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k SYSTEM OF MEDICINE.

SYSTEM OF MEDICINE.

EDITED BY

J. RUSSELL REYNOLDS, M.D., F.R.S.

FELLOW Or THK ROYAL COLLEGE OF PHYSICIANS OF LONDON
FELI/>*' OF THK IMFKRIAL LFOPOLD-CAROL1NA ACADEMY OF GERMANY
FELLOW OF I'NIVERSITV COLLEGE, LONDON ;
PROFESSOR OK THE PRINCIPLES AND PRACTICE OF MEDICINE IN UNIVERSITY COLLEGE ;

PHYSICIAN TO I'NIVERSITY COLLEGE HOSPITAL.

VOLUME THE FOURTH,

rONTAlKISC

DISEASES OF THE HEART.

£ onbon :
MACMILLAN AND CO.

1877.

[AUBighU Reserved.)

LONIXJN ;

ll. CLAY, BUNS, AND TAYI.OR, 1'KINI'KKH,

HK£ AD STREW UILL,

Vll'EEN VICTORIA STItltKr.

PREFACE.

It has been found necessary to divide into two volumes the
remainder of the "System of Medicine," which I have the honour
to edit; and this division has been determined mainly by the
causes which have led to the delay in its appearance.

The Articles on Position and Malposition of the Heart, on
Angina Pectoris, on Pericarditis, and Endocarditis, were begun by
their respective authors some years ago, and several distinct por-
tions of each of those articles were at once committed to the press.
But both Dr. Gairdner and the late Dr. Sibson held that much new
matter must be introduced into them ; and by far the largest con-
tributor to this volume, the late Dr. Sibson, found a mass of facts
at his disposal, the analysis and representation of which occupied
an amount of time and space that far exceeded his anticipation.
The entire originality of his work, the subtlety of thought which
it displayed, the carefulness of the observations upon which it was
based, the catholicity of the views which it expressed, the honest,
kind, although keen criticism that it contained of the opinions of
other workers, and the intimate and important relations of all its
parts, decided me not to reduce its magnitude beyond that which
it now presents, and to wait for its completion. Those who know

yi PREFACE.

what it is to give a concise account of facta derived from their
personal observation, and represented by the statistical method, will
appreciate the years of labour that have been bestowed upon the
articles, Position and Malposition of the Heart, upon Pericarditis
and Endocarditis. Their Author, when he left England during this
past autumn, had left one table uncorrected, and three pages on
Carditis unwritten ; I have endeavoured to correct the table, and
Dr. Gowers has written the article on Carditis.

We have, in this volume, the results of many years of Dr. Sibson's
ardent toil, and the last, and, as I think, the best production of
that earnest, industrious, enthusiastic worker, and most kind and
genial friend.

Another of the contributors to this volume has also passed away
since his papers were printed, and happily in the main corrected
by himself; I refer to the late Dr. Warburton Begbie, whose work
was as good as his heart was large, and who never spared any
pains to carry to the highest point of his ability even the smallest
fragment of labour that he undertook to perform.

J. RUSSELL REYNOLDS.

38, GR08VENOR Street,
December, 187C.

CONTRIBUTORS To THE FOURTH VOLUME.

J am eh Warblrton Begbie, M.D., F.R.C.P., Edinburgh ; Professor of the Institutes
of Medicine in the University of Edinburgh.

C. HiLiuN Fagge, M. D.f F. R.C P., London; Senior Assistant Physician to Guy's
Hospital.

William Tbnnant Gairdner, M.D., F.R.C.P., Edinburgh : Professor of the
Practice of Physic in the University of Glasgow.

William R. Goweiib, M.D., London; Assistant Physician to University College
Hospital, and to the Xntioiial Hospital for the Paralysed and Epileptic.

Thomas Bevill Peacock, M.D., Edinburgh, F. R.C. P., London; Physiciau to St.
Thomas's Hospital.

Francis Sibs>on, M.D., F.R.C.P., F.R.S., London ; formerly lecturer on Medicine,
and Physician to St. Mary's Hospital.

ERRATA.

Page 216, 5th line from bottom, for " 10 " read " 19."

Page 216, 9th lino from bottom, for " 1 mitral aortic " read " 5 mitral-aortic. "

Page 216, 12th line from bottom, for " 1 " read " 6 "

Page 249, note 2, for " pages 250-253," read "pages 274-279."

Page 268, 15th line from top, for " In that case/' read " In three casos."

Page 477, 5th line from top, for " 30th," read " 36th. "

Page 485, 15th line from bottom, for " fixed " read "flexed."

LOCAL DISEASES (continued).

§ IV. Diseases of the Organs of Circulation.

A The Heart.

Weight and Size of the Heart.

Position and form of the Heart and great Vessels.

Malpositions of the Heart.

Lateral or Partial Aneurism of the Heart.

Adventitious Products in the Heart.

Pneumo-Pbricardium.

Pericarditis.

Adherent Pericardium.

Endocarditis.

Carditis.

Hydropericardium.

Angina Pectorls and Allied States; including certain
binds of sudden death.

Diseases of the Valves of the Heart.

Atrophy of the Heart.

Hypertrophy of the Heart.

Dilatation of the Heart.

Fatty Diseases of the Heart.

Fibroid Disease of the Heart.

CONTENTS.

PAKT II. (continued.)

LOCAL DISEASES, OR AFFECTIONS OF PARTICULAR ORGANS,

OR SYSTEMS OF ORGANS.

§ IV. DISEASES OF THE ORGANS OF CIRCULATION,
A. THE HEART :—

PACK

WEIGHT AND SIZE OF THE HEART, by Thomas B. Peacock,
M.D., F.R.C.P.

Of the Healthy Heart 3

Of the Diseased Heart 8

. POSITION AND FORM OF THE HEART AND GREAT
VESSELS, by Francis Sibson, M.D., F.R.S.

Front View after Deatli . 14

Front View during Life 64

Side View after Death 89

Side View during Lif<* 92

Back View after Death 99

Back View during Lift* 100

Notes from Pirogoff ami Brauu 109

^ MALPOSITIONS OF THE HEART 125

Vertical Displacement 125

Lateral Displacement 135

Forward Displacement 148

Backward Displacement \A&

xii CONTENTS.

PAttK

LATERAL OR PARTIAL ANEURISM OF THE HEART, by

Thomas Bkvill Peacock, M.D., F.R.C.P 149

Aneurism of the Left Ventricle 150

Aneurism of the Left Auricle 162

Aneurism of the Valves . 163

ADVENTITIOUS PRODUCTS IN THE HEART, by Thomas

Bevill Peacock, M.D., F.R.C.P 165

Tubercle in the Heart, and Tubercular Pericarditis 165

Cancer 169

Simple and other Cysts 171

Entozoa 172

Fibrinous Deposits : Syphilitic Affections of the Heart .... 176

Fibro-Cartilaginous and Osseous Degeneration 177

Polypoid Growths 179

\S PNEUMOPERICARDIUM, by J. Warburton Beobib, M.D. . . 182

PERICARDITIS, by Francis Sibson, M.D., F.R.S 186

Clinical History of Pericarditis as it occurred in the Author's

Practice in St. Mary's Hospital 186

Rheumatic Pericarditis 186

Sex, Age, and Occupation 187

The Affection of the Joints 202

The Degree of the Joint Affection during the Acme of Effusion . 205

Time in the Hospital 207

Occurrence of previous Attacks 208

Time of the first Observation of Friction-sound in relation to the

Pericarditis and the Joint Affection 209

The Presence or Absence of Endocarditis 212

Progressive changes in the Organs 217

Over- Action of the Heart, and of the Limbs as Causes of

Rheumatism with Heart Affection 218

Pain 223

Irregularity and Failure of the Heart 235

Difficult and Quickened Respiration 237

Difficulty in Swallowing 239

Loss of Voice 240

Effects on the Pulse 241

Fulness of the Veins 242

Appearance of the Face 243

Condition of Face when Effusion at its Acme 248

CONTENTS. xiii

PAOS

PERICARDITIS continued—

Affections of the Nervous System 249

In Rheumatic Pericarditis with high Temperature .... 254

In Endocarditis with high Temperature 262

High Temperature without Inflammation 204

In which Temperature was not Observed 273

Coma 282

Delirium 283

Temporary Insanity, Melancholia, and Hallucinations . . . 283

Chorea, Choreiform and Tetaniform Movements 292

In Pericarditis without Rheumatism or Bright's Disease . . 295

The Physical Signs of Rheumatic Pericarditis 304

Percussion 309

Prominence over the Region of the Pericardium 332

Position of the Impulse 334

Vibration or Thrill 343

Auscultation 349

The Character and Tests of Pericardial Friction Sound . . 388

Physical Signs of Pericarditis in Bright's Disease . . . . 413

Pericarditis, neither Rheumatic nor from Bright's Disease . . 419

Treatment of Pericarditis 430

ADHERENT PERICARDIUM, by Francis Sibsun, M.D., F.R.S. . 438

Anatomical Description 438

Physical Signs 442

Clinical History 446

ENDOCARDITIS, by Francis Sibson, M.D., F.R.S 456

Anatomical Appearances 456

Clinical History in Rheumatism 460

Clinical History in Chorea 511

„ „ Pyaemia 516

„ „ Bright's Disease 517

„ „ Valvular Disease 519

Pathological Evidence of Endocarditis in Cases of Valvular Disease

of the Heart 519

Treatment 52,p

CARDITIS, by W. R. Gowers, M.D 529

HYDROPERICARDIUM, by J. Warburton Beobik, M.D 532

xiT CONTENTS.

PAOR

ANGINA PECTORIS AND ALLIED STATES; INCLUDING
CERTAIN KINDS OF SUDDEN DEATH, by Professor

Gairdner, M.D 536

General Description 535

Diagnosis 542

Causes 548

Illustrations of sudden death without pain 551

Pathology 569

Treatment 586

^- DISEASES OF THE VALVES OF THE HEART, by C. Hilton

Fagoe, M.D., F.R.C.P 601

History 601

Description and Anatomy 603

Etiology 612

Effects 627

Diagnosis 670

Prognosis 676

Treatment 680

ATROPHY OF THE HEART, by W. R. Gowers, M.D 687

Definition and Historv 687

Varieties : Causes 688

vSymptoms 690

Diagnosis. Prognosis, Treatment 691

/ HYPERTROPHY OF THE HEART, by W. R. Gowers, M.D. . . 692

Synonyms, Definition. History 692

Varieties, Causes, Pathology 694

Pathological Anatomy ... 706

Symptoms 712

Diagnosis 720

Prognosis 722

Treatment 724

y, DILATATION OF THE HEART, by W. R. Gowers, M.D. ... 729

Synonyms, Definition, History 729

Varieties, Causes 730

Pathological Anatomy . 741

Consequences 743

Symptoms 747

Diagnosis 751

Prognosis, Treatment 752

CONTENTS. xv

PAOS

FATTY DISEASES OF THE HEART, by W. R. Gowers, M.D. . 760

Fatty Overgrowth 760

History, Causes 761

Pathological Anatomy 762

Symptoms, Diagnosis, Treatment 763

Fatty Degeneration 764

Synonyms, Definition, History 764

Varieties 765

Etiology- 766

Pathological Anatomy 771

Consequences, Symptoms 778

Course and Terminations 782

Diagnosis 783

Prognosis, Treatment 784

Rupture of the Heart 786

Symptoms, Diagnosis 789

Prognosis, Treatment 790

FIBROID DISEASE OF THE HEART, by W. R. Gowers, M.D. > 791

Synonyms, Definition, History 791

Etiology, Pathological Anatomy 792

Consequences, Symptoms 793

Diagnosis : Treatment 794

INDEX 797

LIST OF CHIEF AUTHORS REFERRED TO 809

DISEASES OF THE HEART.

VOL. IV. »

WEIGHT AND SIZE OF THE HEART.
By Thomas B. Peacock, M.D., F.RC.P.

1. Of the Healthy Heart. — From an early period pathologists have
felt the necessity of some standard by which the size of the heart
might be estimated, and its healthy and diseased conditions compared.
Corvisart was unable to suggest any such, and Laennec compared the
size of the healthy heart to the fist of the subject — a comparison too
indefinite to afford any satisfactory estimate. Meckel and Kerkring,
as quoted by Senac, were apparently the earliest writers who gave
any estimate of the normal weight of the heart; and Lobstein and
Bouillaud were the first to suggest the employment of the balance as
a means of comparison between the healthy and diseased organs.
The latter writer, in the first edition of his work, published in 1835,
gave some observations of the weight both of healthy and diseased
hearts, but they were too few in number to form the basis of
satisfactory conclusions. Bizot conceived that the dimensions of the
organ would furnish a better standard; and in 1837, in the M^moires
of the " Society Medicale d'Observation," published a large series of
very careful measurements. Dr. Glendinning, in 1838, contributed
numerous observations of the weight of the heart in a paper in the
" Medico-Chirurgical Transactions ; " and Dr. Ranking, in 1849, pub-
lished in the Medical Gazette a series of measurements, both of
healthy and diseased organs. In 1843 the late Professor Reid ap-
pended to his paper on the weights of the different organs of the
human body, tables of the weight and dimensions of the heart ; and
in 1854 I published a considerable number of observations of the
weight and size of the organ, under different circumstances of health
and disease ; together with various tables compiled from them.
Both these sets of observations were published in the Edinburgh
Monthly Journal. More recently, Dr. Boyd has recorded in the " Phi-
losophical Transactions " a larger and more complete series of obser-
vations than liad been published by any previous writer.

It is useless to refer to the estimates of the weight of the healthy
heart given by any of the earlier writers, for we have no means of
knowing the number of observations upon which they are based ; the
age and sex of the subjects ; the condition of the organs weighed, or the
precise weight employed. Of the more recent observers, M. Bouillaud

b 2

4 A SYSTEM OF MEDICINE.

estimated the weight of the healthy heart in adults, not distinguishing
the two sexes, as ranging from 8 oz. 10 drachms to 9 oz. 11 drachms
imperial. Dr. Glendinning inferred that the mean weight of the
healthy organ was in adult males 8f oz., and in females 7f oz. ; and
Dr. Eeid deduced the average in males as 11 oz. 12 drachms, and in
females as 9 oz. These estimates are sufficient to show how wide the
differences may be according to the mode in which the calculations are
made. It is evident that the weight of the heart must vary consider-
ably according to the cause producing death ; the organ being heavier
when the patient dies suddenly or after only a short attack of illness,
and lighter when death has taken place from lingering diseases, pro-
vided the diseases are not such as interfere with the functions of the
organ, and so give rise to over-nutrition. Thus, while Dr. Eeid, as
just stated, estimated the average weight of the male heart at about
11 oz., he found that in twelve men who were killed the weight
attained an average of 12 oz.; and, on the other hand, I have ex-
amined the hearts of persons who have died from cirrhosis of the liver
and cancer of the pylorus, &c, which were only 5 or 6 oz. in weight.
To form, therefore, an accurate estimate, not only must the age and
sex be taken into consideration, but the weight of the organ must
be given in acute and chronic diseases separately ; and the cases in
which the nutrition of the heart may have been materially modified
by the disease causing death must be excluded from the calculation.
The size of the heart will also be similarly influenced, and especially
the dimensions must vary with the degree of distension of the cavi-
ties at the time of death. To form a thoroughly satisfactory estimate,
the weight and dimensions of the heart must therefore both be given,
and the previous circumstances must be taken into consideration.

In the following tables I have endeavoured to carry out these
views. In the first table the weight of the heart in the adult is given
separately, for males and females, and for acute and chronic diseases.
In the second, the dimensions of the organ, also in the adult and in
males and females, are stated, in Paris lines, millimetres, and parts
of English inches. The third table gives the average weight of the
heart in males and females at different ages.

TABLE I.

Average Weight of the Healthy Heart in Males and Females, and in Acute and Chronic

Diseases, from Twenty to Fifty-five Years of Age.

Malks —

Mean weight 9 oz. 8 drs.

Ordinary range in acute cases . . . 9 oz. to 11 oz.

,, ,, chronic cases . . 8 ox. to 10 oz.

Fkmaler —

Mean weight 8oz. 13 drs.

Ordinary range in acute cases . . . 8 oz. to 10 oz.

,, ,, chronic cases . . 7 oz. to 9 oz.

WEIGHT AND SIZE OF THE HEART.

From the first table it will be seen that in adult males who have
died from acute diseases, or from the effects of accident, the ordi-
nary weight of the heart is from 9 to 1 1 oz. ; and in those who have died
from chronic diseases, 8 to 10 oz. In females, the ordinary weight
of the heart in acute cases may be estimated at from 8 to 10 oz.,
and in chronic diseases from 7 to 9 oz. Occasionally, however, in
persons of small and delicate frame, who have died from emaciating
diseases, such as cancer of the stomach, bowels, or mesentery, or
chronic affections of the liver, the heart will be found to weigh only
5 or 6 oz. ; and in large and powerful men who have been killed or
have died after short illnesses, the organ may weigh 12 oz. or even
more, without exceeding the limit of health. Some writers have given
calculations of the relation of the weight of the heart to that of the
whole body, but the bulk of the body, and also, as before stated, the
size of the heart, vary so greatly from the duration of illness and the
mode in which death occurs, that such calculations do not possess
much value. The height of the subject and the weight and size of
the heart probably bear a more just relation.

From the second table it will be seen that the girth of the right
ventricle, measured externally, exceeds that of the left, in males by
about one-sixth, and in females by one-fifth. The length of the cavity
of the right ventricle is greater than that of the left, in males by one-
seventh, and in females by one-sixth. In both sexes the thickness of

TABLE II.
Dimensions1 of the Healthy Heart (in French Lines, Millimetres, and English Incites) in

Males and Females.

Circumference of heart

Girth of right ventricle

„ left „

Length of cavity of right ventricle

„ left ,

Thickness of walla of right ventricle, base . .

midpoint
apex -
left

.»
it
•»
•»
»»

»»
»•

base . .
midpoint
apex . .

Thickness of aeptum

Circumference of right auriculo-ventricular aperture

left

pulmonic aperture

aortic

»»
»»
»»

»»

HALES.

Lines.

1037
55 4
48-3
43*3
37 6
185
1'98
1*42
5 15
6

2 4
5 73
53*4
45-2
40
35-6

Milli-
metres.

233-32
12385
10867
96 42
846
416
4 35
3-19
11-58
135
5-4
12 89
12015
101-7
90
80 1

Inches.

9-209
4-919
4 289
3821
3-333
164
176
125
■425
•532
•214
•61
4 74
4

3 552
3 146

FEMALES.

Lines.

104
58-4
45 6
44*3
37 1
185
2 0
13
4-9
6 6
2
4
51
45
39-3
34

5
•7
•4

Milli-
metres.

284
131-4
102-6
99 67
83 47
416

4 5
2 92

1102
126

5 62
10 57

115 65

10125

88 42

70 5

Inches.

9236

5184

4 049

3925

3197

•164

177

118

•432

•497

•222

•421

4562

3-996

3 493

3 019

the walls of the right ventricle is about one-third that of those of the
left. The thickness of the septum is intermediate between that of the

1 The dimensions of the orifices are taken by balls, the first of which is 12 lines in
circumference, which increase in circumference three Paris lines, and are numbered
from 1 to 20.

A SYSTEM OF MEDICINE.

external walls of the right and left ventricles. In males the pulmonic
orifice is about one-eighth more in circumference than the aortic. The
left auriculo- ventricular aperture is one-fourth more than that of the
aorta, and the right auriculo-ventricular aperture one-half larger. In
females the differences between the aortic and other orifices are some-
what greater.

It has been generally supposed that the heart increases in weight
with the progress of life ; and this opinion is supported by the facts
recorded relating to males, in the third table. It may, however, be
dpubted whether the result thus indicated is applicable to the heart
in its strictly healthy state. It is well known that in advanced age
there is a decided diminution in the weight of the brain, and there
seems no reason why a similar decrease of weight should not occur
in the heart, provided that organ be not the seat of disease inter-
fering with its normal nutrition. As we well know, but few elderly
persons, especially men, are entirely free from any form of disease
which, by occasioning obstruction, might lead to over-action, and so

TABLE III.
Weight* of the Healthy Heart at Different Ages in Male* and Female*.

Ages

10 to 14

inclusive -

-Mean weight

15 „ 20

•t

i> >•

! From 20 „ 30

»»

»> >»

! „

80 „ 40

»•

• » »»

»»

40 „ 50

»>

»> >»

50 „ 60

• i *•

»>

00 ., 70

»♦

• » >»

Malkh.

oz drs.
6 1-5
8 2 6<5

8 014

9 71W
9 1111
9 12

10 13 33

Femalks.

, oz.

drs.

1 5

1-66

10 42

13 94 .

3 1

7'33 ,

0 1

Mean weight between 20 and 55 year* of age— in 76 males .

„ „ „ „ in 49 females
Difference

9 oz 8 74 drs.

8 oz. 13 16 drs.

11 68 drs.

to some degree of hypertrophy. And even if the heart be not itself
diseased, there are few old persons who do not display some affec-
tion of the lungs, kidneys, or other parts of the system, which might
more or less interfere with the functions of the heart, and so lead to
its enlargement. That this is the more correct view is supported by
the diminution in the weight of the organ in elderly females, as also
shown in the table.

2. The alterations in the weight of the heart in disease are illus-
trated by Tables IV and V.

It was supposed by Dr. Glendinuing, that the heart in cases of
phthisis, contrary to what would & priori have been expected,
acquires an increase of weight, while the rest of the body becomes
•emaciated. This idea appears to have arisen from a misapprehension
of the facts which he collected. The effect of the pulmonary affection

1 The weight employed is Avoirdupois or Imperial.

WEIGHT AND SIZE OF THE HEART. 7

upon the nutrition of the heart appears to vary with the form of the
disease. In cases of uncomplicated constitutional or tubercular
phthisis, the progress of which is generally rapid and which is
usually attended with great emaciation, the heart is found to weigh
considerably below the healthy average, and the organ, on examination,
often displays the appearance of atrophy. In cases of chronic phthisis,
whether tubercular or inflammatory, on the other hand, and especially
when one or both lungs are considerably contracted, or when there
have been marked bronchitic symptoms, so that the blood has for a
long time been transmitted with difficulty through the lungs, the
heart is generally found to be enlarged, or, at least, not to have under-
gone any marked diminution in size ; its weight equalling or exceeding
the healthy standard. So also when, in cases of phthisis, there is any
great impediment to the transmission of the blood from the heart

TABLE IV.
Range of Weight of Heart, in Different Forms of Disease, and when Diseased.

Mean.

Extremes.

j Phthisis. Males

oz. drs.
9 3-4

8 606
14 8

12 2 0

9 12
10 5'4

ox.
6
5

11
9
7

12
10

8
14
13
14
16
14
13
14

drs.
45t<

» .
8 ,
0 ,
4 ,
4 .

0 ,
0 ,
8 ,
0 ,
0 ,
0 ,
0 ,
0 ,

0 ,
8 ,
8 ,

or., drs :
> 11 0 •

, 11 o 1

, ai 0 ;

, 12 8

, 14 8 ;

, 15 8 i

, 40 12 !

, 24 0 j

, 20 0 '

, 21 0 |
, 18 8
, 34 0
, 23 0
, 17 0
, 18 8
, 21 0 i
, 23 0

Mitral valvular obstruction or regurgitation, or both. — Males

„ „ „ „ ,, Females
Combined aortic and mitral valvular disease.— Males . . .
»t »t >$ »» »i Females . .

from valvular or aortic disease, notwithstanding the general tendency
to emaciation, the organ may exceed even very greatly the natural
size.

Chronic Bronchitis. — When there is long-continued obstruction to
the pulmonary circulation from chronic bronchitis, with or without
deformity of the spine, the right side of the heart becomes hypertrophied ;
but, even a great increase in the thickness of the walls of the right
ventricle does not very much augment the weight of the heart, and it
is only after the left side has become implicated that the weight is
found much to exceed the healthy standard. In some such cases,
however, the organ may attain a weight considerably greater than the
natural, amounting, in hearts I have weighed, to 15 or 16 oz.

Morbus JRenum. — Dr. Bright noticed that the heart in cases of
chronic disease of the kidneys was frequently found increased in size

A SYSTEM OF MEDICINE.

without there being any valvular disease to explain the enlargement ;
and the occurrence of simple hypertrophy in such cases has been
noticed by other pathologists. Of eighteen cases in which the organ
was weighed by myself, in seven the weight was below the average of
chronic diseases, while in eleven it exceeded it, attaining in some cases

TABLE V.
Extreme Dimensions of the Heart, with the Dijferent Forms of DUeate in which they occur.

Circumference. — Males

„ Females

Thickness of walls of right ventricle.— Males .

„ „ Females

left „ Males .

Females

f»
•f
tf

>»
»»
»»

Cireumf. right aurieulo ventricular apert. Males

Fern.
Males
Fein.

»»
»»
»»

i>
ii
•i

i>
i>
ii

left

ii
pulmonic aperture. — Males

» i. Fem.

aortic ,, Males

Fem.

• i
ii

Lines.

Milli-
metres.

Inches

182
127
6 76

409 6
2<5 75
12 93

1616

11-27

•61

15 75

•62

31-5

1-24

24-75

•97

63
60
60
46
64

14176

135

10125

121-5

5-50
5 32
5 32
399
4 79

87 78

3 46

101-25

399

78-85

In simple hypertrophy.

Mitral disease.

(Congenital obstruction at
I pulmonic orifice.

Aortic valvular disease.
(Combined aortic and mitral
( -disease.

Simple hypertrophy

Aortic valvular obstruction.

Simple hypertrophy.

Aortic valvular obstruction.

Simple hypertrophy,
r Mitral valvular disease,
J chronic bronchitis, and
( defonned spine.

Aortic valvular disease.

(Aortic valvular disease and
combined aortic and mi-
tral disease.

in males the weight of upwards of 14 or 15 oz. In these cases the
hypertrophy is doubtless due to the over-action of the heart from its
efforts to overcome the obstruction to the transmission of the blood
through the capillaries.

3. — WEIGHT AND DIMENSIONS OF THE DISEASED HEART.

Simple Hypertrophy. — The most remarkable case of increase in the
weight and size of the heart which I have myself met with was in a
case of hypertrophy, without any material valvular disease or any
obvious source of obstruction in the aorta, to explain the condition.
In this instance, which, however, is a very extreme one, the organ
weighed 40 oz. 12 dr.; but in various other cases I have found the
weight considerably to exceed the average or extreme limit of health.'
In a heart which I examined with Mr. Hutchinson, the weight
attained was 26 oz. ; and Dr. Bristowe exhibited one at the Patho-
logical Society which weighed 27 oz. The ages of these patients
were sixty-five, thirty-five, and forty-one respectively. It is difficult
to explain the great enlargement which exists in some cases of this
description. It may depend on some disease of the smaller arteries
which may have escaped observation, or on obstruction in the capil-
laries ; but, in other instances, it is probably due to habitual over-
action from athletic pursuits, and possibly in some cases to palpitatior,

WEIGHT AND SIZE OF THE HEART. 9

at first originating in emotional causes. Enlargement unconnected
with valvular disease is, however, rarely seen except in men, and in
no instance have I found the heart much hypertrophied in females
without there being some obvious source of obstruction to which
the change was referable.

Aortic Obstruction and Aortic Valvular Disease. — The occurrence
of obstruction in the aorta, and especially in the upper portion of
that vessel, is generally attended by considerable increase of weight
in the heart. In various cases of this description I have found the
heart to range from near the natural standard to 24 oz. in males, 17 oz.
in females. In the Transactions of the Medico-Chirurgical Society, a
case is recorded by Dr. Eisdon Bennett, in which the heart weighed
22 J oz. in a man fifty-three years of age, who died from rupture of
the aorta, giving rise to dissecting aneurism and hemiplegia. The
increase of size in the heart was apparently due to atheromatous
disease of the aortic coats.

In aortic valvular disease still greater increase of weight is often
met with. In cases of obstructive disease, 1 have weighed hearts
ranging from 14 oz. to 21 oz. in males, and from 13 oz. to 18 oz.
8 drs. in females. In cases of aortic valvular incompetency, I have
found the heart to weigh from 14 oz. to 34 oz. in males, and from
16 ozs. to 23 ozs. in females. Dr. Van der Byl, in a paper in the
"Pathological Transactions," relates instances in which the heart
weighed 36 oz. in a case of aortic valvular incompetency, in a man
of twenty-eight ; 30 oz. in a case of aortic disease with aneurism of
the aorta, in a man of thirty-three ; and 30 oz. in a case of aortic
and mitral disease, in a man of sixty-two.

In the cases of incompetency of the aortic valves, it is often
impossible to say how much of the great enlargement of the heart
is due to the obstruction, and how much to the incompetency of the
valves ; for the latter condition is generally only the final stage of the
former. In cases of rupture of the aortic valves during violent effort,
we have, however, the opportunity of seeing the remarkable changes
which may occur in the heart even during short periods of time,
when, in organs previously healthy, the valves are rendered incompe-
tent and the left ventricle rapidly becomes hypertrophied and dilated.
Thus, in a case of this description which occurred to myself, the patient,
a man of thirty-three years, survived the accident only twenty-seven
months, yet the heart was found to weigh 17| oz. In a case related
by Dr. Quain, the patient lived two years, and the heart weighed 22J
oz. ; and in another case which I had the opportunity of examining
after death, though the patient, a man thirty-six years of age, only
survived three-and-a-half months, the weight was 23 oz. If, in this
instance, the heart was sound at the time of the occurrence of the
injury, the process of enlargement must have been most rapid ; but
it may be doubted whether the organ was not more or less hyper-
tropliied before the accident, though the patient stated that he was
previously quite welL

10 A SYSTEM OF MEDICINE.

In some cases of disease, also, the enlargement must take place
very rapidly. In a boy of eighteen, who died of aortic valvular dis-
ease originating in malformation, the duration of active illness was
only three-and-a-half years, yet the heart weighed 28 oz. In a case
of aortic valvular incompetency, with probably, regurgitation through
the left auriculo-ventricular aperture from maladjustment of the valves,
described by Dr. Bristowein the "Pathological Transactions," the heart
weighed 46£ oz. avoirdupois, though the subject of the disease was only
twenty-two years of age. In an instance of very great obstruction
at the aortic valves, doubtless from malformation, which I have
recently exhibited at the Pathological Society, the heart weighed
24 oz., the patient being only twenty-three yeafs of age. These ex-
amples show that the heart may attain a veiy great increase of size
even in comparatively young subjects ; but, usually, those in whom
the heart is very large are advanced in age. Probably, also, in most
cases, the disease must be of long duration for the organ to become
very greatly hypertrophied, and this great prolongation of life is only
compatible with comparatively slight disease, or with disease which
has been very slowly progressive, though at the time of death it may
have become extreme.

In mitral valvular disease, whether consisting in obstruction and
regurgitation, from contraction of the orifice and rigidity of the
valves, or in free regurgitation from expansion of the aperture or mal-
adjustment of the valves, the heart does not ordinarily attain by any
means so great an increase of weight as in cases of aortic diseasa In
the former class of cases, the hypertrophy is chiefly limited to the right
ventricle, and only affects the left ventricle secondarily, though in the
latter the left ventricle also partakes of the change from the first. In
cases of mitral disease, the wreights have ranged from 14 oz. 8 drachms
to 17 oz. 8 drachms in males, and from 12 oz. to 18 oz. in females.

As might be expected, in combined aortic and mitral valvular disease,
the weight of the heart is intermediate between that which obtains
in the two separate forms of disease, the organ being lighter than in
aortic, heavier than in mitral disease. In males, in cases of this kind
the heart was found to weigh 14 oz. 8 dr. to 21 oz. 8 dr., and in females
from 17 oz. to 23 oz.

In cases of obstruction at the right side, consisting in congenital
contraction of the pulmonic orifice, the effect produced on the nutrition
of the heart is very similar to that which results from chronic
bronchitis. In the first instance the right ventricle is chiefly hyper-
trophied, but subsequently the left also becomes involved ; and similar
changes ensue in the cases in which the aorta communicates with both
ventricles, provided the life of the patient be sufficiently prolonged.
In a male of twenty, in whom the pulmonary orifice was contracted
from adhesion of the valves, the heart weighed 12 oz. ; and in a female
of nineteen, in whom there was similar disease of the pulmonic valves,
and the aorta arose from both ventricles and the ductus arteriosus was
open, the organ weighed 17£ oz.

WEIGHT AND SIZE OF THE HEART. 11

The effect produced by adhesions of the pericardium on the functions
and nutrition of the heart has been the subject of much discussion.
On the one hand, adhesions have been supposed to interfere with the
free movement of the heart, and so to give rise to hypertrophy ; on
the other, it has been thought that by the compression exercised upon
the organ they might cause atrophy. The question is one which it is
very difficult to decide, for there are few cases in which the pericar-
dium is entirely adherent, in which the valves are not also more or
less involved, and in which therefore the effects produced by the one
condition may not be modified by the other. I find, however, that in
three men in whom the pericardium was entirely adherent, while the
valves were free from disease, the hearts weighed 16 oz., 17 oz. 4 dr.,
and 18 oz. ; but I have examined other organs under similar circum-
stances in which the weight did not exceed the healthy standard. The
general rule is, however, that in cases of adhesion the heart becomes
hypertrophied.

General Remarks on the Weight of the Heart. — M. Bouillaud has
collected some cases in which the heart otherwise healthy weighed
considerably less than natural ; and others in which in various states
of disease it exceeded that point. The former are all cases in which
the OTgan was reduced in weight with the progressive emaciation
of cancer, consumption, &c. The lighest heart, that of a female of
forty-five, weighed 4 oz. 5 dr. in a case of cancer ; the heaviest organ
weighed 24 oz. 4 dr. in a case of obstructive and probably also regurgi-
tant disease of the aortic valves, in a female of fifty-three. From these
observations, and his estimate of the average weight of the healthy
organ as ranging from 8 oz. 10 drs. to 9 oz. 11 drs., he infers that the
heart may attain when diseased three times the weight of the average
healthy organ, and five times that of the most atrophied organ. These
estimates are, however, considerably less than the variations of weight
which actually obtain. I have found the heart to weigh only 5 oz. in
a man fifty-three years of age who died of cirrhosis of the liver, and
6 oz. in a man of thirty-nine who had cancer of the pylorus. The
average weights I have estimated in males at 9 oz. 8 drs., and the
heaviest heart weighed was 40 oz. 12 drs. It follows therefore that in
men the heart may attain a weight which is four times that of the
healthy and eight times that of the atrophied organ. In females, the
variations in the weight of the heart are sufficiently remarkable,
though considerably less than in men. The average weight has been
shown to be 8 oz. 13 drs. : the lightest hearts weighed 5 oz. 8 drs. in cases
of phthisis in twenty-five and thirty years of age ; the heaviest organ
was 23 oz. The most enlarged heart was therefore three times the
weight of the average, and four times that of the atrophied organ.
It has also been mentioned that Dr. Bristowe has placed on record a
case in which the heart of a man twenty -two years of age weighed
46J oz. ; and Dr. Church has recently exhibited at the Pathological
Society the heart of a female forty-seven years of age, who died of
cancer of the pylorus, which weighed only 3 oz. 1 dr.

12 A SYSTEM OF MEDICINE.

The heart described by Dr. Bristowe is, as far as I know, the
heaviest on record- Dr. Hope says that he examined at St. George's
a heart which weighed 2£ lbs., which, if the weight employed were
avoirdupois, would nearly equal the size of the largest heart which
I have myself weighed— 40 oz. 12 drs. M. Lobstein refers to a heart
which weighed 34 oz., and Dr. Vanderbyl to one of 36 oz.

The dimensions of the heart in different forms of disease bear a
general relation to the weights of the organ in similar conditions.
Of the observations which I have myself made, the greatest weight was
attained in cases of simple hypertrophy, obstruction in the course of
the aorta, and obstructive, or obstructive and regurgitant disease of the
aortic valves. It is equally in these forms of disease that the
dimensions of the organ are most considerably enlarged, the cavities
and orifices, especially those of the left side, being the most expanded,
and the walls the most remarkably increased in thickness. There are,
however, differences in the condition of the organ in these several
forms of disease. In cases of obstruction, on whatever cause
dependent, the heart is not generally so large as in cases of incom-
petency, and the form of the organ is also somewhat different. In the
former class of cases the heart is peculiarly long and pointed at the
apex, and the wralls attain the greatest width near the base. In the
latter the ventricle is usually of larger size and rounded at the apex,
and the thickening is more equally diffused over the walls. In both
forms of disease, the enlargement, though most marked on the left
side of the heart, affects the right also very considerably.

In cases of mitral valvular disease, the size of the organ is
considerably less than in the former class of cases, and the shape is
very different, but the precise condition of the organ varies with the
form of disease. In cases of great contraction of the left auriculo-
ventricular aperture, the stress falls chiefly on the left auricle and the
right cavities, and they are all found expanded and the walls increased
in thickness, and much firmer than natural ; the orifices also being
dilated ; while the left ventricle is not much if at all enlarged, and its
walls are not materially hypertrophied. It has, indeed, been supposed
that the left ventricle becomes atrophied. In cases, on the other hand
in which the defect consists chiefly or to a marked degree in incom-
petency of the valves, on whatever cause dependent, the left ventricle
is found to be considerably dilated and hypertrophied, and the changes
on the right side are less marked. . In both these forms of disease,
however, the alteration in the shape of the heart is very marked, the
organ being wide and blunted at the apex — in the one case chiefly in
consequence of the expansion of the right side, in the other of the
dilatation of the left ventricle, and especially the widening of its apex.
In cases of combined aortic and mitral valvular disease, the enlarge-
ment is intermediate, both in shape and extent, between the other two
forms. In cases of chronic bronchitis, chronic phthisis, deformity of
the chest, and pulmonic valvular obstruction, the hypertrophy and
dilatation are at first limited to the right side, but subsequently, if

WEIGHT AND SIZE OF THE HEART. 13

life be much prolonged, involve the left also. Table V. shows some of
the extreme dimensions which I have recorded in different forms of
disease.

It will be observed that not only do the size of the cavities and
the width of the walls vary greatly in different forms of disease, but
the capacity of the orifices also undergoes remarkable change ; and
this not only in cases of old disease, but even during comparatively
short periods of illness. Thus it will generally be found in cases of
acute bronchitis and veiy acute phthisis, that the pulmonic aperture,
which ordinarily exceeds the aortic somewhat in capacity, is dispro-
portionately larger than the aortic, and the right auriculo- ventricular
aperture equally out of proportion with the left. I have also reason
to believe that the apertures may not only expand in a short time,
but may have their dimensions reduced without being otherwise
diseased, and thus it is possible that in some forms of valvular
defect the size of the orifice may be reduced and the incompetency
diminished.

A SYSTEM OF MEDICINE.

POSITION AND FORM OF THE HEART AND GREAT

VESSELS.

By Francis Sibson, M.D., F.B.S.

CONTENTS.

FRONT VIEW, AFTER DEATH

FRONT VIEW, DURING LIFK

8IDE VIEW, AFTER DEATH

SIDE VIEW, DURING LIFE

BACK VIEW, AFTER DEATH

BACK VIEW, DURING LIFE

NOTE8 FROM PIROGOFF AND BRAUN

Page 14
64
89
92
99
100
109

FRONT VIEW; AFTER DEATH.

The following observations on the position and anatomical relations
of the healthy heart and great vessels after death are founded on the
examination of a number ,of diagrams showing the position of the
internal organs after death. This examination was restricted to those
instances in which the heart was healthy and was not enlarged. The
diagrams were made by drawing the outlines of the organs on a
piece of lace or net, stretched upon a frame and placed over the body.

The heart and great vessels present great variety in form and posi-
tion both after death and during life.

During the illness or injury that ends in death, at the time of
death and after death, the heart and great vessels undergo a series of
changes in position and form. According to the nature and direction
of these changes, the heart after death may, in different instances, be
(I.) higher or lower in position ; or (II.) it may deviate more to the
right or more to the left.

(I.) The Higher ok Lower Position of the Heart and Great

Vessels.

Three main conditions may influence the higher or lower position
of the heart after death : (1). The contraction or expansion of the
lungs : (2). The distension or flaccidity of the abdomen : and (3).
The state of the heart itself.

POSITION AND FORM OF THE HEART. 15

(1). When death is associated with bronchitis, or pneumonia, or
affections of a like nature, in which the lungs are large, and are ex-
panded after death, the chest is broad and deep, the diaphragm is
low, and the heart, which is charged with blood, especially in its right
cavities, is large, and occupies a low position. As a rule, however,
the lungs, when they are not thus affected, lessen in size and contract
during the final expirations. The cage of the chest then becomes more
flat and narrow ; it lengthens downwards, and the sternum and costal
cartilages and ribs in front are all lowered in position. The diaphragm
at the same time is elevated. While the front of the chest is thus
lowered, the heart, resting on the diaphragm, is raised, and the whole
organ, and the great vessels occupy a higher position. We thus have
a double and contrary movement in the descent of the bony frame-
work of the front of the chest, and the ascent of the heart immediately
behind that framework. As the heart within, and the sternum and
cartilages without are both thus elevated by the distension of the
abdomen, the actual elevation of the heart and great vessels is much
greater than their apparent elevation, estimated as that usually is by
the relation of those parts to the walls of the chest immediately in
front of them.

(2). When the abdomen is distended, whether by fluid or air in the
cavity itself, by an accumulation of gas in the stomach and intestines,
or by other causes, the whole diaphragm is forcibly elevated, and
the heart, resting as it does on the central tendon of the diaphragm,
is lifted upwards. The sternum and costal cartilages in front of the
heart are, at the same time, also raised in position, and the lower ribs
on either side are pressed outwards. Although the actual elevation of
the heart is, in these cases, often very great, its apparent elevation,
which is measured by the relation of the heart to the walls of the
chest in front of it, may be slight, owing to the simultaneous eleva-
tion of the heart and the sternum and cartilages in front of the heart
caused by the distension of the abdomen.

When the abdomen is flaccid, owing to the stomach and intestines
being empty, the reverse effects take place. The diaphragm descends,
the heart drops downwards, the sternum and costal cartilages are
lowered in position, and the inferior ribs fall inwards.

(3). During the final illness or injury that precedes death the heart
may lessen or enlarge. Fatal haemorrhage or wasting disease reduces
the size of the heart and great vessels. On the other hand, the heart
is swollen, especially on the right side, under the influence of suffo-
cation or bronchitis ; while its left ventricle may be thickened and
enlarged in cases of Bright's disease with contracted kidney. Thus
the right or the left side of the heart may be enlarged when the
obstacle to the flow of blood is respectively in the lungs or the body.

At the time of death, the left ventricle usually closes firmly upon
itself ; while then or soon afterwards the right cavities of the heart
become permanently swollen with blood.

After death the heart shrinks upwards to a greater or less extent.

16 A SYSTEM OF MEDICINE.

This is owing partly to the diminution of the organ, but mainly, I be-
lieve, to the contraction of the arch of the aorta, for the shortening of
that vessel draws the heart upwards, just as its lengthening pushes
the organ downwards.

The exact extent to which the heart is thus raised, is measured by
the space that is left between the lower boundary of the heart, and
the lower boundary of the front of the pericardium. During life
these two adjoining parts fit each other exactly ; but after death
they are separated by a space that varies according to the degree to
which the heart shrinks upwards. Thus in the body of a youth who
died from haemorrhage after fever, and in that of a man who expelled
two or three pints of blood from a cavity in the left lung, an inch of
space intervened between the lower edge of the heart and that of the
lower boundary of the front of the pericardium. In another instance
that space was only the tenth of an inch. As a rule the space varied
from a quarter to seven-tenths of an inch (in 38 of 44 instances) and
its average measurement was nearly half an inch (046 inch). (Note
1, page 109.)

The heart and the great vessels mainly occupy the centre of the
chest, being protected in front by the sternum and the adjoining
costal cartilages. It is, however, my present object, not so much to
describe the relative bearings of those parts after death, as to in-
dicate the variation in the anatomical situation of the more important
boundaries or landmarks of the healthy heart and great vessels observed
by myself in different instances after death.

The lower Boundary of tlie Heart — In one instance, a woman who
died from starvation, the lower boundary of the heart was situated
behind the ensiform cartilage an inch and a half below the lower end
of the sternum (that term being restricted here and elsewhere to the
manubrium and blade or osseous part of the sternum), while in
another it was almost as much (1*4 inch) above that end of the bone.
Between these two extreme points this boundary occupied every
variety of position. In one-fifth of the instances observed (15 in 71) the
lower boundary of the right ventricle was just behind the lower end
of the sternum, while in two-fifths of them it was above (30 in 71),
and in two-fifths of them it was below (26 in 71) that end of the
bone. (Note 2, page 109.)

As we have already seen, the lower edge of the heart usually shrinks
upwards after death for nearly half an inch, the extent varying from
one inch to one-tenth of an inch. The position of the lower border
of the front of the pericardium, which points out the position of the
lower border of the heart at the time of death was indicated in four-fifths
of the cases (55 in 71) in which the inferior boundary of the heart was
observed after death. In one-fifth of these instances (11 in 55) the
lower limit of the pericardium was on a level with the lower end of
the sternum ; while in two-thirds of them (37 in 55) it was below
that point, being situated behind the ensiform cartilage ; and in only
one-eighth of them (7 in 55) was it above that point. We thus see

POSITION AND FORM OF THE HEART. 17

that at the time of death, in the great majority of instances (40 in 59)
the inferior border of the heart was below the lower end of the
sternum, being situated behind the ensiform cartilage. (Note 3,
page 110.)

The seat of the lower boundary of the apex in relation to the left
fifth space is a more important landmark for the clinical observer
than that of the lower boundary of the heart in relation to the lower
end of the sternum.

The lower edge of the heart at the apex was on a level with the
lower edge of the left fifth cartilage in one-seventh of the instances
observed (9 in 69), it was below that edge in two-fifths of them (26 in
69), and it was above that edge in almost one half of them (34 in 69).
In five instances the lower boundary of the apex was situated one
inch above the lower edge of the fifth cartilage, and in four it was
fully one inch below that edge. (Note 4, page 110.)

The lower border of the pericardium just below the apex, which
corresponds with the seat of the lower border of the apex at the time
of death, was on a level with the lower edge of the fifth cartilage in
one-sixth of the instances observed (9 in 55), was situated below that
edge in three-fourths of them (41 in 55), and was above that edge in
only one eleventh of them (5 in 55). (Note"5, page 110.)

We thus see that there was a general, but not a constant correspond-
ence between the relation of the inferior boundary of the right ven-
tricle to the lower end of the sternum, and that of the inferior boun-
dary of the apex to the lower edge of the fifth cartilage, both at the
time of death, and after death when the examination of the body was
made. This correspondence would have been more constant but for
variation in (1) the comparative height of the fifth cartilage and the
lower end of the sternum, (2) the degree of inclination from above
downwards and from right to left of the lower boundary of the heart,
and (3) the extent to which the right ventricle is situated to the right
and to the left of the middle line of the sternum.

(I). In the great majority of instances (60 in 71) the inferior edge of
the left fifth cartilage was lower in position than the inferior extremity
of the sternum, to an extent varying from a quarter of an inch to an
inch and a quarter ; in five cases those two parts were on the same
level ; and iu six the lower edge of the fifth cartilage was higher by
from a quarter to three quarters of au inch than the lower end of
the sternum.

The height of the fifth cartilage in relation to that of the lower end
of the sternum is influenced by (1) respiration, (2) abdominal disten-
sion, and (3) natural and acquired formation. (1) Inspiration raises
and expiration lowers both the sternum and the fifth cartilage attached
to the sternum, but as the cartilage has an additional movement of
its own, during the double act of breathing it is more lowered during
expiration and more raised during inspiration than the sternum. The
artificial distension of the lungs after death elevates the fifth carti-
lage from the sixth to the third of an inch more than the correspond-

vol. rv. c

18 A SYSTEM OF MEDICINE.

ing part of the sternum. If the chest is broad the left fifth cartilage
is higher, and if the chest or the left side of it is narrow, the left
fifth cartilage is lower in relation to the lower end of the sternum than
it would have been otherwise. (2) Abdominal distension raises, and
abdominal collapse lowers both the sternum and the fifth cartilage,
but the raising or lowering of the fifth cartilage under these circum-
stances is greater than the respective raising or lowering of the ster-
num. (3) In some persons the fifth cartilage is naturally higher or
lower than in others. Thus the fifth cartilage is sometimes integrally
attached to the sixth cartilage and it is restrained by and shares its
movements. When this ig so the fifth cartilage tends to be lower in
relation to the lower end of the sternum than when that cartilage is
free. In robust persons with ample chests the fifth cartilage is higher
relatively to the sternum than in thin persons with contracted chests,
in whom the cartilage tends to be low in position in relation to the
end of the sternum.

(2). In nearly all instances (67 in 70) the lower boundary of the heart
inclined downwards from the auricle to the apex, in a direction from
right to left. In one instance the lower boundary of the heart was an
inch, and in another it was only the tenth of an inch lower at the
apex than at the lower end of the sternum. Between these two ex-
tremes there was every variety, the average dip of the lower boun-
dary of the heart from that point to the apex being about half an
inch. (Note 6, page 1 10.)

The inclination or dip of the lowTer boundary of the right ventricle
ceased at the apex, and thence the lower boundary of the heart curved
gently upwards.

(3). The lower boundary of the heart usually extended from two
inches to two inches and three quarters to the left of the middle line
of the sternum, (in 43 instances in 65) but in one-third of the cases
(20 in 65) it only extended from an inch and a quarter to an inch
and three quarters, while in five instances it extended as much as
three inches to the left of the middle line of the sternum. (Note 7,
page 111.)

The Top of the Arch of (he Aorta. — The top of the arch of the aorta,
which is indicated by the adjacent origin of the innominate and left
subclavian arteries, forms the upper limit of the system of the heart
and great vessels. The position of the top of the arch, like that of
the lower border of the heart, is subject to great variety.

In one instance the top of the arch was an inch and a half below
the top of the manubrium, so that it was buried deep down in the
chest and the innominate artery did not appear in the neck. In
another, the top of the arch was seated in the neck, being half an inch
above the top of the sternum, so that before the chest was opened the
whole innominate artery was visible in the neck, coursing upwards and
from left to right across the front of the trachea. The summit of the
aorta occupied in different instances every variety of position between
these two extreme limits. In five cases it was above, and in six it

POSITION AND FORM OF THE HEART. 19

was on a level with the top of the manubrium ; while in seven, in-
stead of being thus almost or quite visible in the neck, it was
situated quite an inch below the top of the manubrium and the whole
of the innominate artery was shielded by that bone. In two-thirds of
the instances, (30 in 48) however, the top of the aorta occupied an
intermediate place behind the upper half of the manubrium, its aver-
age position being half an inch below the top of that bone. (Note 8,
page 111.)

In forty-eight instances the position both of the lower boundary of
the heart and the upper boundary of the arch of the aorta was ob-
served, and, as might have been looked for, there was a general corre-
spondence in the position of these two boundaries in those cases in
which they occupied respectively a very high or a very low position.
Thus, of the five cases in which the top of the arch of the aorta rose
above the top of the sternum, the lower boundary of the heart was
situated above the lower end of the sternum in three, at that point in
one, and less than half an inch below it in one. Again, the top of
the arch of the aorta was situated below the upper end of the manu-
brium in the whole of six cases in which the lower boundary of the
heart was from half an inch to an inch and a quarter below the lower
end of the sternum. Again, of seven instances in which the top of
the arch was deep in the chest, being more than an inch below the top
of the manubrium, in three the lower boundary of the heart was
below the lower end of the sternum, in one at that point, and in three
above it Here the correspondence of the upper and lower boun-
daries is rather indicated than kept up, but this correspondence can
scarcely be recognized when we compare these boundaries with each
other in those cases in which they occupied a less extreme position.
(Note 9, page 111.)

Tht Boundary-line between the Upper Border of the Heart and the
Lower Limit of the Great Arteries. — The origin of the pulmonary artery
and the top of the auricular portion of the right auricle may be re-
garded as the upper boundary of the heart and the lower boundary of
the great arteries. The highest position of the origin of the pul-
monary artery was at the top of the second cartilage, while that of
the top of the auricle was a little higher or on a level with the first
space. The lowest position of the origin of the pulmonaiy artery was
the upper edge of the fourth cartilage, while that of the top of the
auricle was a little less low, or on a level with the lower border of
the third space. Between these two extreme limits the origin of the
pulmonary artery and the top of the right auricle occupied every
variety of position, but their favourite seat was at or on a level with
the second space and the third costal cartilage, which was the situa-
tion of those parts in two-thirds of the instances (36 in 49 for the
pulmonary artery ; 43 in 63 for the top of the auricle).

In the majority of instances there was but little difference between
the height of the origin of the pulmonary artery and the top of the
right auricle, the height of the two being identical in one-fourth of

c 2

20 A SYSTEM OF MEDICINE.

the instances (10 in 44), and the difference in their height being
respectively less than the third of an inch or the third of the breadth
of a space or cartilage in one-half of them (21 and 20 in 44). Of the
remaining instances, in twelve the difference of the height of those two
parts varied from one-third to two-thirds of an inch or two-thirds
of a space or cartilage, and in one the difference of their height
amounted almost to an inch. As a rule,- the origin of the pulmonary
artery tended to be higher in position than the top of the right
auricle, the former part being the higher of the two in twenty
instances, and the latter part being the higher of the two in fourteen
instances. (Note 10, page 111.)

The varying position, higher or lower, of (1) the pulmonary artery,
(2) the aorta, (3) the right ventricle, and (4) the right auricle, in
relation to the costal cartilages and the spaces between them, and to
the sternum will next be considered.

The Pulmonary Artery. — A knowledge of the position of the pul-
monary artery is important to the clinical worker, because it is near
the surface of the chest, and because the signs afforded by it reveal
the condition of the cavities and valves of the heart, and the ease or
difficulty with which the blood finds its way from and to those cavi-
ties, the lungs, and the body. Among those signs are, the character
of the first sound, whether loud and sharp, or feeble and almost silent,
or presenting a pulmonic murmur ; the character of the second sound,
whether feeble or intense, blunt or sharp, or presenting a double
sound, giving in quick succession the aortic and the pulmonic second
sounds or the reverse, the later sound being the louder of the two.

The trunk of the pulmonary artery varied in length from three-
quarters of an inch to two inches and a half. In more than a third
of the instances (17 in 46) the artery was from an inch to an inch
and a half in length, while in less than a third of them it was below
(15 in 46), and in less than a third of them (14 in 46) it was above
that length.

The vertical measurement of the right ventricle, from the origiu of
the pulmonary artery to the lower boundary of the heart, varied in
these instances from two inches and a half to a little over four
inches. The length of the ventricle thus measured was from three
inches to three inches and a half in less than one-half of the cases
(20 in 46).

The proportion between the length of the pulmonary artery and
the length of the right ventricle, measured from above downwards,
presented great variety. In one instance the length of the artery
was nearly equal to the length of the ventricle, that of the former being
two inches and a half, that of the latter scarcely three inches ; while
in two others the vertical measurement of the ventricle was five times as
great as that of the artery, the length of the latter in one instance being
three-quarters of an inch, and that of the former being fully four inches.
The average length of the ventricle in relation to that of the artery

POSITION AND FORM OF THE HEART. 21

was as three to one. As a rule, the length of the pulmonary artery
regulated the proportion in length which that vessel bore to the ven-
tricle ; thus in the whole of the fifteen instances in which the length
of the pulmonary artery was less than an inch, the length of the right
ventricle was more than three times that of the artery ; while in the
whole of the fourteen in which the artery was an inch and a half in
length and upwards, the length of the right ventricle was less than
three times that of the vessel. (Note 11, page 112.)

As we have already seen, the origin of the pulmonary artery varied
in position from the second to the fourth cartilage, its usual situation
being the second space and the third cartilage. The top of the pul-
monary artery was in one instance almost as high as the clavicle, and
in almost one half of the cases (25 in 63) it was situated behind the
manubrium or the first rib ; while in one case it was so low as to be
almost on a level with the upper edge of the third cartilage. In
more than one half of the cases (33 in 63) it was seated behind the
first space or the second cartilage. (Note 12, page 112.)

The situation of the pulmonary artery during its course is regu-
lated by the length of the vessel and by the position of its starting-
place and upper end. In one instance it was so high as to be entirely
concealed by the manubrium, while in another it was so low as to be
entirely covered by the third cartilage and third space. The artery was
rarely limited in position to one space or one cartilage : thus in but one
instance it only occupied the first space, and in but one it was quite
covered by the second cartilage. The artery usually lay behind one
space and one costal cartilage (35 times* in 60), but in one-third of
the instances (21 in 60) it extended to an additional space or cartilage.
In two-thirds of the instances it was present behind the second carti-
lage (43 in 60) ; in more than half of them it lay behind the first
space (35 in 60), and in nearly as many behind the second space (32
in 60) ; while in one-fourth it was covered by the third cartilage (15
in 60), and in one-sixth by the manubrium (9 in 60). (Note 12,
page 112.)

When the pulmonary artery was long (it was so in 14 of 46 in-
stances), its origin occupied, as a rule, a low position. Thus in
sixteen instances the origin of the artery was entirely above the
second space, and in only two of these was it long, while in seven
it was short. • On the other hand, in thirty instances the pulmonary
artery at the first part of its course was at or below the second space,
and in twelve of them the artery was long, while iu eight it was
short. (Note 12, page 112.)

The Arch of the Aorta. — The arch of the aorta is not, like the
pulmonary artery, visible in its whole course from its root to its
summit, being hidden at its root by the right auricle and ventricle.
I shall, therefore, not speak here of the whole of the ascending aorta,
but of that portion of it which comes into view above the right
auricular appendix and between it and the beginning of the pul-
monary artery and the arterial cone of the right ventricle.

22 A SYSTEM OF MEDICINE.

The arch of the aorta, from the part in its course just spoken of
where it first becomes visible, to its highest point at the origin of the
innominate and left carotid arteries, varied much in length. In two
female subjects, one aged nine the other a few years older, the
arch was an inch and a half in length, but in the adult subject its
length ranged from an inch and three quarters to three inches. The
arch, measured from the lower to the higher points just named, was
from just over two inches to two inches and a half in length in two
fifths of the instances (19 in 47), that being about the average or
standard length ; from an inch and three quarters to two inches in
more than one fifth (11 in 47), and from two inches and a half to three
inches in less than two fifths of them (17 in 47). (Note 13, page 112.)

Viewed in proportionate relation to the length of the body,
measured approximately from the chin to the pubes, the vertical
measurement of the arch varied from one seventh to one fourteenth
of the vertical measurement of the body thus taken, and in one half
of the instances (23 in 45) the length of the aorta was one tenth of
that of the body.

In three instances the vertical measurement of the arch of the
aorta was the same as the vertical measurement of the right ventricle
taken from the part at which the aorta was visible to the lower
boundary of the organ. In two instances the arch was longer than
the ventricle in the proportion of ten to niue, but in the remainder
the length of the ventricle was greater than that of the aorta, the
relative proportion varying from 10 to 101 to 10 to'19'17, so that in
the last example the ventricle was nearly twice as long as the arch.
The average length of the arch in proportion to that of the right
ventricle was about 10 to 14 (14 in 47).

The variation in the proportionate length of the arch of the aorta
and the right ventricle, although thus considerable, is not nearly so
great as the variation in the proportionate length of the pulmonary
artery and the right ventricle ; since that artery varied in length from
more than one half to less than one fifth of the vertical measurement
of the ventricle, while the arch was about the same length as the
vertical measurement of the ventricle at one end of the scale, and was
of half that length at the other end.

There was some correspondence between the length of the aorta
and that of the pulmonary artery. Thus the pulmonary artery was
short, long, or of medium length in two fifths of the instances in
which the aorta was respectively short, long, or of medium length
(13 in 33). In the remaining instances (20 in 33) this strict propor-
tion was not maintained, but in only two of them was the difference
in the proportionate length of the vessels great, the aorta being long
while the pulmonary artery was short.

The position of the lower boundary of the heart in relation to the
lower end of the sternum, whether above, at or below that point is,
as a rule, governed to a considerable extent by the length of the arch of
the aorta. Thus in nine instances in which the arch was short, measur-

POSITION AND FORM OF THE HEART. 23

ing two inches or less, the lower boundary of the heart was above the
lower end of the sternum in seven instances and below that point in
two. The other circumstances that regulate the position of the lower
boundary of the heart in relation to the lower end 'of the sternum are
(1) youth; (2) the distension or collapse of the right ventricle; (3) the
length of the sternum ; (4) the important influence of the higher or
lower position of the sternum, higher when the chest is ample, being
of an inspiratory type, and lower when the chest is narrow and flat,
being of an expiratory type ; (5) the higher or lower position of the
top of the arch of the aorta which is often ruled by (4) the lower or
higher position of the sternum; (6) the extent to which the heart
shrinks upwards after death which is evinced by the space intervening
between the lower boundary of the heart and the lower boundary of
the front of the pericardium ; and (7) the elevation or depression of
the diaphragm, which is the most important influence in producing
respectively the elevation or depression of the heart, and which may
be caused by (a) the contraction or expansion of the lungs, or (b) the
distension or collapse of the abdomen. These points are illustrated
by the two exceptional cases just cited, in which, although the arch of
the aorta was short, the lower boundary of the heart was below the
level of the lower end of the sternum. Both of these cases were quite
young (1); in both the vertical measurement of the right ventricle
was long, while in one of them that cavity was distended and large
(2) ; in both of them the sternum wa9 short, its length being less than
four inches in one, while in the other it was four inches and a half (3);
again in one of them the sternum was high, the length of the neck
being only two inches, that of the sternum four inches and a half, and
that of the abdomen fourteen inches, while in the other instance in
which the right ventricle was large, the sternum was low in position,
the length of the neck being almost four inches, that of the sternum
less than four inches, and that of the abdomen only ten inches and a
half (4). In neither of these examples was the position of the lower
boundary of the heart lowered owing to the low position of the top of
the arch, for in one of them that point was above the top of the
sternum and in the other is was a little way below it (5). In fact
this influence, which tended to elevate the lower boundary of the
heart in relation to the lower end of the sternum was more than
counter-balanced by the combined influences of which I have just
spoken, all working in the opposite direction so as to lower the
inferior border of the heart.

In further illustration of this point, the influence, namely, of the
shortness or length of the arch in respectively raising or lowering the
lower boundary of the heart, we find that of seventeen cases in which
the aorta was long, measuring two and a half inches and upwards, in
ten the lower boundary of the heart was below the level of the lower
end of the sternum, in four it was at that point, while in only three was
it above the lower end of the sternum. The three exceptional cases in
which the lower boundary of the heart was above the level oi the

24 A SYSTEM OF MEDICINE,

lower end of the sternum were adults of full size (1) ; the right
ventricle was narrow and contracted in two of them (2) ; and in two
the heart deviated to the left so that the lower border of the right
ventricle was situated to the left of the lower end of the sternum,
instead of being to the right, as is usual. The sternum was long in
two of them, measuring in one case over seven inches (3) ; in all of
them the sternum was low in position, the length of the neck being
five inches and a half, four inches, and three inches and a half
respectively, while that of the abdomen was in each instance less
than fourteen inches (4) ; in one of them the top of the arch was
situated above the top of the sternum (5) ; in one of them the space
between the lower limit of the heart and the lower limit of the front
of the pericardium was nearly an inch, while in another it was fully
half an inch in width, showing that the upward shrinking of the heart
after death had been considerable (6) ; and finally one of them, that
in which the space between the heart and the lower rim of the peri-
cardium was small, the stomach was globose and much distended so
as to push the heart upwards (7b).

In twenty-three cases the arch of the aorta wras of intermediate
length, or from a little over two inches to two inches and a half, and
in these the lower boundary of the heart was in equal relative propor-
tion above, at, and below the level of the lower end of the sternum.

It is evident and is illustrated by what has just been said that if
we group the cases as I have just done, according to the actual length
of the arch of the aorta without relation to age or the dimensions cf
the body, we shall include some instances in which the arch of the
aorta is relatively short or long with those in which it is respec-
tively actually long or short. I have therefore grouped the
whole cases anew, and according to the proportional length of the aorta
in relation to the length of the body. It will suffice here if I say that
the results thus obtained are exactly confirmatory of those that I have
just related, and show that the higher or lower position of the lower
boundary of the heart in relation to the lower end of the sternum
is to a considerable extent governed by the proportional shortness or
length of the arch of the aorta. They show those results indeed more
strikingly, for the conflicting element of (1) youth has been removed.

Two exceptional instances have been brought into the group in
which the arch of the aorta was long in proportion to the length of
the body, that were not included in the parallel group in which the
arch was actually long. In these two examples the lower boundary
of the heart was above the level of the lower end of the sternum,
although the aorta was proportionally long. The heart was lifted
directly upwards to a great extent in both of these instances, in one of
them by very great enlargement of the liver, upwards, as well as
downwards, owing to the presence of malignant disease in the organ,
the sternum being in this case very long (68 inches) ; and in the other
by excessive distension of the stomach and intestines owing to
peritonitis, the sternum in this instauce being short (47 inches) and

POSITION AND FORM OF THE HEART. 25

the top of the aorta being situated in the root of the neck, a third of
an inch above the level of the top of the sternum (7b).

The Rigid Auricle. — The right auricle is, as a rule, hidden from ob-
servation by the couch of lung that is interposed between it and the
sternum and cartilages. It comes, however, to the surface in cases of
pericarditis when the effusion into the sac accumulates in sufficient
quantity to press aside that portion of lung with which the auricle is
covered. With the exception of the important point just considered,
the right auricle cannot be recognized locally by the clinical observer,
the condition of that cavity being in fact best told by the state of the
veins in the neck. The right auricle, measured from the top of its
auricufar portion to its lowest point, varied in length from one inch to
four inches and a half. Its length was usually from two and a half to
three and a half inches (in 41 of 62 instances). In one-fifth of the
cases (12 in 62) its length was less than two and a half inches ; but
one-half of these were youthful subjects (7 in 12). The vertical
measurement of the right ventricle was longer than that of the right
auricle in more than two-thirds of the cases in which the comparison
was made (35 in 49) ; in one-fifth of them the two cavities were nearly
or quite of equal length (10 in 49) ; and in one-twelfth of them the
auricle was longer than the ventricle. (Note 14, page 112.)

The auricular portion of the auricle, which during life laps, like a
tongue, to and fro, from right to left and back again, was usually
nearly on the same level as the top of the right ventricle, the top of
the auricle being of the same height as that of the ventricle in ten
instances, higher than that of the ventricle in fourteen instances, and
lower in twenty. It was at the lower boundary that the right auricle
failed. In one case, in which there was fatal haemorrhage, the auricle,
which was quite insignificant in size, was only half as long as the
ventricle. Usually, however, the auricle was shorter than the ventricle
by from one-tenth to one-third of its vertical measurement (in 29 of
35 instances).

The right auricle, from the variable extent to which, on the one
hand it receives blood, and on the other retains or parts with it before,
during, and after death, and from its passive nature, is more variable
in form and size than any.other cavity of the heart. This point will
be briefly illustrated when the lateral dimensions of the cavities are
considered.

Tlu Right Ventricle. — The vertical measurement of the right ven-
tricle in relation to the pulmonary artery and the aorta has already
been considered.

The right ventricle, measured from the origin of the pulmonary
artery to the lower boundary of the cavity, varied in length from two
inches and three quarters to four inches. In one-fifth of the instances
(9 in 46) the length of the ventricle thus measured was less than two
inches, the msgority of these being youthful subjects (5 in 9) ; in
nearly one-half of them (20 in 46) this measurement was from three
inches to nearly three inches and a half; and in the remainder it was

26 A SYSTEM OF MEDICINE.

three inches and a half and upwards, being fully four inches in six
of them. The variable dimensions and form of the ventricle will
be briefly noticed when its lateral measurements are considered.
(Note 15, page 112.)

The extent of the vertical measurement or length of the right ventricle
produces a marked influence on the position of the lower boundary of
the heart in relation to the lower end of the sternum. Thus, of the nine
cases in which the ventricle was short, its lower boundary was above
the level of the end of the sternum in live instances, and below that
level in only one ; while of the sixteen instances in which the ventricle
was long, in ten of them its inferior border was below the end of the
sternum, while in only six of them was it above that point. It is,
indeed, self-evident that the lower border of the ventricle must be
lower in position when the cavity increases, and higher when it lessens
in size.

The extent to which the upper part of the bony sternum covers the
great arteries, and the lower part of it, the heart, is very variable. In
one instance the great arteries occupied only the upper fourth of the
sternum, while the heart occupied its lower three-fourths. In another
instance this proportion was to a considerable extent reversed, for the
vessels lay behind the upper five-eighths of the bone, the heart itself
being limited to its lower three-eighths. In three-fourths of the in-
stances (39 in 52) the greater share of the sternum lay in front of the
heart, but in one-fourth the greater share of the bone was given to the
great vessels. On an average, the position of the heart was behind
the lower four-sevenths, and that of the great arteries was behind the
upper three-sevenths of the sternum. (Note 16, page 112.)

(II.) The Position of the Heakt and Great Vessels from Side

to Side.

Relation of the Breadth of the Heart to the Breadth of the Chest. —
The proportionate transverse diameter of the heart, compared with the
transverse diameter of the chest, varied considerably. Thus in one
instance, in which death was the result of haemorrhage, the width of
the heart was less than one-third of the width of the chest, on a level
with the lower end of the ensiform cartilage (32 to 10 inches); while
in another instance the measurement across the heart was nearly two-
thirds of that across the chest (5*1 inches to 8-2 inches).

In a large number of the cases observed (39 in 65) the breadth of
the heart was somewhat less than one-half of the breadth of the
chest, the proportion varying from 10 to 4 to 10 to 5. In one-sixth
of the instances (11 in 65) the width of the heart was less than two-
fifths (10 to 3 to 10 to 3-9), and in one-third of them (15 in 65) it
was more than one-half (10 to 5 to 10 to 62) of the width of the
chest. The size of the chest from side to side did not appear to exer-
cise any material influence on the proportional breadth of the heart,

POSITION AND FORM OF THE HEART, 27

but the heart was more frequently of the average proportional width
in those instances in which the chest was of medium breadth (9 to
9*9 inches) than in those in which it was either wide (10 to 12
inches) or narrow (6 to 89 inches). Thus, the heart was of the
average proportional breadth in five-sixths of the instances in which
the chest was of the medium breadth (10 in 12) ; in one-half of
those in which the chest was wide (12 in 22) ; and in two-thirds of
those in which the chest was narrow (19 in 31). The heart was com-
paratively wide and comparatively narrow in equal numbers in
those instances in which the chest was wide (6 of each kind in 22);
while the organ was more frequently comparatively wide than narrow,
in those in which the chest was narrow (wide in 8, narrow in 4, of 31).
Great distension and great collapse of the abdomen produced a marked
effect on the proportionate width of the heart in relation to that of the
chest. Thus, in fully two-thirds of the instances in which the heart
was proportionally narrow, the abdomen was distended (8 in 11), and
in one-half of these the distension was very great (4 in 11) ; while in
one of the three remaining cases the abdomen was large, in one it was
of moderate size, and in only one was it small. Then the reverse took
place in those cases in which the heart was proportionally wide, since
in only one- fifth of them was the abdomen distended (3 in 15), and
in but one of these was the distension very great. Distension of the
abdomen seemed to produce this effect by acting in two directions,
one upon the chest, by widening it, the other upon the heart itself,
by lessening it. The chest is widened because the distended abdomen
pushes the ribs outwards on either side, and elevates the lower border
of the chest in front and at each side ; and the heart is lessened
because the distended abdomen compresses the heart upwards into the
contracting space of the higher part of the cone of the chest, and so
lessens the amount of blood in the organ. (Note 17, page 113.)

The proportional size of the anterior transverse diameter of the
combined right auricle and ventricle, compared with that of the left
ventricle, exercises a marked effect on the proportional breadth of the
heart in relation to the breadth of the chest. This might indeed be
anticipated, for when the proportional width of the combined right
auricle and ventricle is great in relation to the width of the left ven-
tricle, the right cavities are distended with blood, and the whole
heart is consequently large, measured from side to side. In more
than one-half of the cases (7 in 12) in which the proportional breadth
of the heart to that of the chest was great, the proportional breadth
of the combined right auricle and ventricle to the left ventricle in
front was very great, the former being about ten times wider than
the latter ; and in none of them was the proportional breadth of the
right cavities small. Again, in almost one-half of the instances (5
in 11) in which the proportional width of the heart in relation to
that of the chest was small, the proportional width of the right
auricle and ventricle in relation to that of the left ventricle was also
small, the ratio being about 10 to 4. (Note 18, page 113.)

28 A SYSTEM OF MEDICINE.

Extent to which the Heart occupied the Bight and the Left Sides of the
Chest. — The extent to which the heart occupied respectively the right
and the left sides of the chest varied much in different instances.
Thus in one example, the heart extended one inch and a tenth to
the right and four inches to the left of a vertical line drawn down the
middle of the sternum ; and in another the organ extended nearly
two inches and a half to the right, and only two inches and a quarter
to the left of that line ; while in two other instances the heart occu-
pied the right and the left sides of the chest in exactly equal pro-
portions. Thus, taking the two extreme cases, in one of them one-
lifbh of the heart occupied the right side, and four-fifths of it the left
side of the chest ; while in the other fully one-half of the heart was
lodged in the right side, and less than one-half of it in the left side
of the chest.

There was every gradation of difference between these two extreme
examples. In fully two-fifths of the instances (27 in 67) one-third of
the heart or less was situated in the right side, and two-thirds of the
heart or more, in the left side of the chest ; while in fully two-fifths
of them (28 in 67), three-fifths of the heart or less was seated in the
left side, and two-fifths of it or more in the right side (literally 16
to 10).

In twelve intermediate and standard instances, the heart was dis-
tributed to the right and to the left of the middle line of the sternum
in the proportion respectively of ten and eighteen, and this was the
average position of the organ in sixty-seven bodies, so that nearly
two-thirds of the organ lay in the left side, and more than one-third
of it in the right side of the chest. (Note 19, page 113.)

The influences that cause the deviation of the heart towards the
right or the left side of the chest, are (1) before all others, the difference
in size of the right lung and the left ; (2) the encroachment upwards of
the liver or the stomach to an unusual extent on the right or the left
side of the chest respectively ; (3) the position of the patient before
death on the right side or on the left, an occurrence that may take
place in certain rare cases, such, for instance, as bed-sores and
affections of one side of the chest ; (4) the shrinking of the heart
upwards after death, as evinced by the extent of the space intervening
between the lower boundary of the heart and the lower boundary of
the front of the pericardium ; (5) the shortening of the aorta ; (6) the
relative size of the heart and of its cavities, measured from side to
side. There are doubtless other influences at work to produce the
effect in question, but I have not discovered them.

(1.) Of the small number of instances (6 in 66) in which the heart
swerved very far to the left, so as to occupy that side of the chest to
a greater extent by from three to four times than the right side of the
chest, the two lungs were equal in size in one-third (2 in 6), while the
right lung was greater than the left in the remaining two-thirds. On
the other hand, of the cases in which the heart was lodged equally in
the right and the left sides of the chest (3 in 66), and those in which

POSITION AND FORM OF THE HEART, 29

it bore only a little more to the left than the right side of the chest
(12 in 66), the two lungs were of equal size in one-fourth, and the
left lung was larger than the right in the remaining three-fourths.
Thus in none of the instauces in which the heart deviated greatly to
the left was the left lung larger than the right ; and in none of those
in which the heart tended towards the right side of the chest was the
right lung greater than the left. In the whole of the remaining
instances, with a few exceptions, an analogous condition obtained, the
right lung being the larger when the heart was lodged to an unusual
extent in the left side of the chest, and the left lung being the larger
when the heart was lodged to an unusual extent in the right side of
the chest, (Note 20, page 113.)

(2.) The position of the upper surface of the liver, covered by the
diaphragm, was higher in the right side of the chest than that of the
stomach in the left side of the chest in all but a fraction of the
instances observed (57 in 61). On an average, the liver at this
situation was higher than the stomach by more than half an inch
(*6 inch). In two-fifths of the cases (25 in 61) the heart occupied
the left side of the chest to an unusual exteut ; of these, in nearly
two-thirds the height of the liver in relation to that of the stomach
was above the average (14 in 25) ; in nearly one-third it was below
the average (7 in 25) ; aud in a fraction it was at the average (3 in
25). In all but one of the five instances in which the heart was very
far to the left, the relative height of the liver was above the average.
In one-fourth of the cases (14 in 61) the heart occupied the right
side of the chest to an unusual extent, and in nearly three-fifths of
these (8 in 14) the height of the liver was below the average, while
in fully two-fifths of them (6 in 14) it was above the average. When
the top of the liver encroached to an unusual proportional extent on
the right side of the chest, it may be said that the unduly-elevated
organ tended to displace the heart to the left. There were, however>
a few remarkable exceptions to this rule. Thus, in one instance the
heart occupied equally the right and the left sides of the chest, and
yet the top of the liver rose higher by nearly an inch and a half into
the right side of the chest than the stomach did into the left side of
the chest. The reason of this was obvious. There was contraction
of the right lung in this case, owing to phthisis, with the effect of
drawing both the heart and the liver unduly into the space previously
occupied by the right lung.

(3.) I have no after -death evidence to show that the position of the
patient on the right side or the left during the period preceding death
caused the heart to occupy unduly the right or the left side of the
chest. We know, however, that during life the heart falls towards
the side on which the person lies. At the same time that side of the
chest expands less during inspiration than the opposite side, owing to
the restraint offered to the movement of the ribs that bear the weight
of the chest, while, to compensate for the deficient expansion of the
restrained side, the free side of the chest expands to an increased ex-

30 A SYSTEM OF MEDICINE.

tent. After deatli, the organs, as a rule, retain pretty nearly the place
they occupied during life, and the effect of position during life in
displacing the heart more towards the right side or the left, is retained
after death.

(4.) When the heart shrinks upwards, so as to leave a considerable
space between the lower boundary of the organ and the lower
boundary of the front of the pericardium, the heart, as a rule, bears
more towards the right than the left side of the chest. Thus the
space below the heart was large in two-thirds of the cases in which
that organ bore unusually to the right (8 in 12) ; and in only two-
fifths of those in which it bore unusually to the left (8 in 19).

(5.) I am of opinion that in those cases in which the heart shrinks
thus upwards, and bears unusually to the right, the contraction and
shortening of the aorta is one of the principal agents that draws the
apex and the body of the heart to the right as well as upwards.

(6.) The relative size of the heart and of its cavities, measured
from side to side, exercised much less influence than the relative size
of the right and left lung, and the relative height of the liver and
stomach, on the extent to which the heart occupied after death the
right and left sides of the chest respectively.

When the heart is laTge, the lungs necessarily make way for it, to
the right and left equally if the development of the lungs is equal ;
but when one lung is expanded and the other is contracted, the heart
when large encroaches more upon the contracted than the expanded
lung, for that lung offers the least resistance. The stronger influence
of the greater size of one lung overrides then the weaker influence of
the size of the heart. But it is evident that the size of the heart
must produce an influence supplementing and modifying the in-
fluence of the greater size of one lung. When the heart is large it
enhances the influence of the greater size of one lung, and the heart
encroaches more on the side containing the contracted lung ; and
when the heart is small it lessens the influence of the greater size
of one lung, and the heart encroaches less on the side containing the
contracted lung. Thus in the large group of cases in which the
heart occupied the left side of the chest to an unusual extent (1 to
3*9 to 1 to 2, in 23 in 60), and in the equally large group in which
the heart was distributed in the average proportion to the right
and left sides of the chest (1 to 1-5 to 1 to 1*9 in 23 in 60), the heart
was large in fully one-fourth of the respective instances (6 in 23 and
7 in 23), while in no instance was the heart large in the group in
which that organ occupied the right side of the chest.

The heart was small in two of the three instances in which the
organ occupied the right and the left sides of the chest to an equal
extent. The heart is attached at the centre of the chest, behind, to the
roots of the lungs by the pulmonary veins and pulmonary arteries ;
and above and in front, to the great arteries and the descending
vena cava from which it is suspended. The heart, therefore, when
it does not bear to the left or to the right owing to the greater or

POSITION AND FORM OF THE HEART. 31

less size of the right or left lung, hangs directly downwards from the
points of its suspension at the centre of the chest, and tends to
occupy a central position, bearing equally to the right and to the left

Breadth of the Combined Right Auricle and Ventricle in Relation to
tliat of the Left Ventricle as seen in Front — The breadth of the com-
bined right auricle and ventricle in relation to the breadth of the left
ventricle as seen in front, varied from 10 to 1 to 10 to 4J. Thus the
right cavities occupied almost the whole front of the heart in some
examples, and little more than two-thirds of it in others. Every shade
of variation existed between these two extreme instances; but the
average or standard proportion between the breadth of the right cavities
and that of the left ventricle in front was as 4 to 1. (Note 21, page
114.)

Breadth of the Right Auricle. — The auricular portion of the right
auricle varied in breadth from a little over half an inch (55 inch) to
two inches and a third (23 inch), its average breadth being one inch
and a third (1-3 inch). (Note 22, page 114.)

The body of the right auricle1 varied in breadth from a quarter of
an inch to an iuch and a half, its average breadth being four-fifths of
an inch (8*1 inch). (Note 23, page 114.)

The left edge of the auricular portion of the right auricle extended
to the left of the left edge of the sternum in four instances ; it was
placed nearer to the left than the right edge of the sternum in
twenty-four cases ; it was situated about midway between the left
and the right edge of the sternum in eight instances ; and it was
nearer to the right than the left edge of that bone in fourteen.
(Note 24, page 114.)

The right edge of the right auricle extended to the right of the
right edge of the sternum to an extent varying from a quarter of an
inch to an inch and three-quarters, so that to that extent the auricle
lay behind the right costal cartilages. The right auricle extended on
an average from half an inch to a little over an inch to the right of
the sternum. (Note 25, page 114.)

The auricular portion of the right auricle was wider than the body
of the auricle in all but two instances, in which instances their
breadth was the same. As a rule, the auricular portion was wider
than the body of the auricle in the proportion of ten to six and a
half (10 to 6*4), but in two instances that portion was nearly three
times as wide as the body of the auricle. (Note 26, page 114.)

The proportional breadth of the auricular portion of the right
auricle varied from two-fifths to one-fifth of the breadth of the
heart itself. The width of the heart was, on an average, nearly four
times as great as that of the auricular portion of the right auricle.
(Note 27, page 114.)

1 The right auricle is about half an inch wider, and the right ventricle is about half
an inch narrower than the measurements given in this article. Those measurements
have been necessarily taken from the right auriculo- ventricular furrow, which is the
apparent boundary-line between the right auricle and ventricle, but is situated half an
inch to the right of the real boundary-line between those cavities.

32 A SYSTEM OF MEDICINE.

The proportional breadth of the body of the right auricle varied
from about a fourth (10 to 36) to a ninth (10 to 86) of the breadth of
the heart. In one exceptional case in which death took place from
haemorrhage, the heart was twelve times as wide as the right auricle,
that cavity being quite empty. The width of the heart was, on an
average, nearly six times as great as the width of the right auricle.
(Note 28, page 114)

Breadth of the Right Ventricle. — The breadth of the right ventricle *
varied from four-fifths (in 6 of 38 instances) to a little over one-half
(in 11 of 38 instances) of the whole breadth of the heart. The
average or standard breadth of the right ventricle was two-thirds of
the breadth of the heart (10 to 15;, and in one-half of the cases
observed the proportional width of the right ventricle in relation to
that of the heart was above (19 in 38), and in one-half of them it
was below that average (19 in 38). (Note 29, page 114.)

The breadth of the arterial cone of the right ventricle a little way
below the origin of the pulmonary artery varied from four-fifths to
two-fifths of the breadth of the right ventricle at its middle, the
average width of the arterial cone being nearly three-fifths of that
of the body of the right ventricle. As a rule, when the body of the
right ventricle was wide or narrow in relation to the heart, the arterial
cone was respectively narrow or wide in relation to the body of the
right ventricle. (Note 30, page 114)

The vertical diameter or length of the right ventricle,2 measured
from the origin of the pulmonary artery to the lower boundary of that
cavity, was somewhat shorter than the transverse diameter or breadth
of the ventricle in one-sixth of the cases (5 in 30). In the rest of
them the length of the right ventricle was greater than its breadth.
In one instance the length of the ventricle wa3 to its breadth as 17*3
to 10, but the average or standard measurement of the length to the
breadth of that cavity was as 4 to 3. (Note 31, page 114.)

The breadth of the right ventricle in relation to that of the right
auricle l below its auriculaT portion varied from 10 to 1 4 to 10 to 52,
the average proportion being 10 to 3. (Note 32, page 1 14)

The actual breadth of the right ventricle2 in adults, without
distinction of sex, varied from two to four inches. In three-fifths of
them the width of the ventricle was from three to three and a half
inches (in 14 in 24) ; in one-fifth of them it was above three and a
half inches ; and in two-fifths of them it was less than three inches.
(Note 33, page 115.)

1 The right ventricle is about hulf an inch narrower, and the right auricle is about
half an inch wider than the measurements of those cavities given in this article, for
the reason stated in the foot-note at page 31.

9 As the breadth of the body of the right ventricle is about half an inch narrower
than the measurements of that cavity given in this article, for the reason stated in the
foot-note at page 31, the actual relation of the trausverse diameter or width of the body of
the right ventricle here stated to that of the conns arteriosus, and to the vertical diameter
or length of the ventricle, is half an inch narrower than the proportional measurements
here given.

POSITION AND FORM OF THE HEART. 33

In one instance the right ventricle extended further to the right than
to the left of a vertical line drawn down the middle of the sternum,
but in every other instance the ventricle extended more to the left
than to the right of that line. In one case, nine-tenths of the right
ventricle was situated in the left side of the chest, and only one-tenth
of it in the right side ; but, on an average, the ventricle extended
nearly three times farther to the left than the right of the middle
line (27 to 10). (Note 34, page 115.)

The limits of the body of the right ventricle and of its arterial cone
are indicated, (1) to the left by the position of the longitudinal furrow
between the ventricles ; and (2) to the right by the position of the
transverse furrow between the right ventricle, including the right
edge of the origin of the pulmonary artery and the right auricle, in-
cluding its auricular portion.

(1). As a rule, the inter- ventricular furrow takes an oblique direc-
tion outwards, or to the left from above downwards, so that the ven-
tricle occupies a wider space below than above (in 26 of 39 instances).
In a small number of cases (6 in 39) the reverse takes place, and the
furrow tends inwards, and then outwards with a peculiar double curve
as it descends. In these instances the right ventricle was in a state
of contraction, and the left ventricle was exposed to a large extent,
while in those in which the septum inclined markedly outwards
during its descent, the right ventricle was distended so as to cover all
but a small portion of the left ventricle. The greatest inclination of
the longitudinal furrow to the left was one inch, and its greatest
inclination to the right was half an inch (45 inch). (Note 35,
page 115.)

In one instance, a case in which the right ventricle was contracted,
the longitudinal furrow in its descent curved to the right, and the
body of the right ventricle towards its left border was completely
shielded by the sternum ; but in every other instance that cavity was
covered in front to a greater or less extent by the cardiac costal carti-
lages, to the left of the lower half of the sternum. In a small pro-
portion of the cases (6 in 36) the right ventricle lay behind the costal
cartilages from end to end, from the sternum, namely, to the ribs to
which they are united ; and in half of these (3 in 6) the ventricle
extended to the left, beyond the cartilages and behind the ribs. In
the majority of the cases (19 in 36) the longitudinal furrow extended
either up to the ends of the cartilages, a little beyond them, or half
an inch or less to the right of them, so that in all these cases the cardiac
cartilages covered the right ventricle almost or quite from end to end.
In the remaining instances (17- in 36) a considerable portion of the
cartilages, varying from less than an inch to more than an inch and
a half (-7 to 17 inch) extended beyond the right ventricle. (Note 36,
page 115.)

The body of the right ventricle, starting from a vertical line drawn
down the middle of the sternum, extended to the left in all the cases,
from a little over half an inch (-6 inch) to almost four inches (3*8 inch).

34 A SYSTEM OF MEDICINE.

Between these two extreme instances there was every shade of differ-
ence. In the great majority of the cases (35 in 52; the right ventricle
extended from one inch and a half to two inches and a half to the
left of the middle line of the sternum, and behind the cardiac carti-
lages. (Note 37, page 115.)

(2). x The transverse or right auriculo- ventricular furrow was situ-
ated to the right of the right edge of the lower portion of the sternum,
and behind the right costal cartilages, in fully two-thirds of the cases
(36 in 51), at that edge in a fraction of them (3 in 51), and to the left
of that edge, and therefore behind the lower portion of the sternum, in
one-fourth of them (12 in 51). In one instance the right auriculo-
ventricular furrow extended an inch and a third (1*3 inch) to the right
of the right edge of the sternum, so as to lie behind the right costal
cartilages to that extent, and in. five instances its right limit was
situated behind the middle line of the sternum. Between these two
extreme limits there was every gradation in the position of the right
auriculo-ventricular furrow.

The left edge of the auricular portion of the right auricle gives, as
a rule, very nearly the position of the right edge of the arterial cone of
the right ventricle, where it is about to end in the pulmonary artery.
The right edge of the arterial cone, starting from the triscupid orifice,
invariably inclines, as it ascends, from right to left. There was con-
siderable difference in the degree of its inclination, which was measured
by the distance between the right limit of the auriculo-ventricular
furrow and a line drawn downwards from the right edge of the pul-
monary artery. The right edge of the arterial cone swerved as it-
ascended from right to left in one instance, a man, to the extent of
two inches, and in another, also a man, to that of a little over half an
inch (*6 inch). There was every variety of inclination between these
extreme instances, but in the great majority of cases (34 in 51) the
curved line of the right border of the arterial cone bent downwards,
with an inclination from left to right of from an inch to an inch and
a half, the boundary line starting above from the right border of the
origin of the pulmonary artery, and ending below in the auriculo-
ventricular furrow. (Note 38, page 115.)

Breadth and Position of the Pulmonary Arteri/. — As the origin of the
pulmonary artery is the point of convergence towards which the right
ventricle propels its blood, this is the natural place for examining the
position of that artery. The pulmonary artery forms, indeed, the pointed
apex of a triangle, the body of which is constituted by the front of the
right ventricle, its base by the lower boundary of that cavity, resting
on the central tendon of the diaphragm, its left side by the longitudinal
furrow, and its right side by the auriculo-ventricular furrow.2

The breadth of the pulmonary artery varied from a little over half

1 The transverse furrow, which is the apparent boundary-line between the right auricle
and the right ventricle, is about half an inch to the right of the real boundary-line
between those cavities. See note at pace 31.

* Or rather by a line half an inch to the left of the furrow. See note at page 31.

POSITION AND FORM OF THE HEART. 35

an inch (*6 inch) to a little under an inch and a half (1*45 inch).
Between these two extreme limits, both of which occurred in men,
there was every kind of variation in the breadth of the artery. The
width of the artery depended as much on the amount of blood that it
happened to contain as on the natural size of the vessel. In one-
third of the cases (18 in 45) the breadth of the artery varied from
three-quarters of an inch to less than an inch, and of these three were
boys and four were young people ; and in one-third of them (17 in 45)
the breadth varied from an inch to an inch and a quarter, and of these
the youngest was a girl of 16, the rest being adults. The pulmonary
artery was wider than the aorta in twenty-seven cases, narrower
than the aorta in eleven, and of the same width as the aorta in six.
(Note 39, page 115.)

In one instance the right border of the. pulmonary artery at its
origin lay two-thirds of an inch to the left of the sternum, and in
another it was covered by the sternum to the extent of an inch,
so that a mere rim of the artery (-25 inch) appeared in the second
left space. Between these two extreme instances there was every
degree of difference in the position of the origin of the pulmonary
artery to the right or to the left.

In two-thirds of the cases (31 in 45) the pulmonary artery was
situated partly behind the sternum, and partly behind the upper
cartilages and spaces to the left of the sternum ; but in one-third of
them (14 in 45) the vessel lay entirely to the left of that bone, and
behind the upper spaces and cartilages.

Of those instances in which the artery lay completely to the left of
the sternum, in three-fourths (11 in 14) the right border of the vessel
was on a line with or a little beyond the left border of the bone, and in
the remainder (3 in 14) it was placed from one-third to two-thirds of
an inch to the left of that bone. Of the instances in which the artery
lay partly behind the sternum, partly behind the cartilages and their
spaces, in all but one-fifth (6 in 31) the vessel was situated to a greater
extent behind the spaces than the sternum. In no single instance was
the artery entirely covered by that bone. In the large majority of the
cases, therefore, the greater part (in 25 of 45 instances), or the whole
(in 14 of 45 instances), of the artery bore to the left of the sternum
and presented itself behind the upper costal cartilages and their
spaces from the first cartilage to the third space. (Note 40, page 115.)

Breadth of the Left Ventricle. — The breadth of the left ventricle as
it is seen in front where it extends from the septum between the
ventricles to the left border of the heart, varied from almost half an
inch (#4 inch) to almost an inch and a half (1*4 inch). The average
width of the ventricle was four-fifths of an inch (-8 inch). The pro-
portion that the width of the left ventricle at its anterior aspect bore
to the width of the whole heart varied from less than one-tenth (08
to 10) to more than three-tenths (32 to 10). As a rule, when the
ventricle was actually narrow, it was also proportionally narrow in
relation to the breadth of the heart ; and when the ventricle was

p 2

36 A S YtiTEM OF MEDICINE.

actually wide, it was also proportionally wide in relation to the
breadth of the heart. The exceptions to this rule are so few that
I need not give the details here. (Note 41, page 116.)

Position of tht Apex of the Heart. — The line of junction of the fourth
and fifth ribs to their cartilages is a landmark of some clinical im-
portance, for, aided by knowledge, this line may be pretty nearly
ascertained during life. A downward bow is made by the descending
curves of those ribs and of their cartilages, and their junction usually
corresponds to the deepest part of the bow. The left boundary of the
heart at the apex was situated in one instance an inch to the left,
and in another instance an inch to the right of the junction of the
fourth or fifth rib to its cartilage ; in five cases out of forty-two this
left boundary was at that junction, in eighteen it extended to the left
of it, and in six it was seated to the right of it.

The relation of the lower anterior edge of the upper lobe of the left
lung to the apex of the heart is a point of clinical value. The
septum between the upper and lower lobes is situated a little way
to the left of the apex of the heart, and this portion of the upper lobe
is detached as it were from the body of the lung and dips downwards
and forwards, so that it may devote itself to the protection of the
apex around which it is folded, being situated outside, behind and in
front of, above and slightly below the apex. A small tongue of lung,
the existence of which I pointed out in 1844, frequently interposes
itself between the front and under surface of the apex and the walls
of the chest. This tongue of lung and the adjoining structure of
the lower portion of the upper lobe play backwards and forwards
with the forward and backward play of the apex of the heart. When
the apex comes forward towards the ribs and spaces during the con-
traction of the ventricle, the tongue of lung retracts ; when the apex
retracts, the tongue of lung expands ; and thus those two structures
interchange with and adapt themselves to each other during the move-
ments of the heart and the lungs. This tongue of lung that thus
laps round and in front of the apex was present in two-fifths of the
series of cases under observation (24 in 61), was absent in one-half of
them (31 in 61), and was just indicated in the form of an inward
curve in one-tenth of them (6 in 61). This tongue was strongly
marked in one -third of the instances in which it existed (8 in 24),
was slightly marked in another third (9 in 24), and was of inter-
mediate form in the remaining third (7 in 24). Besides these in-
stances, this tongue was present in eighteen additional examples in my
possession : in one-half of these it was large and pronounced (9 in 18),
in four of them it was of medium size, and in four it was small.

During and after death the apex contracts in one direction, or
upwards and to the right towards the centre of the heart, and the left
lung retracts in another direction or to the left. The heart is there-
fore more exposed after death than during life. This especially applies
to the apex of the heart. As a rule, however, in these cases, the apex
and the adjoining portion of the heart are still covered to a certain

POSITION AND FORM OF THE HE A RT. 37

extent by lung (in 34 instances out of 58). In two of these instances
the lung covered the heart from the apex towards the sternum to the
extent of two inches and a half, but in the rest of them the extent of
lung in front of the apex varied in breadth from an inch and a
quarter to the tenth of an inch. In one-sixth of the cases (9 in 58)
the edge of the lung was on a line with or crossed the apex, and in one-
fourth of them (15 in 58) it was situated to the left of the heart, so as
to expose the apex. The space thus left between the lung and the apex
varied from one inch to the eighth of an inch. (Note 42, page 116.)

The Breadth and Position of tlie Ascending Aorta. — The breadth
of the ascending aorta varied from half an inch to an inch and-a-
half (1*45), its average breadth being nearly one inch (.96 inch).
(Note 43, page 1 16.)

The aorta was usually narrower than the pulmonary artery, (in 27
of 44 cases), but it was sometimes wider than that vessel (11 in 44),
aud in a few instances (6 in 44), the two arteries were of equal
breadth. When the aorta was less than an inch in width, it was very
seldom wider than the pulmonary artery (in 2 of 36 cases) ; but
when the aorta was an inch or more in breadth, it was more often
the wider of the two arteries, in the proportion of nine to eight.
(Note 44, page 116.)

The ascending aorta was completely covered by the sternum in
nearly one half of the cases (19 in 45), and of these instances, in
one-third the artery was central (6), in one-third (6) it inclined to
the right, and in one-third (7) it inclined to the left.

In one-third of the cases (15 in 45) the ascending aorta was
visible to a greater or less extent to the right of the sternum, and in
six of these the exposure of the artery to the right was great, the
whole artery being brought into view in one case in which there was
excessive distension of the abdomen.

In -one-fourth of the cases (11 in 45), the ascending aorta was
partially visible to the left of the sternum, but in only one instance
did the breadth of the portion of the artery thus exposed amount to
more than the third of an inch. (Note 45, page 116.)

The Position of the " Root of the Aorta" l including the Orifice, Valve,2

1 I have adopted the terra '* root of the aorta" at the suggestion of Mr. Marshall aud
with the approval of Dr. Sharpey.

* Haller, writing in Latin, correctly designates the valves of the heart under the term
" valvule," derived from " valvse," folding doors, thus — " valvulae scmilunares," " val-
vals mitrales," "valvulae in quas annulum venosum diviserunt." Senac (Structure
du Cceur), speaking of the valves of the heart, uses the terms "valvules tricuspidales,
mitrales, et sigmoides ; " and Douglas, in his translation of Winslow, describes the
" tricuspid valves," the "mitral valves," and the "semilunar valves."

Portal was apparently the first to speak of the auriculo-ventricular valves in the
singular number, under the name respectively of "valvule mitrale " and "valvule
triglochine," on the ground, long previously recognised by anatomists, that the flaps of
each of those valves are attached to a valvular ring.

The English word "valve" has been applied by engineers and in common use to the
mechanism, as a whole, for preventing the back-How ol fluid, and not to one or other of
the flaps composing that mechanism. I have therefore, here and elsewhere, spoken of
the semilunar flaps of the aortic or pulmonic valve, and not of the semilunar valves.

3S A 8Y8TEM OF MEDICINE

and Sinuses of the Aorta. — I possess only seven illustrations of the
position of the root of the aorta. They, however, show the aortic
valve in a variety of situations, and as the anatomical relations of
the " root of the aorta " to the root of the pulmonary artery, and to the
visible portion of the ascending aorta are very definite, it is easy to
infer the position of the aortic valve, when we know that of the
pulmonic valve, and that of the ascending aorta.

The ascending aorta, as it mounts upwards, curves first to the right
and then to the left. The upper and lower ends of the curve bear to
the left, and the centre of the curve bears to the right. When, there-
fore, the visible portion of the ascending aorta is situated far to the
left or far to the right, the sinuses and valve of the aorta are also
situated far to the left or far to the right, their bearing being always
more to the left than that of the ascending aorta. The lower boundary
of the pulmonic orifice corresponds with the upper boundary of the
aortic orifice at the junction of the anterior and the left posterior flaps
of the aortic valve. Nearly one half of the root of the pulmonary
artery is situated just above the left posterior aortic sinus, and more
than one half of it extends to the left of the root of the aorta. The
root of the aorta extends obliquely downwards to the extent of
about one inch below, and fully half an inch to the left of the
pulmonary artery, the extent being greater or less in accordance with
the oblique diameter of the root of the aorta.

In one instance the greater part of the anterior aortic sinus was
situated behind the second left space from its upper to its lower bound-
. ary, while the remainder of the root of the aorta was covered by the
left border of the sternum. In this case the ascending aorta occupied
the left half or three-fifths of the sternum, the right side of that bone
being occupied by the descending cava, and the pulmonic valve was
situated entirely to the left of the sternum behind the second car-
tilage and the upper third of the second space.

In another instance the right border of the right posterior sinus
of the aorta was present in the third right space close to the right
edge of the sternum, and the whole of the rest of the root of the
aorta was covered by the right three-fifths of the sternum, its left
two-fifths being occupied by the arterial cone of the right ventricle.
In that case the whole heart lay more to the right than to the left of
the median line, the ascending aorta extended four-fifths of an inch
to the right of the right edge of the sternum, and four-fifths of the
origin of the pulmonary artery, which was on a level with the third
cartilage, was covered by the sternum.

In the first of these two cases, the situation of the ascending aorta,
and that of the origin of the pulmonary artery were high and much to the
left, and the situation of the root of the aorta was correspondingly
also high and much to the left. In the second of them, the ascend-
ing aorta and the origin of the pulmonary artery were low in situa-
tion, and were placed very far to the right ; and the root of the aorta
was also low in situation, and was placed very far to the right.

POSITION AND FORM OF THE HEART. 39 -

Of the remaining five instances, in two the root of the aorta was
situated for one-fifth of its breadth in the second left space, and for
four-fifths of its breadth behind the sternum on a level with the
second space and the third cartilage. In two other cases, the propor-
tion of the root of the aorta behind the sternum and to the left of
that bone was about the same as in the two cases just quoted ; but
in one of them it was situated behind the third left cartilage and the
upper third of the third left space ; while in the other instance it was
still lower, being on a level with the lower border of the third car-
tilage, the third space, and the upper border of the fourth cartilage.

The root of the aorta, including as I have said, in that term the
orifice, valve, and sinuses of the artery, was oblique in direction in
all instances. Its longest or oblique diameter ranged from one inch
to almost an inch and a half (14) ; its vertical diameter varied from
*8 inch to 1*05 inch; and its transverse diameter from *8 inch to 12
inch. In three instances the transverse and vertical measurements
were equal ; in two the transverse diameter exceeded the vertical ;
and in two the vertical diameter exceeded the transverse.

Although the observation of the actual position of the root of the
aorta in health has been limited to the seven cases just examined, yet
we are able to infer its proximate position by the knowledge already
obtained of the situation of the right edge of the ascending aorta,
and of that of the, origin of the pulmonary artery. The origin of the
pulmonary artery was in one case as high as the upper border of the
second cartilage, and in another it was as low as the upper border
of the fourth cartilage. In the former case the root of the aorta
must have been on a level with the second cartilage and the upper
portion of the second space, while in the latter case it must have
been on a level with the fourth cartilage and the upper portion of the
fourth space. The usual position of the origin of the pulmonary
artery was behind the second space or the third costal cartilage, and
the usual position of the root of the aorta, following in the wake of its
companion great artery, must have been on a level with the third
cartilage and the third space. The average situation of the root of
the aorta must therefore have been on a level with the lower portion
of the third cartilage and the third space. In the seven cases just
examined, the right edge of the ascending aorta was situated on a line
to the right of the right edge of the root of the aorta, to an extent vary-
ing from the eighth of an inch to more than half an inch. In the
same instances the left edge of the ascending aorta was situated on $
line to the right of the left edge of the root of the aorta, to an extent
varying from one-third (*3 inch) to three-fifths of an inch. The
extent to which the ascending aorta bore to the right in relation to
the root of the aorta was governed by two circumstances : (1) the
degree to which the ascending aorta was situated to the right or to
the left : and (2), the distension or collapse of the artery. (1) The
root of the aorta was situated further to the left in relation to the as-
cending aorta, when the position of the ascending aorta was far to the

40 . A SYSTEM OF MEDICINE.

left tlian when it was far to the right. (2) The root of the aorta was
further to the left in relation to the ascending aorta when the breadth
of the artery was great owing to distension, than when it was small
owing to collapse.

In one instance, a case with great intestinal distension, the whole
of the ascending aorta was situated to the right of the sternum,
and in that instance the greater portion of the root of the aorta must
have been also situated to the right of the sternum. In another
instance, the ascending aorta was situated to the extent of more
than one half of its breadth to the left of the sternum, and in that
instance, the greater portion of the root of the aorta must hav«
been also situated to the left of the strrmnn.

»|H'it of the heart.

In one half of the cases (19 in 45), the whole of the aorta was
covered by the sternum, and in most of these the greater part of the
root of the aorta must have been also covered by the sternum, but
its left border must have usually passed a little to the left of that
bone, being situated behind one of the cartilages or spaces close to the
left edge of the sternum.

Under these circumstances the average or standard position of
the root of the aorta must have been behind the left two-thirds or
half of the sternum on a level with the third cartilage and the third
space, its left border being placed behind and below that cartilage at
its articulation to the sternum. (Note 40, page lit!.)

POSITION AND FOUM OF THE HEART. 41

The Position of the Aortic Sinuses, and the Flaps of the Aortic Valve.1
— The aortic orifice looks towards the apex of the ventricle in a direc-
tion to the left downwards, and slightly forwards. The aspect of the
orifice is therefore oblique, its obliquity being usually quite as great
from above downwards, as from left to right. When the heart bears
unduly to the left, the downward obliquity of the aortic orifice is
greater than when it bears unduly to the right.

The root of the aorta, including the aortic orifice, valve, and
sinuses, projects forwards, in front of the mitral valve and the cavity
of the left ventricle, so as to interpose itself between the orifice of
the pulmonary artery above and the tricuspid orifice below. The
root of the aorta thus separates those two openings from each other,
the conns arteriosus being situated v< f;.;!'!. of it. When a section is

made through the auricles across the base of the heart, so as to
expose the four great openings of the heart, the pulmonic, the aortic,
and the tricuspid orifices, viewed in their natural position, are seen
to range themselves in a line from above downwards, the mitral orifice
being situated behind the lower half of the aortic and the upper two-
thirds of the tricuspid orifice. This line is not, however, straight, but
is somewhat convex, the convexity looking backwards, so that the pul-
monic and tricuspid orifices which are situated at the upper and lower
portions of the line are somewhat in advance of the aortic orifice,
which occupies the central position. When the line of the three
orifices is looked at in front, it is seen to take an oblique direction
from above downwards, and from right to loft, the pulmonic orifice
1 See Fig*. I, 2, nnd 3.

M A SYSTEM OF MEDICINE.

at the upper end of the line being situated partly behind and chiefly
to the left of the left edge of the sternum at the second left cartilage
and space, and the tricuspid orifice being situated behind the right
half of the sternum at its lower portion.

The "Aortic Vestibule," or Intervalvular Space of the Left Ventricle.
— When the semilunar flaps of the aortic valve meet together so as to
shut the aortic aperture, they fall backwards into a short space that
I have described in my " Medical Anatomy " under the name of the
" intervalvular space of the left ventricle." I have here, however, at

Pig. 3.— Aortic valve shut, seen in the Fm. 4.— Other half of the heart repre-
aortic vestibule of the left ventricle, Banted in Fig. 5, showing the mitral ml

which parts an exposed by cutting a tricuspid valves and the fleshy septum

flap in the anterior cusp of the mitral (n) with its continuation in the form of

valve and pinning it backwards. ft " fibrous septum," which is also seen

in the companion figure.

the suggestion of Dr. Sharpey, adopted the appropriate name of the
" aortic vestibule " for this space, which is well seen in the preparation
from which Fig. 3 was taken, in which the semilunar flaps of the
aortic valve are seen through an opening cut in the anterior flap of
the mitral valve. The aortic vestibule bends forwards and to the right
from the upper part of the left ventricle, and forms the channel
between the cavity of that ventricle and its outlet at the aortic
aperture. The walls of the aortic vestibule are rigid and unyielding,
and it therefore retains its size during every stage of the action of

POSITION AND FORM OF THE HEART. 43

the heart These walls are muscular in front and to the left, where
they are lined by rigid fibrous tissue, and where the space is situated
immediately behind the conns arteriosus of the right ventricle ; fibro-
cartilaginous on the right, where they are formed by the central fibro-
cartilage and " fibrous septum " of the heart ; and fibrous behind, where
they are formed by the base of the anterior flap of the mitral valve
and the adjoining wall of the left auricle, upon which the posterior
sinuses of the aortic valve are implanted.

The aortic vestibule occupies the centre of the heart, and is sur-
rounded by all the more important parts of the organ. The conies
arteriosus and the orifice of the pulmonary artery are in front of it ;
the tricuspid valve and right auricle are to the right of it ; and the
mitral valve and left auricle are behind it. During the ventricular
diastole, when the left ventricle is of full size, the aortic vestibule is
the narrowest portion or bent neck of the ventricle, and it then
receives the flaps of the closed aortic valve which fall back into its
cavity. During the ventricular systole, on the other hand, when the
ventricle has completely contracted upon its contents so as to present
an almost solid mass, the aortic vestibule moves downwards and to
the left towards the apex, and becomes the widest part of the small
remaining cavity, and the presence of this space then allows the
mitral valve to remain closed up to the end of the systole by the
pressure of the blood on its anterior flap.

The " aortic vestibule," as Mr. Marshall suggests, is a short conns
arteriosus, since it corresponds in relative position and function, though
not in shape or size, or in the structure of its walls, to the conns
arteriosus of the right ventricle, immediately behind which it is
situated. These two analogous parts take opposite directions in
relation to each other, and respectively to the ventricle from which
they spring and the great artery to which they proceed. The right
conns arteriosus ascends with a bearing to the left, and curves back-
wards to end in the pulmonary artery ; while the aortic vestibule or
left conns arteriosus ascends with a bearing to the right and bends
forwards to terminate in the root of the aorta. Those two great
arteries, following the direction of the conns arteriosus from which
they respectively spring, cross each other in their onward and up-
ward course, so that the pulmonary artery proceeds backwards to the
left and then to the right, while the ascending aorta proceeds for-
wards to the right and then to the left. If the two cavities be looked
at as a combined whole, each with its ventricle, its conus arteriosus,
and its great artery, they resemble somewhat the curious double oil
and vinegar flask that is met with so commonly in the most beautiful
parts of South Germany.

The central fibro-cartilage and " tendinous septum " of the heart
form, as I have just said, the right wall of the aortic vestibule. The
fleshy septum terminates at its base in a strong tendinous aponeurosis
or fibro-cartilage, which forms a part of great importance in the
structure of the heart, and which is well seen in the preparation from

44 A SYSTEM OF MEDICINE,

which Figs. 3 and 4 have been taken. The muscular septum (d) is,
in fact, converted at this region into a fibrous septum ; but while the
muscular septum separates the two ventricles, the fibrous septum
separates the left ventricle from the right auricle as well as from the
top of the right ventricle. Higher up this fibrous septum is con-
verted into the central fibro-cartilage, which corresponds to the
central fibro-cartilage and bone of the heart of the ox (Fig. 6), and
which is converted into bone iu a human heart in my possession.
The central fibro-cartilage, a3 may be seen in Fig. 2, forms a firm
bond of connection between the tendinous rings of the mitral and
tricuspid orifices, the central or inner angles of the mitral and tri-
cuspid valves, the right posterior sinus of the aorta, and tho aortic
vestibule. It also gives insertion to muscular fibres from the left aud
the right ventricles (Fig. 5 a), which, sweeping round from the left and

Fie. 5. — Showing tbo muscular fibioa unravelled uf the left and right ventricW
s. Fibres from the left uud right ventricles going to the central fibro-cartilage of
the beart, and forming a [wrtiou of the sqituin.

the right respectively, blend together toward the base of the posterior
longitudinal furrow, so as to form short central bands of fibres, which
dip forwards at right angles to the circular fibres, deepening as they
advance, enter and go to form the septum and end in the central fibro-
cartilage, which gives origin to numerous muscular fibres, to the inter-
auricular septum, and the right and left auricles. During the ventricular
systole the central fibro-cartilage, and with it the aortic vestibule and
all the adjacent parls.are drawn downwards and to the left towards the
itpex by the contraction of the ventricular fibres inserted into the ten-
dinous ring and especially into the central fibro-cartilage, which thus
becomes the focus and movable pivot of the heart, which binds toge-
ther all those important parts and gives' to them a common movement.
The setting of the orifice of the aorta is muscular anteriorly and to

POSITION AND FORM OF THE HEART 45

the left, and fibrous posteriorly and to the right. The muscular setting
is made by the anterior half of the base of the left ventricle, and the
fibrous setting by the anterior cusp of the mitral valve and its con-
tinuation towards the left auricle, and by the central fibro-car-
tilage. During the diastole the anterior cusp of the mitral valve
divides the ventricle into two portions, each with its own aperture,
an anterior or aortic portion, out of which the blood pours during the
systole through the aortic orifice, and a posterior or mitral portion, into
which the blood flows during the diastole through the mitral orifica

There is one anterior, and there are two posterior and lateral aortic
sinuses. The right or anterior coronary artery springs from the an-
terior sinus, and the left or posterior coronary artery from the left
posterior sinus. The right posterior sinus is sometimes called the
intercoronary sinus. OwTing to the obliquity downwards, forwards,
and to the right of the orifice of the aorta, the right posterior flap of
the aortic valve is much lower in position than the other flaps. Thus
the lower boundary of that flap was in two instances half an inch
lower than the lower boundary of either of the other flaps. In another
example, in which the aoita was far to the right, the lower edge of
the right posterior cu?p was only a quarter of an inch lower than
that of the left posterior cusp, but it was half an inch lower than the
lower edge of the anterior cusp.

The root of the aorta is buried in the centre of the heart, and
is therefore incircled bv all the cavities of the heart and the two
other great vessels. The crescentic edge of the anterior sinus is
attached throughout to the central fibro-cartilage which forms the
summit of the interventricular septum. The anterior sinus is
covered in front by the conns artirio'irt nnd, higher up, on the right
side, to a varying extent, by t!i j av.rio-.ihir portion of the right auricle,
and on the left side by the pulmonary artery.

The left and right halves respectively of the right and left
posterior flaps of the aortic valve are attached at their junction, and
along their lower border to the anterior cusp of the mitral valve,
.and to the aponeurosis that is continuous with that cusp. At this
situation the two posterior sinuses of the aorta are in front of the
left auricle. (Figs. 3 and 4.)

The left half of the left posterior sinus is attached at its root to the
muscular base of the left ventricle, and is covered, going from right to
left, first by the auricular portion of the right auricle, and then by the
inner or right wall of the pulmonary artery. The junction of the
anterior to the left posterior flap of the aortic valve is usually a little
in front of the junction of the posterior and the left anterior flaps of
the pulmonary artery, so that a pin thrust through that artery at the
junction of the flaps in question into the aorta, appears about the
tenth of an inch behind the junction of those aortic flaps; but in
one instance the pin, thus inserted, pierced through the junction of
the aortic flaps as well as through that of the pulmonic flaps. The
left or posterior coronary artery at its origin is, in one of my prepara-

4fl A SYSTEM OF MEDICINE.

tion8, #25 inch from the left edge of the left posterior cusp, and *4 inch
from its right edge, and I believe it will be found that this represents
the usual position of the origin of the artery.

The relations of the right posterior sinus of the aorta are of re-
markable extent and importance. The centre and right side of the
root of that sinus is firmly attached to or incorporated with the central
fibro-cartilage and fibrous septum of the heart that crown the inter-
ventricular septum. To the left of this attachment to the fibro-cartilage,
the right aortic sinus is united, as we have just seen, to the anterior
cusp of the mitral valve, and it is seated in front of the left auricle.
To the right and in front of this attachment, it is closely connected
with the inner or left angle of the tricuspid valve. The right wall
of the right posterior sinus, as it advances to join the right edge of
the anterior sinus, is covered first by the inner or left wall of the
right auricle, and finally by the inner or posterior wall of the arterial
cone of the right ventricle.

This right aortic sinus is thus closely connected with every
important part of the heart, except the pulmonary artery. The right
and left ventricle, the right and left auricle, the mitral and tricuspid
valves are all of them attached to or in contact with it ; and the
central fibro-cartilage of the heart, as we have seen, with which
the base of this sinus is incorporated, acts as a tie that binds to-
gether the allied movements of those parts.1 The descending vena
cava also comes into contact with the upper portion of this sinus.

Mr. Thurnam brought into notice, thirty-three years ago, the
extensive and important bearings of the sinuses of the aorta, in
especial relation to aneurism of those parts.

It is customary for authors on anatomy, following the original
error of the great Valsalva, unfortunately repeated by Mr. Thurnam,
and more recently by that great anatomist, Henle, to describe the
aortic sinuses as being two of them anterior, and one posterior. I
have examined the heart in situ in many bodies, with regard to this
point, and I have always found those sinuses and the corresponding
flaps of the aortic valve in the position I have described, one being
anterior, and two posterior. A little consideration as to the known
relation of these sinuses to other parts, the position of which is well
ascertained and admitted, will show that two of these sinuses are
posterior and lateral, and that only one of them is anterior.

The right and left posterior flaps of the aortic valve are attached
in about an equal degree to the anterior mitral cusp, as is shown
in drawings and many hearts now around me, and in Dr. John
Reid's figure.2 The anterior cusp of the mitral valve is on a level
with the posterior wall of the root of the aorta, and it is therefore
impossible that either of the aortic sinuses that are attached to that
flap can be situated at the anterior aspect of the aorta ; they must,
indeed, both be posterior in position. Again, while the right or anterior

1 See Fig. 4.

1 " Cyclopaedia of Anatomy," vol. i. p. 588. See alsoFigs. 1, 2, and 8.

POSITION AND FORM OF THE BE ART. 47

coronary artery arises from the anterior aortic sinus, the left or pos-
terior coronary artery arises from the left posterior sinus ; and while
the right artery advances to the right of the pulmonary artery, the
left artery passes to the left behind the pulmonary artery. Further,
the origin of the left coronary artery is nearer to the left or anterior
and lateral edge than to the right or posterior edge of the left posterior
sinus. I might adduce other points in illustration of what I have
advanced, but these facts, which speak for themselves, are sufficient.1

The error has, I believe, arisen and been perpetuated from the cus-
tom of examining these sinuses, not when the heart is in situ, but
after it has been removed from the body. If the right ventricle with
its arterial cone, and the ventricular septum are carefully removed
without disturbing the position of the heart, and without injuring the
anterior wall of the aorta at its origin, the true position of the aortic
sinuses and of the flaps of the aortic valve may be readily observed.

The right and left posterior aortic sinuses advance forwards on
either side, and finally curve gently inwards and forwards to complete
the circle of the aorta by uniting at either end with the anterior

1 Valsalva's original drawing (V. Opera, tab. ii. fig. 1 ; see Fig. a), in which the
anterior and left posterior sinuses with their respective coronary arteries are represented
in front of the root of the aorta, gives not a front but a side view of the aortic arch.
The artery from which this drawing was taken shows the cut end of the vessel, and has
evidently been removed from the body and placed upon its right side. The effect of this
position would be to place the anterior and left posterior sinuses, each with its coronary
artery, on the same anterior plane. Fig. b is a reduced copy of a similar drawing of the
arch of the aorta after its removal from the body, given by Lower (Tractatus de Corde,
tab. L fig. 4) in which the two coronary arteries, as in Valsalva's drawing, spring
from the front of the root of the aorta.

Nearly all the drawings of the root of the aorta that have been taken from the actual
body, the artery being in situ (reduced copies of several of which drawings are given
below), represent the sinuses in the position that 1 have described, two of them being
posterior in situation and one anterior, and the right posterior sinus being the lowest of the
three sinuses. I find it thus in Tiedemann's " Tabula Arteriarnm," plate xix. (fig. e) ;
John Bell's "Anatomy," vol. ii. p. 283 (fig. f) ; Charles Bell's Engravings of the
Arteries, tab. ii. (fig. o) ; Mr. Quain's " Anatomy of the Arteries," anterior view, fig. 3,
and posterior view, fig. 4, plate xlviii. (figs, h i) ; PirogolTs " Anatomia Topographica,"
in eleven different views (figs, klmn); and Braun's " Topographisch-Anatomisch Atlas"
(tin. o P). Henle, in a much reduced figure of the aorta in situ, represents one anterior
and two posterior sinuses (fig. q), but he gives a seiics of drawings of the heart and aorta
after their removal from the body (one of which I have given on a reduced scale, Fig. d),
in all of which the sinuses are represented and described as being two anterior and one
posterior.

Anatomists, including Morgagni and Senac in former times, and, as I have said above,
the respected names of Thurnam and Henle in our own day, have as a rule described
two of the sinuses of Valsalva and their corresponding coronary arteries as being anterior,
and one of them, or that which is destitute of a coronary artery, as being posterior.

On the other hand, Vesalius and P. Sylvius described the left coronary artery as arising
from behind the posterior valve. Some authors give contradictor)' descriptions of the
origin of the coronary arteiies. Thus, Window in one passage says that there are two
coronary arteries, ** one of which is situated anteiiorly, the other posteriorly" (vol. ii. p. 3) ;
while elsewhere (p. 221) he says that "one of the vessels lies towards the right hand,
the other towards the left, of the anterior third part of the circumference of the aorta."
Portal (" Anatomie Medicale," vol. iii. p. 152) says that the left coronary artery arises from
the left posterior portion of the aorta ; but elsewhere (p. 51) he states that two of the
valves are anterior and lateral and the third is posterior, and that the right and left
coronary arteries are situated above the two anterior valves.

The accurate Hallcr, "Elemental Physiologic," iii. 345, speaking of the aortic valve,

48 A SYSTEM OF MEDICINE,

sinus. The anterior portion of the left posterior sinus is concealed by
the pulmonary artery, while the anterior portion of the right posterior

says : "Situs alequantnm differ!, dute enim 'snperiori loco ponnntur, altera anterior,
posterior altera ; tenia inferior eat. Eamm eaj, qtue superiori loco ponnntur, aodalea
habent arterias coronarias, inferior nullum aortas ramum vicinum habot." Hare that
great anatomist nan given a correct description of Ilia situation of the flaps of the aortic
valve and of the origin of the coronary arteries.

In our own day, Pirogoff and Mr. Heath describe the sinuses as being one of them
1 two of them posterior. Bourgery (fig. C) curiously figures the coronary

POSITION AND FORM OF THE HEART. 49

sinus is. readily exposed by pressing aside the auricular appendix. It
is rather difficult to Bay which of the two posterior sinuses comes
forward to the greater extent at their points of attachment to the
anterior sinus ; I think, however, that the right posterior sinus, which
usually goes by the name of the posterior sinus, comes forward to a
greater extent than the left posterior sinus, which usually goes by the
name of the left anterior sinus. (Note 46, p. 116.)

The Position of the Mitral Valve. — In seven instances the size and
position of the mitral valve are given, and in three of them accurate
details of its structure are represented. These points are further
illustrated by preparations and dissections. (Note 40, p. 118.)

Fid. 6. — C«Ifa heart boiled, showing the aortic (c) nnd mitral (n) orifices thrown
iuto one by Ihe removal of the mitral valve, the lower a beiiijj the central fibro-
cartilage, B the tricnaijid orifice, and p the orifice of the pulmonary artery.

The setting of the mitral orifice is muscular in its two posterior
thirds, and fibrous in its anterior third. In these respects the mitral
and aortic orifices balance each other. The setting of the mitral orifice
is muscular behind, while that of the aortic orifice is muscular
in front, the two openings being separated by the interposed anterior
flap of the mitral valve and its short fibrous continuation to the two
posterior aortic sinuses, and by the central fibro-cartilage of the
heart. When the heart is boiled for a sufficient length of time
this interposed fibrous partition softens and separates from its attach-
ments, and the aortic and mitral apertures are thrown into one large
irregular opening (see Fig. 6). The base of the ventricles then pre-
tents not four but three great apertures, the tricuspid, the pulmonic,
and the mitral-aortic.

tol. rv. F

60 A SYSTEM OF MEDICINE.

The apparatus of the mitral valve occupies the whole of the pos-
terior part of the left, ventricle, and when its anterior walls are
removed, the whole of this apparatus is brought into view.

The anterior cusp or flap of the mitral valve is alone visible in one
of the three drawings giving the anatomical details of the valve, while
in the two others the lower border of the posterior cusp is likewise
brought into view.

The whole apparatus of the valve takes an oblique direction from
right to left and downwards. The right end or base of the apparatus
of the valve corresponds with the junction of the left auricle with the
left ventricle, and its left end corresponds with the interior of the apex
of the left ventricle. The apparatus of the valve thus forms a long
triangle, its base being at the base of the ventricle, its apex at the
apex of the ventricle, its upper side being slightly curved upwards

Fio. 7.— Showing the mitral orifice, the Fio. 8.— Systole of the left ventricle.

anterior flap of the mitral valve, and
the right and left posterior flaps of the
aortic valve Diastole of the ventricles.

or outwards, and its lower side being slightly bent inwards or upwards
at its middle. The flaps, the tendinous cords, and the papillary
muscles, which are connected by the cords to the flaps, form the
three component parts of the valve. (Figs. 7,10, 11, 12, and "Medical
Anatomy," Plate VI.)

The convex base of the anterior flap of the mitral valve is attached
on the one hand to the junction of the left ventricle to the left auricle,
and on the other to the roots of the right and left posterior flaps of
the aortic valve. This attachment of the mitral to the aortic valve
is effected through the fibrous structure that extends from the base of
one valve to the base of the other, and by the central fibro-cartilage
of the heart, which forms a triple bond of connexion that ties the
mitral, the aortic, and the tricuspid valves to each other. (Fig. 2.)

POSITION AND FORS^OF THE HEART.

When the mitral valve is shut, the anterior flap of the valve pre-
sents a convex edge, shaped like a horseshoe, which falls back upon
and fits like a lid into the posterior flap of the valve, which flap, being
crescentic in shape, presents a concave edge.1 Each flap adapts itself
to the other by a notched lip, made up of small hemispherical
eminences. The eminences of one lip fill up the notches of the other
lip. These eminences, thus seen on the auricular surface of the valve,
are cells when seen on its ventricular surface, and as these cells are
distended with blood when the ventricle contracts, and ajce exactly
maintained in their places by the tendinous cords and papillary
muscles, the distended cells or eminences at the opposite lips of the
valve adapt themselves to and press against each other during the
systole, so as to shut the valve. (Figs. 2, 9, 10, 12.)

Mitral valve shut ; auric ulur mr-
jilcrior or convex and posterior
'' flaps; ventricular systole.

systole.

-Mitral valve shut; ventricular

; anterior flip, with tendinous
ind papillary must-Ira ; tiro pos-
flapa of aortic valve ; ventricular

The anterior flap is simple, and when closed is shaped like a three-
quarters moon. The posterior flap is compound, and when closed ia
shaped like a quarter or crescent-shaped moon. The compound pos-
terior flap is usually made up of one central and two lateral sub-
segments, the latter being sometimes subdivided. These sub-segments
adapt themselves so to each other, that the concavity of the crescentic
border of the posterior compound flap is preserved entire; for it
would have been impossible, by means of one simple fold of
membrane, to fill up without a break the whole of the crescentic
border.

1 need scarcely give a description of the arrangement of the ten-
dinous cords in relation to the flaps of the valve, and of the papillary
muscles in relation to the cords and the flaps. It will be sufficient if
1 Figs 2, a.

K 2

52 A SYSTEM OF MEDICINE.

I here say that they are so arranged that when the muscular walla
of the ventricle contract, the papillary muscles, which are really semi-
detached portions of those walls, also contract with equal steps ; that as
the walls shorten so as to approximate the base and the apex by
a double movement to each other, the papillary muscles shorten to an
exactly parallel degree ; and that thus while they hold the naps of the
valve, through the medium of the cords, in apposition, they steadily draw
the whole valve towards the apex, and the apex towards the valve, to
exactly the same extent that the base and apex of the ventricle are
drawn towards each other. The mechanical arrangements are com-
plicated, for there are many parts to be adjusted to each other; but
the principle on which those parts are adjusted to each other is simple,
for it is by one single contraction of the whole single muscle of the
left ventricle, made up in its component part3 of walls, columns, and

Fig. IS. — Diagram of the shut mitral
valve, with the anterior cusp A A inclose
muscles, contact with the posterior cusp (b, 6).

The tendinous cords and papillary
muscles are shown, the direction of the
current and pressure of the blood being
indicated bj arrows.

papillary muscles, that the base of the ventricle (including the mitral
aperture and valve and the aortic aperture and valve) and the apex of
the ventricle are approximated steadily to each other during the
systofe.

When the convex anterior flap of the mitral valve falls back upon
and tills up the concave posterior flap of the valve, the anterior flap
and its membranous continuation to the left and right posterior aortic
flaps form a smooth scooped channel or hollow, along which the blood
flows noiselessly from the ventricle into the aorta during the systole.
(Kg. 7.)

The mitral orifice extends downwards, with an inclination to the
left, immediately behind and below the aortic orifice; and, like that

POSITION AND FORM OF THE HEART. 53

orifice, it looks towards the apex of the left ventricle, or to the left,
downwards and slightly forwards. The line of direction of the mitral
orifice, viewed from the front, is therefore from above downwards, with
a slight obliquity from left to right. The upper and left boundary of
the mitral orifice is about half an inch above the level of the lower
edge of the right posterior flap of the aortic valve. The lower border
of the mitral orifice is about three-quarters of an inch below the
lower border of the aortic orifice. The upper or left edge of the
mitral orifice is not so far to the left, while its lower or right edge is
about as far to the right, as are the left and right edges respectively
of the aortic orifice. The mitral orifice is situated deep behind the
sternum, a little below the middle of that bone. Its upper or left
boundary, in four instances, was on a level with the third cartilage,
just within the left edge of the sternum; and it3 lower or right
boundary was on a level with the fourth cartilage, behind a line
drawn down the middle of the sternum. This is probably higher than
the average position of the mitral orifice after death. In one other case
the top of the mitral orifice was on a level with the lower border
of the secoud space, its situation otherwise corresponding to that in
the cases just described. In two other instances, the mitral orifice
was comparatively low and was situated unusually to the right,
its upper border being on a level with the lower edge of the third
cartilage or upper border of the fourth space, behind the middle line
of the sternum, and its lower or right border being on a level with the
lower portion of the fourth space, or the top of the fifth cartilage
behind the right edge of the sternum. As a rule, the mitral orifice
occupied a space behind the left half of the sternum, extending down-
wards for more than one inch below the middle of the bone ; but in
occasional cases it was present behind the right half of the bone.

The tendinous cords and papillary muscles of the mitral valve, as
they extended to the left with an inclination downwards, retained, as
a rule, their situation behind the space or cartilage that was on a
level with their starting-point from the valve.

Thus in the four instances in which the upper rim of the orifice
was on a level with the third cartilage, the upper or left cords lay
behind the third left cartilage, and the upper or left papillary muscle
behind the third space ; and in the same instances the lower rim of
the orifice was in two of them on a level with the third space, and in
two of them on a level with the fourth cartilage ; and in these two
sets of cases the lower or right cords and papillary muscle lay re-
spectively behind the third space and the fourth cartilage, with a final
dip to the space or cartilage below.

In the other cases in which the position of the upper and lower
edges of the mitral orifice were higher or lower in relation to the
spaces and cartilages than in those just quoted, the upper and lower
cords and muscles retained their bearing throughout in relation to the
space or cartilage on the level of which they started, until they also
usually made a final dip so as to occupy a relatively lower position.

54 A SYSTEM OF MEDICINE.

In two of the instances there was a space of half an inch between
the right and left papillary muscles, the width of the interior of the
ventricle being an inch and a half; and in the other instance, in
which the systole of the ventricle was more pronounced, the space
between the muscles was the fifth of an inch, the width of the cavity
being a little over an inch (1-2 inch).

In one instance, in which the heart and all its parts lay unduly
to the right, and in which the flaps, cords and muscles of the valve
took a very oblique direction downwards, the right papillary muscle
was situated behind the left border of the sternum and the sternal
half of the fifth cartilage, and the left papillary muscle crossed the
third cartilage and space midway between the sternum and the junc-
tion of the cartilages to their ribs.

This instance was throughout exceptional in the position of the
heart and all its parts, and the great vessels ; but the other instances
offer fair average examples of the position of the mitral valve. I need
not, therefore, further analyse additional cases. It is sufficient to bear
in mind that when the origin of the pulmonary artery is high or low
in position, the aortic and mitral valves are also correspondingly high
or low in position ; and that when the ascending aorta and the origin
of the pulmonary artery are far to the right or far to the left of their
usual situation, the aortic and mitral valves are also correspondingly
far to the right or far to the left of their usual situation.

The Tricuspid Valve. — The apparatus of the mitral valve occupies
the whole of the posterior part of the left ventricle, but the
apparatus of the tricuspid valve fills up the whole body of the right
ventricle, the narrowing comes arteriosus being the only portion of
the ventricle unoccupied by it. (Note 46, page 119.)

The reason for this diffusion of the apparatus of the tricuspid
valve and this concentration of that of the mitral valve is obvious.
It depends on the form of the two ventricles and the relation to each
other of their apertures of ingress and egress.

The leit ventricle is the central cavity of the heart, and is flask-
shaped ; and its walls on a transverse section are shaped like a ring, and
surround a circular space, the mitral valve being behind (see Fig. 3).
The right ventricle is applied upon the anterior and inferior walls of the
left ventricle, which project into the cavity of the right ventricle and
form its inner or posterior wall. The right ventricle on a transverse
section is crescent-shaped, its inner wall being convex, while the inner
aspect of its outer wall is concave or angular, for it presents at its
lower border and outer aspect a projecting angle. The whole cavity of
the right ventricle looked at in front is triangular in form, the base
of the triangle resting on the central tendon of the diaphragm, its
apex pointing to the top of the pulmonary artery, its right side
being formed by the junction of the right auricle to the right ventricle
and by the tricuspid orifice, and its left side by the septum between
the ventricles.

The three cusps of the tricuspid valve are visible when the cavity

POSITION AND FOllM OF TBE EEART. 55

is opened, the anterior and inferior flaps being completely exposed
while the posterior flap is partially concealed (Figs. 13, 14, 15).

The whole apparatus of the tricuspid valve, like that of the mitral
valve, takes a direction from right to left; but while the apparatus
of the mitral valve concentrates itself as it recedes from the flaps, the
papillary muscles pointing towards the apes, and the whole structure
forming a long triangle, the apparatus of the tricuspid valve spreads
itself out as it recedes from the flaps, like the rays of a fan.

Fira. IS, 14, and 15 are views of the interior of the right ventricle and of a portion
of the left ventricle : A, anterior flap ; n, posterior flap ; c, inferior flap ; and d,
one of the long sub-aegments of the inferior flap of the tricuspid valve, f, anterior
papillary muscle ; □, superior papillary muscle ; h n, inferior papillary muscles ;
a, sub-segment occupying the angle between the anterior and posterior naps of the
valve ; 0, ™™ arUrwma ; p, pulmonary artery ; b, upper or left papillary muscle,
and «, lower or right papillary muscle belonging to the left ventricle and mitral

The anterior flap gives attachment at its upper edge to a group
of cords which converge upon the small superior papillary muscle,

36 A SYSTEM OF MEDICINE.

which is incorporated with the posterior wall of the cavity at the
lowor portion of the arterial cone. The cords from the lower edge of
the anterior flap converge upon the anterior papillary muscle, which
muscle also sends a radiating scries of cords that attach themselves
to the upper and anterior edge of the lower flap of the valve. The
anterior papillary muscle is not immediately connected either with
the front or the back wall of the ventricle, hut is attached inter-
mediately to both of them by fleshy columns. A strong and rather long
column curves hackwards to he attached by outspreading roots to the
posterior wall of the ventricle near the septum ; while an interlacement
of shorter and thinner columns advances forward and to the left, ex-
tending from the base of the anterior papillary muscle to the anterior
wall of the ventricle, also near the septum (Fig. 13). Thus the roots

of the anterior papillary muscle spread both backwards and forwards,
the base of the muscle being, however, nearer to the front than the
back of the ventricle. J!y this beautiful arrangement a purchase is
given for this muscle to act upon the centre of the valve from the
middle of the cavity.

The inferior flap of the valve is not formed, like the anterior flap,
of one sheet of membrane, but is a compound flap, which is sub-
divided into four or five sub-segments, two of which are longer than
the rest, which, by meeting together and adapting themselves to
each other, fill up the large rounded space of the tricuspid orifice,
at its inferior portion. The cords from these sub-segments converge
upon o series of papillary muscles that are conveniently situated

POSITION AND FORM OF THE BEART. 67

around the lower portion of the ventricle, some, or one, being
seated in front, Borne below, and some behind. The inferior papillary
muscles are attached, like the anterior papillary muscle, not imme-
diately to the walls of the ventricle, but intermediately by inter-
lacing fleshy columns. The posterior papillary muscles of this
group, which are thus connected with the inferior flap of the tri-
cuspid valve, are immediately attached to the inner or convex wall
of the ventricle.

The posterior flap is attached behind by a series of radiating cords
to the inner walls of the ventricle, sometimes by means of small
papillary muscles, sometimes by the immediate insertion of the cords
into the walls.

The upper portion of the tricuspid orifice is narrow and angular,
while its lower portion is wide and circular; and thus, therefore, the

simple anterior and posterior flaps, with the intervention of one
anterior and one superior sub-segment, fill up the upper and narrow
part of the orifice ; while the inferior and compound sub-segments
adapt themselves to the large and rounded inferior portion of the
orifice. (See fig. 2, p. 40.)

The whole of these segments of the valve meet together at the centre
of the orifice, and hence arises the necessity for an array of papillary
muscles, the points of which converge towards the centre of the valve,

58 A SYSTEM OF MEDICINE.

and that are attached at their roots by fleshy columns that connect
them with both the outer and the inner walls of the ventricle.

The tricuspid orifice is situated behind the lower portion of the
sternum and in front of the mitral orifice and the left ventricle. The
direction of the tricuspid orifice is from above downwards with a
slight inclination from left to right. The upper boundary of the
tricuspid orifice is immediately below the orifice of the aorta, and
in front of the mitral valve.

The four great orifices of the heart — the pulmonic, the aortic, the
mitral, and the tricuspid — are situated in that order, one above another,
the pulmonic orifice being the highest and the tricuspid the lowest.
The lower portion of each of the first three orifices is lower than the
upper portion of the orifice below it. Thus the pulmonic orifice, when
looked at in front, covers the upper part of the orifice of the aorta on
its left side ; the lower border of the aortic orifice is lower than the
upper border of the mitral orifice ; and in like manner, the lower
two-thirds, or three-fifths, of the mitral orifice lie behind the upper half
of the tricuspid orifice, the lower half of which is below the level
of the lower edge of the mitral valve.

The posterior aspect of the tricuspid orifice is attached to the anterior
wall of the left ventricle, not on a level with the mitral orifice, but
about half an inch nearer to the apex. The wall to which it is thus
attached is convex, and the posterior surface of the tricuspid valve
where it fits upon the left ventricle is therefore concave. The shape
of the tricuspid orifice is, in consequence, angular above, concave
behind, convex in front, and rounded and broad below. The tricuspid
orifice thus maintains the crescentic form of the cavity of the right
ventricle when a cross section is made through its walls.

In five of the cases, the upper and left boundary of the tricuspid
valve was situated about the third of an inch to the left, and its
lower and right boundary about a third of an inch to the right of a
line drawn down the middle of the sternum. In two instances the
lower and right boundary of the tricuspid valve extended to the
right of the right edge of the sternum.

The right transverse or auriculo-ventricular furrow which corre-
sponds with the right edge of the right ventricle, as I have already
remarked, is situated about half an inch to the right of the right edge
of the tricuspid valve, and when therefore we know the position of the
furrow, we can infer the position of the right edge of the valve. As we
have already seen (page 34) the transverse furrow was situated to the
right of the right edge of the sternum in nearly three-fourths of the
cases (36 in 61), at that edge in three of them, and to the left of that
edge, behind the right half of the sternum, in one fourth of them (12
in 51) ; and it extended in one instance for an inch and a third to the
right of the right edge, and was situated in five instances behind the
middle line of the sternum. The transverse furrow occupied every
variety of position between these two extreme points. We may there-
fore infer that the right border of the tricuspid valve occupied every

POSITION AND FORM OF THE HEART. 59

range of position between a line three-quartera of an incli to the right
of the right edge of the lower portion of the sternum, and a line half
an inch to the left of its middle line ; the average situation of the
right border of the valve being behind the right edge of the sternum.

In like manner we can infer approximately the position of the
lower border of the tricuspid valve if we know the position of the
lower boundary of the right ventricle. We have already seen that
the lower boundary of the right ventricle varied in situation from
an inch and a half below, to an inch and a half (14 inch) above, the
lower end of the sternum. The lower border of the tricuspid valve
is from half an inch to nearly an inch above the level of the lower
boundary of the right ventricle, and we may therefore infer that the
lower border of the valve varies in position from a point nearly two
inches above, to a point three-quarters of an inch below the lower
end of the sternum.

The top of the tricuspid orifice and valve was situated on a level
with the third cartilage in three cases, with the third space in one, and
with the fourth cartilage in two ; its lower edge being in those cases
on a level respectively with the fourth cartilage, the fourth space,
and the fifth cartilage. In each of those cases the upper edge of the
tricuspid orifice and valve was lower, and its lower edge was much
lower than the corresponding edges of the mitral orifice and valve.

The tendinous cords and papillary muscles of the tricuspid valve, as
they radiated to the left, slightly upwards, downwards and outwards,
retained, as a rule, their situation behind the space or cartilage that
was on a level with their starting-point from the valve. Thus, the
inferior cords and muscles maintained their relative position through-
out, behind the fourth space or fifth cartilage, which was on a level with
the lower edge of the tricuspid valve, while the anterior group of cords
and the anterior papillary muscles lay behind the fourth cartilage or
the fourth space. The upper group of cords retained its relation to
the third cartilage or space, or the fourth cartilage, on a level with
which the upper edge of the valve was situated, but the superior
papillary muscle radiated upwards to a somewhat higher relative posi-
tion than that from which it started, so that, as, for instance, in two
cases, the top of the valve being on a level with the third or fourth
cartilage, the superior papillary muscle was behind, respectively, the
second or third space.

In the remaining instance, that in which the heart was placed to
an unusual extent to the right, the flaps of the valve were situated
behind and to the right of the right portion of the sternum, the valve
extending from the level of the upper edge of the fourth cartilage
to that of the lower edge of the fifth. The tendinous cords, and the
papillary muscles took an oblique direction downwards, and they
were seated almost entirely behind the right half of the sternum.

The position of the tricuspid valve corresponds with the position
of the right ventricle, the valve occupying about the lower two-thirds
of the cavity.

60 A SYSTEM OF MEDICINE. '

The relation of the Lungs to the Heart.

The extent to which the lungs covered the heart varied much in
different examples. In two instances the heart was almost concealed
by the lungs, the edges of which were separated over the lower
portion of the right ventricle by a mere chink, which widened out to
three-quarters of an inch at the inferior border of the heart. In other
instances the lungs had receded from before the heart to such an
extent that almost the whole organ and the great vessels were exposed
to view, though in no instance were they entirely uncovered.

The space where the heart comes to the surface, which is bounded
above and at the sides by the lungs, and below by the liver and
stomach, was sometimes triangular in shape (in 10 of 60 cases), but
was usually four-sided (50 in 60).

The superficial "cardiac space" was triangular in shape in the
two instances just noticed in which that space was very small, the
width at the lower boundary of the heart being three-quarters of an
inch ; and in an instance of an opposite kind in which the base of the
triangle, which always corresponded with the lower boundary of the
heart, was four and a half inches wide. In this instance the lower
boundary or base of the superficial space of the heart was wider than
in any other. The base of the triangular superficial cardiac space
presented every intermediate gradation of breadth between the ex-
treme instances just noticed. This triangular shape is favourable
to the covering of every part of the heart with lung except the
right ventricle, for, while the anterior wall of the right ventricle was
laid bare to a greater or less extent in these cases, as it was in every
case under observation, in but one of them was the apex of the
heart exposed, while in only two of them the right auricle, the aorta
and pulmonary artery were also somewhat uncovered.

The superficial cardiac space was in all these cases actually triangu-
lar in shape, the lower limit or base of the triangle being the lower
border of the heart. If, however, the lower boundary of the heart had
occupied a lower position in relation to the adjoining margins and the
lower boundaries of the lungs, then that space would have been four-
sided in shape in the majority of these instances (6 in 10); for in them
the inner border of the left lung, after it had left the heart., curved in
a downward direction. If, therefore, the heart had not shrunk upwards
in these instances, the superficial cardiac space would, like the other
cases, have been four-sided in shape.

When, as is usually the case, the superficial space of the heart
is bounded by four sides,1 the heart, which moulds for itself a place
between and within the lungs, conies forwards to the surface at
that part where the organ is massive and its walls are powerful. The

1 I have grouped the remainder of the cases, amounting to fifty, under the common
heading of those in which the superficial space of the heart was bounded by four sides,
but in seven of those cases the space was almost triangular in shape, and in a few
other instances irregularity in outline modified the typical four-sided form of the space.

POSITION AND FORM OF THE HEART. 61

inner edge of the right lung descends in a straight line behind the
sternum, but the edge of the left lung leaves the right lung, and
deviates to the left at a variable point. This deviating edge of the
upper lobe of the left lung, which is suspended like a curtain above
the upper margin of the superficial space of the heart, describes a
double curve, first convex, where it leaves the right lung, and then
concave, where it begins to dip downwards to form the outer edge
of the space. It then, as I have already observed, again tends to curve
inwards, and to form the tongue of lung that enfolds the apex of
the heart. The breadth of the cardiac space, measured along its base
at the lower boundary of the heart, varied from an inch and a half to
four inches and a third (4*3 inch). The breadth of the lower boun-
dary of the superficial cardiac space varied in three-fourths of the
cases (37 in 50) from two to four inches ; it was less than two inches
in one-fifth of them (9 in 50), two-thirds of these being youthful ;
and it was above four inches in four of them.

The superficial cardiac space wras, as a rule, narrower at its upper
than at its lower boundary (in 35 of 50 cases) ; but sometimes this
was reversed, the space being narrower below than above (in 10 of 50
cases). In a few instances (5) the space was of equal breadth above
and below.

The lower boundary of the superficial cardiac space measured less
than three inches in all but one of those instances in which it was
narrower than the upper boundary of that space.

The inner borders of the right and left lungs were in contact with
each other behind the upper portion of the sternum so as to cover
the great vessels in three-fifths of the cases under examination (in
35 of 59). In the remaining two-fifths of the cases (24 in 69) a space
varying in width from the eightli of an inch to an inch and a half wras
interposed bctwreen the inner borders of the right and left lungs at the
upper part of the front of the chest. In one-third of these instances (7
in 24) the space between the edges of the lungs was less than the third
of an inch, so that, practically, these cases may be added to those in
which the edges of the lung were in contact, which brings up their pro-
portion to three-fourths of the total number of cases observed (42 in 59).
The point of separation and divergence of the left and right lungs
in these cases, including those in which the lungs were nearly in con-
tact, varied from the level of the first intercostal space to that of the
fifth cartilage. In three-fourths of the cases this point of separation
varied in position from the level of the second space to that of the
fourth cartilage.

In the seventeen cases in which the lungs were separated from each
other over the great vessels to an extent ranging from almost half an
inch to an inch and a half, the position of the point of divergence
of the right and left lungs varied from the level of the first cartilages
to that of the third, the level of the second cartilages and second spaces
being the more usual situation of the point of divergence in this group
of cases.

02 A SYSTEM OF MEDICINE.

There was much variation in the relative size of the right and left
lungs. The two lungs were about of equal size in more than one-
fourth of the cases (17 in 59), the right lung was larger than the left
in nearly one-half of them (27 in 59), and the left lung was larger than
the right in one-fourth of them (15 in 59).

Although the right lung was so often larger than the left, yet the
base of the left lung was lower at the side than that of the right lung
three times more often than the reverse, the bases of the two lungs
being on the same level in one- fourth of the cases (14 in 57).

When the right and left lungs met together behind the upper half
of the sternum to form a covering over the great vessels, the margin
of the right lung extended to the left of a line drawn down the middle
of the bone more often than that of the left lung extended to the right
of that line in the proportion of 35 to 15, while in nine instances
the edges of the two lungs lay in contact behind the middle line of
the sternum.

Below the point of separation of the two lungs, while the left lung
deviated, as we have seen, extensively to the left, the right lung
usually (in 42 of 60 cases) deviated at first very slightly and then
more definitely to the right, so that at its lower anterior border the
left inner margin of the right lung at the level of the lower boundary
of the heart was usually situated to the right of the middle line of
the sternum, the extent to which it did so varying from the tenth of
an inch to an inch and three-quarters. In less than one-third of the
cases (18 in 60) the left margin of the right lung, at or a little above,
the level of the lower boundary of the heart, extended to the left of
the middle line of the sternum.

When the superficial cardiac space was small, measuring less than
two inches across, the inner margin of the right lung extended to the
left of the centre of the chest in three-fifths of the cases (10 in 18).
When, however, the space was of medium size (2 to 3 inches wide),
the right lung passed to the left of the middle line in less than
one-fifth of the cases (4 in 21) ; and when the space was large (above

3 inches wide), the right lung extended thus to the left of the middle
line over the superficial cardiac space in only one-tenth of the cases
(2 in 21).

The upper boundary of the superficial cardiac space, whidi is an
important landmark to the clinical worker, is formed by the lower
anterior border of the upper lobe of the left lung after it deviates
from its point of separation from the right lung. 1 have already
described the direction and nature of this curve.

The margin of lung, which thus forms the upper boundary of the
superficial cardiac space, lay immediately behind one or other of the
left costal cartilages or their spaces, and it generally took the down-
ward direction of the cartilage behind which it lay, or was somewhat
more inclined. It generally lay behind one cartilage or space, from
the point at which it left the sternum to the point where it curved
downwards to form the left border of the superficial cardiac space.

POSITION AND FORM OF THE HEART. 63

It sometimes, however, took a more oblique direction downwards, and
crossed from behind one cartilage to behind the next space below,
and then, after crossing that space, it spent itself behind the next
cartilage below. The upper boundary of the cardiac space varied in
position from the level of the second left costal cartilage to that of
the fifth, but it was most frequently present behind the third or
fourth cartilage or the fourth space, being thus situated in three-fifths
of the cases (35 in 60).

In three of the cases the surface of the heart exposed below
the lower edge of the left lung was a mere belt composed of the
lower boundary of the right ventricle, this belt being from two inches
to two inches and a half in diameter from side to side, and from
a fifth to a little over one-half of an inch from above downwards.
The heart had been lifted upwards behind the lungs by great disten-
sion of the stomach and intestines in these three cases, and the
front of the cage of the chest had been also lifted upwards by the
same agency, while the lungs had expanded downwards under the
influeuce of the forward movement of the ribs.

Extent to which the Surface of the Heart is Exposed.

In every instance more or less of the right ventricle was uncovered.
A very small portion of the right ventricle was exposed in the two
instances in which there was a narrow longitudinal chink over the
front of the heart, and in the three in which the exposed surface of
the organ was a very narrow belt extending from right to left along
the lower border of the ventricle.

In nearly one-half of the cases (25 in 60) the right ventricle was
the only part of the heart that was exposed at the superficial cardiac
space. In five other cases the apex of the heart was the only addi-
tional part brought into view by the lateral withdrawal of the lung.
In almost one-half of the cases (25 in 60) the apex of the heart was
in contact with the walls of the chest, the pericardium intervening ;
and in one-third of them (19 in 60) the higher portion of the left
ventricle was also exposed to a greater or less extent In only one
instance was the whole of the narrow anterior portion of the left ven-
tricle laid bare. In the rest of the cases, more or less of the upper
portion of the left ventricle was covered by the edge of the left lung
where it overlaps the front of the heart.

The right auricle was uncovered to a greater or less extent in one-
fifth of the cases (11 in 59,) and in all but three of these its auricular
appendix was also apparent. In one instance the whole of the auricle
was exposed. The tip of the auricle was just visible in eight addi-
tional cases.

The whole of the ascending portion of the aorta was exposed to
view in nine instances, and it was visible on its right side in three,
on its left side in four, and at its middle in one. Thus the aorta was
more or less exposed in nearly one-fourth of the cases.

64 A SYSTEM OF MEDICINE.

The whole of the pulmonary artery was laid bare in only one
instance, but in eight other cases the right side of the vessel, and in
five others the left side of the vessel, was respectively exposed. The
arterial cone of the right ventricle was completely covered by the lungs
in one-third of the cases (20 in 59). In certain cases (10) a very small
portion of the cone was uncovered just below the point of separation
of the right and left lungs. These cases may practically be added
to those in which the cone was completely concealed, so that, with
this reservation, it may be said that the cone was covered with lung
in one-half of the cases (31 in 59). In several instances, only one-
fourth of the arterial cone was exposed, while in one instance the
whole of it was uncovered. Between these extreme cases there was
every variety in the extent to which the cone was brought into view.

FRONT VIEW; DURING LIFE.

We have just seen that after death the healthy heart and great
vessels, and the different parts composing them, present great variety
in position ; and that although perhaps in no two instances do those
parts occupy precisely the same relative situation, yet in a consider-
able proportion of the cases, and within certain limits, they present a
standard or average position.

During life in like manner the healthy heart and great vessels vary
much in relative situation, yet those parts, within certain orderly
limits, regulated and modified by the various demands of life, main-
tain a standard or average position.

It is evident that during life, when the heart is at work and in
motion, sending blood to and receiving blood from the lungs and every
part of the frame, the position of the heart and great vessels is dif-
ferent from what it is when observed in the dead body. A knowledge
of the position of the heart and the great vessels during life, when in
active motion, is essential to the clinical worker, and not merely that
of the anatomy of the dead organ.

I shall here, therefore, endeavour to describe the average position of
the heart and great vessels in the living frame, from the study of the
situation of those parts after death and during life, and of the move-
ments of the heart when in action, and when influenced by respira-
tion.

When the exertions of the body are prolonged and powerful, the
heart acts with corresponding power ; it receives and distributes more
blood than when the body is at rest, and its size, and that of its
great vessels, become enlarged. When, however, the body is in repose
the heart's action is weakened ; it receives and sends out less blood,

POSITION AND FORM OF THE HEART. 65

and its size and that of its great vessels are diminished. The used
power and the size of the heart, and the supply of blood to and from
the organ, strictly balance the actual demands of the body, whether
in action or at rest

Under the like circumstances the lungs, answering to the demands
on respiration, enlarge or lessen in size, and the volume of the cage
of the chest is correspondingly larger or smaller, while the pitch of
the diaphragm is lower or higher, so as directly to depress or elevate
the heart. As the result, therefore, of these changes, thus induced by
respiration, the heart, when it enlarges during exertion, is low and
deep, and when it lessens during rest, is high and superficial.

In a corresponding manner, and for the same reasons, the heart is
large, low, and deep in strong labouring men, while it is small, high,
and shallow in weak youths of sedentary habits. In women and in
children the heart is proportionally smaller and higher than in adult
men ; and in the scale of life, from infancy to old age, the heart tends
proportionally to increase in size, and to become lower and deeper in
position.

In order that we may have before us the movements of the heart
and great vessels during the varied exercises of life, I shall, before
describing the position of those parts in the living body, give a brief
account of the action of the heart, of the currents of blood through
the cavities of the heart, and of the movements of the heart caused
by respiration.

Movements of the Heart. (See Figs. 16, 17, 22, 23.)

I have observed, with the valuable assistance of Dr. Broadbent, the
movements of the heart in the dog and the donkey, when under the
influence of chloroform; and from those observations, and the
careful examination of the human heart in many subjects, I have con-
structed figures 16, 17, 22 and 23, representing the heart in man in
the opposite conditions of complete ventricular contraction and dila-
tation. In figures 16 and 17, the direction and extent of the move-
ments of the walls during the ventricular systole are represented by
arrows.

The appearance of the heart in motion is very striking. The ven-
tricles during their systole, contract from all sides upon their own
centre and become wrinkled, and the arteries and veins on their
surface are full and tortuous, while the auricles become purple,
plump, and glistening. During the diastole, the aspect is reversed.
The ventricles enlarge and become smooth, their superficial vessels
almost disappearing, while the auricles shrink, and become pale and
wrinkled.

The Systole of the Ventricles.— During the systole, the ventricles,
when looked at in front, contract from all sides towards a given
centre, which is situated on the right ventricle a little to the right
of the septum, about midway between the origin of the pulmonary

VOT,. TV. F

6B A SYSTEM OF MEDICINE.

artery and the lower boundary of the ventricle, where it rests upon the
diaphragm. The contraction of the right ventricle, owing to its
position at the front of the heart, and its consequent complete ex-
posure, is marked and vigorous. The whole right margin of the
ventricle, at its juncture to the auricle, moves extensively from right
to left ; while its left margin, at the longitudinal furrow or septum
between the ventricles, moves to a comparatively slight degree from
left to right At the same time the top of the ventricle, at the
origin of the pulmonary artery, descends, while its lower border,
where it rests on the diaphragm, ascends.

Fig. 16.— Front view. Fio. 17.— Side view.

The amtmwnu lines indicate the position of the outlines of the various pert* of the
heart during the systole of the ventricle* ; the interrupted lines indicate the position
of the same part* during the diattole of the ventricles ; the arrows point out the
direction and extent of the movements or the walls of the heart during the tytoU.
Via. 1A ahnwa tlis transversa, vertical, and nhlinna mnuniwm«n»i in tnillimatM*

The point of rest towards which these various movements converge
corresponds closely with the attachment of theanterior papillary muscle.

The right auricle and superior vena cava are distended, and the
pulmonary artery is enlarged and lengthened simultaneously with the
contraction of the ventricle. The auricle, which just before was
wrinkled, becomes full ; and its auricular portion and left edge move
rapidly inwards, and to the left, so as to replace the ventricle. The
movement of the auricular portion is remarkable. It suddenly en-
larges and becomes purple, and its tip moves from the right to the
left edge of the sternum, at the level of the third costal cartilage.

POSITION AND FORM OF THE HEART. 67

The vigorous contraction of the left ventricle is only visible at its
apex and along its left border, since the rest of the cavity is hidden
by the right ventricle. The apex has a revolving movement, upwards,
forwards, and to the right The left border ' of the ventricle, like the
apex, moves forwards and to the right ; but while the portion of the
ventricle near the apex ascends, the portion near the base descends.
The appendix of the left auricle, which during the diastole of the ven-
tricle is scarcely visible, descends during the systole, and moves rapidly
forwards and downwards, so as to replace the retreating ventricles.
and to fill up the angle between them and the pulmonary artery.

When we remove the left ribs and look at the heart from the left side
□ as to obtain a profile view, the animal lying upon the back, we see
; the whole left ventricle moves forwards during the systole, the
«rior wall advancing much more than the anterior; and that the
a of the ventricle descends, while the apex ascends, so that apex
1 base approximate. It is difficult to fix upon the precise zone of
i of the ventricular walls towards which the apex ascends and the
t descends, but it is somewhere about the middle of the ventricle,
•, perhaps, to the apex than the base. This region of stable
riuui corresponds to a similar point of rest in the papillary
s. Owing to this arrangement, the ventricles and their valves
t themselves to each other during the ventricular contraction.
1 auricle, like the right, enlarges during the systole, and as
of the ventricle then descends and advances, the ventricular
nient of the swollen auricle descends likewise, apparently, as it
■, pushing the base of the ventricle before it
"en the left ventricle propels its contents into the aorta, the arch
j aorta is distended and lengthened, and its root, like that of
_e pulmonary artery, descends. The arch of the aorta enlarges both
i length and breadth, and becomes tense and rigid. Its lateral en-
largement is small, but its elongation is considerable ; and its orifice,
like , of the pulmonary artery, descends during -the systole.

Dsring the systole, the auricles aud great vessels enlarge, and
descend into the place just left by the retreating .ventricles ; there is,
therefore, more blood at the base of the heart at thelend of the systole
than at the end of the diastole. Since, however, during the systole,
both ventricles contract, the increase of the blood at the base probably
balances its diminution towards the apex. During the pause which
follows the dilatation of the ventricles, the blood continues to flow
into the auricle so that the amount of blood in the heart and great
vessels is greater just before the ventricular systole than at any
other period. *

Movements of the Papillary Muscles. — That I might observe the
action of the papillary muscles, I removed the anterior wall of the
right veutricle when the heart was beating in situ; and I found that
the tip of the anterior papillary muscle of the right ventricle con-
tracted towards the septum during the systole.
I then removed the septum, so as to expose the two papillary muscles

v 2

68 A SYSTEM OF MEDICINE.

of the left ventricle, and I noticed that both the muscles, which
during the diastole were wide apart, approximated and came close
together during the systole. At the same time the muscles shortened
towards their own centre, so that their tips and their tendinous cords
descended to the left towards the apex of the ventricle, while their
roots of attachment near the apex ascended to the right towards the
base of the ventricle. The fixed point towards which the two ends
approximated corresponded apparently to the zone of rest, or stable
equilibrium, in the walls of the ventricle, towards which the base
and the apex of the ventricle approximate during the systole.

Action of the Mitral and Tricuspid Valves. — In order that I might
see the movements of the mitral and tricuspid valves, I cut out the
heart when beating vigorously, and immersed it in water. The
ventricles contracted with force, and expelled the water from the
great arteries during each systole. The jet from the aorta was six
inches in length. The segments of the mitral and tricuspid valves
were seen to come together at their notched and bead-like margins,
so as to close the valves during the systole, and prevent the efflux
of a drop of liquid.

At the beginning of each diastole the margins of the valves
separated quickly from each other, so as to admit the flow of water
freely into the cavity.

Direction of the Currents of Blood in the Cavities of the

Heart. (See Figs. 18, 19.)

In the left ventricle, the aperture of entrance, the mitral orifice, is
contiguous to the aperture of exit, the aortic orifice, the two orifices
being separated by a membranous septum consisting of the anterior
flap of the mitral valve. In the right ventricle, the aperture of
entrance, the tricuspid orifice is at a distance from the aperture
of exit at the pulmonary artery, the two orifices being sepa-
rated by the muscular channel of the conns arteriosus. In the left
ventricle the current of blood inwards, which descends during the
diastole behind the anterior segment of the mitral valve, is parallel in
direction to the current of blood outwards, which ascends during the
systole in front of that segment. (Fig. 18.) In the right ventricle
the current of blood inwards is at right-angles to the current of blood
outwards, since the blood enters the cavity from right to left, and
leaves it from below upwards (Fig. 19). During the systole the stream
of blood in the left ventricle takes a spiral direction towards the aortic
orifice, in accordance with the diiection of the aorta itself. The stream
of blood in the right ventricle, as it ascends, mounts over the bulging
septum, being restrained by the concave anterior wall of the ventricle.
This upward stream, which narrows as it ascends, thus takes the
curved direction upwards, backwards, and inwards of the conns arte-
riosus and the pulmonary artery. In the left ventricle, the anterior
segment of the mitral valve and the right and left papillary muscles,

POSITION AND FORM OF THE HEART.

form a hollow channel for the stream of blood, which, as it ascends to
the aorta, presses upon the under-surface of the valve. In the right
ventricle the stream of blood, as it ascends, sweeps onwards at right
angles to the under-surface of the tricuspid valve, and rushes between
and across the papillary muscles, and through the tendinous cordage
that connects the muscles to the flaps of the valve.

Fig. 18. — Showing the direction of the
currents of the blood in the left side
of the heart.

Fio. 19. — Showing the direction of the
currents of the blood in the right side
of the heart.

The Movements of the Heabt caused by Respiration.

(See Figs. 20, 21.)

During inspiration the diaphragm in its descent draws downwards
the fibrous sac and floor of the pericardium, and the whole of its
contents. The heart rests upon the central tendon of the diaphragm
which forms the floor of the pericardium, and it therefore necessarily
rises and falls with the rise and fall of the diaphragm. The descent
of the diaphragm is accompanied by the advance of the anterior
wall of the chest, which produces the corresponding expansion of
the lungs anteriorly. The central tendon of the diaphragm forming
the floor of the pericardium presents an inclined plaiie, upon which
the heart glides forwards and downwards during inspiration, under
the combined influence of the descent of the diaphragm and the
forward movement of the ribs and sternum. Whatever be the cause
of the altered level of the diaphragm, whether it contracts and
descends, as in inspiration, or is pushed downwards by fluid or

70 A SYSTEM OF MEDICINE.

tumours in the chest — whether it is raised during expiration, or
pushed upwards by distension- of the stomach and intestines, by
fluid in the abdomen, by abdominal tumours, or by abscess or other
affections of the liver ; whatever, in short, be the cause producing
the ascent or descent of the diaphragm, a corresponding ascent or
descent of the heart must ensue. The only exception is .the displacement
downwards of the central tendon of the diaphragm by means of effusion
into the pericardial sac, when the fluid interposes itself between the

heart and the diaphragm, with the effect of pushing the diaphragm
downwards and the heart upwards. An important part is played by
the pericardium in the influence of respiration on the position of the
heart The central tendon of the diaphragm forms the base of the peri-
cardium, upon which the heart rests as upon a floor. The aponeurotic
structure of the pericardium, which takes its origin from the central
tendon, ascends so as to form a strong fibrous pouch which envelopes
the whole heart, and gives off a fibrous investment to each of the great

POSITION AND FORM OV THE HBART

vessels as they enter or leave the pericardial sac. Through the
medium of this aponeurotic structure, the diaphragm, during its de-
scent, acts so as to draw downwards the great vessels simultaneously
with the heart

The respiratory movements of the heart are vertical. The organ
and all its parts and great vessels move downwards during inspiration,
and move upwards during expiration. While, therefore, the vertical
relations of the heart and great vessels to the parietes of the chest

Fig. 21.— Showing the u

d relation to the w«l'i of

Kale. —The lower bonndiry of the heart ought to have been somewhat lower in this figure.

are altered, the lateral relations of the various parts of the heart and
great vessels to each other are unaltered, and their relative positions
to the surrounding organs are not materially changed.

While the diaphragm descends during inspiration, carrying with it
the heart, the front and sides of the cage of the chest, formed by
the ribs and sternum, ascend. The change in the position of the heart
in relation to the ribs and sternum is, therefore, doubled in extent by the

72 A SYSTEM OF MEDICINE.

twofold operation of the descent of the diaphragm and the heart
simultaneously with the ascent of the cage of the chest.

Inspiration, besides causing the descent of the heart, produces also
a lengthening and general enlargement of the organ and its great
vessels. The lengthening of the heart and its vessels tells with
decreasing effect from below upwards. The descent of the great
vessels in the neck is much, but not completely, restrained by the
attachments of those vessels. The innominate, the left carotid and the
subclavian arteries, and the ascending aorta are elongated and straight-
ened to a considerable extent, and as less blood is sent into those
vessels during inspiration than during expiration, they are lessened
in width at the same time that they are increased in length. The
enlargement of the cavities of the heart is limited to the right side.
The right auricle receives in increased quantity the blood which has
been stored up in the hepatic and portal vessels and the great veins
during expiration. The space in the vessels of the expanded lungs for
the reception of blood is increased ; the blood is sent with greater ease
through the pulmonary artery from the right ventricle, in consequence
of the enlargement of the pulmonary capillaries, and is at the same
time sent in greater quantity from that cavity, because its supply of
blood, derived from the auricle, is materially increased during inspira-
tion. The venae cav*e, the right auricle, the right ventricle, and the
pulmonary artery are therefore enlarged both in length and width.
The supply of blood to and from the right cavities of the heart,
which is thus increased during inspiration, is then probably
associated with a corresponding diminution in the supply of blood to
and from the left cavities of the heart The blood is retained in the
pulmonary vessels in augmented quantity during inspiration. We may
infer that less blood is sent then into the left auricle, and we know
that less blood is sent then into the system through the arteries from
the left ventricle, than during expiration.

The result of the various co-operating and contending forces which
I have just considered are exhibited with, I believe, an approach to
accuracy in Figs. 20 and 21, representing the position of the heart and
great vessels in relation to the cage of the chest and the lungs at the
end of a forced expiration, and at the end of a deep inspiration.

The greatest change in the relative position of the heart during inspi-
ration takes place at its lower boundary, the descent of which is equal
to that of the central tendon of the diaphragm, or at least one inch.
The upward movement at the same time of the lower end of the
sternum and the adjoining cartilages is about one inch also. The
resulting change in the relative position of the lower boundary of the
heart and the external walls ought to be, and I believe is, though I have
not ascertained it by exact demonstration, about two inches. The
ascertained change in the relative position of those parts is such, that
the lower boundary of the right ventricle, at the end of expiration, is
situated behind the lower end of the sternum, and at the end of in-
spiration, behind the lower end of the ensiform cartilage. The result

POSITION AND FORM OF THE HEART. ?3

during life, in a robust man, is that at the end of expiration, the im-
pulse of the right ventricle may be perceptible to the left of the lower
end of the sternum ; while at the end of inspiration it is to be seen and
felt beating with considerable force over, below, and to the left of the
ensiform cartilage, or in other words, at the epigastrium. The heart
has in fact descended into the space previously occupied by the liver
and stomach, and instead of being protected at the part sppken of by
a bony framework, is at the end of a deep inspiration only covered
to each side of the ensiform cartilage by the abdominal muscles. The
apex of the left ventricle descends to the same extent during a deep
inspiration, or from the fifth rib to the seventh costal cartilage. The
impulse at the apex, which at the end of expiration is often felt
beating with force in the fourth intercostal space, is at the end of a deep
inspiration quite imperceptible. I need not go through the whole of
the details of the altered relative positions of the heart and great
vessels in relation to the ribs and sternum during expiration, and at
the end of a deep inspiration. They speak for themselves, and are
exhibited in the accompanying figures. It will suffice, if I describe the
altered bearings of the principal landmarks. A transverse boundary-
line drawn across the top of the right auricle and right ventricle cor-
responds with the attachment of the great vessels to the heart. This
transverse line, which marks the position of the aorta above the
right auricle, and the commencement of the pulmonary artery,
extends at the end of expiration across the second intercostal
spaces, and the intervening portion of the sternum a little below
the manubrium ; while at the end of inspiration it crosses the lower
boundary of the third intercostal spaces and the intermediate portion
of the sternum. The pulmonary artery descends from the second to
the third intercostal space, and the visible commencement of the
aorta makes a corresponding descent behind the sternum. The top of
the arch of the aorta which at the beginning of a deep inspiration is
a little below the top of the manubrium, is, at the end of it, at or a
little above the lower end of that bone.

The vertical and forward respiratory movements of the heart explain
the difference in the position of the heart in relation to the walls of
the chest in weak persons with flat chests on the one hand, and in
those who are full-chested and robust on the other. The relations of
the heart and great vessels to the cage of the chest follow the type of
expiration in the feeble, and the type of inspiration in the strong.

Front View of the Heart and Great Vessels in a Healthy
Man with a well-formed Chest. (See Figs. 22, 23.)

The heart and great vessels occupy the central region of the chest.
The lower boundary of the right ventricle is situated behind the
ensiform cartilage, and is about half an inch or more below the lower

74 A SYSTEM OF MEDICINE.

end of the osseous sternum ; 1 and the top of the arch of the aorta,
at the origin of the innominate and left carotid arteries, is about half
an inch or more below the upper end of the sternum.

Note.— The fifth cartilages were unusual

The breadth of the heart is about one-half of the breadth of the
chest. The heart, at its extreme limits, extends for a little more than

i All the works on the diagnosis of the discuses of the heart with which I im

POSITION AND FORM OF THE SBART. 75

one-third of its breadth into the right aide of the chest, and for &
little less than two-thirds oi' its breadth into theleft side of the chest,
or in that proportion to the right and left of a vertical line drawn
down the middle of the sternum.

Fig. 23.— Showing the position and relative size of the var
of the great vessels during the diastole, of the ventricles a

During the systole of the ventricles the proportion of the heart in
the left side of the chest lessens, owing to the inward contraction of

dead body from which it was taken. It gives, however, on that very account, an inac-
curate view of the relative position of the heart io the living man.

I have just stated that the lower boundary of the heart is situated behind the enai-
form cartilage, about half au inch or more below the lower end of the osseous sternum,
and have done so on the following grounds : —

(1.) At the time of death tbe heart is raised by the elevation of the diaphragm during
the final expiration. After death the heart contracts upwards towards its higher points

76 A SYSTEM OF MEDICINE.

the left border of the left ventricle, while that in the right side of the
chest increases, owing to the outward expansion of the right border of
the right auricle.

The boundary line across the sternum, between the upper border
of the heart and the lower limit of the great vessels, is on a level
with the third costal cartilages.

The lower boundary of the heart extends, with a slight inclination
downwards, from about half an inch below the lower end of the
sternum to the fifth left space, just above or on a level with the upper
edge of the sixth left cartilage. The lower boundary of the heart
ascends during the systole of the ventricle, and descends during its
diastole; it descends also during ordinary inspiration, and ascends
during ordinary expiration for about the third of an inch. A deep
inspiration may bring down the lower border of the heart to the lower
end of the ensiform cartilage, and a forced expiration may raise it to
or above the level of the lower end of the sternum.

The left boundary of the heart at its apex is situated to the left of
the junction of the fifth rib to its costal cartilage, and behind or to
the left of a vertical line drawn downwards from the left nipple.1 The
right boundary of 'the heart extends about an inch to the right of the
right edge of the sternum.

The Right Side of tlie Heart. — The right cavities occupy the whole
front of the heart with the exception of its left portion, where the

of attachment, so as to leave an average space of half an inch between the lower boundary
of the heart and the lower boundary of the front of the pericardium ; that space being
the exact measure of the upward shrinking of the heart afler death. The lower boundary
of the heart was situated behind the end of the osseous sternum in one-fifth, and below
that point in two-fifths of my cases, while it was above that point in two-fifths of them.
The lower boundary of the front of the pericardium, which marks the position of the
lower boundary of the heart itself at the time of death, was behind the lower end of the
sternum in one-fifth, and below that point (being situated behind the upper portion of the
ensiform cartilage) in two-thirds of my cases, while it was above that point in only one-
eighth of them.

(2). We have already seen (pp. 16, 17) that there is a general correspondence between the
relation of the lower boundary of the right ventricle to the end of the osseous sternum,
and the relation of the lower border of the apex of the heart to the inferior edge of the
fifth costal cartilage and rib. The inferior edge of the junction of the fifth cartilage and
rib was on a lower lovel than the end of the sternum by from a quarter of an inch to
an inch and a quarter in 60 out of 71 cases, was on the same level in five, and was
above that level in six instances. It is evident that, with few exceptions, the apex-beat
could not be felt in the fifth space if the lower boundary of the heart were situated above
the end of the sternum.

(3). The lower edge of the anterior portion of the right lung at its left border corre-
sponds, as a rule, with the lower boundary of the heart at the same situation. In six
cases the lower edge of that portion of the right lung was behind or on a level with the
lower end of the sternum ; in three it was above that point to the extent of half an inch ;
and in twenty it was below that point to an extent varying from a quarter of an inch to
an inch and a half, or, in one exceptional case, two inches. We may therefore infer
that the lower boundary of the heart was situated in two-thirds of these cases behind
the ensiform cartilage, in one-fifth of them, behind the lower end of the osseous
sternum, and in only one-tenth of them above that end of the bone.

1 I have made comparatively few observations as to the position of the left nipple in
relation to the junction of the adjoining ribs to their cartilages and the left boundary of
the heart at its apex.

POSITION AND FORM OF THE HEART. 77

left ventricle comes into view from behind the right ventricle to the
extent of an inch in breadth. The transverse or auriculo- ventricular
furrow forms the external apparent separation between the right au-
ricle and right ventricle. The auriculo-ventricular furrow sweeps
backwards and forwards to so great an extent, to the left during the
systole, and to the right during the diastole, that it presents no fixed
position during life, but ranges to and fro between certain limits.
The upper end of the furrow may be situated at the left edge or at
the middle line of the sternum, on a level with the third cartilage ;
and its lower end may be placed a little below and to the right of
the lower end of the sternum, being behind the sternal end of the
seventh cartilage, but it may extend for fully half an inch to the
right of this position. The transverse furrow thus crosses behind the
lower half of the sternum obliquely from left to right, and from above
downwards. The upper third of the transverse furrow forms a true
line of separation between the auricular appendix and the arterial
cone of the right ventricle ; but the lower two-thirds of the furrow
lie about half an inch to the right of the tricuspid orifice and the
line of division between the right auricle and the right ventricle.
The right transverse or " auriculo-ventricular " furrow is not there-
fore at this part of its course a true line of separation between the
right auricle and ventricle, but is thrown half an inch to the right
of that line by the presence there of the right coronary vessels, and
the couch of fat in which they are embedded.

The Right Auricle — The right auricle is broad above, where it
widens out into the auricular appendix, especially during the systole,
and lies behind the middle of the sternum, reaching from its right
often to its left edge, on a level with the third cartilages ; and it is
narrow below, where it appears to come to a point at the lower end
of the transverse furrow, to the right of the lower end of the sternum.
The real or internal breadth of the right auricle is, as I have just
explained, greater than its apparent or external breadth along the
line of the transverse furrow. When, therefore, the lower portion
of that furrow is situated a little to the right of the sternum, the
lower portion of the tricuspid orifice is covered by the lower
end of the sternum, a little to the right of the middle .line of
that bone. The right boundaiy of the auricle extends behind the
. right costal cartilages for about an inch beyond the right edge of the
sternum.

The right auricle undergoes more change in form during the action
of the heart than any other portion of the organ. During the systole
of the ventricles the auricle retains its length, but it becomes twice
as wide, and its whole surface, instead of being pale and wrinkled, is
purple, plump, and glistening. The ventricular border moves ex-
tensively to the left, so as to pass from the right margin to the middle
line of the sternum, while its right border expands a little to the
right. There is a slight descent of the upper and lower borders of
the right auricle during the contraction of the ventricles. During

78 A SYSTEM OF MEDICINE.

the diastole of the ventricles these appearances and movements are
reversed.

The Bight Ventricle. — The right ventricle forms the solid muscular
front of the heart, and is flanked to the right by the right auricle,
and to the left by that small portion of the left ventricle that comes
into view in front of the heart, and forms its left border.

The right ventricle, when exposed to view in front of the heart,
presents a pyramidal shape. The base of the pyramid is formed by
the lower boundary of the ventricle, which rests on the central tendon
of the diaphragm, and extends, with a slight obliquity downwards
and from right to left, from the right auricle to the apex of the left
ventricle ; its upper border is crowned by the pulmonary artery,
which forms the apex of the pyramid; its left border is formed
by the longitudinal furrow, which divides the right from the left
ventricle; and its ostensible right border by the transverse furrow
which apparently separates the right auricle from the right ventricle,
the actual separation of those two cavities at the tricuspid orifice
being situated, as I have just stated, about half an inch to the left
of the transverse furrow.

The right ventricle, in its vertical diameter or length, extends from
the third left cartilage to the sixth, which are the cardiac cartilages. In
its transverse diameter, or breadth, the right ventricle extends from
the transverse furrow, at or to the right of the right edge of the ster-
num below, and somewhat to the right of the left edge of the sternum
above, to the anterior longitudinal furrow, which is situated behind
or a little to the right of the junction of the left costal cartilages to
their ribs from the third to the fifth.

The length or vertical measurement of the ventricle is greater
than its breadth or transverse measurement, in the proportion of
about four to three. The body of the ventricle forms about the
lower two-thirds of the cavity extending from the fourth left carti-
lage to the sixth, and the conus arteriosus forms about the upper
third of the cavity extending from the third left cartilage to the
fourth. The arterial cone of the right ventricle narrows from
below upwards until it ends in the pulmonary artery, and the
breadth of the cone a little below the origin of the pulmonary artery
in relation to that of the body of the right ventricle, is in the pro-
portion of nearly three to five, or in other words, the width of the cone
is nearly three-fifths of the width of the body of the right ventricle.
Owing to the arterial cone being so much narrower than the body
of the right ventricle, especially at its right border, the transverse
furrow extends further to the left at its upper than at its lower
border by more than an inch. In consequence of this great deviation
towards its upper end the transverse furrow presents a double curve,
which, looking to the right, is concave above, where the rounded auri-
cular appendix fits into the hollow profile of the arterial cone ; and
convex below, where it is situated half an inch to the right of the
tricuspid orifice.

POSITION AND FORM OF THE HEART. 79

The longitudinal furrow takes a downward direction, with a slight
inclination to the left, this inclination to the left increasing rapidly
towards the lower end where it approaches the apex. In consequence
of this, the longitudinal furrow also presents a double curve, which,
looking to the left is convex above, concave below. The deviation
to the left of the lower end of the longitudinal furrow is caused by
the deviation to the left of the cavity of the right ventricle as it
approaches the apex of the heart. The furrow between the ventricles
turns to the left at its inferior extremity, and, so to speak, cuts
through the apex of the heart. The apex of the heart is thus com-
posed of the apex of the left ventricle and the adjoining left end of
the lower border of the right ventricle.

During the contraction of the right ventricle its four sides approxi-
mate towards a point of rest or stable equilibrium, which is situated
on the anterior wall of the cavity, over or close to the attachment of
the anterior papillary muscle, a little to the left of the longitudinal
furrow, and slightly nearer to the lower than the upper border of the
ventricle. The movement of the transverse furrow to the left is ex-
tensive, and that of the longitudinal furrow to the right is slight ; the
downward movement of the upper border at the origin of the pul-
monary artery is considerable, and the upward movement of the lower
bolder of the ventricle is somewhat less. The right border of the
eonus arteriosus moves less to the left than the right border of the
ventricle at the tricuspid orifice. At the same time the surface
of the ventricle becomes wrinkled, and its coronary vessels start out
from the surface and become tortuous. During the dilatation of the
ventricle the reverse movements take place, its surface becomes
smooth, glistening, and rounded, and the vessels on its surface cease
to be prominent. (See Fig. 16, page 66.)

The Ltft Ventricle. — The left ventricle, where seen in front, comes
into view to the left of the right ventricle, and forms the convex left
border of the heart. The left ventricle forms here a comparatively
long, narrow slip, extending from the third left space down to the
fifth, and from the longitudinal furrow behind or to the right of the
junction of the corresponding ribs to their cartilages, to the left
border of the heart, which reaches up to or just beyond the left nipple.
This visible anterior portion of the left ventricle is of the greatest
width at and below its middle, behind the fourth space and the fifth
cartilage. Above and below this region the ventricle narrows, coming
to a point at the apex below, and above bearing to the right, where it
is finally hidden by the appendix of the left auricle. The breadth
of the anterior visible portion of the ventricle at its widest part is
about one-fifth of the breadth of the heart.

The apex of the heart occupies the fifth space, its lower border
being situated just above or behind the upper edge of the sixth car-
tilage and rib, and its left border being at or a little beyond a vertical
line drawn down from the nipple.

During the contraction of the left ventricle the right and left borders

80 A SYSTEM OF MEDICINE.

of its visible anterior portion both move a little to the right, its base
and upper portion descend, and its lower portion and apex ascend, both
portions moving forwards and to the right. (See Fig. 17, page 66.)

The Appendix of the Left Auricle is situated behind the third left
cartilage close to its junction with the third rib, and tills up the angle
or space between the upper end of the left and right ventricles, at the
top of the longitudinal furrow, and the left boundary of the origin
of the pulmonary artery.

The left auricular appendix is much more prominent and extensive
during the contraction of the ventricles, when its right and lower
borders move respectively considerably to the right and downwards,
and its left and upper borders move obliquely to the right and slightly
downwards, than it is during the dilatation of the ventricles, when
the auricular appendix shrinks inwards upon itself.

The Great Vessels, — The great vessels lie side by side, the ascending
aorta being in the centre, the pulmonary artery to the left, and the
superior vena cava to the right, behind the upper portion of the
sternum and the adjoining costal cartilages, at and above the level
of the third cartilage.

The Arch of the Aorta. — The root of the aorta, including the aortic
orifice, valve, and sinuses, is hidden in the centre of the heart. The
ascending aorta comes into view just above the appendix of the right
auricle, on a level with the third costal cartilages, and is covered by
the sternum, the right border of the artery being situated behind or a
little to the left of the right edge of the sternum ; and its left border,
which is partially covered by the right border of the pulmonary
artery, being about a quarter of an inch or less to the right of the left
edge of the sternum. As the arch of the aorta ascends, it bears to
the left, and at the point where it gives origin to the innominate
artery, it is exactly behind the middle line of the sternum. From this
point the transverse aorta ascends slightly until it gives origin to the
left carotid artery, whence it curves backwards and slightly down-
wards, with an inclination to the left, and gives off the left sub-
clavian artery, the last of its three great branches. The left carotid
arises just within a line drawn downwards from the sternal end of the
left clavicle, and the left subclavian just without that line. The part at
which the innominate and left carotid arteries take their origin is the
highest point of the arch, and is situated about three quarters of an
inch or rather less below the top of the manubrium, as far as the breadth
of the innominate artery to the left of a line drawn down the middle
of that bone, and in front of the lower portion of the body of the
third or the upper portion of that of the fourth dorsal vertebra,
which corresponds with the third dorsal spine, which is situated mid-
way between the spines of the scapulae. The transverse aorta, as it
curves backwards, to the left and downwards, rests first on the front
and left side of the trachea, and then upon the left side of the
oesophagus, and is situated between the manubrium, just to the left of
the middle line, from three-quarters of an inch or less below the top

POSITION AND FORM OF THE HEART. 81

of the bone down to its lower end in front, and the left side of the body
of the fourth and the upper portion of the fifth dorsal vertebra
behind. The relations of the transverse aorta to the manubrium in
front are very variable, but those to the dorsal vertebrae behind are
less so.

The deep left border of the descending portion of the arch may be
seen in a front view, and this border is situated in succession behind
the left and lower portion of the manubrium, near its junction to the
first rib, the first space and the sternal portion of the second left costal
cartilage, and the adjoining portion of the sternum. The relations of
this important portion of the arch will be considered when the side
and back views of the heart and great vessels are described.

The ascending aorta just above the right auricular appendix
descends slightly during the contraction of the ventricles ; but the top
of the arch, at the origin of the innominate and left carotid arteries,
is scarcely moved during the contraction of the heart. Inspiration
causes the descent of the ascending and transverse aorta and its
great branches. This descent is slight during ordinary breathing, but
is considerable on a deep inspiration. The inspiratory descent of the
arch of the aorta is much less than that of the root of the aorta
and heart.

Tlie Pulmonary Artery. — The origin of the pulmonary artery is
situated behind the upper portion of the third left cartilage, and its
top lies behind the second left cartilage. As the artery ascends to the
left of the ascending aorta, it occupies the second left space and
cartilage for four-fifths of its breadth, and is covered by the left
border of the sternum for the remaining fifth. The pulmonary
artery, at its origin, is situated just above and within the appendix
of the left auricle ; and, as it proceeds on its course, it makes for
the hollow of the arch of the aorta, through which it sends its right
branch. Its direction is therefore much more from before backwards
than from below upwards. The remaining course of the artery cannot
be seen in front, and will be considered when the side and back views
of the heart and great vessels are described.

During the contraction of the right ventricle the pulmonary artery
descends at its origin to a considerable extent, and the higher parts of
the artery also descend, but less and less from below upwards. At
the same time the whole artery enlarges and lengthens. The pulmonary
artery descends also during inspiration, but to a less extent than the
body of the right ventricle, and less at its upper part than at its origin.

The Superior Vena Cava. — The superior vena cava receives the
right and left innominate veins a little below the level of the top of
the arch of the aorta, behind the right portion of the manubrium,
midway between the upper and lower end of the bone. The
right innominate vein descends behind the sternal end of the right
clavicle, and the left innominate vein crosses in front of the three
great arteries, just at or above their origin from the arch of the aorta.
The superior vena cava descends immediately to the right of the

vol. tv. r,

82 A SYSTEM OF MEDICINE.

sternum behind the first space, the second cartilage and the second
space, and it opens into the right auricle behind the third right costal
cartilage.

The superior vena cava descends slightly at its point of entrance
into the right auricle during the contraction of the ventricle. It
descends also during the inspiration, but to a greater extent.

The Relation of the Lungs to the Heart in Front. — The lungs cover
the great vessels and the whole of the heart except the more pro-
minent portion of the right ventricle which is behind the cardiac
cartilages.

The inner margins of the right and left lungs in front meet together
behind the upper two-thirds of the sternum, the right lung, as a
rule, passing to the left of the centre of the sternum, so as to encroach
somewhat on the left side of the chest. The inner margin of the left
lung separates from that of the right lung, ani diverges to the left on
a level with the fourth left costal cartilage. Thence, the lower border
of this portion of the lung extends to the left, lying behind the lower
edge of the fourth cartilage or the upper border of the fourth space,
and in front of the body of the right ventricle. Before this border of
the lung reaches the longitudinal furrow and the junction of the
cartilages to the ribs, it curves downwards, crossing within the fourth
space and the fifth cartilage, where it again curves to the right
so as to form a hollow space for the lodgment of the apex of the
heart. After crossing the fifth space the inner margin ends in the
lower border of the upper lobe, which is situated behind the upper
edge of the sixth cartilage and rib, where it soon ends in the
septum that divides the upper from the lower lobe of the left lung.
Owing to the outward and inward curve thus made by the inner
margin of the left lung where it crosses the heart to form the left
and lower border of the superficial cardiac space, a remarkable
tongue of lung is formed by the inner and lower borders of the
upper lobe of the left lung. This tongue of lung, owing to its free
position just in front of the interlobular septum, wraps round the
apex of the heart, being above, below, outside and in front of it, so as to
adapt itself to every movement of the apex. When the apex advances
it recedes, when the apex recedes it advances, and thus it allows free
play to the apex at the same time that it softens the impulse of the
apex upon the walls of the chest, and shields it, when it becomes
again flaccid, and retires within its nest.

The inner margin of the right lung, after that of the left lung ha3
deviated to the left, continues its course downwards, behind the
sternum, being nearer to the left than the right edge of that bone.
It thus completely covers the transverse fuiTow, the right border
of the right ventricle, and the tricuspid orifice. This inner margin
of the right lung inclines to the left before it reaches the lower
boundary of the heart, where it soon ends in the lower margin of the
right lung ; which margin lies at first behind the upper part of the
ensiform cartilage, then crosses behind the sternal portion of the

POSITION AND FORM OF THE HEART. 83

seventh and sixth right cartilages, and afterwards takes its course to
the right, behind or just above the sixth cartilage.

It is evident, from what has just been stated, that the lungs are
moulded by a natural adaptation to the form and structure of the
heart and great vessels. They thus cover the soft and yielding right
auricle, which requires the additional protection of the soft covering in
which it is thus imbedded ; they thus cover the great vessels, which do
not advance so far forwards as the body of the heart ; they thus cover
the circuit of the ventricles around the three sides of the superficial
cardiac space ; and they thus leave uncovered the most prominent and
powerful portion of the right ventricle. Obeying thi3 law of adapta-
tion, the inner margin of the right lung extends inwards and to the
left along its whole length, more than that of the left lung extends
to the right ; for the greater prominence of the pulmonary artery, of
the conus arteriosus, and of the centre of the right ventricle, parts that
are situated to the left of the middle line of the sternum, offers
resistance to the free inward expansion to the right of the margin of
the left lung. On the other hand, the less prominence of the ascend-
ing aorta, the soft and yielding character of the right auricle and its
appendix, and the less prominence of the right border of the right
ventricle, parts that are situated behind and to the right of the
sternum, allow and even invite the more free inward expansion to
the left of the inner margin of the right lung. The inner margins of
the lungs, in short, advance freely where they meet with the least
resistance, and stop or even recede where they meet with the greatest
resistance.

The Orifices and Valves of the Heart and (lie Great Arteries. — The
orifices and valves of the heart may be considered in two orders : (1)
As they are superficial or deep in situation, when the pulmonic and
tricuspid orifices and valves would come first, and then the aortic and
mitral orifices and valves ; and (2) as they are ranged from above
downwards when the pulmonic orifice and valve come first in order,
then the aortic, then the mitral, and last the tricuspid orifice and
valve. I shall consider them in detail according to the first and most
natural of those orders, namely, the superficial and deep orifices and
valves, which are also the orifices and valves of the right or anterior
and the left or posterior cavities. After doing so, I shall briefly
indicate them, for the sake of their common connexion, in their order,
from above downwards.

The orifice of the pulmonary artery is the highest of the four orifices,
and its anterior portion is situated mainly behind the third left carti-
lage, its right border being covered by the adjoining edge of the
sternum. During the systole of the ventricles the anterior portion
of the orifice of the pulmonary artery descends into the third space.

The root of the pulmonary artery consists of two anterior sinuses
and one posterior sinus, and its valve consists of two flaps in front
and one behind, each in its own sinus. The position of the anterior
flaps is higher than that of the posterior flap. The anterior or super-

o 2

Hi A SYSTEM OF MEDICINE.

ficial convex wall of the right ventricle is much longer than its
posterior or internal convex wall, owing to its outer wall being a
section of a much larger sphere than its inner one. When, therefore,
the right ventricle contracts, its anterior and outer wall shortens and
draws downwards the anterior flaps of the pulmonic valve to a much
greater extent than the posterior and inner wall shortens and draws
downwards the posterior flap. The result is that when the right ven-
tricle is in a state of complete contraction, the anterior and posterior
flaps of the pulmonic valve are nearly on the same level ; and that
when the ventricle is in a state of distension the anterior flaps may
be an inch higher than the posterior flap. This is well seen in
several of Pirogotfs vertical sections.

The tricuspid orifice, is the lowest as well as the most superficial
of the four orifices, and is separated from the orifice of the pulmo-
nary artery by the conus arteriosus of the right ventricle. In a
healthy active man with a well-formed chest, the tricuspid orifice is
situated behind the lower fourth of the sternum to the right of the
middle line of that bone, its upper bonier being on a level with
the lower edge of the fourth cartilage, and its lower border being
behind the lower end of the sternum, and the articulation to it of the
right sixth cartilage.

The tricuspid orifice is situated about half an inch to the left of
the right transverse auriculo-ventricular furrow. It is impossible
to assign accurately a fixed position to the tricuspid orifice, owing to
its extensive movement to the left during the contraction, and to the
right during the dilatation of the right ventricle. The limits of the
range of this movement may, however, be defined to the right by a
line a little to the right of the sternum, and to the left by a line a
little to the left of the middle line of that bone, the orifice playing
backwards and forwards behind, and to the right of the right half of
the lower portion of the sternum.

The position of the flaps, the tendinous cords, and the papillary
muscles of the tricuspid valve have been already described in detail.1
It will, therefore, be sufficient to say here that the papillary muscles
radiate like a fan upwards, outwards, and downwards from the cords
and flaps of the valve ; that the superior papillary muscle, when
present, ascends behind the fourth cartilage ; that the anterior papillary
muscle takes the direction outwards of the fifth cartilage ; and that
the inferior papillary muscles descend behind the sixth cartilage.

The root of the aorta,2 including its orifice, valve and sinuses, occu-
pies the space between the pulmonic and tricuspid orifices. The root
of the aorta, and the aortic vestibule, which is the channel or chamber
with rigid walls that leads to it from the cavity of the left ventricle,
project forwards in front of that cavity and of its mitral orifice, so that
the orifice of the aorta, covered by the posterior wall of the conns arte-

1 See pages 54-59.

* I have already described the anatomical relations of the root of the aorta. (See
pages 37-42).

POSITION AND FORM OF THE HEART. 86

riosus, interposes itself, as has just been stated, between the pulmonic
and tricuspid orifices. By this arrangement the aortic orifice advances
more nearly to the front of the chest, the shallow comes arteriosus being
in front of the orifice, and the deep cavity of the right ventricle being
below it. Hence the murmur of aortic regurgitation, and an intensified
aortic second sound, and coincident doubling of that .sound, are
heard loudly over and to the left of the middle third of the sternum
in front of the arterial cone and the root of the aorta ; and feebly
over and to the left of the lower third of the sternum, in front
of the cavity of the right ventricle. The root of the aorta is
somewhat overlapped above and to the left by the root of the pul-
monary artery, and is situated accordingly below and to the right of
the pulmonic orifice, behind the left half or three-fifths of the sternum,
on a level with the third space, the left portion of the aortic orifice
extending beyond the sternum so as to lie within that space. The
upper and left border of the aortic orifice, especially during the
diastole, is seated behind the lower portion of the third cartilage,
near the sternum ; and its lower and right border, especially during
the systole, is situated behind the middle line of the sternum, on a
level with the upper portion of the fourth cartilage.

The root of the aorta descends considerably and moves to the left,
so as to approach towards the apex during the contraction of the left
ventricle, and at the same time the apex moves to a less degree
upwards, and to the right, so as to approach towards the aortic orifice.

The mitral orifice is situated partly behind, and partly below the
level of the aortic orifice, its upper third or upper two-fifths being
behind, and its lower two-thirds or three-fifths below the level of
that orifice ; and partly behind, and partly above the level of the
tricuspid orifice, its lower two-thirds or three-fourths being behind,
and its upper tliird or fourth being above the level of that orifice.
The mitral orifice is seated behind the left half of the sternum, at
the upper two-thirds of the lower third of that bone, on a level
with the fourth cartilage, the fourth space, and the upper portion of
the fifth cartilage. It is impossible to assign a fixed position to the
mitral orifice, for it, like the tricuspid orifice, plays to and fro during
the contraction and dilatation of the ventricles. The limits of its
movement may, however, be approximately defined by a line a little
to the right of the middle line of the sternum on the one hand
and a line corresponding to the left edge of the sternum on the
other. I have already described the anatomical relations of the
mitral valve,1 and it will therefore be sufficient to state here that
the left or upper and the right or lower papillary muscles, starting
from their attachments through their tendinous cords to the flaps
of the valve, concentrate themselves towards their roots at the
apex, instead of radiating from the flaps upwards, outwards, and
downwards, as in the instance of the tricuspid valve. The left or
superior papillary muscle usually follows the course of the fourth

1 See J age* 49-54.

86 A SYSTEM OF MEDICINE.

cartilage and space, and the right or inferior papillary muscle that of
the fifth cartilage, both muscles dipping downwards towards the lower
cartilage or space as they approach the apex.

It may be gathered, from what has just been said, that each of the
higher orifices overlaps in position the orifice immediately below it.
Thus the pulmonic orifice at its lower and right edge is situated to a
slight extent in front of the upper and left edge of the aortic orifice ;
the right posterior or lower flap of the aortic valve is situated in
front of the upper third or two-fifths of the mitral orifice; and
the lower two-thirds or three-fourths of the mitral orifice is behind
the corresponding upper portion of the tricuspid orifice.

The position of the orifices and valves of the heart in relation to
the deeper parts of the heart and of the chest, and to the spinal
column, will be considered when the side and back views of the
heart and great vessels are described.

The Position of the Heart and Great Vessels in Robust

and Feeble Persons.

(See Figs. 20, 21, 22, 23, 24.)

We have just seen that respiration materially alters the position
of the heart and the great vessels, and that at the end of a deep
inspiration the lower boundary of the heart may be two inches lower
in relation to the walls of the chest than at the end of a forced
expiration. Thus, the lower boundary of the heart is situated
behind or even above the lower end of the sternum at the com-
pletion of a forced expiration ; while it may be situated at the lower
end of the ensiform cartilage at the termination of a deep in-
spiration. Again, the top of the arch of the aorta may be situated
behind the upper end of the manubrium at the end of a forced
expiration, and behind its lower end on the completion of a deep
inspiration.

This great change is produced by a double agency, acting in
opposite directions : one, the descent of the diaphragm which lowers
and lengthens the heart and great vessels, and lengthens the lungs
by lowering their base ; the other, the ascent and advance of the walls
of the chest in front. This combined downward movement of the
heart and arteries, and upward movement of the sternum and carti-
lages, doubles the effect on the position of the organ in relation to
the cartilages and sternum.

In robust persons, who lead an active and laborious life, the amount
of reserved air constantly in the lungs is great, the chest is high, deep
and broad, and the heart and arteries are low in position in relation
to the anterior walls of the chest. In such persons the chest and
its organs present the form and position of inspiration, and they have
therefore the inspiratory type of chest. (See Figs. 20,21, 22, 23.)

In feeble persons, on the other hand, who lead an indoor sedentary

POSITION AND FORM OF THE HEART, 87

life, the amount of reserved air constantly in the lungs is small, the
chest is flat and narrow, and the heart and arteries are high in posi-
tion in relation to the anterior walls of the chest. In such persons
the chest and its organs assume the form and position of expiration,
and they present the expiratory type of chest. (See Fig. 24.)

In robust persons, such as sailors, miners, labourers and smiths,
the lower boundary of the heart may be situated quite an inch below
the lower end of the sternum, so that the heart may be felt beating
in the epigastrium to the left of the ensiform cartilage and the apex
of the heart may be situated behind the sixth left cartilage or space.
The lungs at the same time enlarge forwards and downwards, so as to
interpose themselves between the heart and the walls of the chest, all
but a small space bounded above by the fifth cartilage, on the right
by the ensiform cartilage, and on the left by the sixth and seventh
cartilages near their attachment to the sternum. The heart's impulse
is, therefore, quite imperceptible over the front of the chest, that
of the right ventricle being sometimes transferred, as I have just said,
to the epigastrium, and the apex beat is lost, being enveloped in the
folds of the enlarged lung. In such persons, also, the top of the arch
of the aorta is low in position, being perhaps situated quite an inch
below the top of the manubrium.

The position of the lower boundary of the heart and the summit
of the arch of the aorta being unusually low, the position of every
part of the heart and the great arteries is also correspondingly low.
It is not necessary to describe the situation of the various anatomical
points in detail, but it will be well to name that of the leading land-
marks of the heart and great arteries.

The boundary-line across the third cartilage that indicates the upper
border of the right auricle and ventricle and the lower limit of the
great arteries may be shifted downwards to the level of the fourth
cartilages. The position of the origin of the pulmonary artery in
front being thus given, that of the aperture and valve of the aorta,
being a degree lower and to the left, may be inferred, it being situated
behind and a little to the left of the left half of the sternum, on a level
with the fourth cartilage and the fourth space. The mitral and tricuspid
orifices in their descending order take each of them a lower position
the mitral orifice being situated behind the lower fourth of the sternum,
its upper boundary being on a level with the fourth space and its
lower border, a quarter of an inch above the lower end of the ster-
num ; and the tricuspid orifice being behind the lower sixth of the
sternum and the upper portion of the ensiform cartilage.

In feeble, thin persons, of sedentary occupation, or in those who have
only recently recovered from illness, the lower boundary of the heart
may be situated behind the lower end of the sternum, or somewhat
higher, and its apex may be present behind the fifth left cartilage, and
may be felt, therefore, beating, not in the fifth, but in the fourth space.
Each lung at the same time lessens at its base, and shrinks away
from before the body of the heart, uncovering the apex and the left

88 A SYSTEM OF MEDICINE.

ventricle, the whole of the right ventricle, and a portion of the auricu-
lar appendix, of the pulmonary artery, and even of the ascending aorta.
The heart's impulse is, therefore, diffused to an unusual extent over
the front of the central part of the chest, from the second space to the
fourth, and from the right of the lower portion of the sternum to the
apex, being felt not only over the apex, but with considerable force
over the right ventricle, where it is usually feeble or absent. A
double pulsation may alt>o be often felt over the pulmonary artery,
feeble and soft with the first sound, but sharp and sudden with the

> the front of tlie chest ami

second sound. In such persons also the top of the arch of the aorta
is high, being situated behind or even above the top of the manubrium.
The position of the other parts of the heart and great vessels is
correspondingly high. The boundary-line between the upper border
of the right auricle and ventricle and the lower limit of the great
arteries may be on a level with the middle of the second space,
behind which the origin of the pulmonary artery m^y be seated.
The orifice and valve of the aortn, being a stage lower and to the

POSITION AND FORM OF THE HEART. 89

left, may be on a level with the lower portion of the second space
and the third cartilage, behind the left half of the sternum. The
mitral orifice may be situated behind the left half of the sternum,
behind and just below the central portion of the bone, its upper
border being on a level with the upper edge of the third carti-
lage, and its lower border with that of the upper edge of the fourth
cartilage ; and the tricuspid orifice may be situated behind the right
half of the sternum just below the centre of the bone, so that its upper
border may be on a level with the lower edge of the third cartilage
or the upper portion of the third space, while its lower border may
be on a level with the fourth space.

In many well-formed women of active, healthy habits, the heart
and great vessels maintain their proper position. But this is not
so in the large class of women who work indoors with the needle,
and in whom the chest is wont to be flat, the position of the heart
being high.

The effect of tight stays is to lessen the descent of the diaphragm,
and to increase, for the sake of compensation, the expansion and ele-
vation of the upper part of the front of the chest. In such persons
a double and opposite effect maybe produced. The lower boundary of
the heart in relation to the lower end of the sternum may be high, but
the top of the aorta in relation to the higher costal cartilage may
be low.

In children of both sexes the position of the heart in relation to the
walls of the chest is high.

SIDE VIEW; AFTER DEATH.

LEFT SIDE. (Fig. 25.)

The ninth plate of my Medical Anatomy represents a side view,
looked at from the left side, taken from the body of a robust well-
formed man. In this body the lower boundary of the heart was
situated behind the ensiform cartilage, an inch and a half below the
lower end of the sternum.

In this instance the top of the manubrium was on a level with the
middle of the body of the third dorsal vertebra, and the lower end of
the sternum was on a level with the upper border of the ninth ver-
tebra. The middle of the sternum corresponded in level to the lower
portion of the body of the fourth vertebra ; the lower end of the
manubrium, to the lower portion of the fifth vertebra ; and the top of
the lower third of the sternum, to the middle of the body of the
seventh dorsal vertebra. The ensiform cartilage was of great length,
measuring nearty 3 inches (2'8 inches), and its lower end was about
on a level with the upper border of the body of the twelfth dorsal
vertebra.

90 A SYSTEM OF MEDICINE.

This drawing and Plate X. of the same work show well the great
anatomical importance of the somewhat neglected ensiform cartilage,
especially to the clinical worker. The front of the diaphragm, and
the floor of the pericardium, which is formed by the central tendon of
the diaphragm, take their origin in part from the tip of the ensiform
cartilage by means of a strong slip of muscular fibres. The lower
boundary of the pericardium and of the heart, and the lower
boundary of the diaphragm, and with it that of the cavity of the right
side of the chest and the right lung, may be brought down on a deep
inspiration almost to the extremity of the ensiform cartilage, when
that point forms the lower boundary of the chest. In this drawing,
the lower boundary of the pericardium and the lower margin of the
right lung were situated an inch above the end of the ensiform carti-
lage, and nearly two inches below the lower end of the sternum, and
the lower boundary of the heart at the apex, as I have already
remarked, was an inch and a naif below the level of the lower end of
the sternum.

The top of the arch of the aorta at the adjacent origin of the inno-
minate and left carotid arteries was in this instance four-fifths of an
inch (*8 inch) below the top of the manubrium, and was on a level
with the upper portion of the body of the fourth dorsal vertebra.

The lower end of the descending portion of the arch of the aorta
was in front of the upper portion of the body of the sixth dorsal
vertebra, and was on a level with a point a little below the lower end
of the manubrium.

The top of the pulmonary artery was a little higher in position
thau that of the lower end of the descending portion of the arch of
the aorta just described ; the origin of the pulmonary artery was
three-quarters of an inch below the centre of the sternum, and
within the third space, and was on a level with the lower portion of
the body of the seventh vertebra ; and the pulmonary artery occupied
in its ascent the upper portion of the third space, the third cartilage,
and the second space.

The top of the appendix of the right auricle was nearly half an
inch below the centre of the sternum, and on a level with the
cartilage between the sixth and seventh vertebrae. The top of the
appendix of the left auricle, and the upper boundary of the left ven-
tricle, which would be a little above the lower boundary of the orifice
of the aorta, were about on a level with the middle of the body of the
seventh dorsal vertebra behind, and the top of the lower third of the
sternum, or about the fourth costal cartilage in front. The lower
boundary of the left auricle, which would nearly correspond with the
lower boundary of the mitral valve, was in front of the top of the
ninth vertebra, and on a level with a point a quarter of an inch
above the lower end of the sternum. The lower boundary of the
posterior part of the left ventricle was in front of the top of the
tenth dorsal vertebra, and about on a level with a point four-fifths of
an inch below the lower end of the sternum ; while the lower boun-

POSITION AND FORM OF THE HEART. 91

dary of the left ventricle at the apex was on a level with the lower
portion of the body of the tenth dorsal vertebra, and with a point
about an inch and a half below the lower end of the sternum.

RIGIIT SIDE.

The tenth plate of my Medical Anatomy represents a side view,
looked at from the right side, taken from the body of a strong man
with a well-formed chest of the inspiratory type. In this body the
heart was distended with water, and the lower boundary of the
swollen right ventricle was situated behind the ensiform cartilage,
three quarters of an inch (*7 inch) above the tip of that cartilage, and
an inch and a half (14 in.) below the lower end of the sternum.

The top of the manubrium in this instance corresponded in level
with the lower border of the body of the second dorsal vertebra ; the
lower end of the sternum, with the lower border of the ninth vertebra ;
the middle of the sternum at the level of the third cartilage, with
the body of the sixth vertebra; the lower end of the manubrium,
with that of the fifth vertebra; and the upper border of the lower
third of the sternum corresponded in level with the body of the
seventh dorsal vertebra.

The commencement of the superior vena cava in this instance was
on a level with a point below the middle of the manubrium in front,
and with the body of the fourth dorsal vertebra behind ; and the ter-
mination of the vein in the right auricle was in front of the cartilage
between the sixth and seventh vertebrae, and on a level with a point
half an inch below the middle of the sternum, and with the third space.

The top of the appendix of the right auricle was on a level with
the middle of the sternum and the third cartilages in front, and the
l>ody of the sixth dorsal vertebra behind ; the attachment of the lower
boundary of the appendix to the body of the right auricle, at the
transverse furrow, which corresponds closely to the upper boundary
of the tricuspid valve, was on a level with a point an inch and a
quarter above the lower end of the sternum in front, and the upper
border of the eighth dorsal vertebra behind ; and the lower boundary
of the right auricle, which corresponds closely to the lower boundary
of the tricuspid orifice, wfas on a level with a point half an inch
below the lower end of the sternum in front, and the upper portion
of the tenth dorsal vertebra behind.

The origin of the pulmonary artery and the upper boundary of
the right ventricle were on a level with a point half an inch below the
centre of the sternum and the third space in front, and with the*lower
border of the sixth vertebra behind; and the lower boundary of the
right ventricle in front was situated behind the ensiform cartilage,
an inch and a half (14 in.) below the lower end of the sternum,
and three quarters of an inch above the tip of the ensiform carti-
lage in front, and about on a level with the lower border of the
body of the tenth dorsal vertebra behind. The lower boundary of

02 A SYSTEM OF MEDICINE.

the right ventricle was about three-quarters of an inch higher behind
than in front.

The lower boundary of the pericardium was about an inch and
three-quarters below the lower end of the sternum, and about half
an inch above the tip of the ensiform cartilage.

Although I possess other drawings showing a side view of the
heart and the other internal organs, these are the only ones that
give the relation of the heart and its various parts to the walls of
the chest in front and the spinal column behind. Both of these
drawings were taken from the bodies of men of a robust frame, with a
chest of the inspiratory type, and with a heart well developed and
low in position. The relations of the heart to the front of the chest
in all their variety have been already abundantly illustrated, and its
relations to the spinal column will be further described when the
position of the heart and great vessels looked at from the back is
considered. PirogofF gives numerous sections, both vertical and
horizontal, showing the position of the various parts of the heart and
great vessels in relation to the anterior walls of the chest and the
spinal column, and I therefore refer the reader to the notes describ-
ing those sections and two others that are figured in Braun's work.
(Note 46, page 116 ; Note 47, page 121.)

SIDE VIEW; DURING LIFE.

In a Healthy Man with a well-formed Chest.

left side. (Fig. 25.)

The heart and great vessels occupy the space in the centre of
the chest, between the sternum in front and the bodies of the dorsal
vertebrae behind. The margins of the lungs fill up the unoccupied
spaces in front of the great vessels and the heart ; and the oesophagus
aud descending aorta are interposed between the heart and the bodies
of the vertebrae, behind.

It is evident that in the recumbent posture and during the ventri-
cular systole, the heart would press backwards upon the oesophagus and
the descending aorta so as to render swallowing difficult, and to inter-
fere with the flow of blood to the lower part of the body, unless the
heart were supported by some special contrivance. Such support is to
be found in the walls of the pericardial sac. The floor of the pericar-
dium is formed by the central tendon of the diaphragm, which is sus-
pended in its place, in the middle of the partition between the chest
and the abdomen, by means of the great converging circuit of the
muscular fibres of the diaphragm, arising from the ensiform carti-
lage and the ribs ; and is supported firmly from below by the liver

POSITION AND FORM OF THE HEART. 93

and stomach. The heart rests upon the floor of the pericardium,
formed by the central tendon of the diaphragm, and this supplies a
smooth inclined plane, upon which the heart glides forwards and
downwards during inspiration, and backwards and upwards during
expiration, so as to adapt itself to the various modulations of respira-
tion. The strong fibrous walls of the pericardium arise from the cen-

Fio 26. -Side view, looked at from Hip Ipft niile, shotting tlie heart and great vessels in
relation to the wall* of the chest and the spinal column.

tral tendon of the diaphragm. Those walls are endowed with a fibrous
■tincture which is of especial strength posteriorly, where it is firmly
incorporated with the coats of the pulmonary veins as they enter the
pericardium. A fibrous covering is also contributed by the pericar-
j° *^e kferior and superior venae cavae where they enter the
sac, and to the pulmonary artery and ascending aorta where they leave

02 A SYSTEM OF MEDICINE.

the right ventricle was about three-quarters of an inch higher behind
than in front.

The lower boundary of the pericardium was about an inch and
three-quarters below the lower end of the sternum, and about half
an inch above the tip of the ensiform cartilage.

SIDE VIEW; DURING LIFE.

In a Healthy Man with a well-formed Chest.

left side. (Fig. 25.)

The heart and great vessels occupy the space in the centre of
the chest, between the sternum in front and the bodies ol the dorsal
vertebrae behind. The margins of the lungs fill up the unoccupied
spaces in front of the great vessels and the heart ; and the oesophagus
aud descending aorta are interposed between the heart and the bodies
of the vertebrae behind.

It is evident that in the recumbent posture and during the ventri-
cular systole, the heart would press backwards upon the oesophagus and
the descending aorta so as to render swallowing difficult, and to inter-
fere with the flow of blood to the lower part of the body, unless the
heart were supported by some special contrivance. Such support is to
be found in the walls of the pericardial sac. The floor of the pericar-
dium is formed by the central tendon of the diaphragm, which is sus-
pended in its place, in the middle of the partition between the chest
and the abdomen, by means of the great converging circuit of the
muscular fibres of the diaphragm, arising from the enatfonu carti-
lage and the ribs; and is supported firmly from

POSITION AND FORM OF THE HEART. 95

inclination to that of the ribs, they, as well as the transverse fuiTow
between them, are covered throughout by the fourth, fifth, and sixth
ribs. The left auricle and ventricle start from the back of the centre
of the chest in front of the bodies of the seventh, eighth, and ninth
dorsal vertebrae, and the left ventricle crosses from the back to the
front of the chest with a definite leaning to the left, so that its apex
points at the left fifth space. The left auricular appendix and the
left pulmonary veins, where they enter the auricle at its higher part,
are situated in front of the adjoining portions of the bodies of the
seventh and eighth dorsal vertebne and their intervening cartilage,
and on a level with the third and fourth costal cartilages and the third
space in front.

The anterior longitudinal furrow presents a convex outline, looking
forwards towards the pulmonary artery at its upper thircl, and towards
the right ventricle at its lower two-thirds ; and a concave outline
looking backwards and downwards towards the left auricular appendix
and the left ventricle. The upper end of this furrow is in front of
the body of the seventh dorsal vertebra and behind the third costal
cartilage or space, and the lower end of the furrow at the apex of the
heart is situated behind the lower border of the fifth space, and is on
a level with the body of the tenth dorsal vertebra behind.

During the ventricular systole, the left ventricle and auricle change
remarkably in form, size, and position (Fig. 17). The ventricle con-
tracts and shortens, and the auricle expands and lengthens to a great
extent. The base of the ventricle and the adjoining edge of the
auricle, the transverse furrow and the mitral orifice advance to a con-
siderable extent forwards, to the left and downwards away from the
spinal column and towards the apex of the left ventricle. The apex
at the same time moves forwards, upwards and to the right, towards
the base, so that the base and apex of the ventricle both approximate
towards each other, and towards a zone of rest in the walls of the
ventricle, situated nearer to the apex than the base. The anterior
wall of the ventricle, at the anterior longitudinal furrow, advances
forwards and becomes more convex ; while the posterior wall of the
ventricle also advances forwards, but to a much greater extent, espe-
cially at its middle, where it becomes hollow, the apex pointing
downwards ; so that the posterior wall of the ventricle, previously
convex, becomes concave towards the apex and convex at the base,
thus presenting a double curve. All the systolic movements of the
left ventricle converge forwards, towards the poiut of rest on the
surface of the right ventricle, about its middle and near the septum.

During the ventricular systole the left auricle becomes greatly
distended and expands upwards, forwards and downwards, along its
upper, anterior and lower borders respectively, the amount of move-
ment of the auricular appendix being greater than that of the trans-
verse furrow. The posterior wall of the auricle which rests on the
back of the pericardium remains stationary.

The right ventricle extends in front from the third cartilage to the

96 A SYSTEM OF MEDICINE.

•

sixth, and from the middle of the sternum to the lower portion of
the upper third of the ensiform cartilage, and is on a level behind
with the body of the seventh dorsal vertebra at its upper boundary,
and with the upper portion or middle of the body of the tenth dorsal
vertebra at its lower boundary.

During the systole of the ventricles, the right ventricle advances,
while the upper portion of its walls contracts downwards and the
lower portion of its walls contracts upwards, those movements con-
verging towards a point situated near the longitudinal furrow and the
Attachment of the anterior papillary muscle.

The pulmonary artery conceals the ascending aorta in the first half
of its course, when we look at the left side of the heart. By remov-
ing the fat between the pulmonary artery and the left auricular
appendix, the left posterior sinus of the aorta and the left or posterior
coronary artery are brought into view, deep behind and beyond
the posterior surface of the pulmonary artery. The mode in which
the pulmonary artery in its progress backwards, and the ascending
aorta in its progress upwards, cross each other, is now well seen.
When the arch of the aorta is looked at in front, it does not present
the appearance of an arch, since the left border of the ascending
aorta is situated almost in front of the deep right border of the de-
scending aorta ; and the pulmonary artery covers the left edge of the
ascending and almost the whole of the descending aorta, the deep left
edge of which is alone visible in front. When, however, the left side
of the arch of the aorta is looked at, its arched form is at once
apparent, the ascending aorta forming the front, the descending aorta
the back, and the transverse aorta the top of the arch.

The pulmonary artery as it ascends makes for the hollow of the
arch of the aorta, through which it sends its right branch, and its
direction is therefore much more from before backwards than from
below upwards.

The origin of the pulmonary artery is situated just behind the
third left cartilage, and is on a level with the body of the seventh
dorsal vertebra. The uppar boundary of the pulmonary artery, at
the top of its point of bifurcation, which is also its most posterior
portion, is situated in front of the lower portion of the body of the
fifth, or the upper portion of that of the sixth dorsal vertebra, and on
a level with the second costal cartilage; and the left and right
branches of the pulmonary artery are situated in front of the body of
the sixth dorsal vertebra, on a level with the second space.

The pulmonary artery in its course from before backwards and
upwards presents a convexity on. its anterior and upper surface, and
a concavity on its posterior and lower surface, and is on a level
with the third left cartilage and the second space. The posterior
sinus of the pulmonary artery is somewhat lower in position than
the two anterior sinuses, and is situated behind the upper portion of
the third space. The left bronchus separates the left pulmonary
artery from the left pulmonary veins.

POSITION AND FORM OF THE HEART. 97

During the systole of the ventricles, the whole pulmonary artery
lengthens and enlarges. The origin of the artery moves to a consi-
derable extent downwards and forwards, the higher parts of the
artery sharing this movement, but to a less and less extent from
below upwards. The two anterior sinuses of the pulmonary artery
descend more during the systole than its posterior sinus, so that the
anterior or higher valves are then more nearly on a level with the
posterior or lower valve than during the diastole.

The arcli of the aorta, like the pulmonary artery, lengthens and
enlarges dining the systole, so that the whole arch widens. The
orifice of the aorta, which is situated at the centre of the heart,
moves to a considerable extent downwards and to the left, the direc-
tion of its movement, like that of the mitral valves, being towards the
apex. The walls of the ascending aorta also move downwards, but to
a less and less extent from below upwards.

The position of the ascending, transverse and descending portions
of the arch of the aorta in relation to the sternum, the adjoining
parts, and the spinal column has already been described.

The pulmonic, the aortic, and the mitral orifices and valves are
situated in their relative position on an inclined plane, each being one
above and behind the other in the order named, the orifice of the pul-
monary artery being the highest and most anterior, the mitral orifice
the lowest and most posterior, and the aortic orifice holding an inter-
mediate position. The upper and anterior boundary of the pulmonic
orifice and valve is behind the third costal cartilage and on a level with
the lower third of the body of the sixtli dorsal vertebra ; and the lower
boundary of the mitral valve is on a level with the fifth cartilage and
is situated in front of the lower border of the body of the eighth
or the upper border of that of the ninth dorsal vertebra. The aortic
orifice, being a stage lower than the pulmonic orifice, by which it is
overlapped, is in front of the body of the seventh dorsal vertebra,
and the intervertebral cartilage just below it. The mitral orifice is
in front of the same intervertebral cartilage, the body of the eighth
and the upper border of the body of the ninth dorsal vertebi*a. The
position of the sternum and costal cartilages in relation to those
valves need not be here repeated.

The position that I have assigned to the various parts of the heart *
and great arteries, is that which usually exists in a healthy, well-
formed man, but those parts change in position during the systole
and diastole of the ventricles, and during inspiration and expiration,
in the manner and to the extent that I have already described. In
those who are robust and possess a broad and deep chest of the
inspiratory type, the position of the heart and arteries and of all
their parts are lower, while in those who are slender and possess a
narrow and flat chest of the expiratory type, the position of those
parts is higher, than in the average man whom I have taken as an
example. During inspiration the whole of the anterior walls of the
chest ascend considerably, but the spinal column, owiug to.. the

VOL. IV. H

96 A SYSTEM OF MEDICINE,

sixth, and from the middle of the sternum to the lower portion of
the upper third of the ensiform cartilage, and is on a level behind
with the body of the seventh dorsal vdrtebra at its upper boundary,
and with the upper portion or middle of the body of the tenth dorsal
vertebra at its lower boundary.

The origin of the pulmonary aiiery is sitmted just behind the
third left cartilage, and is on a level with the body of the seventh
dorsal vertebra. The upp3r boundary of the pulmonary artery, at
the top of its point of bifurcation, which is also its most posterior
portion, is situated in front of the lower portion of the body of the
fifth, or the upper portion of that of the sixth dorsal vertebra, and on
a level with the second costal cartilage; and the left and right
branches of the pulmonary artery are situated in front of the body of
the sixth dorsal vertebra, on a level with the second space.

MSITION AND FORM OF THE HEART, 99

The tricuspid orifice is the most anterior and the lowest in posi-
tion of the four orifices of the heart and great vessels, and is sepa-
rated from the spinal column by the left ventricle and auricle. The
tricuspid orifice is situated, as we have already seen, behind the right
half of the lower fourth of the sternum, and i.s on a level with the
bodies of the eighth and ninth dorsal vertebra}.

The descending vena cava is situated to the right of the ascending
aorta and on a deeper plane. The commencement of the vein, at the
confluence of the two innominate veins, is on a level with the body
of the fourth dorsal vertebra, and it enters the right auricle behind its
appendix in front of the body of the seventh dorsal vertebra, the
right pulmonary artery being just above its termination, the superior
right pulmonary vein just below it, and the oesophagus just behind it
or to its left. The vein, as it descends, rests upon the right side of the
trachea near and at its bifurcation, and upon the right bronchus.

BACK VIEW; AFTER DEATH.

I made observations some years ago on the position of certain
parts of the heart and great vessels in relation to the spines of the
dorsal vertebra} in eleven different bodies.

The top of the arch of the aorta was situated in front of a point
below the spine of the second dorsal vertebra in one instance, just
above the spine of the third dorsal vertebra in seven instances, and
below the spine of that vertebra in three instances. In other words, in
one instance the top of the arch was in front of the upper portion of
the body of the third dorsal vertebra, in seven cases it was in
front of its lower portion, and in three it was in front of the body of
the fourth dorsal vertebra. The lower boundary of the left ventricle was
on a level with the spine of the ninth dorsal vertebra in one instance,
with a point just above that spine or below that of the eighth vertebra
in eight cases, with the spine of the eighth vertebra in one, and above
it in one. In other words, the lower boundary of the left ventricle
varied in position from the level of the lower edge of the body of the
eighth to that of the upper third of the tenth dorsal vertebra. In five
instances the upper boundary of the left auricle was on a level with
the spine of the fifth dorsal vertebra (in one), or just above that spine
(in one), or just below that spine (in three) ; and its lower boundary
was on a level with (in one), above (in one), or below (in three) the
spine of the seventh dorsal vertebra. In other words, the upper
border of the left auricle was situated in front of the upper part of
the seventh dorsal vertebra, or just above it, and its lower border in
front of the tody of the eighth vertebra.1

1 Note 4f>, i>. 116 ; Note 47, p. 21.

II 2

10(» A SYSTEM OF MEDICINE.

BACK VIEW; DURING LIFE.
In a Healthy Man with a well-fokmgd Chest. (See Fig. 20.)

When the back of the heart and great vessels is exposed, the left
cavities of the heart are brought into view, the lower boundary of the
left ventricle resting upon the floor of the pericardium, which conceals
the under surface of the heart. When the floor of the pericardium is
withdrawn, the under surface of the heart is visible from behind. The
under surface of the heart inclines from behind downwards and for-
wards, and it presents posteriorly, the lower border of the left ventricle
from base to apex ; auteriorly, the lower surface of the right ventricle ;
and intermediately, the posterior longitudinal furrow.

The lower boundary of the left ventricle is on a level with or higher
than the spine of the ninth and the upper portion of the body of the
tenth dorsal vertebra ; the top of the arch of the aorta at the origin of
the innominate and left carotid arteries is in front of the spine of
the third and the lower edge of the body of the third or the upper
edge of that of the fourth dorsal vertebra or it may be somewhat
higher; and the boundary line between the heart and the great
arteries, at the lower border of the division of the right and left
pulmonary arteries and the upper border of the left auricle, is in front
of the spine of the fifth and the lower border of the body of the
sixth dorsal vertebra. The level of the boundary-line between the
heart and the great arteries is somewhat higher behind, where it
follows the line of the lower border of the division of the pulmonary
artery, than it is either in front or at the sides, where it follows the
line of the origin of the pulmonary artery or that of the top of the
right auricle.

The Left Auricle and Ventricle. — The left auricle and ventricle main-
tain the same relation to each other and to the spinal column at the
back of the chest that the right auricle and ventricle do to each
other and to the sternum at the front of the chest, but each por-
tion of the left side of the heart bears more to the left behind,
than the corresponding portion of the right side of the heart does in
front.

The left auricle at its upper and posterior portion, which in-
cludes the auricular appendix, is central, being situated in nearly
about equal proportions to the right and left of the middle line of
the spinal column. The auricular appendix, which is a semi-detached
wing of the auricle, leaves the body of the auricle at its left upper
corner and advances forwards and to the left, so as to fill up the deep
furrow between the pulmonary artery and the base of the left ventricle.
The lowest portion of the left auricle lies entirely to the right of the

POSITION AND FORM OF THE HEART. 101

middle line of the spine, while the left ventricle lies almost completely
to the left of it, and the transverse furrow where it separates the two
cavities occupies an intermediate position, its' upper portion lying
considerably to the right, and its lower portion slightly to the left of
the middle line of the spine. The left auricle at its anterior aspect lies,
when at rest, almost entirely to the right of the middle line of the
chest, but its left boundary moves to the left of the middle line when
the ventricles contract, and to the right of that line when they dilate.
The transverse furrow takes an oblique direction from above down-
wards and from right to left, and as it sweeps to and fro, from one
side to the other and back again, during the contraction and dilatation
of the ventricle, it occupies a position in front of the spines of the
fifth, sixth, and seventh, and the bodies of the seventh and eighth
dorsal vertebra?, and the upper part of that of the ninth.

The heart is attached to the roots of the lungs by the entrance of
the right and left pulmonary veins into the upper part of the left
auricle at either side of the spine. The left pulmonary veins are as
a rule higher in position, and enter the auricle nearer to the centre
of the spine than the right, while the right lower pulmonary vein is
larger and lower in position than the left, the right lower vein being
sometimes double. The prcater size of the lower lobe of the rioht
lung compared with that of the left, evidently accounts for the greater
size of the right lower pulmonary veins. The higher position of the
left side of the auricle owing to the presence on that side of the base
of the ventricle, and the general inclination downwards of the heart,
its longitudinal parts following the line of the longitudinal furrows
from right to left, and its transverse parts following the oblique direction
of the transverse furrow from left to right, explain, I consider, the
lower position of the right than the left pulmonary veins. The pul-
monary veins have, in short, more room to deploy on the right side of
the left auricle, wdiere no object interferes with their freedom, than on
the left side of the auricle at its upper angle, where the veins and the
auricular appendix are pushed up into a corner by the close proximity
of the upper border of the left ventricle. The downward inclination
from left to right of the upper boundary of the left auricle, between
the left and right pulmonary veins, although quite definite, is very
much less than the downward inclination from left to right of the
posterior transverse furrow. The right pulmonary veins are on a level
with the spines of the fifth and sixth dorsal vertebra, and the two left
pulmonary veins, holding a higher position, are respectively just abeve
the level of those two spines.

The left ventricle lies to the left of the spinal column, and extends
in a direction to the left, downwards and forwards, from its base at
the back of the chest where it is in front of the spinal column, on a
level with the sixth and seventh dorsal spines, to its apex at the
front of the chest where it is behind the fifth left intercostal
space. The upper boundary of the left ventricle is more rounded
and more inclined from above downwards than ts lower boundary

100 A SYSTEM OF MEDICINE.

BACK VIEW; DURING LIFE.
In a Healthy Man with a well-foiimed Chest. (See Fig. 26.)

When the back of the heart and great vessels is exposed, the left
cavities of the heart are brought into view, the lower boundary of the
left ventricle resting upon the floor of the pericardium, which conceals
the under surface of the heart. When the floor of the pericardium is
withdrawn, the under surface of the heart is visible from behind. The
under surface of the heart inclines from behind downwards and for-
wards, and it presents posteriorly, the lower border of the left ventricle
from base to apex ; anteriorly, the lower surface of the right ventricle ;
and intermediately, the posterior longitudinal furrow.

The left auricle at its upper and posterior portion, which in-
cludes the auricular appendix, is central, being situated in nearly
about «qual proportions to the right and left of the middle line of
the spinal column. The auricular appendix, which is a semi-detached
wing of the auricle, leaves the body of the auricle at its left upper
corner and advances forwards and to the left, so as to fill up the deep
furrow between the pulmonary artery and the base of the left ventricle.
The lowest portion of the left auricle lies entirely to the right of the

POSITION AND FORM OF THE HEART. 101

middle line of the spine, while the left ventricle lies almost completely
to the left of it, and the transverse furrow where it separates the two
cavities occupies an intermediate position, its' upper portion lying
considerably to the right, and its lower portion slightly to the left of
the middle line of the spine. The left auricle at its anterior aspect lies,
when at rest, almost entirely to the right of the middle line of the
chest, but its left boundary moves to the left of the middle line when
the ventricles contract, and to the right of that line when they dilate.
The transverse furrow takes an oblique direction from above down-
wards and from right to left, and as it sweeps to and fro, from ono
side to the other and back again, during the contraction and dilatation
of the ventricle, it occupies a position in front of the spines of the
fifth, sixth, and seventh, and the bodies of the seventh and eighth
dorsal vertebrae, and the upper part of that of the ninth.

The heart is attached to the roots of the lungs by the entrance of
the right and left pulmonary veins into the upper part of the left
auricle at either side of the spine. The left pulmonary veins are as
a rule higher in position, and enter the auricle nearer to the centre
of the spine than the right, while the right lower pulmonary vein is
larger and lower in position than the left, the right lower vein being
sometimes double. The greater size of the lower lobe of the right
lung compared with that of the left, evidently accounts for the greater
size of the right lower pulmonary veins. The higher position of the
left side of the auricle owing to the presence on that side of the base
of the ventricle, and the general inclination downwards of the heart,
its longitudinal parts following the Hue of the longitudinal furrows
from right to left, and its transverse parts following the oblique direction
of the transverse furrow from left to right, explain, I consider, the
lower position of the right than the left pulmonary veins. The pul-
monary veins have, in short, more room to deploy on the right side of
the left auricle, where no object interferes with their freedom, than on
the left side of the auricle at its upper angle, where the veins and the
auricular appendix are pushed up into a corner by the close proximity
of the upper border of the left ventricle. The downward inclination
from left to right of the upper boundary of the left auricle, between
the left and right pulmonary veins, although quite definite, is very
much less than the downward inclination from left to right of the
posterior transverse furrow. The right pulmonary veins are on a level
with the spines of the fifth and sixth dorsal vertebrae, and the two left
pulmonary veins, holding a higher position, are respectively just abcve
the level of those two spines.

102 A SYSTEM OF MEDICINE.

along the line of the posterior longitudinal furrow, whore it is more

nearly straight and horizontal.

The posterior and left border of the mitral orifice is situated about
or fully half an inch to the left of the posterior transverse furrow.
This orifice looks towards the apex of the left ventricle, or in a direc-
tion to the left, forwards and slightly downwards. Its superior or left

column, tlio ribs, i

vessels in relation to tlio npiiii]

angle is a little behind the auricular appendix, on a level with a
point above the spine of the sixth, and with the middle of the body
of the seventh dorsal vertebra, and about half an inch, more or less,
to the left of the middle line of the spine. Its inferior or right
boundary is on a level with the spine of the seventh, and the lower
portion of the body of the eighth dorsal vertebra, and with a point
between the scapula;, just above their lower angles, and a little

POSITION AND FORM OF THE HEART. 105

ventricle behind from the right ventricle in front, on the under
surface of the heart, and when that organ rests upon the floor of the
pericardium, the transverse furrow and the right ventricle are hidden.
When, however, the floor of the pericardium is lowered so as to
bring into view the under surfrce of the heart, which inclines from
behind, forwards and downwards, the posterior longitudinal furrow,
and the under surface of the right ventricle beyond and in front of
it, are rendered visible. The posterior longitudinal furrow, resting
upon and adapting itself as it does to the floor of the pericardium, is
comparatively horizontal in direction ; but it is slightly convex near
the base of the ventricle, owing to the shoulder formed there by tho
muscular walls. During the contraction of the ventricle, when its
base and apex approximate, the transverse furrow changes in direction
both toward the base and the apex. The furrow then becomes more
convex than before at the base, because the base of the ventricle itself
becomes more convex, and it turns or twists downwards in a peculiar
manner towards the apex, because the apex itself twists downwards,
so as to form a concavity towards that end. The longitudinal furrow
then presents, therefore, an outline with a double curve.

The posterior longitudinal furrow at its auricular extremity comes
very close to the posterior border of the heart, and I think that
it is visible from behind at that point, even when the heart rests
upon the floor of the pericardium. Thence the furrow advances
forwards and to the left to the apex of the heart, where it divides
the left ventricle from the right, and where it joins the anterior
longitudinal furrow.

The under surface of the heart contracts gradually from its auri-
cular portion or base, where it is wider than at any other part, to its
apex, where it is narrower than at any other part. The under
surface of the right ventricle is thus triangular in form, the base of
the triangle being at the nuriculo-ventricular furrow, and its apex at
the apex of the heart. The posterior longitudinal furrow which is
Straight, forms the posterior side of the triangle, and the lower
boundary of the right ventricle, which is somewhat convex, forms its
anterior side. This lower boundary of the right ventricle at the front
of the heart, which is on a level with the body of the tenth and the
spine of the ninth dorsal vertebra, is lower in position than the lower
border of the left ventricle at the back of the heart, which is situated
in front of the cartilage between the bodies of the ninth and tenth
dorsal vertebrae, or a little lower, and is on a level with the space
between the eighth and ninth dorsal spines.

The apex of the heart is lower in position than the lower boundary
of the right ventricle, and is on a level with the body of the tenth, and
with a point above the spine of the ninth dorsal vertebrae, and with
the lower angle of the left scapula.

The Great Vessels. — The position of the boundary line between the
upper border of the heart and the lower limit of the great vessels is,
as I have already stated, higher at the back than at either side or in

104 A SYSTEM OF MEDICINE.

mitral orifice and valve over the dorsum. The left ventricle is
situated to the left of this region, aud extends below its level.
During the diastole of the ventricle, the stream of blood from the
auricle into the ventricle pours across this region in a direction from
right to left, forwards and somewhat downwards. To the right of,
and rather above this region, is situated the left auricle ; and in cases
of mitral incompetence, the reversed stream of blood pours across
this region from left to right and somewhat upwards, as it regurgi-
tates from the left ventricle into the left auricle.

In cases of mitral regurgitation, one might be led, & priori, to
expect that the mitral murmur would be always audible over the
back at the region of the mitral orifice, or midway between the
scapulae, just above the level of their lower angles. This is, how-
ever, not usually the case, and especially when the mitral murmur is
soft in character, the lungs and chest are of full size, and respi-
ration is free. This is, I believe, to be explained by the great space
that intervenes, owing to the presence of the vertebrae, between the
mitral orifice and the ear when applied over that region, by the
extent to which the lungs envelope the heart and fill the chest
backwards, and by the position of the descending aorta and the oeso-
phagus between the mitral orifice and left auricle in front and the
spinal column behind. When, however, the mitral murmur is grave,
vibrating or musical in character and loud, and when the lungs and
chest are contracted and respiration is limited, then the mitral
murmur is audible over the back at the region of the mitral valve,
and in many cases with great intensity.

The Right Auricle and Ascending Vena Cava. — The inferior and pos-
terior portion of the right auricle, and the entrance of the ascending
vena cava into that portion of the auricle are situated at the back of the
heart. The right auricle is here separated at its upper boundary
from the left auricle below the entrance of the lower right pulmonary
vein by a septum, which often makes but little mark externally. The
lower boundary of the right auricle is defined by the continuation
backwards of the posterior transverse furrow between the base of the
left ventricle and the right auricle, until it reaches the posterior longi-
tudinal furrow. The posterior and inferior portion of the right
auricle thus fills up the angle formed between the lower border of the
left auricle and the base of the left ventricle posteriorly. This angle
is formed by the downward prominence and thickness of the
muscular wall of the left ventricle at its base.

The ascending vena cava penetrates the diaphragm on a level with
the eighth or ninth dorsal spine, where it is situated nearly half an
inch to the right of the descending aorta, and of the middle line
of the spine ; and after ascending to the extent of an inch or less, it
enters the right auricle on a level with the seventh dorsal spine,
about three-quarters of an inch to*the right of the descending aorta.

The Under Surface of the Heart ; the Longitudinal Furrow and the
Right Ventricle. — The posterior. longitudinal furrow divides the left

POSITION AND FORM OF THE HEART. 105

The under surface of the heart contracts gradually from its auri-
cular portion or base, where it is wider than at any other part, to its
apex, where it is narrower than at any other part. The under
surface of the right ventricle is thus triangular in form, the base of
the triangle being at the auriculo-ventricular furrow, and its apex at
the apex of the heart. The posterior longitudinal furrow which is
Straight, forms the posterior side of the triangle, and the lower
boundary of the right ventricle, which is somewhat convex, forms its
anterior side. This lower boundary of the right ventricle at the front
of the heart, which is on a level with the body of the tenth and the
spine of the ninth dorsal vertebra, is lower in position than the lower
border of the left ventricle at the back of the heart, which is situated
in front of the cartilage between the bodies of the ninth and tenth
dorsal vertebrae, or a little lower, and is on a level with the space
between the eighth and ninth dorsal spines.

The Great Vessels. — The position of the boundary line between the
upper border of the heart ami the lower limit of the great vessels is,
as I have already stated, higher at the back than at either side or in

108 A SYSTEM OF MEDICINE.

between the mitral orifice find the base of the left ventricle in front
and the spine behind. The oesophagus lies in front of the right side
of the spinal column until it reaches the bodies of the eighth, ninth,
and tenth dorsal vertebrae, which are on a level with the seventh,
eighth, and ninth dorsal spines, where it gradually passes over the
front of the aorta. It is thus interposed between the left auricle
and the right side of the spinal column, and finally between the base
of the left ventricle in front and the aorta and spinal column behind.

The right and left lungs at the back of the chest fill up the deep
hollow in front of the angles of the ribs, and their inner margins
overlap respectively the right and left borders of the bodies of the
dorsal vertebra.

The lungs at the back and both sides completely envelop the
heart and great vessels, with the exception of those parts that lie at
the very centre of the chest, in front of the anterior portion of the
bodies of the dorsal vertebrae.

POSITION AND FORM OF THE HEART. 1 09

NOTES.

Notk 1. — PirogofF, in his valuable " Anatoiiiia Topographica," Biaun, in
his beautiful " Topograph iscli- A natomisclier Atlas ;" and Le Geudre, iu his
" Anatouiie Chirurgicale Homolographiquo," give drawings taken from sections
of the frozen dead body representing the position of the internal organs. In
this and the following notes I shall briefly describe the position of the heart as
it is represented iu those various drawings. 1 may remark that many of theso
drawings are evidently not of the size of nature.

PirogofF represents vertical sections of twelve different bodies, the sec-
tion being made cither through the centre of the sternum iu front and the
spinal column behind or to the right or left of the centre. Iu these instances
the front of the pericardium was lower in position than the front of the heart to
an extent varying from *8 or *9 inch to '02 inch. Between these two extreme
instauccs there was every variety of difference from '2 inch to '7 inch, the
average extent to which the front of the pericardium was lower than the front of
the heart being *4 inch, or less than half an inch.

These drawings of PirogofF represent, which mine do not, the relation of the
whole under surface of the heart to the floor of the pericardium. In two of
them, the whole lower surface of the heart, including both ventricles aud the
longitudinal furrow between them, rested upon the pericardium ; while in one of
these, with healthy organs, the front of the pericardium was *7 inch, and iu
another with ascites it was '35 inch below the front of the right ventricle. In
the latter case the fluid in the abdomen pressed the pericardium upwards into
close contact with the heart, aud elevated that organ. In four other cases the
right ventricle rested upon the pericardium, while in all of these the interventri-
cular furrow was separated by fluid from the pericardium from *2 in. to *65 iu.,
and in three of them the left ventricle was higher than the pericardium from
•3 in. to *4 in. In the six remaining cases, a film of fluid, varying from
•1 in. to #5 in., separated both ventricles and the longitudinal furrow from the
pericardium ; in two of those cases the separation of the two surfaces was equal
throughout ; in two it was greater at the furrow than the ventricles, and greater
below the left ventricle than the right ; and iu two it was greater below the
right ventricle than the left.

Notk 2. — PirogofF represents the exact position of the lower boundary of the
front of the heart in relation to the lower end of the bony sternum in five instances
in which a vertical section was made through the centre of the sternum in front
and the spinal column behind. In two of these instances the lower boundary of
the heart was above the lower end of the sternum to an extent varying from *8 in.
to '7 in., and in three of them it was below the lower end of the sternum to an
extent varying from one inch to half an inch. He also gives thirteen cross,
sections of the body that show whether the lower boundary of the heart was
higher or lower thau the lower end of the sternum. In three of these cases the
heart was below, in four it was above, and in six it was either at, a little above,
or a little below the lower end of the sternum. In one instance the lower
border of the heart was very much below, aud in another it was very much
above the lower end of the sternum. The latter case stood alone. The

110 A SYSTEM OF MEDICINE.

section was made through the lower margin of the nipples and the middle of
the third space, and only a small piece of the ventricles towards the apex re-
mained frozen in the pericardial fluid ; the heart being absent from behind the
centre of the sternum. The stomach and the oesophagus were enormously dis-
tended with food, and both the stomach and the liver rose high into the cavity of
the chest, above the level of the section. In eight other cases the section was
made, as in this one, through the third cartilage, in nine others through
the fourth, and in four others through the fourth space ; and in all of these,
amounting to twenty-one, the heart was present in the section of full size.

Braun gives vertical sections of the body through the centre of the sternum
and the spine in two instances, in one of which the lower boundary of the heart
is half an inch above, and in the other is an inch and a third below the level of
the lower end of the sternum.

Note 3. — The position of the lower boundary of the pericardium in relation
to the lower end of the sternum is represented by PirogofF in the two groups of
sections, vertical and transverse, referred to in Note 2. Tn two of the vertical
sections the lower boundary of the front of tho pericardium was above the level
of the lower end of the sternum from the tenth to the third of au inch, and in
three of them it was below the lower end from 1*2 in. to *88 in. Tn the
thirteen cross sections the lower border of the pericardium was above the level
of the lower end of the sternum in only one case, and below it in twelve case?.

Note 4. — PirogofF represents the position of tho apex in relation to the
fourth, fifth, and sixth spaces and cartilages in the two groups of vertical and
transverse sections. Tn one of the vertical sections, a case of ascites, the apex
was situated in the fourth space ; in another, it was situated behind the fifth
rib, and in a third behind the sixth rib ; while of the cross sections, in five the
apex was situated in the fifth space, in five behind the fifth cartilage, and in one
behind the fourth cartilage or the third space. Five vertical sections also repre-
sent the relation of tho lower boundary of the right ventricle to the cartilages and
spaces, at a point intermediate between the lower boundary of the sternum and
the apex ; in two of these the inferior margin of the right ventricle was behind
the seventh cartilage, in one behind the sixth cartilage, in one behind the fifth
space, and in one behind the fifth cartilage.

Note 5. — PirogofF, in the three vertical and eleven cross sections referred to
in Note 4, shows the relation to the cartilages and spaces of the lower boundary
of the pericardium below the apex. In two of the three vertical sections repre-
senting the apex, the inferior border of the pericardium was lower than the
inferior border of the apex from two-thirds of an inch (*7 in.) to half an inch
(•4 in.) ; and in the remaining one the pericardium fitted close upon the apex.
Tn two of these cases the lower boundary of the pericardium below the apex
was behind the sixth cartilage, and in the third, that affected with ascites, behind
the fifth cartilage. Tn three of the cross sections the lower boundary of the
pericardium below the apex was situated behind the sixth cartilage, in fi^re of
them it was behind the fifth space, in two behind the second cartilage, and in
the remaining one behind the fourth cartilage. In two of the Qve vertical sec-
tions in which the relation of the lower border of the right ventricle to the car-
tilages aud spaces is shown, the lower boundary of the pericardium below the
ventricle was situated behind the seventh cartilage, in two behind the sixth space,
and in one behind the sixth cartilage.

Note G. — PirogofF gives a series of deepening sections made downwards and
from side to side, presenting a front view of the organs. Tn two of the more super-
ficial of these sections there was an inclination of two-thirds of an inch (*7 in.)

POSITION AND FORM OF THE HEART. Ill

from right to left extending from the lower boundary of the right auricle to the
apex of the heart. In a third section, a case of ascites, there was no inclination,
the apex being on the same level as the lower border of the right auricle. When
the sections deepened, the inclination was still maintained, but the dip from auricle
to the apex was less great. Thus in three sections in which the lower border
of the left ventricle was .exposed, the dip from auricle to apex was respectively
one-half ('4 in.), one-third ('3 in.), and one-sixth (15 in.) of an inch, the latter
section being progressively deeper than the former. In like manner, but with
a different effect, in two other sections of the case of ascites, the lower boundary
of the apex was higher than that of the auricle, in one section by the fifth
of an inch (2 in.), and in a deeper section by half an inch ("5 in.)

Note 7. — Pirogoff shows the extent to which the heart extends to the left of
the middle line of the sternum in four (or five) vertical, and in eighteen (or
seventeen) cross sections. The heart extended to the left of the centre of the
sternum from two inches to two and three-quarters (28 in.) in two-thirds of these
cases (14 in 22); from an inch and a third (1*4 in.) to an inch and three-
quarters (1- 85 in.) in one-third of them (7 in 22); and three inches and a
third (3*4 in.) in one additional instance.

Note 8. — Pirogoff indicates approximately the position of the top of the
arch in five vertical and four cross sections. In two of the vertical sectious the
top of the arch appeared to be respectively a quarter and a tenth of an inch
above the top of the manubrium, on a level in one with the top of the second, and
in the other with the top of the third dorsal vertebra. In the three other vertical
sections the top of the arch was three-quarters of an inch (•(> to '8 in.) below
the top of the manubrium, and on a level with the lower portion of the third
dorsal vertebra. In one of the four cross sections the top of the arch at the
origin of the innominate and left carotid arteries was on a level with the
lower edge of the sterno-clavicular articulation, and with the lower border
of the second or upper border of the third dorsal vertebra ; while in three of them
it was on a level with the first space, and in the individual cases respectively
with the lower border of the second, the lower border of the third, and the
upper bonier of the fourth dorsal vertebra. Braun gives two vertical sections,
in one of which the top of the arch of the aorta was from a quarter to half an
inch below the top of the manubrium and on a level with the third dorsal
vertebra, while in the other it was more than an inch below the top of the
sternum and on a level with the fourth vertebra.

Note 9. — The lower boundary of the heart was from two-thirds of an inch
(•(J in.) to an inch below the lower end of the sternum in Pirogoff 's three ver-
tical sections in which the top of the aorta was three-quarters of an inch (6 in.
to '8 in.) below the top of the manubrium ; and was an inch and a quarter
below the end of the sternum, reaching, indeed, to the tip of the ensiform cartilage
in Braun's case, in which the top of the aorta* was more than an inch below the
top of the sternum. On the other hand, the lower boundary of the heart was
three-quarters of an inch (*8) above the lower end of the sternum in one of
Pirogoff 's cases, in which the top of the aorta was above the top of the sternum,
and was fully half an inch above that bone in Braun's ease, in which the top
of the aorta was from a quarter to half an inch below the top of the sternum.

Note 10. — Pirogoff shows in his vertical sections the position of the origin
of the pulmonary artery in eight instances, and that of the top of the auricular
portion of the right auricle in seven. The origin of the pulmonary artery was
situated behind the second cartilage in one instance, and behind the fourth car-
tilage in another; in three cases it lay behind the third cartilage, and iu one

112 • A SYSTEM OF MEDICINE.

behind the second space ; while in two it lay from two to two-and-a-half inches
below the top of the manubrium. The top of the right auricle was seated
behind the second cartilage in two cases, behind the third cartilage in two, and
below the top of the manubrium from an inch and a half to an inch and three-
quarters in three. In one of the instances in which it lay behind the third car-
tilage, it was three inches below the top of the manubrium.

Note 11. — In five of Pirogoff 's vertical sections referred to in Note 10 the
vertical length of the pulmonary artery and the right ventricle is shown. In
two cases the vertical length of the pulmonary artery was about half an inch, and
in these two cases the vertical length of the right ventricle was respectively three
inches (32 in.) and two and a third (2'3 in.). In the three other cases the vertical
length of the pulmonary artery was about one inch ('9 in., 1*05 in., 1*2 in.),
that of the right ventricle in those cases being about three inches (2 8 in.,
3*1 in., 3 5 in.). In the three latter cases, in which the pulmonary artery was
relatively long, the length of the ventricle to that of the artery was as three to
one ; while in the two others in which the vessel was short, the ventricle was
from four-and-a-half to six times the length of the artery.

Note 12. — In one of Pirogoff s transverse sections, referred to in Note 1 1 ,
the top of the pulmonary artery was situated just above the secoud cartilage,
and the artery, in its short upward course (*4 in.), was covered by the second
cartilage ; in another, the top of the artery lay behind the third cartilage, and
the artery ascended within the third space. In the three other cases the artery
took an intermediate and average position within the second space, its top being
seated behind the second cartilage, and its origin behind the third cartilage, or,
in one instance, the second space.

The origin of the pulmonary artery was the lowest in position, being behind
the fourth cartilage, in the one among these five cases in which the vessel took
the longest upward course (1*2 in.) ; while on the other hand, the origin of the
artery was the highest, being behind the second cartilage, in the one in which the
vessel was the shortest (*4 in.)

Note 13. — The arch of the aorta, measured from the point at which it came
into view above the right auricle to the adjacent origin of the innominate and left
carotid arteries, in Pirogoff *s vertical sections, varied in approximate vertical
length from about one inch to more than two inches (about 2 2 in.), its average
length being about an inch and a half. In two cases, in which the vessel was short
(about 1 in.), the vertical length of the arch, from the point at which it came
into view, was less than that of the heart, measured from the same point, in
the proportion of 10 to 25 ; while in three cases, in which the vessel was long
(1*8 in., 2 in., 2*2 in.), the ratio of the length of the vessel to that of the heart
was about 10 to 18.

Note 14. — Pirogoff shows the vertical length of the right auricle in six
sections. In three of these the length of that cavity was two inches and three-
quarters (2-6 in., 2 7 in., 2 8 in.) ; and in three it was from three inches and a
third to almost four inches (3*3 in., 3*4 in., 3*8 in.)

Note 15. — Pirogoff represents the vertical length of the right ventricle in
eleven cases. In two of these the cavity was two inches and a third (2*3 in.),
and in one it was four inches in length. There was considerable variation in
the other cases between these limits, the average length of the cavity in the
eleven cases being three inches.

Note 16. — The great vessels occupied the upper half of the sternum, and
the heart its lower half, in two of Pirogoff 's and in one ofBraun'a sections.
In one of Braun's sections the great vessels lay behind the upper third of the

POSITION AND FORM OF THE HEART. 113

bone, and the heart behind its lower two-thirds ; in three of PirogofF's sections
the great arteries were covered by the upper three-sevenths of the sternum, and
the heart by its lower four-sevenths (1*5 in. to 2*1 in. ; 2*7 in. to 3in. ; l*4in.
to 2*3 in.) ; while in one of PirogofF's the great vessels occupied the sternum to
a greater extent than the heart in the proportion of eight to seven (3 1 in. to
2-7 in.).

Note 17. — The width of the healthy heart was one-half of the width of the
chest in two of PirogofF's cross sections (78 in. to 3*9 in. and 7-2 in. to 3*5 in.) ;
it was one-third of that of the chest in four of them (7*4 in. to 2*4 in., 9*4 in.
to 3*2 in., 9a2 in. to 3*2 in., 7*2 in. to 2*6 in.), and in six of them the proportion
between the width of the heart and that of the chest varied from 10 to 3*9 to
10 to 4*6. In no instance was the breadth of the healthy heart greater in pro-
portion than one-half of that of the chest In this respect PirogofF's cases
differ from mine, for, as I have said above, in one-third of my cases the width
of the heart was greater than one-half of that of tho chest (10 to 5 to 10 to
6 2). This may partly be accounted for that in PirogofF's drawings the section
was not as a rule made across the widest part of the heart, and that the breadth
of the heart was measured from precisely opposite points ; whereas in mine the
measurement was taken from the point of the heart furthest to the left, which
was near the apex, to the point of the heart furthest to the right, which was
about the middle of the right auricle ; and I need scarcely say that these points
were never precisely opposite to each other.

Note 18. — In some of Pirogoff 's sections the right ventricle and auricle were
proportionally broad in relation to the front of the left ventricle when the heart
itself was wide in relation to the width of the chest, while the right cavities
were relatively narrow when the heart itself was relatively narrow. In other
instances, however, it was the reverse, the heart being relatively narrow or wide,
when the right cavities were respectively relatively wide or narrow.

Note 19. — In one of Pirogoff 's cross sections the heart extended one inch
and a tenth into the right side of the chest, and nearly three inches (28 in.)
into its left side ; while in another of them the heart occupied the right side of
the chest for a little less than two inches (1*85 in.), and its left side for a little
more than two inches (2*15 in.). In one of these extreme instances nearly
three-fourths of the heart occupied the left side, and over one-fourth of
it the right side of the chest ; while in the other more than one-half of the
organ lay in the left side, and less than one-half of it in the right side.

In twenty-five cross sections nearly two-fifths of the heart occupied, on
an average, the right side, and fully three-fifths of it the left side of the
cheat (10 to 17). These sections were made across the heart at all levels,
from just below the origin of the great vessels to a little above the lower
boundary of the organ. In at least four instances more sections than one were
made through the same body at different heights, and in these instances the
heart, as a rule, lay more to the right in the higher than in the lower sections.
This was due to the greater proportionate prevalence of the right auricle in the
higher and middle sections ; and of the right and left ventricles in the lower
sections of the heart. There were, however, three marked exceptions to this
rule, which seemed to be due to the greater extension of the right auricle to
the right at its middle than at its higher region.

Note 20. — The right lung was more developed in front than the left in
eight out of nine cases, in which two-thirds of the heart or more occupied the
left side, and one-third of it or less the right side of the chest ; and the develop-
ment of the two lungs was about equal in seven out of eight cases in which

TOL. IT. 7

114 A SYSTEM OF MEDICINE.

two-fifths of the heart or more lay in the right side, and three-fifths of it or
less in the left side of the chest, the right lung being, however, larger than the
left in the two exceptional cases.

Note 21. — The breadth of the combined right auricle and ventricle in
relation to that of the left ventricle as seen in front in fifteen of Pirogoff's
croso sections, varied from 10 to 1 '4 to 10 to 4*4, the average proportion being
10 to 3-3.

Note 22. — The auricular portion of the right auricle varied in breadth
in Pirogoff's cases from nearly an inch and a half (1*4 in.) to four-fifths of an
inch (*8 in.), its average breadth in ten cases being one inch.

Note 23. — The body of the right auricle varied in breadth in Pirogoff's
cases from nearly an inch and a half (1*4 in.) to the fifth of an -inch (*2 in.), its
average breadth in twenty-one cases being two-thirds of an inch ('66 in.).

Note 24. — The left edge of the auricular portion of the right auricle
extended almost to the left edge of the sternum (*1 in. from left edge) in one
instance ; almost or quite to the centre of the sternum, so as to lie behind its
right half, in four instances ; . and in one instance it was covered by the right
third of that bone.

Note 25. — The right edge of the right auricle extended to the right of the
right edge of the sternum from the third of an inch to an inch, and, on an
average, for two-thirds of an inch in sixteen of Pirogoff's cross sections.

Note 26. — The auricular portion of the right auricle was from one-third to
two-thirds wider than the body of the auricle in five hearts represented by
Pirogoff.

Note 27. — The width of the heart in ten of Pirogoff's sections varied from a
little more than twice (22 to 10) to almost four times as great as that of the
auricular portion of the right auricle ; the heart being on an average fully three
times as wide as the auricular appendix.

Note 28. — The heart was from three to nine times wider than the exposed
portion of the body of the right auricle in twenty of Pirogoff's cases ; the
heart being on an average nearly six times as wide as the auricle.

Note 29. — The breadth of the right ventricle varied from four-fifths (10 to
12*5) to a little less than one-half (10 to 20*5) of the breadth of the heart in
twenty-one of Pirogoff's drawings, sixteen of which were from cross sections of
the body, and five from front views of the heart. The average breadth of the
right ventricle in these drawings was two-thirds of the breadth of the heart (10
to 15), and in one-half of them (10 in 21) the proportionate width of the heart
was at or above, and in one-half of them (11 in 21) it was below that average.
The average proportionate breadth of the right ventricle in relation to that of
the heart was 10 to 16 in the sixteen cross sections, and 10 to 14 in the five
front views of the heart.

Note 30. — The breadth of the upper part of the conus arteriosus varied from
one-half (10 to 20) to four-fifths (10 to 17-2) of the breadth of the right ventricle
at its middle, in Pirogoff's five front views of the heart ; the average width of
the comes arteriosus being in those cases fully three-fifths of that of the right
ventricle (10 to 18*6).

Note 31. — The length of the right ventricle was equal to that" of its
breadth in one, and was greater than that of its breadth in four of Pirogoff's
five front views of the heart, the average proportion of the length to the
breadth of the right ventricle being in those four cases as 5 to 6 (10 to
11-75).

Note 32. — The breadth of the right ventricle in relation to the right auricle

POSITION AND FORM OF THE HEART, 115

in Pirogoff's Qve front views of the heart varied from lOto 1*3 to lOto 3*4,
the average proportion being 10 to 2*2.

Note 33. — The breadth of the right ventricle varied from an inch and two-
thirds (1*65 in.) to nearly three inches (29 in.) in sixteen of Pirogoff's cross
sections, its average breadth being just over two inches (2*1 in.) ; while in his
five front views of the heart, its breadth varied from two inches and a half to
three and a third, its average breadth being almost three inches (2*9 in.). The
cross sections were somewhat reduced in size, while the front views appeared to
be of the natural dimensions.

Note 34. — In one of Pirogoff's sections the right ventricle extended further
to the right than the left of the middle line of the sternum (1*4 in. to 1* in.
to left) ; in one it occupied the right aud left sides of the chest in equal pro-
portions (1*2 in. to 1*2 in.); but in fourteen other sections the right ventricle
extended more to the left than the right of the vertical centre of the sternum.
In two instances six-sevenths of the ventricle lay to the left, and one-seventh of
it to the right of the central line ; but on an average, two-thirds of the ven
tricle occupied the left, and one-third of it the right side of the chest.

Note 35. — In three of Pirogoff's five front views of the healthy heart, the
longitudinal furrow during its descent took a direction slightly to the left or
outwards during its whole course, so that it was about half an inch more to the
left at its lower than its upper portion ; but in two of them the furrow curved
first to the right for the third of an inch (*3 in.), and then to the left for, in
one instance, the same, and in the other for a greater extent (*5 in.)

Note 36. — In oue of Pirogoff's cross sections the right ventricle extended
for only a quarter of an inch to the left of the sternum ; but in every other
instance that ventricle was covered to a greater or less extent by the costal
cartilages. The exact extent to which they were so is not indicated, but I
judged that in one-fifth of the cases (3 in 16) the right ventricle extended
almost as far to the left as the junction of the cartilages to their ribs ; that in
one-fourth of them (4 in 16) the ventricle was covered by the two sternal thirds
of the cartilages ; that in two of them it extended to midway between the
sternum and the ribs; and that in one-third of them (6 in 16) it was only
covered by the sternal third of the cardiac costal cartilages.

Note 37. — The body of the right ventricle extended to the left of the
middle line of the sternum from four-fifths of an inch ('85 in.) to two inches
(2*1 in.), and on an average for an inch and a half (1*45 in.), in sixteen of
Pirogoff's cross sections.

Note 38. — The right auriculo-ventricular furrow, starting from the right
edge of the origin of the pulmonary, as it descended, extended to the right to
an amount varying from one inch to one inch and four-fifths, and on an average for
an inch and a half (1*45 in.), in Pirogoff's five front views of the heahhy heart.

Note 39. — The breadth of the pulmonary artery at its origin varied from an
inch to an inch and a half, and was on an average an inch and a quarter, in
Pirogoff's five front views of the healthy heart ; and in the same cases the
breadth of the pulmonary artery a little above its origin varied from three-
quarters of an inch to an inch and a quarter, and was on an average about
one inch. The pulmonary artery was wider than the aorta in four of these
instances, and narrower than the aorta in one of them.

Note 40. — The right edge of the pulmonary artery was covered by the
sternum to the extent of the third of an inch in one instance, and the tenth
of an inch in another, and the remainder of the artery, amounting to three-
fourths of its diameter in one instance (*8 in., '11 in.), and six-sevenths of it»

T 2

116 A SYSTEM OF MEDICINE.

diameter in the other, occupied the second left space or the second costal
cartilage.

Note 41. — The approximate breadth of the left ventricle as seen in front of
the heart varied from almost half an inch (*4 in.) in two instances to an inch and
one-fifth (1*2 in.) in three cases, and was on an average three-quarters of an
inch in nineteen of Pirogoff's cross sections and five of his front views of the
heart. The proportion that the width of the left ventricle at its anterior aspect
bore to that of the whole heart in those cases varied from one-eighth (10 to 1*25)
to one-third (10 to 3 2).

Note 42. — The apex was covered by the inner margin of the left lung to the
extent of from half an inch to three-quarters in three of Pirogoff's cross sections,
and to the extent of the tenth and the fifth of an inch respectively in two of
them; while in two others the outer edge of the lung was not covered by the
lung, which, however, was close to it ; and in one other instance the apex was
completely exposed, the left edge of the lung being '6 in. to the left of the apex
and *3 in. to the left of the outer left border of the pericardium.

Note 43. — The ascending aorta varied in breadth from three- Quarters of an
inch ('7 in.) to an inch and a fifth (1*2 in.) in Pirogoff's five front views of the
health j heart, its average breadth being one inch.

Note 44. — The aorta was narrower than the pulmonary artery in four and
wider in one of Pirogoff's cross sections.

Note 45. — The ascending aorta was covered by the sternum in four of
Pirogoff's five cros9 sections showing that vessel, and of these instances, in three
the artery was central and in one it inclined to the right In the remaining
case the ascending aorta extended a quarter of an inch to the left of the sternum,
being present to that extent within the left second space.

Note 46. — Pirogoff, whose work is rich in illustrations of the root of the aorta,
including its valve and sinuses, represents those parts in eight cross sections, five
vertical sections, made through the sternum or cartilages in front, and the spinal
column or adjoining ribs behind, and two vertical sections made from side to side.
In the eight cross sections the root of the aorta, including its sinuses and the
flaps of its valve, was in part covered to a very varying extent by the sternum, and
was in part situated behind the corresponding cartilage or space to the left of the
sternum. In one of them four-fifths of the artery lay behind the sternum
('8 in.),. and one-fifth of it extended to the left of that bone ('2 in.) ; while in
one of them only one-fifth of the vessel (-8 in.) was covered by the sternum,
while four-fifths of it occupied the adjoining third left space. There was
every gradation between these two extreme instances ; and, on an average, less
than three-fifths of the root of the aorta lay behind the left portion of the sternum,
and more than two-fifths of it behind the corresponding left cartilage or space.

The upper part of the root of the aorta, including its sinuses and the flaps
of its valve, was situated in two of the cross sections on a level with the second
space, its lower portion being on a level with the third cartilage ; in three of
them its upper portion was on a level with the middle or lower edge of the third
cartilage, its lower portion extending to a greater or less extent to the level of
the third space ; in one of them its lower border was on a level with the upper
half of the third space ; and in two of them its upper portion was on a level
with the third space, at and above its middle, while its lower portion extended to
the level of the upper part of the fourth cartilage. In an additional cross section
made through the third space the lowest portion of the right posterior flap of
the aortic valve remained, showing its attachment to the anterior flap of the
mitral valve

POSITION AND FORM OF THE HEART. 117

Pirogoff shows the root of the aorta, including its sinuses and the flaps of
its valve, in five vertical sections, of which, (1) two sections were made through the
left costal cartilages in front, close to their articulation to the sternum, and the
ribs behind near their attachment to the transverse processes of the vertebrae ;

(2) one through (he left side of the sternum and the fifth and sixth cartilages
near their attachment in front, and the bodies of the vertebra behind ; and

(3) two through the centre of the sternum and ensiform cartilage in front, and
that of the spinal column behind.

The relations of the anterior and left posterior flaps of the aortic valve
were shown in three of those sections (1, 2), and those of the three flaps,
including in addition the right posterior flap, in two others (3). In one sec-
tion the top of the angle of junction of the anterior and left posterior flaps
was situated behind the left third cartilage, in one of them the tenth of an
inch (*1 in.) below its upper edge, and in another of them the third of an
inch (*3 in.) above its lower edge. In two of them the lower boundary of
the section of the aortic valve was half an inch (*5 in. and '45 in.) below the lower
edge of the third cartilage or about the middle of the third space. As, how-
ever, in these instances the right posterior flap had been removed, the lower
boundary of the valve and of the origin of the aorta must have been about half
an inch lower than the lowest point of the section, or behind the upper portion
of the fourth left costal cartilage. In the third instance (2), in which also the
inferior flap had been removed, the top of the angle of junction of the two
superior flaps lay behind the sternum, three-quarters of an inch (*7 in.) below
the lower end of the manubrium, or about on a level with the lower border of
the second space ; and the lowest portion of the section through the aortic
valve was situated behind the sternum an inch and a half (15 in.) below the
lower end of the manubrium, or about on a level with the top of the third
space, so that in this instance the lower boundary of the aortic valve would be
about on a level with the lower border of the third space. In these three cases
the measurement of the section of the aortic valve, the lower portion of those
valves being removed, varied from two-thirds of an inch in one instance (*6 in.) to
almost an inch (*9 in.) in two instances. In the two remaining sections, however,
in which the whole valve was exhibited, its measurement from above downwards
amounted to a little over an inch (I'l in.) in one instance, and to an inch and a
half (1*5 in.) in the other. In one of these cases, in which the lower boundary
of the heart was four-fifths of an inch (;8 in.) above the lower end of the
sternum, the upper boundary of the aortic valve was situated about half an inch
(•4 in.) above the middle of the sternum, or about on a level with the second
space, and its lower boundary about three-quarters of an inch (-7 in.) below the
middle of the sternum, or about on a level with the lower edge of the third car-
tilage or upper border of the third space. In another case, in which the
lower boundary of the heart was situated behind the ensiform cartilage, about an
inch ('95 in.) below the lower end of the sternum, the upper boundary of the
aortic valve was situated behind the sternum four-fifths of an inch (8 in.) below
the middle of the bone, or about on a level with the lower edge of the third car-
tilage or upper border of the third space, and the lower boundary of the valve was
situated behind the sternum, fully two inches (2*2 in.) below the middle of the
bone, and two-thirds of an inch (*65 in.) above its lower end, or about on a level
with the fifth cartilage. Keeping out of view this unusual case, it may be said
that in PirogofTs sections, on an average, the root of the aorta, including its
sinuses and the flaps of its valve, was situated on a level with the third cartilage
and the third space.

118 A SYSTEM OF MED r CINE.

Mitral Valve. — In one of PirogofTs vertical sections the top of the mitral
valve was fully half an inch ('55 in.) and in another of them it was a third of an
inch (*3 in.) above the lower border of the right posterior flap of the aortic
valve. In three other sections, the right inferior flap of the aortic valve had
been removed, the other flaps being retained ; and in one of these sections the
top of the mitral valve was the third of an inch, in another it was tho fifth
of an inch (*2 in.), and in the third it was about the tenth of an inch above the
lower edge of the left posterior flap of the aortic valve.

The lower border of the mitral valve was about an inch below the lower border
of the left posterior or the anterior flap of the aortic valve in the three instances
in which the right posterior flap had been removed ; and it was from fully half
an inch to fully three-quarters of an inch below the lower edge of the right
posterior flap in the two other instances. In one of PirogofTs front vertical
sections the top of the mitral valve was fully half an inch (*6 in.) above the
level of the lower border of the right posterior flap of the aortic valve.

In two of PirogofTs vertical sections, and probably in a third, the top of the
•mitral valve was about half an inch (-6 in.) below the level of the middle of the
sternum, but it was an inch and three-quarters below that point in another
instance in which the lower boundary of the heart was an inch below the lower
end of the sternum.

In one of PirogofTs vertical sections the top of the mitral valve was on a
level with the lower edge of the third cartilage ; and in three of them it was
behind the third space, these occupying respectively the upper, the middle, and
the lower portion of that space. If we combine the cases in which the vertical
section was made through the cartilages with those in which it was made
through the sternum, and estimate in the latter cases the approximate relative
position of the valve to the cartilages by its position in relation to the sternum,
we find that in two cases the top of the mitral valve was on a level with the lower
portion of the third cartilage ; in three, with the upper third of the third space ;
in two, with the middle or lower portion of the third space ; and in one, with
the fourth space.

In one of Braun's vertical sections (a woman aged 25), in which the lower
boundary of the heart was half an inch above the lower end of the sternum, the
top of the mitral valve was half an inch (*4 in.) below the centre of the
sternum; and in another section (a soldier aged 21), the lower boundary
of the heart was an inch and a fifth (1'2 in.) below the lower end of the
sternum, and the top of the mitral valve was nearly an inch and a half (1 '4 in.)
below the middle of the sternum.

The lower border of the mitral valve was situated an inch and a half above
the lower end of the sternum in one vertical section, and in two it was as low as
half au inch above that point ; while in three other vertical sections it was on a
level with the fourth space, and in two with the fifth cartilage. If we group the
two sets of cases together, it may be estimated that in four of them the lower
end of the valve was behind the fourth space, and in four behind the fifth
cartilage.

In one of Braun's vertical sections, from a woman aged 25, in which the lower
boundary of the heart was half an inch above the lower end of the sternum, the
lower boundary of the mitral valve was an inch and a half (1*4 in.) above
that end of the bone; and in another, from a soldier aged 21, in which the
lower boundary of the heart was an inch and a fifth below the lower end of the
sternum, the lower border of the mitral valve was less than half an inch ('4 in.)
ahove the end of the bone.

POSITION AND FORM OF THE HEART. 119

Pirogoff represents nine cross sections through the second space, the whole of
which were above the mitral valve; four through the third cartilage, two of
which were above the mitral valve, and two were made through the upper part
of the valve ; eight through the third space, one of which was above and one
below the mitral valve, while five were made through the upper portion of the valve,
and one through the middle of the mitral orifice ; nine through the fourth car-
tilage, of which two were made through the upper portion and two through the
middle of the valve, while five were made below the valve ; six through the
fourth space, of which one was made through the top of the valve, and three
through its middle, while two were made below the valve ; and seven through the
fifth cartilage, of which six were below the valve, and one was made through
the middle of the mitral orifice.

It is self-evident that, in these cases, the top of the mitral valve occupied the
space or cartilage above that in which the section passed through the middle of
the mitral orifice, and that the top of the valve was relatively still higher in those
cases in which the section was made below the mitral valve.

Estimating the position of the top of the mitral valve approximately in these
sections on this view, I consider that the upper boundary of the valve was
situated in one case on a level with the second space ; in nine, on a level with
the third cartilage ; in two, with the third cartilage or third space ; in nine, with
the third space ; in two, with the third space or fourth cartilage ; in three,
with the fourth cartilage ; in six, with the third cartilage or space or the fourth
cartilage ; and that iii one instance the top of the mitral valve was ou a level
with the fourth space.

In these cases, on the basis of the calculation just made, it may be approxi-
mately estimated that the aveiagc position of the top of the mitral valve was
about on a level with the upper half of the third intercostal space.

In the same transverse sections, on a similar approximate calculation, the lower
border of the mitral valve was situated about on a level with the third cartilage in
one instance ; the third space in six instances ; the fourth cartilage in two ; the
fourth space in four ; the third space, fourth cartilage, or fourth space in six ; the
fifth cartilage in four instances ; and below that cartilage in one.

The average position of the lower boundary of the mitral valve in these cases
appears to me, from as close an estimate as I can make, to be about on a level
with the lower edge of the fourth cartilage and the upper border of the fourth
space.

Pirogoff represents the mitral valve or orifice in seven cross sections, and in
all of them the anterior wall of the mitral orifice was situated more to the right
than its posterior wall to an extent varying from one- third (35 in.) to four-fifths
(•8 in.) of an inch.

In four of these sections the mitral orifice was situated behind the left half
of the sternum ; and in three of them it was placed partly behind the left
portion of the sternum, partly behind the cartilages and spaces to the left of that
bone. In no instance was the anterior wall or border of the mitral valve seated
to the right of the middle line of the sternum.

Tricuspid Valvk. — In two of Pirogoff's vertical sections the top of the tri-
cuspid valve was nearly the third of an inch (a3 in.), and in two others it was
nearly half an inch (*4 in. and 45 in.) below the level of the top of the mitral
valve.

The lower border of the tricuspid valve was below the level of tho lower border
of the mitral valve from half an inch, in the first two cases noted above, to three-
quarters of an inch (65 in. and *75 in.) in the other two cases

120 A SYSTEM OF MEDICINE.

The top of the tricuspid valve was situated, in one of PirogofPs vertical sections,
half an inch, and in two of them one inch, below the centre of the sternum ; in
another instance it was an inch above the lower end of that bone. In one of
Braun's vertical sections, in which the lower boundary of the heart was high, the
top of the tricuspid valve was on a level with the centre of the sternum.

The top of the tricuspid valve was on a level with the top of the third space
in one vertical section, with the fourth space in another, and with the fifth car-
tilage in a third instance.

The lower border of the tricuspid valve was one inch above the lower end of
the sternum in two of PirogofPs vertical sections, and an inch and a half above
that point in one of Braun's vertical sections, in which the lower boundary of the
heart was above the lower end of the sternum ; and it was a third of an inch
(*3 in.) below the lower end of that bone in two of Pirogoff *s sections, in which
the inferior boundary of the heart was behind the middle of the ensiform car-
tilage. The lower border of the valve was on a level with the fourth space in
one of PirogofTs sections, and with the sixth cartilage in two of them.

Pirogoff represents four cross sections through the third cartilage, all of which
were above the tricuspid valve ; eight through the third space, four of which
were above that valve, three were made through its upper portion, and one below
it ; nine through the fourth cartilage, of which three were above the valve, one
was made through its middle, three through its lower portion, one through the
bottom of the valve, and one below it ; six through the fourth space, of which
one was above the valve, three through its upper portion, one through its lower
portion, and one below it ; and seven through the fifth cartilage, of which one
was made through the middle of the tricuspid orifice and six below it.

Estimating approximately the position of the top of the tricuspid valve in these
cross sections, T consider that the upper boundary of the valve was situated on a level
with the second space, or third cartilage in one instance ; with the third cartilage
or space in two ; with the third space in seven ; with the third space or fourth
cartilage in ten ; with the fourth cartilage in three ; with the fourth cartilage or
space in four ; and with the fourth space in two.

I think that we may estimate that in these sections the top of the tricuspid
valve was on an average situated behind the lower portion of the third space, or
the upper edge of the fourth cartilage.

In the same cross sections, and on a similar approximate calculation, the lower
border of the tricuspid valve was about on a level with the third cartilage in one
instance ; with the third space in one ; with the third space or fourth cartilage
in one ; with the fourth cartilage in one ; with the fourth cartilage or space in
six ; with the fourth space in seven ; with the fifth cartilage in three ; and with
the fifth cartilage or space or lower in ten.

The approximate average position of the lower boundary of the tricuspid valve
in these transverse sections appears to me to be about on a level with the lower
portion of the fourth space, or upper portion of the fifth cartilage.

Pirogoff represents the tricuspid orifice in eleven cross sections, and in all of
them the anterior edge of the tricuspid orifice was more to the right than its pos-
terior edge to an extent varying from a quarter (25 in.) to four-fifths (-85 in.)
of an inch.

The left edge of the tricuspid valve was situated more to the right than the
right edge of the mitral valve in six of seven instances in which the section went
through both valves, to an extent varying from the tenth to the third (*3 in.) of
an inch ; while in the seventh instance the left edge of the tricuspid was imme-
diately in front of the right edge of the mitral valve.

POSITION AND FORM OF THE HEART. 121

In five of the eleven sections the tricuspid valve was situated behind the right
half of the sternum ; in one of them it was behind the right third of that bone ;
in one it lay partly behind the right portion of the sternum and partly to the
right of it ; in two it was central, occupying equally the right and left sides of the
sternum; and in the remaining two it lay to the left of the middle line of that bone.

Note 47. — Pirogoff shows the relation of the sternum and costal cartilages
in front to the vertebrae behind in twelve antero-posterior vertical sections and in
sixty-two cross sections.

In five of the vertical sections the top of the sternum was on a level with the
lower border of the body of the second or the upper border of the third dorsal
vertebra, or the cartilage between these two vertebrae ; in one of them it was on a
level with the top of the fourth dorsal vertebra ; and in one of them, an instance
that stands alone, it was according to Pirogoff's description, on a level with the
upper portion of the first dorsal vertebra. This description is however evidently
an accidental error, and I, therefore, for the first, read the second vertebra.
In Braun's two vertical sections the top of the sternum was on a level with
the cartilage between the second and third dorsal vertebrae.

I examined eleven human skeletons in the Museum of the Royal College of
Surgeons, with the valuable assistance of Mr. Wright, of the Museum, and I
found that in eight of them, including one in the Hunterian Museum, the top of
the manubrium was on a level with the second dorsal vertebra,1 the point varying
from its upper to its lower border ; and that in three of them it was on a level
with the first dorsal vertebra.

Jn two of Pirogoff's vertical sections the top of the sternum was on a level
with the lower border of the third rib, near the spine, in one of them it was on a
level with the upper border of the fourth rib, and in one it was above the level of
the first rib. In this last instance there was evidently an accidental error.

The lower end of the osseous sternum was on a level with the middle of the
eighth dorsal vertebra in two of Pirogoff's vertical sections, in one of which the
sternum and ribs had been elevated by a large accumulation of fluid in the
abdomen ; in one of them it was on a level with the middle of the ninth vertebra,
and in one with the cartilage between the ninth and tenth vertebra?.

In Braun's two sections the lower end of the sternum was on a level respec-
tively with the middle and lower border of the ninth vertebra.

In one of the skeletons in the Museum of the Royal College of Surgeons the
lower end of the sternum was on a level with the seventh dorsal vertebra, in one
with the cartilage between the seventh and eighth vertebra?, in three with the
middle of the eighth vertebra, in two with the cartilage between that vertebra
and the ninth, and in three with respectively the top, middle, and lower border of
the ninth vertebra, the last instance being the skeleton in the Hunterian Museum.

The middle of the sternum which corresponds with its articulation to the third
costal cartilages was on a level with the middle of the fifth dorsal vertebra in
one of Pirogoff's vertical sections, with the cartilage between the fifth and sixth
vertebras in two of them, and with the middle of the sixth vertebra in another
of them, and in Braun's two sections.

The bottom of the manubrium which corresponds with the second cartilage
and with the lower end of the upper third of the sternum was on a level with
the lower half of the body of the fourth dorsal vertebra in two of Pirogoff's
vertical sections, and in two of them and in Braun's two sections with the middle <
of the fifth vertebra.

1 The body of the dorsal vertebra is referred to here and elsewhere, unless it is other-
wise specified.

122 A SYSTEM OF MEDICINE.

The lower end of the middle third of the sternum which corresponds as a rule
with its articulation to the fourth costal cartilages was on a level with the lower
half of the body of the sixth dorsal vertebra in two of Pirogoff's vertical sections
and with the middle of the seventh vertebra in two of them and in Brauu's
two sections.

In one of Pirogoff's cross sections the sternum at the junction to it of the
first costal cartilages was on a level with the upper border of the body of the
fourth dorsal vertebra ; in four of them the sternum at the spaces between the
first and second cartilages was on a level respectively with the upper and lower
borders of the second vertebra and the upper border of the third ; the sternum
was on a level — at the second cartilages, in three instances, with the fifth vertebra ;
— at the second space, in eight instances, with respectively the fourth, fifth, and
sixth vertebrae ; — at the third cartilage, in four instances, with the top of the fifth
vertebra in one and with the seventh in three ; — at the third space, in eight
instances, with respectively the cartilages between the fifth, sixth, seventh and
eighth vertebra, and with the bodies of the seventh, eighth, and ninth
vertebrae ; — at the fourth cartilage, in ten instances, with respectively the
cartilages between the sixth, seventh, eighth and ninth vertebrae, and with the
seventh and eighth vertebrae and the top of the ninth ; — at the fourth space, in
six instances, with the cartilages between the sixth, seventh, eighth and ninth
vertebrae, and with the bodies of the seventh and eighth ; — at the fifth cartilage,
in eight instances, with respectively the lower border of the seventh vertebra,
the upper border of the tenth, and the two intermediate vertebra) ; — at the fifth
space, in two instances, with respectively the eighth and tenth vertebra ; and
finally, in four instances, the lower end of the osseous sternum or base of the
ensiform cartilage at the sixth cartilage, was on a level respectively with the lower
third of the ninth vertebra, the cartilage between that and the tenth, and the
upper border of the body of the eleventh dorsal vertebra.

The lower boundary of the front of the heart was situated in one of Pirogoff's
vertical sections on a level with the middle of the body of the eighth or, accord-
ing to an evidently erroneous reference, the seventh dorsal vertebra, behind, and
the sixth cartilage in front; in two of them on a level with the cartilage
between the eighth and ninth vertebra? ; in three of them with the top, and in
one of Braun's sections with the middle of the ninth vertebra ; and in one of
Pirogoff's sections with the lower border, and in one of Braun's with the
middle of the body of the tenth vertebra. In the last two instances the lower
boundary of the heart was situated behind the ensiform cartilage, an inch below
the lower end of the sternum, in another instance it was half an inch below, and
in two others from half to three quarters of an inch above the lower end of the
sternum.

The lower boundary of the pericardium was on a level in one of Pirogoff's vertical
sections with the cartilage between the seventh and eighth dorsal vertebrae ; in
three of them with the cartilage between the eighth and ninth vertebrae ; in one
with the upper, and two with the lower portion of the ninth, and in one with the
top of the eleventh vertebra.

In these cases the lower boundary of the pericardium was situated from a
third of an inch above to fully ono inch below the lower end of the sternum, and
from a third of an inch above the level of the sixth cartilage to that of the lower
portion of the seventh cartilage.

The top of the arch of the aorta was about on a level with the upper portion
of the body of the third dorsal vertebra in three of Pirogoff's vertical sections,
and with its middle in one of his aud in one of Braun's sections, and with

POSITION AND FORM OF THE HEART. 123

respectively the top and middle of the fourth vertebra in one of Pirogoff's and
the other of Braun's vertical sections. In these seven cases the top of the arch
of the aorta was about on a level with a point varying from a quarter of an inch
above the top of the manubrium to an inch and a half below it. In one
of Pirogoff's cross sections the top of the arch, at the origin of the inno-
minate and left carotid arteries, was in front of the upper portion of the third
dorsal vertebra, and in two of them the arch a little below its top was on a level
respectively with the lower border of the third and the upper border of the fourth
vertebra.

The top of the pulmonary artery was on a level with the cartilage between the
fourth and fifth dorsal vertebrae in one of Pirogoff's vertical sections, with the
space between the fourth and fifth ribs near the vertebras in another of them,
with that between the fifth and sixth ribs near the space in a third instance, and m
a fourth with the lower border of the seventh rib at the same situation. In these
four cases the position of the top of the pulmonary artery varied from the level of
the middle of the second left cartilage to that of the lower border of the third. . .
' The origin of the pulmonary artery was on a level with the body of the
fourth dorsal vertebra in one instance, and with respectively the lower border of
the fifth and the upper border of the sixth vertebra in two others of Pirogoff's
vertical sections ; and it was on a level with the top of the sixth vertebra or the
cartilage above it in four of Pirogoff's cross sections.

The lower boundary of the body of the left ventricle, not including its apex,
in three of Pirogoff's vertical sections was respectively on a level with the middle
of the eighth, the top of the ninth, and the two upper fifths of the tenth dorsal
vertebra.

The lower boundary of the body of the left ventricle was on a level with the
upper border of the ninth vertebra in one of Braun's vertical sections, and with
the cartilage between the ninth and tenth vertebra in the other.

The section passed through the left ventricle a little above its lower border
at the apex in Pirogoff's cross sections, in one instance on a level with the carti-
lage above the ninth vertebra, in another of them on a level with that vertebra,
in two others with the cartilage below it, and in one on a level with the upper
portion of the tenth vertebra.

The upper boundary of the root of the aorta, including its orifice, valve, and
sinuses, at the attachment of the angle of junction of the anterior and left pos-
terior flaps of the aortic valve, was situated in one of Pirogoff's vertical sections
as high as the upper third of the fourth vertebra, in two of them it was in front
of the sixth, and in one of them the upper portion of the seventh vertebra. The
lower boundary of the root of the aorta, including the aortic orifice, valve, and
sinuses, was 011 a level in two instances with respectively the middle and lower
border of the sixth vertebra, in one with the upper third of the seventh, and iu
one with the lower border of the eighth vertebra. In oue of Braun's vertical
sections the upper boundary of the root of the aorta was in front of the cartilage
between the fifth and sixth vertebrae, and its lower boundary was in front of the
cartilage between the sixth and seventh vertebras ; and in his other vertical sec-
tion the lower boundary of the root of the aorta was on a level with the lower
border of the seventh vertebra. The upper portion of the aortic valve, including
the anterior and left posterior flaps and sinuses, was situated in three instances in
front of the cartilage above the sixth vertebra, and the top and middle of that
vertebra ; in six instances in front of the top of the seventh vertebra or the car-
tilage above it ; and in one in front of the body of that vertebra.

The lower portion of the aortic valve, or its right posterior flap, was situated

124 A SYSTEM OF MEDICINE.

in four instances in front of the middle or top of the seventh vertebra or the
cartilage above it, and in one in front of the middle of the eighth vertebra.

The upper boundary of the mitral valve was situated in six of Pirogoff's
vertical sections in front respectively of the middle of the sixth dorsal vertebra,
the cartilage between the sixth and seventh vertebrae, the seventh vertebra, and
in one instance the eighth ; and its lower boundary was situated in three of his
vertical sections in front of the eighth, and in one it extended down to the top
of the lower third of the ninth vertebra. In one of Braun's vertical sections the
mitral valve extended from the level of the cartilage below the sixth vertebra
down to that of the upper third of the eighth, and in the other it extended
from the cartilage below the seventh vertebra down to the upper third of the
ninth vertebra.

The mitral valve was situated in front of the cartilage above the seventh dorsal
vertebra in two of Pirogoff's cross sections, the seventh vertebra in probably nine
of them, the cartilage between that vertebra and the eighth in two of them, and in
front of the eighth vertebra in four of them.

The upper boundary of the tricuspid valve was situated in seven of Pirogoff's
vertical sections on a level respectively with the upper and (in a case of ascites)
lower borders of the sixth dorsal vertebra, the cartilage between that vertebra and
the seventh, and the upper border of the seventh vertebra, the lower portion of the
eighth vertebra, and the cartilage below it The tricuspid valve in one of
Braun's sections extended from the level of the top of the seventh vertebra to
that of the middle of the eighth.

The tricuspid valve was on a level with the eighth vertebra in five in-
stances, with the cartilage below it in two, and with the ninth vertebra in two.

MALPOSITIONS OF THE HEART.

The displacements of the heart may be conveniently divided into
the Vertical, Lateral, Forward, and Backward displacements.

THE VEETICAL DISPLACEMENTS OF THE HEART.

Cases in which the Heart is Lowered. — The cause of the vertical
lowering of the healthy heart is in all cases, with the exception of
aneurisms of the arch of the aorta, an unusual lowering of the
diaphragm. Pulmonary emphysema, bronchitis, and spasmodic
asthma ; croup, laryngitis, and laryngismus stridulus ; collapse of the
stomach and intestines ; and aneurism of the arch of the aorta — all
tend to lower the heart. To these may be added certain cases ot
mediastinal tumour, and pleuritic effusion into the left side during
the middle period of its increase.

Pulmonary Emphysema, Bronchitis, and Spasmodic Asthma. —
In Pulmonary Emphysema the right cavities of the heart and the
pulmonary artery are greatly enlarged. The right ventricle often
completely covers the left ventricle. The diaphragm is remarkably
low, its standard position being often lower than it is in health at the
end of the deepest possible inspiration. The enlargement of the
lungs is so extensive that they cover the heart within the chest ; and
they are consequently everywhere interposed between the heart and
the walls of the chest, with the exception of the border of the seventh
costal cartilage (Fig. 27). The heart is invariably enlarged, the en-
largement being almost limited to the right side. The venae cavae
and right auricle are usually distended and of great size ; the right
ventricle is so much increased in volume that it almost or altogether
conceals the left ventricle, its walls being hardened and hypertrophied ;
and the pulmonary artery is greatly increased in length and breadth.
Notwithstanding the enlargement of the heart, its impulse is imper-
ceptible over the walls of the chest ; and in some cases its sounds are
so muffled that they are scarcely audible over the usual cardiac region
owing to the great development of the lungs in front of the heart.
In no instance, however, is the heart absolutely covered by the dilated
lungs. The central tendon of the diaphragm descends almost or quite
to the level of the lower end of the ensiform cartilage, and neces-
sarily draws downwards the enlarged heart. It is customary to
speak of the displacement of the heart downwards as being caused by

126 A SYSTEM OF MEDICINE.

the expansion of the lung. This may be so in some cases, bat as a
rule the unusual descent of the heart, like that of the base of the
lungs, is caused by the unusual descent of the diaphragm. The
lower boundary of the right ventricle is brought downwards into the
epigastrium, so that it is situated behind and to each side of the ensi-
form cartilage. In that position, and to the left of it, the heart is not
covered with lung, and it is therefore iu contact with the ensiform carti-
lage, with the neighbouring margin of the seventh left costal cartilage.

Fin. 27-— Position of the heart and great vessel* in Pulmonary Emphysema. The
heart » displaced downward^ and is covered with the over-developed lung*. The

rx-beat is imperceptible, but the impulse of the right ventricle is teen and felt in
epigastrium.

and with the intermediate abdominal muscles, the pericardium inter-
vening. The result is that, as Dr. Stokes has pointed out, the impulse
of the right ventricle may be felt in the epigastrium ; and as the
right ventricle is hypertrophied, "the heart may be felt pulsating
with a violence that we would not expect from the examination of
the pulse at the wrist, which is often small and feeble, while the
impulses of the right ventricle are given with great strength." • The
form of the chest, the great expansion of the lungs, the low position

' Dr. Stokes on the Diaeawi of the Cheat, p. 17a'

MALPOSITIONS OF THE HEART. 127

of the diaphragm, and the enlargement, elongation, and lowering of
the heart and great vessels, all correspond, though to an exaggerated
degree, with the condition of those parts at the end of the deepest
possible inspiration in health. The presence of the impulse and
sounds of the heart over the epigastrium, and their absence over the
walls of the chest, are the signs that often first direct attention to the
morbidly enlarged condition of the lungs.

In cases of severe bronchitis, the diaphragm is invariably lowered,
the right cavities of the heart are enlarged, and the lungs are
amplified. In those cases, therefore, as in emphysema, the heart is
lowered, its impulse is obliterated over the intercostal spaces by the
interposition of the lung, and the beat of the right ventricle is felt
and seen in the epigastrium. The extent to which the heart ris
enlarged, lowered, and covered by lung is by no means so great in
bronchitis as in emphysema.

When, as is often the case, the patient affected with emphysema is
attacked by bronchitis, the extent to which the heart is lowered, and
enveloped by the lungs is increased.

During an attack of spasmodic asthma, the diaphragm descends, the
lungs are expanded to the utmost, and the impulse of the right ventricle
is lowered into the epigastrium, just as in cases of true pulmonary
emphysema. After the seizure is over, its effect upon the size of the
lungs and the position of the heart does not immediately disappear.
Gradually, however, the organs resume their healthy size and position.
The asthmatic seizure that often attacks those affected with emphy-
sema, is accompanied by an excessive amplification of the lungs and
descent of the impulse ; but in such patients the lungs and heart do
not regain their normal size and position after the cessation of the
attack, and in this important respect true spasmodic asthma is to
be distinguished from the asthmatic seizure of a person affected with
true pulmonary emphysema.

Croup, Laryngitis, Laryngismus Stridulus. — In all those cases in
which there is excessive narrowing of the fauces, larynx, or trachea so
as to contract the channels through which air is admitted into the lungs
and render inspiration exceedingly difficult, the inspiratory efforts
are laborious but ineffectual. Every muscle of respiration is brought
into powerful action. The diaphragm descends as low as possible.
The lungs are consequently lengthened and the heart is drawn down-
wards. As air, in spite of the laboured breathing, #can scarcely enter
the air tubes, the lungs, being lengthened downwards, instead of
expanding, collapse during inspiration, and the walls of the chest
fall inwards. The lungs recede from before the heart, which is in
immediate and extensive contact with the walls of the chest as well
as with the ensiform cartilage. The heart is, therefore, in such cases
to be felt beating with force over and to the left of the lower sternum
and in the epigastrium.

Collapse of the Stomach and Intestines. — When the abdomen is un-
usually spare, the stomach and intestines being comparatively or

128 A SYSTEM OF MEDICINE.

quite empty, the abdominal organs shrink downwards, and the

Fig. 28.— Position of ths heart tad great vessel! in a case with Collapse of At Stomach
and Jntatinti. The heart is displaced downwards, and covered with long to the
fifth cartilage. The apei-beat is present in the fifth apaue, and perhaps in the auth,
and the impulse of the right ventricle is seen and felt in the epigastrium.

diaphragm is permanently lowered. This was well seen in the poor
woman from whom fig. 28 was taken. She hod been unable to

MALPOSITIONS OF TUB HEART. J 29

swallow owing to cancer of the oesophagus for a fortnight before her
death. Her emaciation was extreme. The stomach and intestines
were absolutely empty of gas as well as of food. The liver, though
not enlarged, had dropped downwards, so that its lower border rested
on the bones of the pelvis. The diaphragm necessarily followed the
liver and stomach in their descent, and as the result, the lungs at
their base, and the heart where it rested on the diaphragm, were
unusually lowered, and both organs were remarkably lengthened.
The elongation of the ascending aorta and the pulmonary artery was
very marked.

This was an extreme case, but in all instances of abdominal col-
lapse, the diaphragm descends in exact proportion to the .descent
of those organs upon which it rests, and the lungs and heart are
lengthened downwards to a corresponding degree. In some of those
cases the transfer of the impulse from the iutercostal spaces to the
epigastrium may give rise to the suspicion of pulmonary emphysema
ou the one hand, or aneurism of the abdominal aorta on the other.
In emphysema the chest is unduly developed, and the abdomen,
instead of being retracted, is usually of more than average size. In
aneurism of the lower thoracic or higher abdominal aorta, the im-
pulse or pulsation in the epigastrium is strong during expiration, but
it lessens and even disappears during a deep inspiration. In cases of
abdominal collapse, it is the reverse, for the impulse in the epigas-
trium becomes lower and stronger when the patient takes a deep
breath.

Aneurism of the Arch of the Aorta. — One would have expected
& priori that aneurisms affecting the arch of the aorta, especially
when they are of large size, would cause considerable displace-
ment of the heart downwards. Dr. Townshend saw an instance
of aneurism of the arch thrusting the heart downwards, so that
it pulsated in the epigastrium.1 I possess drawings taken from
thirteen cases of aneurism of the arch of the aorta. In one of
these the lower boundary of the right ventricle was situated more
thau an inch below the lower end of the sternum. In four there
was effusion of blood into the left pleura, displacing the heart to
the right In the remaining seven instances the lower boundary of
the right ventricle was from one-third to three-quarters of an inch
below the lower end of the sternum. It is clear that in the majority
of these cases, although the aneurism was in nearly all of them large,
varying from three to five inches in diameter, the descent of the heart
into the epigastrium was definite, but not proportionately great. In
two of the instances there was cylindrical aneurism or dilatation of the
ascending aorta. In these the transverse diameter of the aorta was
only two inches, while its vertical measurement was four inches.
They must, therefore, be included with the others in estimating the
influence of aneurism of the arch of the aorta in displacing the
heart downwards. The aneurismal sac displaces not so much the

1 Cyclopedia of Medicine, ii. 391. r*

VOL. IV. K

130 A 8Y8TEM OF MEDICINE.

whole heart as those parts of it upon which it makes immediate
pressure, and which are subjected thereby to compression. This
applies especially to the aneurisms of the ascending aorta, which
amount to nine among my cases. In all of these the right ventricle,
and in most of them the right auricle, were compressed from above
downwards, the compression starting from a point at the top of the
transverse furrow between those cavities, where the aorta comes into
view. The difference in the vertical diameter of the right ventricle
below the part in question and just below the pulmonary artery,
amounted in one instance to two inches, the actual measurements
being respectively three and five inches. As a rule the difference was
much less, but this was mostly due to the right ventricle being com-
pressed downwards in its whole breadth by the sac. In five of the
cases the auricular appendix was displaced downwards and to the
right.

The downward displacement of the apex in aneurism of the arch
of the aorta is not considerable, being in fact mainly due to co-existing
hypertrophy of the left ventricle. That condition, however, is not
usual, except in those cases of cylindrical aneurism or dilatation of the
ascending aorta, in which there is free aortic regurgitation, when
the left cavity is greatly enlarged, and when the descent of the apex is
much more due to that cause than to the aneurism.

Mediastinal Turnovers. — Dr. Bennett gives a case of mediastinal
tumour, which will be more fully noticed at page 144, in which there
was considerable displacement downwards and to the right of the
heart, which was seen and felt beating in the epigastrium.

Pleuritic Effusion into the Left Side. — In the middle period of these
cases, when the fluid is steadily increasing, but has not yet reached to
its height, there is displacement downwards and to the right of the
heart, which may be felt beating in the epigastrium. A full account
of such cases, and an explanation of their phenomena, will be found
at page 136.

Cases in which the Heart is Raised. — Abdominal enlargement
from gastro-intestinal distension, ascites, the presence of gas in the
cavity of the* abdomen, abdominal tumours, ovarian dropsy, aneurism
of the abdominal aorta at the cseliac axis, and enlarged liver and spleen,
all tend to elevate the heart. To these may be added certain cases of
mediastinal tumours.

We have just seen that when there is collapse of the abdomen the
diaphragm descends, drawing after it the heart and lungs. When
there is distension of the abdomen, whatever be the cause, the reyerse
of this takes place. The diaphragm is raised, the cavity of the chest
is shortened, and the heart and lungs are elevated and compressed
upwards.

Distension of the Stomach and Intestines. — By far the most frequent,
distressing, and often fatal cause of the elevation of the diaphragm
and compression upwards of the heart and lungs, is the distension

MALPOSITIONS OF THE HBART. 131

of the stomach and intestines with gas. The effect of this condition
is well shown in fig. 29, which was taken from a youth affected with
diabetes, who, for months before his death, suffered from great abdo-
minal distension. The cavity of the chest was materially lessened.
The lower ribs, especially on the left side, were pressed outwards bo

Fhi. 29. — Position of the heart and great vessels in cases with IHMmion of the Stomach
and Intatina, The heart is displaced and compressed upwards, its impulse being
present in the second and third spacee, and perhaps in the fourth.

as to restrain their movements, and the whole cage of the chest was
elevated in front and at the sides. The heart and lungs were com-
pressed upwards and lessened in size, so as to impede respiration and
circulation.

K 2

132 A SYSTEM OF MEDICINE.

When the abdomen is enlarged, it is enlarged in two directions,
one outwards and downwards by the expansion of the walls of the
abdomen, the other upwards by the elevation of the diaphragm.
When the abdomen is extremely distended, the whole cavity becomes
oval in form, or shaped like a balloon ; the outer part of it presses
outwards, and the upper part of it presses upwards. The cage of the
chest is raised by this double movement of distension upwards and
outwards. The wide irregular cone formed by the upper part of the
swollen oval abdomen, acting upon the lower ribs, forces them asunder
to the right and to the left, and lifts up the whole front of the cage
of the chest. The more important effect of this distension of the
abdomen is to lift up the diaphragm, and with it the heart at the
centre of the chest, and the right and left lung on each side of it.
When these organs are thus raised, as the walls of the chest in front
of them, by which their relative position is measured, are raised also,
the apparent elevation of the heart is much less than its real eleva-
tion. The heart and great vessels are compressed upwards, and dis-
placed somewhat to the right, so that the heart takes a central position
in the chest, while the great vessels often bear unduly to the right.
The shape of the heart is altered. It is shortened from below upwards,
and is proportionally though not actually widened. Its apex is
especially tilted upwards, and instead of being, as in health, lower
than the inferior boundary of the right ventricle at the end of the
sternum, is higher than that point by from a third to one-half of an
inch. It is to be observed that the heart and lungs are compressed
upwards into the highest part of the cavity of the chest, and as that
cavity is a cone narrowing from below upwards, those organs, to their
great additional inconvenience, are pushed up into the narrowest part
of the space that they naturally occupy.1

Intestinal distension is usually present in peritonitis, and it be-
comes in many cases the most distressing symptom. As Dr. Stokes
has shown, muscles are paralysed by inflammation. The inflamed
muscular coat of the intestines, being paralysed, yields before the
gaseous distension, which is no longer restrained by the peristaltic
contraction of the intestines. In peritonitis, abdominal respiration is
suspended and the diaphragm is passive. It therefore yields without
resistance to the upward pressure exerted upon it by the distended
intestines, and the heart and lungs are compressed upwards to a
greater degree than in those cases of abdominal distension in which
the diaphragm retains its power. Distension of the stomach and
intestines is very frequent in the dying. It was present to an exces-
sive degree in either the stomach or intestines, or both, in 63 out
of 122 dead bodies observed by me indiscriminately ; and in 28 of
these the stomach and intestines were very much distended. In such
cases the abdominal distension, which is usually one of the secondary

1 For additional details as to this subject, see a lecture by the author on the
" Influence of Distension of the Abdomen on the Functions of the Heart and Lungs,"
in the British Medical Journal for August 2/ 1873, p. 108.

MALPOSITIONS OF THE HEART. 133

effects of the original disease, produces compression of the heart
and lungs, and thereby often hastens death or becomes its immediate
cause. The introduction of the jesophagseal tube from above, or of
O'Beirne's tube from below, or the insertion of a small aspiration
tube through the abdominal walls into the stomach, will in some of
these cases give vent to the flatus and so produce material relief.

Many persons, especially those who have become stout, are subject
to habitual distension of the stomach and intestines, with the effect
of compressing the diaphragm upwards, curtailing its power to descend
freely during inspiration, and so encroaching on the cavity of the chest.
Those so affected do not, in many instances, suffer when they are at
rest, but on any exertion respiration becomes hurried and difficult and
the circulation of the blood is impeded. Such persons generally
present themselves in two classes. One class, complain, of shortness of
breath, the other, of pain or distress in the heart when they make
exertion, especially after a full meal In many cases of angina pectoris,
the distress is most easily excited after food. Some stout people
are unusually subject to distress in breathing or in the heart or both
from comparatively slight distension of the abdomen. In these
persons the cavity of the abdomen is naturally incapable of great
expansion owing to its walls being firm and resisting. The abdominal
fulness, when it passes certain limits, cannot make way forwards and
outwards, and the result is that the diaphragm is pushed upwards
and the lungs and heart are soon subjected to a distressing amount of
pressure.

In dyspeptic persons, the most distressing symptoms induced by
the fulness of the stomach after food are often referred to the heart.
This is apt to be the case also whenever the stomach is greatly
distended. The reason is obvious : the stomach is immediately sub-
jacent to the heart, the diaphragm being interposed, so that the heart,
in fact, rests upon the stomach. Whenever, therefore, the stomach
is greatly swollen by an accumulation of gas and food, the heart is
compressed upwards in an especial manner, and the distress experienced
is often, therefore, almost limited to the heart. I do not of course lose
sight of the additional physiological influence exerted by the stomach
upon the heart through the medium of the eighth pair of nerves.

Ascites. — In ascites, the accumulation of the fluid is gradual. The

patient is usually in bed, and the distress in breathing and in the heart

experienced by the patient, owing to compression of the heart and

lungs, is by no means proportionate to the amount of the distension.

Indeed, those cases of ascites that suffer great distress in the organs

of the chest usually have in addition distension of the stomach and

intestines as well as enlargement of the liver. When this is so,

a small amount of fluid in the peritoneal cavity will produce serious

discomfort, and the removal even of a little of it by tapping will give

immediate and unusual relief. Some years ago I had a patient in St.

Mary's Hospital who was affected with aortic and mitral regurgitation.

The heart was enlarged and the pericardium was adherent. He breathed

134 A SYSTEM OF MEDICINE.

with difficulty, owing to the great size of the abdomen, which was
produced by the triple combination of great enlargement of the liver,
distension of the stomach and intestines, and ascites. The quantity
of urine was scanty, being about eleven ounces daily. The amount of
fluid in the peritoneal cavity was small, but with the view of afford-
ing relief, tapping was resorted to. The intestines were so near the
surface that an incision was made in the parietes of the abdomen,
and the trochar and canula were introduced in a downward direction.
At first only half a teaspoonful of fluid escaped, but by passing a
female catheter through the canula, so as to press the intestines
gently away from the end of the tube, about ninety ounces of serum
were withcfrawn. The relief to breathing was complete. The urine,
before so scanty, now began to flow freely, and from fifty to eighty
ounces were passed daily. By drawing off the fluid the extreme dis-
tension was relieved, and the ligature, so to speak", on the circulation,
caused by the compression of the heart, was removed. Ultimately
the fluid reaccumulated, and the patient died. The result was un-
favourable, but the case was none the less instructive, for it demon-
strated that the encroachment of the abdomen upon the chest checked
the circulation of the blood and so prevented the free secretion of urine.

In all cases of abdominal distension the seat of the impulse of the
heart is a ready and exact measure of the extent to which the cavity
of the abdomen encroaches upwards on the cavity of the chest. The
progress of such distension, whether on the ascending or descending
scale, may be exactly ascertained by noticing the varying position,
upwards or downwards, of the impulse of the heart. It must how-
ever be borne in mind that, when the heart and lungs are raised by
distension of the abdomen, the walls of the chest in front of those
organs is raised also, and that the apparent elevation of the heart,
measured by its relation to the walls of the chest, is much less than
its real elevation.

Escape of Gas into the Cavity of the Abdomen. — The escape of gas
into the cavity of the abdomen, owing to perforation of the stomach
or intestines, produces rapid distension of that cavity and great eleva-
tion of the diaphragm and the heart and lungs, with the effect of induc-
ing great distress in breathing and difficulty in the action of the heart.

Abdominal Tumours, even when they are of considerable size, rarely
produce any material disturbance either in the action of the heart or
in the performance of respiration.

Ovarian Dropsy. — The same may be said of cases of ovarian dropsy,
even when the sac is of very large size, and rises upwards so as to
encroach on the chest, unless that affection be accompanied by intes-
tinal distension. In the female the walls of the abdomen are capable
of great forward expansion, and the result is that large ovarian cysts
as well as the gravid uterus at the full time tend rather to protrude
forwards so as to distend the abdominal parietes anteriorly, than to
rise upwards so as to elevate the diaphragm and encroach upon the
heart and lungs.

MALPOSITIONS OF THE HEART. 135

Simple Enlargement of the Liver and Spleen. — When the liver is
universally enlarged, even when it assumes a very great size, it does
not rise upwards, so as to raise the diaphragm and compress the
heart and lungs, but it tends to grow downwards, so as to displace the
stomach and intestines. The same may be said of the spleen in cases
of leucocythemia, even when that organ attains to a very large size.

The result is, that simple enlargement of the liver or spleen does
not as a rule encroach upon the chest so as to produce serious dis-
turbance in the functions of the heart or lungs.

It is quite otherwise when the upper part of the right lobe of the
liver is occupied by lafge abscesses or hydatid cysts or malignant
growths. These morbid conditions produce a peculiar displacement
of the heart upwards and towards the left subclavicular region, and
I shall therefore consider them under the lateral displacements of the
heart.

Mediastinal Tumour. — Dr. Bennett1 gives a case of mediastinal
cancer involving the bronchial glands and spinal column, in which
the heart was found displaced, being drawn upwards. During life
there was very little impulse to be felt or seen immediately to the
left of the sternum just above the nipple.

THE LATEEAL DISPLACEMENTS OF THE HEAET.

Pleuritic effusion, empyema, and pneumo-thorax of one side of the
chest ; haemorrhage into either cavity of the chest from the rupture
of an aneurism of the aorta ; thoracic tumours ; aneurisms of the arch
of the aorta ; aneurisms of the abdominal aorta at the cseliac axis ;
and large abscesses or hydatid cysts or malignant tumours in the
upper part of the liver ; all tend to displace the heart towards the
side of the chest opposite to that which is affected. Contraction or
cirrhosis of one lung with adhesions of the pleura tends to displace
the heart towards the affected side. To these may be added lateral
curvature of the spine and congenital transposition of the viscera.

The lateral or transverse displacements of the heart, which are some-
times called dislocations, unlike the displacement of the heart upwards
by the encroachment of the cavity of the abdomen upon that of the
chest, do not as a rule produce much distress in the heart itself or
disturbance of the circulation. The lateral displacements of the heart
are, however, valuable and decisive indications of disease, since by the
evidence they afford they often render our diagnosis accurate and
certain.

* Pleuritic Effusion, Empyema, Pneumo-thorax. — The effusion of serum
into either cavity of the chest, owing to pleuritis, acute or chronic, is
the usual cause of the lateral displacement of the heart.

1 Intrathoracic Tumours, p. 127.

13R

A SYSTEM OF MEDICINE.

When extensive effusion takes place into the left side, the heart is
pushed over towards or into the right side of the chest, as may be
seen in fig. 30. This figure, unlike the others, does not represent an
actual case, hut is a diagram, made from drawings of six cases, one

Flo. 30. — Position of the heart and great veaaela in caseu of Plcvrttie Ejfvtion into the
Ltfl cavity of the Chat. The heart is displaced into the right aide of the cheat, its
impuleo being felt in the third, fourth, and fifth space*.

of effusion of serum into the pleura, one of empyema, and the four
others of extensive effusion of blood into the left pleura from the rup-
ture of a thoracic aneurism. In one of these the clot measured three
pints and a half.

The displacement of the heart from the increasing effusion of Quid

MALPOSITIONS OF THE HEART. 137

into the pleura is usually gradual. It may, however, be rapid, and
Dr. Walshe states that thirty-six hours will sometimes suffice for the
heart's impulse to find its way beyond the right nipple. When the
quantity of fluid is so small as to occupy only the back part of the
left side of the chest, the heart is scarcely displaced. When the fluid
increases the left ventricle and its apex are at first thrown a little
forwards, and towards the centre of the chest. The pressure of
the effused fluid is not made directly upon the heart, but upon the
strong fibrous sac of the pericardium, and, through its medium,
upon the heart. If the heart had no sac of its own, and was
present without restraint in, say, the left cavity of the chest, it would
not be forced forward and to the right when the left cavity of the
chest is filled with fluid, but it would, I consider, gravitate backwards
owing to its own dead weight, and sink to the back of the cavity,
just as the liver sinks to the back of the fluid in cases of ascites. The
presence of the pericardium completely prevents such a state of
things. The accumulated fluid distending the left cavity of the
chest presses equally in every direction. It displaces the ribs back-
wards, forwards, and especially outwards, so that they draw the lower
end of the sternum somewhat to the left ; it displaces the left wing
of the diaphragm, the spleen, stomach, and left lobe of the liver down-
wards and to the right; and it displaces the pericardium and the
heart and great vessels inwards and to the right. The lower end
of the pericardium at its attachment to the central tendon of the
diaphragm is stretched downwards by the traction upon it of the
lowered left wing of the diaphragm, to which it is attached by its
central tendon.

The apex forms throughout the lowest part of the heart, and it
describes a segment of a circle or arc as it sweeps round from its
natural position in the left side of the chest to the position of extreme
deviation to which it may attain in the right side of the chest. When
the apex describes this curve, instead of being raised by the resistance
offered by the abdominal organs, it is lowered during the first two-
thirds of its course. The reason for this is obvious. The fluid in
the left pleura, which displaces the pericardium and the heart to the
left, displaces at the same time, as I have just explained, the left
wing of the diaphragm and its central tendon and the subjacent
organs downwards, forwards, and to the right Under these circum-
stances, as the central tendon forming the base of the pericardium is
lowered, there is a free space downwards into which the apex of the
heart, suspended from the arch of the aorta, necessarily drops, so
that it may be felt beating in the epigastrium over, beyond, and even
below the ensiform cartilage. At length, however, the heart, as it
advances further into the light side, meets with increasing resistance
from the solid convexity of the liver ; and the heart, consequently,
again rises, so that it is at length about as high on the right side as it
is in health on the left. The displaced heart may indeed attain to a
higher position if it deviate still farther to the right, when, as in a

138 A SYSTEM OF MEDICINE.

case of Wintrich's,1 it may approach the axilla, and be felt beating
from the second to the fourth spaces.

Information of some diagnostic value is to be obtained by observing
the position of the heart in comparatively early stages in cases of
pleuritic effusion, at a time when the impulse of the apex has already
moved from its natural position and is on its way towards the cen-
tral line. To quote Dr. Stokes, we observe, first, that the apex strikes
in a situation about midway between its natural position and the
upper portion of the ensiform cartilage.2 It is not, however, until
the apex beat presents itself in the epigastrium that much notice is
taken of the altered position of the heart In four of my cases of
displacement of the heart towards the right from effusion into the left
side of the chest, the apex presented itself in the epigastrium, being
in one of these behind the lower end of the ensiform cartilage, and
in two behind its middle. As Dr. Townshend remarks, in speaking
of empyema in the left side, the heart is thrust from its natural
position down into the epigastrium, where it may be seen and felt
beating. There is no difficulty in distinguishing the impulse of the
apex from that of the right ventricle in the epigastrium. When the
latter is present the whole heart has been lowered, owing to the lowering
of the diaphragm. This may occur, as we have already seen, in
cases either of pulmonary emphysema, or croup, or with collapse
of the stomach and intestines, when the presence of pulmonary
resonance over the left side will at once enable us to distinguish
the case. In cases of pleuritic effusion the existence of dulness,
and in those of pneumothorax the presence of amphoric resonance,
over the whole of the left side, and the absence of impulse to the
left of the sternum, will generally suffice to make the case clear.
Cancerous tumours occupying the whole of the left side may also give
rise to displaced impulse and to general dulness on percussion, when
that disease cannot be distinguished from pleuritic effusion or empyema
on those grounds alone. In cases of pneumonia of the whole of the
left lung, it is possible that owing to the enlargement of the pneu-
monic lung from consolidation and the development of the right lung
to compensate for the disablement of the left lung, the impulse of the
apex may disappear from the walls of the chest, while that of the
right ventricle may descend into the epigastrium. In such cases,
however, the impulse is comparatively slight, and it always extends
rather to the left than the right of the ensiform cartilage, while
in cases of pleuritic effusion the impulse is usually strong and marked,
and tends rather to the right than the left side of that cartilage.
As soon as the seat of the impulse disappears from the left side of
the chest and extends to the right of the sternum, every difficulty of
the kind just stated vanishes.

As the heart passes over from the left to the right side of the chest
it gradually and necessarily turns over upon itself, hinging, so to speak,

1 Krankheiten der Respirationsorgane.
1 Dr. Stokes on the Diseases of the H<

Heart and Lungs, p. 500.

MALPOSITIONS OF THE HEART. 139

upon the vessels by which the heart is attached to the lungs and the
system, so that the right auricle is hidden, all but the top of its
appendix, and instead of the right ventricle being in front of the left
ventricle, all but its left border, it is the reverse, for the left ventricle
hides a large portion of the right ventricle (see Fig. 30). The part of
the right ventricle exposed is, however, not that near the apex, but
that near the pulmonary artery. The ascending aorta and pulmonary
artery change their direction ; they move to the right at their respec-
tive origins, but higher up they are retained in their places, the arch
of the aorta at the end of its transverse portion, and the pulmonary
artery at its bifurcation. The aorta and pulmonary artery, therefore,
present not a front but a profile view, with a direction to the right.

I published a case with a diagram showing the position of the
internal organs in the "Provincial Medical Transactions" for 1844
(p. 162), in which effusion in the left side of the chest was limited to
the lower two-thirds of the cavity, owing to the upper lobe of the
left lung being adherent down to the third rib. In this case the
heart was simply displaced to the right, the front of the organ being
still occupied by the right ventricle, and its right and left sides by the
right auricle and the left ventricle. This case shows that the heart
does not turn over upon itself so as to present the left ventricle
instead of the right in front, unless the fluid presses upon the left
side of the pericardium for its whole length, so as to bear upon the
great vessels as well as upon the body of the heart.

The impulse to the right of the sternum is sometimes limited to the
fourth and fifth intercostal spaces, while sometimes it is also present
over the third and even the second space. In the latter case the im-
pulse is double, and is due to the pulsation, followed by the second beat
coincident with the second sound of the pulmonary artery or aorta, or
both. When pulsation is present in the first, second, and third right
spaces, and also in the normal position to the left of the sternum, the
case is one of aneurism of the aorta ; and the distinction of this impulse
or pulsation from that of displaced heart presents therefore no difficulty.

Wintrich 1 states that sometimes, when the effusion is in the left
side, the heart is displaced backwards (and to the right) being covered
by lung, when the displacement of the heart can by no means be dis-
covered. He saw one such case in which an able clinical physician
mistook the disease for pericarditis with very great effusion.

When effusion of fluid takes place into the right cavity of
the chest, the heart is displaced towards the left side. As the im-
pulse, however, is already seated on that side, the change in position
of the impulse of the heart is not nearly so marked or diagnostic
as in cases in which the heart is displaced to the centre or right
side of the chest, owing to effusion into the left side. Important
information, however, is to be obtained in such cases from the position
of the impulse on the left side.

In a patient under my care who had extensive effusion into the

1 Krankheiten der Rwpirationftorgane, p. 255.

140 A SYSTEM OF MEDICINE.

right pleura, the impulse was felt in the sixth space, two inches farther
to the left, and somewhat lower than the natural position. In two
cases of seropurulent effusion in moderate quantity into the right
pleura, of which I possess drawings, the heart was displaced to the
left, and lowered to a slight extent. In one the apex of the heart
was situated behind the seventh rib, more than an inch to the left
of the natural site, and nearly an inch lower. In the other, the
displacement of the heart downwards and to the left also existed,
but to a less degree.

Since the above was in type I have seen three cases of extensive
effusion of fluid into the right side of the chest. In two of these
cases the apex-beat was felt as far to the left as about the seventh rib,
the position of the impulse being somewhat lower than natural. In
the third case, a young woman, whom I saw through the kindness of
Dr. Wane, the amount of fluid in the right side of the chest was very
great. The impulse of the heart was not perceptible to the right of
the mamma, but prevailed along its upper left border from the
third or fourth to the seventh space where it was unusually low in
situation. There was a double impulse over the great arteries at the
left upper border of the mamma, and doubling of the second sound,
the second of the two sounds being that made in the pulmonary
artery. There was also a loud mitral murmur around the region of the,
apex. A large quantity of fluid was drawn off, by means of a glass
syringe through a fine tube, by Mr. James Lane, who performed the
same operation for the two other cases, I watched the position of
the impulse when the fluid was being withdrawn, and noticed that it
soon disappeared from the seventh space, and more slowly from the
sixth, the beat moving steadily to the left and somewhat upwards.
When the full amount of fluid had been withdrawn, the impulse was
present in the fourth and fifth spaces, and perhaps in the third, being
situated to the right of the mamma. The doubling of the second
sound at once disappeared, and later 1 believe that the mitral murmur
also vanished. In the drawing of an instance of great cylindrical dilata-
tion or aneurism of the ascending aorta, in which there was considerable
effusion of fluid in the right side of the chest, the heart, which was
greatly enlarged and lowered in position, was displaced to the left as
far as the ribs would allow, the apex extending to the seventh space,
fully two inches below the level of the lower end of the sternum.

In two cases related by Dr. Gairdner 1 of effusion into the right
pleura, the apex-beat in both was displaced to the left; in one
(p. 329) the impulse probably retained its usual level, being displaced
about one inch to the left. In the other (p. 354), before para-
centesis, the apex-beat was felt in the fifth space, one inch and a
half to the left of the normal site; after the operation it was
present in the fourth space. In this case the impulse was probably
lowered. Dr. Townshend, who was the first to observe the dis-
placement to the left in such cases, felt the apex striking against

1 Clinical Medicine.

MALPOSITIONS OF THE HEART. 141

the stethoscope between the fourth and fifth ribs in the axilla in two
cases of empyema of the right side.1 It is evident, then, that when
considerable effusion takes place into the right side the apex-beat is
always pushed further to the left, and that it is usually lower, some-
times on the same level as, and sometimes higher than the natural
position. I attribute the loweved position of the impulse to two
causes, the displacement downwards of the central tendon of the
diaphragm by the effusion, and the inspiratory lowering of the dia-
phragm to enlarge the left lung, and so to compensate for the disuse
of the right lung.

I do not find that the displacement of the heart from empyema
differs in any respect from that caused by the effusion of serum into
the pleura.

In pneumo-thorax of the left side, the displacement of the heart
is the same as in cases of fluid effusion into the pleura. In general,
fluid is combined with the air in those cases, but air without fluid
will produce displacement of the heart, and it must do so when it
is in sufficient quantity to distend the sac of the pleura, press down
the diaphragm, and so push the pericardium and the heart over to
the opposite side. Dr. Douglas Powell 2 relates a case in which the
right side of the chest was filled with air, and the right border of the
heart was situated to the left of the left sterno-clavicular line.

Wintrich8 states that displacement of the heart takes place in
pneumothorax as in pleuritic effusion ; the only difference being that
in pneumothorax the heart is more frequently displaced from before
backwards.

HoBmorrhage into either Cavity of the Chest from the rupture of an
aneurism of the aorta displaces the heart, as a rule, to the opposite
side, in the same manner, and to the same extent, the quantity of
fluid being alike, as in cases of pleuritic effusion. Two circumstances,
however, tend to modify this result, one, the size and position of the
aneurismal sac ; the other, the lessening of the size of the heart that
may be induced by the haemorrhage. Mr. Sidney Ooupland 4 gives a
case in which a diffuse aneurism of the thoracic and abdominal aorta
ruptured into the left cavity of the chest, which contained twenty-
four ounces of clot. During life the apex was tilted upwards, and
was felt beating in the fourth space, one inch within, and on a line
with the left nipple.

Contraction or Cirrhosis of the Lung with Adhesion of the Pleura. —
When pleuritis with effusion, whether chronic or acute, ends in the
permanent condensation of the lung, fibroid thickening of the pleura,
and binding adhesions, the whole of the affected side contracts and
the ribs are crowded together. That side of the chest, however, is not
obliterated ; it is still much larger than the condensed lung, and the
result is that if, for instance, the right be the affected side, the heart
is permanently drawn over into the right side.

1 CycL of Med. vol. ii. p. 88. • Path. Trans, xix. 77.

* Krankheiten der Respirationsorgaiie, p. 34 i, 347. 4 Path. Trans, xxir. 54.

148 A SYSTEM OF MEDICINE.

Dr. Stokes was the first to draw attention to the displacement of
the heart to the right side, in consequence of the absorption of an
effusion into the right pleura.1

When the left is the affected side, the heart may he drawn quite
over into the left side, the right auricle being situated to the left of

Fro. 31. — Position of the heart and great vessela in a case with Contraction of the Left

the median line. This is well seen in fig. 31, which was taken from

a man in whom, owing to the complete contraction of the left lung,

the heart entirely occupied the left side of the chest in front, no

1 On the Diseases of the Cheat, p. SOI.

MALPOSITIONS OF THE HEART. 143

portion of the left lung being interposed between the heart and the
walls of the chest. The heart is raised towards the infra-clavicular
region and the axilla, and the ribs fit closely upon the heart from
the second to the fifth. In this man the impulse must have extended
from the first intercostal space to the fourth.

It may be observed that here also, as in displacement of the heart
into the right side, the heart revolves upon itself and turns over, but
in the reverse direction. In displacement into the right side, the left
ventricle and auricle are situated in front, the right ventricle being
partially and the right auricle all but its tip being wholly concealed.
In displacement to the left, the right ventricle entirely hides the left
side of the heart. The aorta and pulmonary artery are twisted to
the left, both venae cavae are completely exposed when the right
lung is turned aside, and are situated behind the sternum, and the
whole heart seems to turn to the left upon the two venae cavae as
upon a hinge or pivot.

In cirrhosis of either lung the heart is drawn towards the affected
side. Dr. Hilton Fagge * relates a case of cirrhosis of the right lung
in which the impulse was seen and felt two inches below and one
inch to the left of the right nipple. The heart deviated more to the
right during life than after death, when the apex was two inches to
the left of the middle line, being situated between the fifth and sixth
(cartilages) ; and one-half of the heart was to the left, and one-half
of it was to the right of the middle line. Dr. Greenhow2 gives a
case of contraction of the right lung, the precise condition of which
was unknown, observed by him during life, in which the heart was
displaced very far to the right and upwards, and was felt beating in
the third and fourth spaces over an area of three inches by three and
a half, of which the right nipple formed the central point.

Dr. Wilks 8 communicates a case of cirrhosis of the left lung, in
which that lung was contracted and hard, and had to be cut out.
The right lung was enlarged, and was the only organ observable on
removing the sternum. The heart was drawn towards the left side,
" owing to the pericardium being firmly united to the pleura."

Dr. Bastian 4 gives an analysis of thirty cases of cirrhosis derived
from various sources. The heart was much displaced towards the
affected side in twelve of these, and slightly in three ; while in three
of them there was no displacement, and in the remaining twelve
there was no notice of the position of the heart.

When the left bronchial tube is obliterated by compression, by
its own contraction, or by the admission of a foreign body, the left
lung shrinks, the left side contracts, and the heart is displaced towards
the clavicle and axilla, exactly as in cases of complete contraction
with adhesions of the left lung. Dr. Stokes publishes a case of
Dr. Mayne's of aneurism arising from the front of the transverse
portion of the arch of the aorta, which extended downwards towards

1 Path. Trans, xx. 35. a Ibid. xix. 159.

• Ibid. viii. 80. « Ibid. xix. 47.

144 A SYSTEM OF MEDICINE.

the left lung, compressing and flattening the left bronchial tube. The
left side of the chest was less than the right by two inches, the ribs
were crowded together, and the heart was displaced towards the left
axilla.1

There are many cases of partial contraction of a portion of the
upper lobe of the left lung, whether from phthisis, cirrhosis of the
lung, gangrene of the lung, or other cause, in which the upper part
of the heart and the great vessels, especially the pulmonary artery, are
drawn upwards and to the left towards or into the former seat of the
contracted portion of the lung. In such cases the presence of the
pulmonary artery, elevated in position and drawn to the left, may be
immediately ascertained by its peculiar double impulse. I cannot
say that I have strictly observed the analogous displacement of the
ascending aorta towards the seat of the upper lobe of the right lung,
in cases of contraction of that lobe, but I have noticed cases of this
class in which the vessel evidenced itself by very loud superficial
first and second sounds, which communicated themselves to the ear,
if not to the hand, like a double shock or impulse. Dr. Stokes has
given an interesting account of the displacements of the heart from
the diminished volume of the lung, in his work on Diseases of the
Heart, p. 458.

Intra-thoracic Tumours. — Large cancerous growths in the cavity
of the chest, when they press upon the heart without penetrating
into its structure, necessarily displace it in the direction of the
pressure. The heart is simply pushed aside by the tumour, and its
displacement is in no way influenced by the relation of the heart to
the central tendon of the diaphragm.

* " In the year 1856 I saw," writes Dr. Cockle, in his paper on
intra-thoracic cancer, " a case of intra-thoracic cancer occupying the
whole of the left side of the chest, and encroaching slightly on the
right side, in which the tumour carried the heart before it as far as
the right nipple. The impulse was felt pulsating between the second
and third ribs, and down to, and at a later period beyond, the right
nipple."

Dr. Bennett 2 relates the case, communicated to him by Dr. Sutton,
of a little girl, in whom the entire left side was occupied by a mass of
medullary cancer which had pushed the heart considerably to the
right. During life the heart was displaced and was felt beating at the
right nipple. The diagnosis was " very great effusion into the left
pleural cavity,1* and the chest was twice punctured.

In a case published by Dr. Andrew,8 in which a large malignant
growth occupied the upper lobe of the left lung, the heart was dis-
placed downwards and to the right. Dr. Bennett4 gives a case of
cancer of the anterior and posterior mediastinum involving the anterior
portion and root of the right lung on which the heart was pushed
downwards and towards the right side, so that rather more than half

1 Dr. Stokes on Diseases of the Heart and Aorta, p. 666.

■ Intra-thoracic Growths, p. 100. s Path. Trans, xvi. 51. 4 Loc cit. p. 92.

MALPOSITIONS OF THE HEART. 145

of the organ was to the right of the median line. A fortnight before
death there was manifest and considerable displacement of the heart,
which was beating in the epigastrium. Dr. Douglas Powell l relates
a case in which the left cavity of the chest was occupied by a solid
mass, displacing the heart to the right, and the lung posteriorly.
After death it was found that this tumour was intimately connected
with the heart at its left and posterior aspects. I might cite other
cases of intra-thoracic tumour, published by Dr. Townsend, Boer-
haave, quoted by him, and others, in which the heart was displaced.

On the other hand, cases are recorded in which there was little or
no marked displacement of the heart, although the extent of the
disease was great.

Dr. Graves and Dr. Stokes 2 have published a well-known instance
of this disease, in which there was found, in place of the right lung,
a solid mass, weighing more than six pounds. It encroached upon
the left side of the chest, enveloping and nearly concealing from view
the pericardium, great vessels, and trachea. Notwithstanding the
extent and position of the disease, the heart pulsated in its natural
situation.

Dr. Wilks describes a case in which the whole right lung was
converted into one mass of medullary cancer, which protruded into
the pericardium, ran along the great vessels at the base of the heart,
and pierced the auricles of the organ itself. The superior cava was
almost destroyed by the cancer, the inferior vena cava was closely
surrounded by it but was free, the right pulmonary artery was a
mere slit in the midst of it, and it had entered the heart through the
pulmonary veins. There is no notice of displacement of the heart,
although it is stated that the sounds of the heart were very feeble.

Dr. Quain3 exhibited before the Pathological Society an encepha-
loid mass of the size of a large cocoa-nut, which was situated between
the root of the left lung and the heart. When the patient was first
seen, six weeks before his death, the heart was little displaced. After-
wards effusion took place into the left side, and the heart became
much displaced towards the right side.

It is evident from these cases, that a large intra-thoracic tumour
occupying one side of the chest may in some instances displace the
heart into the opposite side, while in other instances, in which the
tumour is equally large, there may be no displacement of the heart
whatever. The reason is obvious. In those instances in which there
is no displacement, the cancer penetrates into or surrounds the organ,
without pushing it aside.

It is evident, then, that the displacement or non-displacement of
the heart, and the mode and extent of its displacement, in instances
in which there is complete dulness of one side, may sometimes help
us to discover whether the case is one of intra-thoracic cancer or
of simple effusion into the pleura.

1 Path. Trans, xxiv. 28. * Dr. Stokes on the Diseases of the Chest, p. 371.

8 Path. Trans, viii. 64.

VOL. TV. L

146

A SYSTEM OF MEDICINE.

Large abscesses, hydatid cysts, or malignant tumours in. the upper
or convex portion of the Liver. — The patient from whom fig. 32 was
taken was affected with jaundice. On post-mortem examination
several large abscesses were found in the upper portion of the liver,

Flu. 82. — Position of the heart and great vessels in a cane with Large Ahatxaa in the
Upper portion of the Liver. The heart and great vessels are displaced extensively
upwards and to the left towards the left axilla, so as completely to occupy the left
side of the chest. The impulse is present in the second and third loft spaces.

where it ascends into the right side of the chest He also had
peritonitis, and excessive intestinal distension. The whole diaphragm
was raised, and with it the heart was pushed upwards and to the.
left in a remarkable manner. The liver encroached upon the right

MALPOSITION* OF THE BEAUT. 11

-»<

side of the cheat to such an extent that its highest point was on a
level with the lower edge of the second rib. The convexity of the
liver consequently encroached on the left side of the chest as well
as the right, and carried the heart, resting upon its upper surface,
completely over into the upper portion of the left side of the chest

If this figure be compared with fig. 29, in which the diaphragm is
excessively raised by means of distension of the stomach and intes-
tines, it will be seen that while in both the diaphragm is raised to an
excessive degree, there are important points in which they differ
materially from each other. In that figure as well as in this we
fiud that the abdomen is distended, the diaphragm is pushed upwards,
the lower ribs are prominent, and the heart and lungs are pressed
upwards and lessened in size, being encroached on by the abdominal
organs. In universal distension of the abdomen, the heart, while it is
compressed upwards, retains a central position, as it rests on the
central tendon of the diaphragm. It deviates rather to the right than
to the left. But in those cases in which there are large abscesses
or hydatid cysts, or cancerous growths in the upper portion of the
liver, the heart, as it is pushed upwards, deviates extensively to the
left, and occupies a space to the left of the upper half of the
sternum, behind the first, second, third, and fourth ribs. It is to be
remembered that in this case there was peritonitis and great intes-
tinal distension, consequently the compression of the heart upwards
was effected by a double cause.

The deviation of the heart to the left side of the chest from
extensive abscesses in the upper portion of the liver, differs thus from
the deviation caused by effusion of fluid into the right side of the
chest — in effusion into the right side of the chest, the heart and
the impulse at the apex are either lowered or only slightly raised ;
while in cases with abscesses in the upper portion of the liver they are
pushed upwards, being above the fourth rib. The position of the heart
in enlargement of the liver from abscess, and in great contraction and
adhesions of the left lung, corresponds very closely. (Compare figs.
31 and 32.) In both the heart and great vessels are situated behind
the second and two or three upper ribs, in both the heart is pushed
entirely into the left side, the venae cavae being behind the sternum.
But in the following respects they differ. In enlargement of the
liver from abscesses, the anterior aspect of the heart is unchanged ;
the left upper ribs are widened apart and the ribs on both sides
are raised and pushed outwards ; the dulness on percussion is more
extensive on the right side than the left, especially behind, and the
heart and its impulse scarcely appear below the fourth rib. In con-
traction of the left lung, these conditions are reversed. The heart
turns upon the venae cavaB as upon a hinge over towards the left,
the right auricle and both venae cavae being completely exposed, and
the left ventricle being hidden by the right; the ribs are crowded
together, the whole of the left side of the chest being contracted;
there is dulness on percussion over the whole left lung, while the

t, 2

148 A SYSTEM OF MEDICINE.

whole right side of the chest is very resonant, the area of resonance
being increased, owing to the encroachment of the right lung upon the
left side of the chest to the left of the sternum ; and the impulse of
the heart is felt down to the fifth rib.

Extensive effusion in the pericardium in acute pericarditis is an
additional cause of displacement of the heart towards the axilla. Of
this displacement I shall speak in the article on pericarditis.

DISPLACEMENT OF THE HEART FORWARDS.

Dr. Hope relates a case in which the thoracic aorta, extending from
an inch below the left subclavian artery down to the diaphragm, was
enlarged into an aneurismal sac which lay across the spine, and pro-
jected on the right side three inches beyond the vertebrae without
reaching the ribs, while on the left it extended to the ribs, causing
destruction of three and caries of two or niore of them, and at last
formed a considerable tumour on the back. This tumour necessarily
compressed the heart forwards against the front of the chest. The
impulse of the heart was exceedingly vigorous, and was double, con-
sisting of a diastolic as well as a systolio impulse, each of a jogging
character. It was agreed that there must be considerable hypertrophy
of the heart to account for so strong an impulse, and yet the organ
was found by Mr. Caesar Hawkins, who drew up the autopsy, only
"slightly enlarged and thickened/'1 Dr. Hope quotes without refer-
ence, a case mentioned by Dr. Todd, in which the heart was pushed
forward and outwards, and, as it were, compressed against the ribs by
an enormous aneurism of the thoracic aorta. The sounds of the heart
were so modified by this compression as to lead to the erroneous
diagnosis of concentric hypertrophy.

I possess a drawing taken from a case of extensive aneurism of
the abdominal aorta at the coeliac axis, in which the aneurismal sac
extended upwards, behind the diaphragm, in front of the lower dorsal
vertebrae, so as to displace the heart forwards and probably some-
what upwards.

DISPLACEMENT OF THE HEART BACKWARDS.

When abscesses or tumours form in the anterior mediastinum,
behind the lower portion of the sternum, the heart must be displaced
backwards.

The displacement of the heart backwards is also induced by the
very extensive effusion that gradually takes place into the pericardium
in cases of chronic pericarditis.

Wintrich states, as we have already seen, that sometimes when
there is pleuritic effusion in the left side, the heart is displaced back-
wards and to the right, so that its displacement can by no means be
discovered.

1 Dr. Hope on the Diseases of the Heart, p. 447.

LATEEAL OR PARTIAL ANEURISM OF THE

HEART.

By Thomas Bevill Peacock, M.D., F.R.C.P.

Under this term it is proposed to treat of the partial or lateral
sacculated dilatations, in contradistinction to the general enlargements
of the cavities of the heart, to which, and especially in France, the
term aneurism has also been applied. The partial aneurisms differ,
however, from the latter forms of the disease, not only because they
involve only a portion of the parietes of the cavity, but also in that
the structure of the muscular walls is always more or less altered in
the seat of disease.

The real aneurismal tumours affect only the left cavities of th*
heart, the left ventricle and auricle, or the corresponding arterial
and auriculo-ventricular valves. The immunity thus possessed by
the right cavities has been variously explained by different writers.
Bi-eschet, who thought that the aneurismal dilatation was almost
always, if not invariably, situated near the apex of the left ventricle,
and that its production was due to the laceration of the inner
portions of the ventricular walls, supposed that the non-occurrence
of the disease in the right ventricle was owing to the greater relative
power of its walls at the apex. Dr. Thurnam referred the freedom of
the right ventricle from disease to the peculiar action of the valves at
the right auriculo-ventricular oritice, by which, when the ventricle
becomes distended, the aperture is incompletely closed so as to allow
the reflux of the blood into the right auricle. He also contended that
the term aneurism should be restricted to the dilatations of the cavities
of the heart through which arterial blood circulates ; while the term
varix should be applied to the similar enlargements of the venous
cavities, so as to maintain the analogy between the affections of the two
sides of the heart and those of arteries and veins. Rokitansky considers
the dilatations of the right side of the heart as not truly aneurismal,
and ascribes the occurrence of the real aneurisms only on the left side
to the greater frequency of endocarditis in that situation. There seems
good reason to believe that the proneness to inflammation of the
lining membrane of the left cavities, is mainly influential in causing the

150 A SYSTEM OF MEDICINE.

occurrence of aneurism on the left and not on the right side of the
heart ; but it is also probable that the greater tension to which the
walls of the left ventricle are exposed, with the variations of pressure
exerted by the column of blood in the arteries, materially conduces
to the disease. Certainly when from any cause any portion of the
parietes is rendered less resistant and more readily expansible, the
pressure of the blood will tend rapidly to expand the weaker part so
as to form a distinct sac.

In the following notice I shall treat first of aneurisms of the left
ventricle, then of those of the left auricle, and lastly of valvular
aneurisms.

ANEURISM OF THE LEFT VENTRICLE.

The occasional occurrence of partial aneurismal dilatations of the
heart similar to those which are of such frequent occurrence in the
arteries, was first shown by the case recorded by Galeatti in 1757 ; and it
is a curious coincidence that in the same year the condition was brought
to the knowledge of John Hunter by the occurrence of a case, the pre-
paration of which is contained in the Museum of the Royal College
of Surgeons, and of which the description was found by Dr. Thurnam1
in his MS. Catalogue. In 1759 a case of the kind occurred to Walter,
which was published in 1785,2 and in 1793 another specimen preserved
in Dr. Hunter's Museum, was described by Dr. Baillie and figured
by him in the plates which appeared in 1799. Corvisart met with
a case in 1796, which was published in 1806. Hodgson described
one in 1815,8 Zannini in 1816/ Rostan in 1820,6 and Shaw in 1822,6
Sir A. Cooper, in his Lectures published by Tyrrell in 1825, said that he
had met with three cases, of which two were contained in the Museum
of St. Thomas's Hospital. In 1827 the first memoir on the subject was
published by Breschet,7 in which the particulars of ten cases were
collected, including one communicated to him by Cruveilhier in 1816,
two by the Berards which first appeared in a Paris Thesis, and one
by Dance, together with the case of the celebrated Talma and the
description of a specimen in the museum of the Faculty by Breschet
himself. In the same year two other cases of the kind were described
by Adams in Dublin,8 and by Johnson in this country.9

In 1830, Dr. Elliotson, in his Lumleian Lectures, described another
case, of which the preparation is now in the Museum at St. Thomas's,
and referred to sixteen cases as on record at that time. In 1829 two
additional cases were narrated by Bignardi and Reynaud,10 in 1832

i Med.-Chir. Trans, vol. 21. 1838. 7 Rep. Gen. d'Anat. tome 8»« p. 181.

» Nouv. Mem. l'Acad de Berlin. 8 Dublin Hospital Reports, toI. iv.

5 Diseases of Arteries and Veins, p. 84. • Med.-Chir. Key. toI. xt.

* Italian Translation of Bail lie's Morbid Anatomy.

9 Sur lea Rapt, du Cceur, Obs. v. l'° Journal Hebd. de Mod.

• Manual of Anatomy, vol. i. p. 251.

LATERAL OR PARTIAL ANEURISM OF THE HEART. 151

a third was published by Hope, and in 1833 a fourth by Lobstein.
In 1834 a notice of the subject was given by Ollivier,1 in which he
referred to the cases collected by Breschet, together with those of
Adams, Bignardi, and Eeynaud. In 1835, Dr. Thomas Davies re-
ferred to the disease, and stated that there were two specimens in
the Museum of the late Mr. Langstaff. In the same year, Bouillaud
treated of the subject in a section of his work, detailing the more im-
portant observations recorded by Breschet and Ollivier, with two more
recently published cases by Choisy and Petigny. In 1838 Dr. Thurnam
contributed a memoir to the Medical and Chirurgical Society,2 which
was then completely exhaustive of the subject and still leaves little to
supply, and affords the best description of the pathology of these affec-
tions which has appeared. In this memoir he related seven new cases,
of which three were drawn from the MSS. of John Hunter in the pos-
session of the Royal College of Surgeons. He further referred to five
other specimens previously undescribed, which he had found in different
museums. In 1842 a short notice of the subject was published by
Rokitansky, in his work on Pathological Anatomy ; and in 1843, Dr.
Craigie contributed to the Edinburgh Medical and Surgical Journal
a valuable memoir,3 detailing the particulars of twenty-two of the
cases up to that time recorded, all of which had, however, been pre-
viously referred to by Dr. Thurnam, together with a very interesting
example which had occurred in his own practice. In 1846 a case was
described by myself;4 in 1850, Dr. Halliday Douglas6 related the
particulars of four cases ; and in 1852, M. Cruveilhier discussed the
subject in his Pathological Anatomy, illustrating his views by reference
to various examples which had fallen under his own notice.

Since the publication of Dr. Thurnam's memoir, numerous ob-
servations have been placed on record, so that I have had no
difficulty in collecting forty-three fresh cases, together with brief
notices of others not fully reported. Of this number fourteen are con-
tained in the Bulletins of the Soci£t6 Anatomique of Paris, two in the
M(5moires of the Soci£t<$ de Biologie, and sixteen in the Transactions
of the Pathological Society. With the cases collected by Dr. Thurnam,
fifty-eight in number, those on record must at present exceed one
hundred, and I have seen references to several others the particulars
of which I have not been able to obtain.

Nature and Mode of Origin. — Breschet, as the name, false consecu-
tive aneurism, which he gave the affection, indicates, regarded the real
aneurisms of the heart as originating in rupture or ulceration of the
lining membrane of the ventricle and some portion of the muscular
walls, the result of softening from inflammation or atheroma. Reynaud
showed that in his case the dilatation originated in disease of the
endocardium ; and Cruveilhier pointed out that in some cases the

1 Diet, de Med. tome viii. p. 303.

a Transactions, vol. xxi. In Dr. Thurnam's paper references will be found to all the
cases hern named, published up to the period of its appearance.
* Vol. lix. p. 381.
4 Edin. Med. and Surg. No. 169 B Monthly Jour, of Med. Sc.

152 A SYSTEM OF MEDICINE.

whole of the structures of the ventricular walls were dilated, — and
apparently in consequence of the muscular fibres having undergone
conversion into a fibroid structure, which was less resistant to pressure
and more readily admitted of expansion.

Dr. Thurnam to some extent adopted the views of the pathologists
who had preceded him, and contended, that, while the aneurisms did in
some cases originate in rupture or softening of the lining membrane
and muscular walls of the ventricle, they more frequently were con-
nected with the changes in the endocardium and muscular substance
pointed out by Eeynaud and Cruveilhier, and consisted in dilatations
of the whole of the structures constituting the parietes of the
ventricle. He also thought that these changes were probably often
referable to inflammation, and that in some cases the formation of
coagula in the cavity of the ventricle might cause the expansion of
the ventricular wall in the seat of deposition. He further contended
that the aneurisms of the heart presented all the several forms
which are met with in similar affections of arteries. Eokitansky
regards the aneurisms of the heart as always depending upon inflam-
matory processes, either of an acute or chronic character. In the
first or acute form of the affection, the disease originates in recent
inflammation of the endocardium and probably also of the contiguous
muscular substance, and the consequent laceration or breaking down
of the inflamed surface under the pressure of the blood. In the other
variety, the dilatation is the more remote result either of inflam-
mation of the endocardium and a somewhat thick layer of the muscular
substance, or of the whole thickness of the wall of the ventricle
during endo- and peri-carditis. In this form the muscular fibres
become replaced by fibroid structure, the endo- and peri-cardium are
blended with the altered tissue, and the parietes become expanded
under the pressure of the blood. The first of these forms corre-
sponds therefore with the false consecutive aneurism of Breschet ; the
second with the true aneurism of Eeynaud, Cruveilhier, and Thurnam.
While adopting Eokitansky's views as to the inflammatory origin of
the cardiac aneurisms, there is no reason to deny the correctness
of the analogy contended for by Dr. Thurnam, between their various
forms and the different varieties of arterial aneurisms. It is, however,
very doubtful how far the coagulation of the blood in the cavities of
the heart gives rise to partial dilatation. Such coagula form, it is
well known, chiefly on the right side, in which the aneurismal dilata-
tion does not occur ; and the clots which Dr. Thurnam has described
and figured, might as probably have originated in the already dilated
part as have given rise to the dilatation.

It is obviously only by the examination of incipient aneurismal sacs,
or those of small size, that we can form a correct judgment as to their
original modes of development. Confining his assertion only to such
cases, Dr. Thurnam states that of twenty-eight out of the fifty-eight
cases which he collected, twenty-two originated in dilatation of the
structures entering into the composition of the walls of the heart ;

LATERAL OR PARTIAL ANEURISM OF THE HEART 163

while in six there was solution of continuity of the endocardium
and inner stratum of muscular fibres. Of the forty-three cases
which I have myself collected, in thirteen the data are imperfect or
the disease is very far advanced ; of the remaining thirty, in twenty-
five the sac was lined by endocardium, which is stated to have been
opaque, thickened, indurated or ossified in eleven cases ; — and in four
the lining membrane was destroyed. In sixteen of these cases the
subjacent muscular structure had undergone the fibroid degeneration
and was more or less attenuated, in one of them to such an extent as
to present only a trace of the altered tissue ; in five the muscular
substance was thinned but not otherwise altered; and in seven cases it
was wholly wanting and the sac was only bounded by the endo- and
peri-cardium. Both series of facts, therefore, show that in the cases
in which satisfactory opinions as to the mode of origin of the sacs
can be formed, they are usually at first of the true form, or that in
which all the structures are expanded.

From several specimens which I have had the opportunity of
examining, either in the recent state or as preparations, the following
may be stated to be the progressive changes in the development of the
true aneurisms.

1. In the earliest stage in which the affection can be recognised,
we observe thickening and opacity of the endocardium, with slight
dilatation of the corresponding portion of the walls of the ventricle,
and attenuation of the muscular substance without any marked
alteration of its texture.

2. In a more advanced stage there is thickening and opacity of the
endocardium, and conversion of a more or less thick stratum of the
muscular substance into a dense, yellowish or whitish coloured fibroid
tissue intermixed with the muscular structure. The parietes of the
ventricle in the seat of disease have become more atrophied, and the
cavity presents a more marked dilatation.

3. At a still later period, together with the thickening and opacity
of the endocardium, this membrane becomes intimately blended with
the subjacent tissue, so as to be no longer separable from it. The
muscular substance throughout the whole or the greater part of the
thickness of the ventricular parietes, is converted into dense, pale-
coloured fibroid tissue. The attenuation of the walls of the ventricle is
greater, and the dilatation of the corresponding portion of the cavity,
if occupying the outer surface of the heart, occasions a more or less
marked prominence externally.

While these changes are in progress in the parietes of the ventricle,
others are proceeding in its interior. The dilated portion of the cavity
becomes, especially if it be somewhat circumscril)ed and bounded by a
tolerably defined margin, the seat of coagula. These are at first thin,
loose, and dark coloured, subsequently they become more firm and
paler ; and at length the sac is found more or less completely filled
by coagula, of which the outer portions are distinctly laminated and
decolorized, and often adherent to the altered endocardium. As the

152 A SYSTEM OF MEDICINE.

Dr. Thurnam to some extent adopted the views of the pathologists
who had preceded him, and contended, that, while the aneurisms did in
some cases originate in rupture or softening of the lining membrane
and muscular walls of the ventricle, they more frequently were con-
nected with the changes in the endocardium and muscular substance
pointed out by Eeynaud and Cruveilhier, and consisted in dilatations
of the whole of the structures constituting the parietes of the
ventricle. He also thought that these changes were probably often
referable to inflammation, and that in some cases the formation of
coagula in the cavity of the ventricle might cause the expansion of
the ventricular wall in the seat of deposition. He further contended
that the aneurisms of the heart presented all the several forms
which are met with in similar affections of arteries* Eokitansky
regards the aneurisms of the heart as always depending upon inflam-
matory processes, either of an acute or chronic character. In the
first or acute form of the affection, the disease originates in recent
inflammation of the endocardium and probably also of the contiguous
muscular substance, and the consequent laceration or breaking down
of the inflamed surface under the pressure of the blood. In the other
variety, the dilatation is the more remote result either of inflam-
mation of the endocardium and a somewhat thick layer of the muscular
substance, or of the whole thickness of the wall of the ventricle
during endo- and peri-carditis. In this form the muscular fibres
become replaced by fibroid structure, the endo- and peri-cardium are
blended with the altered tissue, and the parietes become expanded
under the pressure of the blood. The first of these forms corre-
sponds therefore with the false consecutive aneurism of Breschet ; the
second with the true aneurism of Eeynaud, Cruveilhier, and Thurnam.
While adopting Rokitansky's views as to the inflammatory origin of
the cardiac aneurisms, there is no reason to deny the correctness
of the analogy contended for by Dr. Thurnam, betwreen their various
forms and the different varieties of arterial aneurisms. It is, however,
very doubtful how far the coagulation of the blood in the cavities of
the heart gives rise to partial dilatation. Such coagula form, it is
well known, chiefly on the right side, in which the aneurismal dilata-
tion does not occur ; and the clots which Dr. Thurnam has described
and figured, might as probably have originated in the already dilated
part as have given rise to the dilatation.

It is obviously only by the examination of incipient aneurismal sacs,
or those of small size, that we can form a correct judgment as to their
original modes of development. Confining his assertion only to such
cases, Dr. Thurnam states that of twenty-eight out of the fifty-eight
cases which he collected, twenty-two originated in dilatation" of the
structures entering into the composition of the walls of the heart ;

LATERAL OR PARTIAL ANEURISM OF THE HEART. 163

2. In a more advanced stage there is thickening and opacity of the
endocardium, and conversion of a more or less thick stratum of the
muscular substance into a douse, yellowish or whitish coloured fibroid
tissue intermixed with the muscular structure. The parietes of the
ventricle in the seat of disease have become more atrophied, and the
cavity presents a more marked dilatation.

While these changes are in progress in the parietes of the ventricle,
others are proceeding in its interior. The dilated portion of the cavity
becomes, especially if it be somewhat circumscribed and bounded by a
tolerably defined margin, the seat of coagula. These are at first thin,
loose, and dark coloured, subsequently they become more firm and
paler ; and at length the sac is found more or less completely filled
by coagula, of which the outer portions are distinctly laminated and
decolorized, and often adherent to the altered endocardium. As the

156 A SYSTEM OF MEDICINE.

septum. In three instances there were two or more sacs in the same
case. In one of them one sac was situated at the apex, and another on
the left side ; in a second, one aneurism was at the apex, the other in
the septum ; in the third, one sac was situated partly in the septum and
partly in the anterior wall, another was situated posteriorly in the
septum, and a third occupied the middle of the external wall. Both
these enumerations concur in showing that the most frequent situations
for the aneurismal sacs are first the apex, then the base, and lastly the
external wall and septum.

The greater liability to the occurrence of aneurisms at the apex of the
ventricle is supposed by M. Breschet to be owing to the relative thin-
ness of the parietes in that situation, exposing them to rupture during
the active contraction of the heart. It is, however, more probably owing
to the tissues being readily involved in inflammatory action, extending
from the peri- or endo-cardium, when, as at the apex, those membranes
are more nearly in contact, than when the layer of muscular structure
is of greater width. The portions of the ventricle near the base are
probably commonly affected, from the frequency of endocarditis
of the aortic valves, leading to induration and thickening, and so
to more or less obstruction to the flow of blood from the ventricle.
Under these circumstances there is a tendency to excavation beneath
the aortic valves, which may proceed to the extent of forming a dis-
tinct aneurismal sac. In some cases the disease is situated in what
has been termed the " undefended spate" the space which intervenes
between the base of the ventricular septum and the convex sides of
the left and posterior semilunar valves. This ordinarily is only
closed by the endocardium of the left ventricle, and by a layer
of fibrous tissue, a thin layer of muscle, and the endocardium of
the right ventricle. Being thus imperfectly protected, the space is
readily expanded under any unduly distending force, and a sac is formed
which will protrude into the right cavities about the auriculo-ventri-
cular aperture. When in Vienna a year ago Rokitansky showed me
one or two cases of the kind ; one was exhibited at the Pathological
Society -during the last session, by Dr. Hare, and I have found the
condition myself. In some cases portions of the ventricular wall in this
situation may be congenitally deficient, and a column of blood flowing
from the left ventricle may distend and dilate the folds of the tricuspid
valves, as shown in a specimen in the Museum of the Royal College of
Surgeons. In other cases, the excavation may occupy some other por-
tion of the base of the ventricle beneath the aortic valves, and a
channel may be formed leading into a small aneurismal sac, situated
external to the origin of the aorta ; and such sac may be still further
prolonged so as to open above into the aorta. Cases of this kind
were first described and figured by Dr. Hope, though he supposed
that the aneurisms originated in connexion with the aorta and
only opened into the ventricle. I have described two cases of
the kind in the Pathological Transactions, and a similar one is also
related by Dr. Bristowe. Aneurism at the base of the ventricle may

LATERAL OR PARTIAL ANEURISM OF THE HEART. 157

also rupture into the right auricle or pericardium. Rokitansky men-
tions having seen a case in which both these results occurred. When
the sacs form in the external wall of the ventricle, they may open into
the left auricle or may burst into the left pleura, as in a case
referred to by Sir A. Cooper. When seated in the septum they may
press upon the right auricle and ventricle and open into one or
other of those cavities, especially the right ventricle, as in the case
related by Dr. Peretra, one existing in the Museum of St. Thomas's
Hospital, and one referred to by Eokitansky. In cases of this kind
a form of aneurism results, whioh, as pointed out by Dr. Thurnam, is
analogous to the " spontaneous varicose aneurisms " of authors.

Form and Size. — Aneurisms of the heart may be either circum-
scribed or diffused ; or, in other words, the apertures by which they
communicate with the ventriole may be more or less constrioted ; or
the cavity of the aneurism may gradually extend from that of the
ventricle without any obvious line of separation. The sacs, when
situated at the apex, are more generally of the diffused form ; those at
the base, and in other parts of the ventricle, are more commonly cir-
cumscribed. In the first series of cases the sacs are inferred to have
been circumscribed in twenty-five cases, and diffused in nineteen. As
far as can be ascertained from the reports of the more recently pub-
lished cases, it appears that of thirty-seven cases, twenty-five were
circumscribed and twelve diffused.

The size of the sacs also varies according to the seat and duration
of the disease. At the base and in the septum the sacs rarely attain
any great size ; on the contrary, when developed in the external wall or
at the apex, they may form tumours of considerable magnitude or
may even equal the dimensions of the heart itself. The acute forms of
aneurism also appear, as might be expected, not to attain the dimen-
sions of the more chronic cases. Dr. Thurnam states that in his cases
the sacs might, in nine instances, be compared to nuts, in twenty to
walnuts, in seven to fowls' eggs, in fourteen to oranges, and in nine their
size almost or quite equalled that of the healthy heart itself. In thirty
of the cases which I have myself collected, in four the aneurisms are
simply stated to have been small ; in five they are compared to hazel
nuts or filberts ; in two to walnuts ; one is said to have been large
enough to hold a plover's egg, one to hold a pigeon's egg, and six are
compared to bantam's or smaller or larger fowl's eggs. One sac is said
to have been as large as a nutmeg, another as a plum ; one is reported
to have been capable of holding the whole end of the thumb, another
to have been as large as an apple, and a third as a small oranga Two
are described as being large. In one case, in which there were two
distinct cavities, both were the size of walnuts ; in a second one was
as large as a hen's egg, the other as a walnut. In a third there were
three cavities, the largest the size of a nut. In several cases the
cavities contained one or more loculi, and in one there were three large
pouches projecting from the main cavity.

State of other parts of the Pericardium and Heart. — The frequency

158 A SYSTEM OF MEDICINE.

of alterations in the pericardium and endocardium and in the walls
of the ventricle in the seat of the aneurismal swellings, has already
been referred to. It must also be mentioned that the occurrence of
thickening, opacity, and induration and ossification of the endocardium
and pericardium, and the fibroid transformation of the muscular
substance, are by no means confined to the immediate seat of disease.
These changes often involve a considerable portion of the heart, and
especially of the left auricle and ventricle. In addition to these morbid
conditions, also, the effects of more recent inflammation are frequently
found. Hemorrhagic pericarditis occurred in one of the first collection
of cases ; and in the recent series, pericarditis, with or without old
adhesions and white patches, is recorded to have been found in four
cases. In two also of the cases, blood was found in the pericardium, and
in a large proportion of both series there was serous effusion in con-
junction with general dropsy. In two cases also of the later collection
there were evidences of recent endocarditis, and in several instances fatty
degeneration of the muscular structure had occurred in different parts
of the heart.

In five of Dr. Thurnam's cases there is stated to have been disease
of the mitral valves, in three of the aortic valves, and in one of both
sets, and in only eight cases are the valves expressly stated to have
been healthy. In my own cases, the valves are stated to have been
healthy in only five cases. The aortic valves are reported to have
been diseased in seven instances, the mitral in two, and both sets
in three, and in two or three other instances the aneurismal sacs were
so situated as to have interfered with the action of the auriculo-
ventricular valves. It must necessarily follow that the state of
the whole heart is affected to a greater or less extent in these
conditions, which necessarily lead to alterations in the size of the
cavities and in the thickness of the walls. From the first series of
cases it was inferred that there was general dilatation of the organ
in three cases, dilatation with hypertrophy in three, dilatation of
the left ventricle only in two, hypertrophy in two, and dilatation
with hypertrophy of both ventricles in nine. In only ten cases was
the heart reported to have presented no other lesion than the aneu-
risms, and in three only was it stated to have been positively healthy.
In the more recent coDection the heart appears to have been greatly
enlarged in seven cases ; there was great enlargement, but especially
hypertrophy and dilatation of the left ventricle in twenty cases ; dila-
tation of the left ventricle in two ; and dilatation of the right ven-
tricle in one. In two cases the separation of the two sides of the heart
was imperfect from the apertures having formed in the fold of the
foramen ovale. In three cases the coronary arteries were diseased; and
in six there existed more or less atheroma, calcification, dilatation, or
aneurism of the ascending portion of the aorta. Of the whole num-
ber of cases, excluding from consideration six in which the reports are
imperfect as to the general condition of the heart, there is not one
in which there was not some alteration in the state of the heart or

LATERAL OR PARTIAL ANEURISM OF THE HEART. 150

pericardium, in addition to the aneurism. In one case the heart is in-
deed said to have been of natural size, but in that instance there was
recent pericarditis and an acute aneurism.

The shape of the heart is stated to have been frequently altered by
the presence of the aneurismal swellings. In some it had an un-
usually wide or globular form ; in others there was a bulging of the
aneurismal sac, separated by a more or less distinct furrow from the
other portion of the ventricular wall ; and in yet other cases there were
obvious tumours projecting from the surface of the organ. These
were sometimes only of small size so as to be compared to a small nut
or thimble ; in others they were of considerable magnitude, and were
separated from the walls of the heart by a distinct constriction or
neck. In one specimen contained in the Museum of St. Thomas's
Hospital, probably one of those referred to by Sir A. Cooper, there is
a tumour with thin parietes as large as an ordinary heart projecting
from the anterior surface of the organ, and separated from it by a
neck which is not half the circumference of the tumour itself.

The existence, however, of an obvious tumour or irregularity on the
surface of the heart depends upon the seat and size of the aneurismal
sac. At the base the tumours are generally, if not always small, and
do not form projections which can be detected till the parts around are
dissected away. Aneurisms in the septum also can produce no marked
alteration in the general form of the organ ; but those on the anterior,
outer, and posterior walls, if at all of large size, necessarily occasion
either some general bulging or form a distinct tumour. Of fifty-four
aneurisms it is inferred that only thirty-five were attended by tumour.

State of other Organs of the Body. — The condition of the other organs
of the body is not recorded by Dr. Thurnam, probably from the histories
of the cases which he collected being defective in these particulars. I
regret also that 1 am not able to supply satisfactory information from
the reports of thfe more recent cases. I find, however, that in a large
proportion of them there was more or less general dropsy, and that
serous effusion had occurred in one or both pleural cavities and in
the peritoneal sac. In one of the cases the fluid in the pleura was
bloody, the lungs being also engorged in the same case. In two cases
there were signs of recent pleurisy, and in eight the visceral and
parietal pleurae were attached by old adhesions. In eight cases there
was pulmonary apoplexy, emphysema, bronchitis, or pneumonia, and
in one of the latter cases the lung was gangrenous. In one instance
there were tubercles in the lungs, and in another old syphilitic disease
of the larynx.

The liver is reported to have been small and pale in one case ; fatty
in one ; and congested, enlarged, granular or indurated in eight cases.
The spleen was large in two cases, small in one, and softened and con-
taining fibrinous or purulent deposits in one. The kidneys were en-
gorged in four cases ; granular, atrophied, cystic, or otherwise diseased
in six : and contained purulent deposits in one.

Symptoms and Cause of Death. — It is impossible to point out any

160 A SYSTEM OF MEDICINE.

symptoms which can, in the present state of our knowledge, be regarded
as characteristic of the lateral or partial aneurisms of the heart ; and,
indeed, it is doubtful whether any such symptoms will hereafter be
ascertained. This will readily be understood when the frequency with
which the affection is associated with valvular diseases and with alter-
ations in the size of the cavities and thickness of the walls of the heart
is considered. On analysing the reports which have been published, it
appears that in several cases the condition was only deteoted on post-
mortem examination, in the bodies of persons who were not known
to be suffering from any form of cardiac disease, and were supposed
to be previously in good health. In by far the largest proportion of
cases, however, twenty-two out of twenty-seven, there is a history of
prolonged indisposition, not unfrequently commencing with acute
rheumatism or in some inflammatory affection of the thoracic organs,
and characterised by the usual symptoms of cardiac disease. Dif-
ficulty of breathing, and sense of suffocation and oppression at the
chest ; pain in the region of the heart, at the sternum, and at the
epigastrium ; palpitation and tumultuous action of the heart, and
irregularity of the pulse; with cough, expectoration, and dropsical
symptoms, are generally mentioned as having been present. Not un-
frequently, also, the sounds of the heart are stated to have been
replaced by morbid murmurs, but these appear to have been chiefly,
if not wholly, referable to coincident valvular affections. The only
symptoms, indeed, which can be regarded as at all of a specific
character are pain and sense of weight in the region of the heart,
which appear to be more constant attendants on these forms of
disease than on any other kind of organic affection of the heart.
It must, however, be concluded, that, at the present time, the diagnosis
of these affections cannot be effected during life, and it is indeed
doubtful whether it will be ever possible, with any exactitude, to
diagnose them.

The cause of death is also often not clearly stated in the reports
which have been, published. It appears, however, that of the cases
collected, in three the patients died suddenly, and probably from syn-
cope, without any obvious reason being detected for the occurrence.
In two, death resulted from cerebral congestion and convulsions. In
one, from more acute disease supervening upon old laryngeal affection.
In one from bronchitis, two from pneumonia, one from pleurisy, and
in one from phthisis. In two cases the patients sank from coma and
other symptoms connected with disease of the kidneys. In four in-
stances death resulted from the rupture of the sac and the escape of
blood into the cavity of the pericardium ; in four from the rupture of
an aneurism of the ascending aorta into the pulmonary artery. In two
cases the patients died from extensive disease of the aortic valves con-
nected with endocarditis ; combined in one with the opening of an acute
aneurism into the left auricle and very nearly externally, and in the
other with purulent deposits in different organs. In the remaining
seventeen, out of the twenty-five cases in which the. particulars are

LATERAL OR PARTIAL ANEURISM OF THE HEART. 161

given, it appears that death resulted from the progress of the general
and dropsical symptoms and the affections of different organs super-
induced by the cardiac defects. Of the cases previously analysed,
the cause of the death was assignable in twenty-four. In twelve of
them death was sudden : in three from syncope, in six from rupture
of the sac into the pericardium, in one into the left pleura, and in one
from rupture of the heart itself. In four, the patients died of apoplexy
or paralysis, and in one from epistaxis. In nine cases death ensued
from the progress of the cardiac symptoms, and six from other coin-
cident complications. Bokitansky mentions the case of a boy of
twelve years of age, in whom a small aneurism at the base of the
ventricle, after having first formed a connection with the right auricle,
opened into the pericardial sac.

It thus appears that there are on record eleven cases in which
the aneurismal cavities have terminated by rupture. In most of
them the affection proved suddenly fatal. Such was the result in
the instance of General Kidd, a gentleman of seventy-three years of
age, whose case is related by Dr. Johnson, and who was found dead in
his bed. Here the aneurism was of small size, and was situated near
the base of the ventricle. In a case related by Dr. Wilks, a girl twelve
years of age, died suddenly when playing, and an aneurism about the
size of a walnut was found about the middle of the anterior wall of the
left ventricle near the septum. In other instances, however, life has
been prolonged for some short time after the occurrence of the rupture.
Thus, in the case related by Galeatti, the symptoms indicating the
rupture appeared about a week before the fatal termination; and
in one which I have myself related, blood appears to have escaped
into the cavity of the pericardium, not, however, by a distinct rup-
ture, five days before death ; more rapid extravasation having been
prevented by adhesions between the layers of pericardium at the seat
of disease.

In some cases the aneurism may be regarded as having under-
gone a partial natural cure. M. Cruveilhier has described cases in
which the process of dilatation seems to have been arrested and the
sac had been converted into bone, or more properly speaking, in
which cretaceous matter had been deposited in its walls. In a
case recorded by Dr. Wilks l the cure appears indeed to have been
almost complete. A man, fifty-two years of age, of very intem-
perate habits, died of phthisis, and on examination after death, the
heart and pericardium were found adherent to the diaphragm at the
apex. In this situation there existed a hard calcified tumour, about
the size of a pigeon's egg, which contained layers of decolorized coagu-
lum. The cavity communicated with that of the ventricle by an
aperture of about the same size as the sac itself. The edges of this
aperture were smooth, and the membrane lining the sac was con-
tinuous with the endocardium of the ventricle. No history of the
case could be obtained; but there is no doubt that the sac was

1 Path. Trans, vol. viii. p. 103.
VOL. IV. M

162

A SYSTEM OF MEDICINE.

aneurismal, and that the progress of the disease had been entirely
arrested some time before the death of the patient

Age and Sex of the Subjects of the Disease. — Dr. Thurnam found the
sex assigned in forty of the cases which he collected, and of them
thirty were males and ten females, and he points out the difference
which this proportion displays to the frequency of aneurismal affec-
tions of the arteries in the two sexes. The facts which I have brought
together show a still larger proportion of cases in females — the num-
bers being thirty-nine — twenty-five males and fourteen females. The
ages of the patients in the first series of cases ranged from eighteen
to eighty-one, and were pretty evenly distributed throughout the
middle and later periods of life, though somewhat more frequent
between twenty and thirty, and in advanced life. The more recent
cases display a tolerably equal distribution from early to advanced age,
and are given in the following table : —

Age. Males.

14 and 16 2

21 to 30 4

81 to 40 4

41 to 50 4

51 to 60 8

61 to 70 3

71 to 77 2

Between 60 and 70 .... 1

Not stated 2

Age. Female*.

12 and 15 2

21 to 80 . . . ... 4

31 to 40 0

41 to 50 0

51 to 60 0

61 to 70 4

71 to 77 2

Between 60 and 70 .... 0

Not stated 2

The most noticeable circumstance in this enumeration is the very
early age at which the cardiac cases occur as compared with different
forms of arterial aneurism ; this being explained by the frequent origin
of the disease in endocarditis, and the frequency of endocarditic affec-
tions, as complications of rheumatism, in early life. It would have been
interesting to have given some more satisfactory information as to the
influence which rheumatism exercises, either immediately or more
remotely, in the production of the partial aneurisms of the heart.
The reports of the cases are, however, very imperfect on this point ;
but they clearly indicate that the aneurisms are not unfrequently
connected with rheumatism. They appear also to be very commonly
predisposed to by habits of dissipation and intemperance, both causes
which we know are very influential in the causation of other forms of
cardiac disease.

Aneurism of the Left Auricle. — An instance of dilatation of the
left auricle with deposition of coagula in the dilated part, the result of
an injury, was related by Dionis in 1716.1 With this exception,
however, the condition does not appear to have been noticed till the

1 L'Anat de 1'Homme, p. 713.

LATERAL OR PARTIAL ANEURISM OF THE HEART. 163

beginning of the present century, when cases of the kind were related
by Abernethy, Burns, and Hodgson, and, more recently, others have
been placed on record by Sir A. Cooper, Elliotson, Hope, Chassaigniao,
and "Virchow, &c. Dr. Thurnam refers to eleven cases, including a
further notice of one previously mentioned by Dr. Thomas Davies.
Since the date of his memoir there have been four or five other cases
published. Of these one is related by Dr. FeDwick,1 another by Mr.
Prescott Hewitt,2 a third by Dr. Bristowe,8 and one by myself.4

The so-called aneurisms of the auricle consist of dilatations contain-
ing coagula and fibrinous deposits of the sinus and auricular appendix,
or both. They may either involve a considerable portion of the walls
of the cavity and pass gradually from the undilated part without any
obvious constriction or separation ; or they may form distinct saccu-
lated expansions. In the largest proportion of instances the sinus
has been the seat of the disease, and the aneurism has been of the
diffused form. In the cases, however, of M. Chassaigniac and Virchow,
and in that of Dr. Fenwick, the cavity was distinctly circumscribed.
Most generally, also, the disease has been found in connection with
some, and often very marked, obstruction at the left auriculo- ventricular
aperture ; but in the instances named the valves were free from disease.
The case of Dr. Fenwick was further interesting from there having
existed during life a loud systolic sound audible at the apex, which was
clearly due to the obstruction caused by the aneurismal swelling.

In two of the cases referred to, those of Mr. Prescott Hewitt and
Dr. Bristowe, the right auricle was greatly dilated as well as the left,
and the cavity contained coagula ; in the former instance, apparently
of similar character to those in the left auricle — in the latter, how-
ever, only the usual amorphous clots. Partial expansions of this kind
should not, however, have the term aneurism applied to them ; but to
maintain the analogy between the similar affections of the arteries
and veins, the dilatations of the right side of the heart should be
termed varicose.

Aneukisms of the Valves. — A dilatation of the mitral valve, to
which the term aneurism may properly be applied, was described by
Morand in 1729; another was mentioned by Laennec and Fizeau at
the beginning of this century. Sir A. Cooper, also, in 1825, referred to
a case then and still existing in the Museum of St. Thomas's Hospital,
and two other instances of the kind have been more fully related by
Dr. Thurnam though previously noticed by others, of which one oc-
curred in the practice of Sir Thomas Watson at the Middlesex Hospital.
More recently specimens have been described by Cruveilhier, by Mr.
Prescott Hewitt,6 Dr. Habershon,6 Dr. Ogle,7 and myself;8 and the
affection has been noticed by Eokitansky in his Pathological Anatomy.

1 Lancet, Feb. 1846.

1 Path. Trans. 1848-50, vol ii. p. 194.

* Ibid. zL 1859-60, p. 65.

4 Ed. Med. and Surg. Journal, 1846.

5 Path. Trans. yoL iii. p. 78.
• Vol. ix. p. 117.

7 Ibid. vol. vi. p. 156

8 VoL iii. p. 71.

M 2

164 A SYSTEM OF MEDICINE.

Aneurisms may occur both in the aortic and mitral valves. Of their
mode of origin in the former situation a very interesting example is
contained in the Museum of St. Thomas's Hospital. In one of the aortic
valves there exists a small distinctly-marginated sac, which would
have contained a small bean ; in a second, there is one of somewhat less
size, and in the third there is simply a deposit of fibrine in one part of
the fold and a very slight dilatation in the same seat. It is evident
that the last is the result of inflammatory action, and indicates the
first stage in the production of the small aneurisms which exist in the
other valves. Dr. Chevers has shown that in cases of contraction of
the outlet of the ventricle and expansion of the inlet, whether relative
or absolute, the aortic valves have a tendency to bulge at their most
dependent parts. If this be unattended by any deposit of fibrine, the
fold ultimately gives way in the weakened portion ; if, however, the
valve be strengthened by a deposit of fibrine the bulging may increase
till a distinct sac is produced. A very characteristic example of the
kind was exhibited by myself at the Pathological Society.

In the mitral valve the disease is, I believe, always found in the
free fold. The dilatation may occupy merely a small part of the
valve, or may be of large size, so as to involve a large portion of the
fold. In some cases the disease seems to originate in the protrusion of
the endocardium of the left ventricle, through the fibrous structure of
the valve, so as to come in contact with the lining membrane of the
left auricle. In other cases all the coats are dilated. In both instances
the sacs generally project into the cavity of the left auricle, and some-
times the base of the sac gives way, and an opening is produced in the
valve as if a piece of the fold had been punched out. The sacs may
vary in size from one which would lodge a pea or bean or filbert, to
one capable of holding a pigeon's egg. Of the former size the cases of
Mr. Prescott Hewitt and myself afford instances. Of the latter, the
specimen in the Museum of St. Thomas's, referred to by Sir A. Cooper,
is a most remarkable example. In several cases two or more sacs have
been found in the same valve. These small aneurisms of the mitral
valve not unfrequently occur in cases of aortic valvular obstruction,
and I have described one which was found in a case of rupture of the
aortic valves. The sacs may contain laminated coagula, and in one
of the cases described by Mr. Keith, a portion of the valve was
entirely wanting, and a small sac was produced by a fibrinous coagu-
lum being attached on the auricular side.

These affections are not only interesting pathologically, but may be
of practical importance, as both at the aortic and mitral valves they
may give rise to the symptoms and signs of incompetency.

I have before referred to a specimen which exists in the Museum of
the Royal College of Surgeons, in which the current of blood flowing
through a congenital aperture existing at the base of the ventricular
septum has expanded portions of the tricuspid valves, so as to form
small sacs or aneurisms ; and I have seen a similar condition of the
tricuspid valve in a recent case of malformation of the same kind

ADVENTITIOUS PRODUCTS IN THE HEART.

By Thomas Bevill Peacock, M.D., F.RC.P.

TUBERCLE IN THE HEART AND TUBERCULAR

PERICARDITIS.

Laknnec1 when alluding to accidental products says, that he had
only three or four times met with tubercles in the substance of the
heart ; and when speaking of chronic pericarditis, he remarks, that a
tuberculous eruption may sometimes be developed in the false mem-
brane and may thereby convert the acute into chronic disease, as
frequently happens in pleurisy and peritonitis, and he states that he
had met with two cases of the kind. In this passage, Laennec indi-
cates the forms in which tuberculous deposits are found in the heart ;
in one of these they take place in the substance of the organ ; in the
other on the surface, in connection with inflammation of the peri-
cardium. The former is certainly a very rare condition. Louis 2 says
that in 112 dissections of phthisical persons he did not meet with a
single instance of the existence of tubercle in the substance of the
heart. Rokitansky 8 also speaks of the extreme rarity of the affection ;
and in the records of 116 post-mortem examinations of persons who
had died of phthisis which I have analysed, I do not find more than
two or three cases in which tubercle is said to have been found in the
heart. The recorded instances of such deposits being at all of serious
importance are also very few in number. The first writer who alludes
to cases of the kind is, I believe, Dr. Baillie,4 who in his " Morbid
Anatomy " says that he " once saw two or three scrofulous tumours
growing from the cavity of the pericardium, one of which was nearly
as large as a walnut. They consisted of white soft matter, somewhat
resembling new cheese," and he adds that " the pericardium is a very
unusual part for any scrofulous affection;" and in his "Dissec-
tions," * in alluding to the same case, he further says that both lungs
were studded with tubercles, and the right in a state of suppuration in
places. . The subject of the dissection was a man twenty-one years of age

1 Diseases of the Chest, Forbes's trans. 4th edit. 1834, pp. 586 and 623.

* Sydenham Society's Trans. 48-50. * Ibid vol. iv. p. 210.

* Morbid Anatomy, and works by Wardrop, 1825, vo.l ii. p. 9.

* Works by Wardiop, vol. i. p. 220.

166 A SYSTEM OF MEDICINE.

Dr. Macmichael,1 in 1826, detailed the history of a man of thirty-five,
who died at the Middlesex Hospital with dropsy and other symptoms
of cardiac disease, and in whom the lungs and bronchial glands were
found tuberculous, and the pericardium, especially at the base, studded
with tuberculous deposits. In 1834, M. Sauzier. as quoted by Bouil-
laud,2 found in a man thirty-four years of age, who died with abscess
from caries of the sternum after accident, the luugs, pancreas, and pleura
tuberculous, and in the substance of the auricles there were two
tubercles, and around them the pericardium was adherent. The most
remarkable case of the kind is, however, that related by Dr. Townsend
in 1852.8 In this instance a large mass described as tuberculous was
connected with the left auricle, and had compressed that cavity and the
entrances of the pulmonary veins, so as to give rise to extreme disten-
sion throughout their course; tubercles existed in the bronchial glands
but not apparently in the lungs. The subject of the disease was a
man sixty-two years of age, who died after an illness of twelve months.
Since this time a case has been recorded by the late Dr. Baly in the
Pathological Transactions.4 It occurred in a prisoner at Millbank, six-
teen years of age, who died with symptoms of sub-acute fever and head
affection, after an illness of about ten days, and tubercular masses were
found in the substance of the brain, and small tubercles in the lungs,
bronchial glands and intestines. A yellow rounded mass, the size of
a man's thumb, projected from the tinter-auricular septum into the
cavities of the right and left auricles, the two projections being parts
of the same tuberculous mass which was situated in the septum. Dr.
Quain also mentions that there were tubercular deposits in the peri-
cardium in a Bosjesman girl, who died of tuberculosis.6

The second form of tuberculous deposit which occurs in connection
with inflammation of the pericardium, is by no means so rare as
that which has just been mentioned. The first instance of the kind that
is recorded is probably that by Corvisart,6 and another was figured by
Cruveilhier, and is further alluded to in the General Pathology more
recently published. The pericardium adhered intimately to the
heart, and in these adhesions a thick and continuous layer of tubercu-
lous matter was deposited, and this enveloped the vessels and had
destroyed the muscular structure of the auricle. M. Fauvel, as quoted
by Aran,7 and by liilliet and Barthez in their work on diseases of
children, met with a case of tubercular pericarditis in a child six
years and a half old, who died with dropsy and symptoms of disease
of the heart. The pericardium was entirely adherent, the heart was
considerably enlarged, and its surface was studded by whitish-yellow
friable nodules, some of them the size of a nut, and as numerous

1 London Medical and Physical Journal, vol. lvi. (N.S. vol. i.) p. 119.

a Maladies du Coeur, 2me edit, tome ii. p. 442.

3 Dublin Journal, vol. i. 1852, p. 176.

« Path. Trans, vol. iii. 1850-51, 1851-2, p. 84.

5 Path. Trans, vol. ii. 1848-49, 1849-50, p. 182.

6 3™ edit. Paris, 1818, p. 26.

7 Aran, Arch. Gen. de M<Sd. 4mo seric, 1846, tome xi. p. 1S1.

ADVENTITIOUS PRODUCTS IN THE HEART. 167

behind as in front. The internal surface of the right ventricle displayed
similar depositions everywhere except at the septum. Since this time
the occurrence of tuberculous deposits in connection with pericarditis
has been made the subject of a special memoir by Sir G. Burrows,1 in
which he details three cases which he supposes to be examples of the
affection ; and in two of them — one of which occurred in his own practice,
the other under the care of the late Dr. Baly — the inference was con-
finned by post-mortem examination. More recently, Dr. Bristowe has
described three other cases in the Pathological Transactions,2 and such
instances cannot indeed be very uncommon. Cruveilhier says that he
has many times met with tubercles, in connection with false mem-
branes, in children with tuberculous lungs.8 Louis also refers to such
cases, and details the particulars of one in his memoir on pericarditis.4
Otto6 mentions having twice seen the condition in children, and Dr.
Walshe * states that it is displayed in one of Dr. CarswelTs drawings
contained in the collection to illustrate morbid anatomy at University
College. I have myself met with three cases of the kind, two while
Pathologist of Edinburgh Infirmary and one at the Victoria Park
Hospital.

Tubercular deposits in the pericardium bear a close resemblance
to the similar disease of the arachnoid, pleura and peritoneum. They
may be of very small size, mere specks, or may attain the dimensions
of a cherry-stone, filbert, or walnut. In consistence they are generally
soft, and they are usually of a greyish or yellowish colour. In one of
m£ own cases, the tubercles, which were thickly spread over the
attached and reflected pericardium, varied in size from that of a pin's
head to a cherry-stone. In another, while there were very small
masses of yellowish tubercle thickly studded over the surface of the
heart, there were also laminated false membranes, in some places a
quarter of an inch, in other parts fully half an inch in thickness, and the
middle layers of this deposit were of a yellowish colour, soft and granu-
lar, and closely resembled what is commonly called tuberculous infil-
tration. In the third case the tuberculous deposit assumed the form
of small granulations of a greyish colour, the two layers of pericardium
being entirely attached by cellular adhesions. The affection in two of
Dr. Bristowe's cases consisted of small miliary granulations, in one with
patches more closely set together in places ; in the other there were
both separate tuberculous masses and laminae of considerable siz£

In the cases which have fallen under my own notice the deposits
were situated beneath the serous membrane, and in one of them there
were masses which were more deeply embedded in the substance of
the ventricles and which were only exposed on section. One of these
cases also, it will be observed, displayed tubercle in the centre of a
thick layer of false membrane covering the heart, thus corresponding

1 Med.-Chir. Trans, vol. xxx. 1847, p 77. a Vol. xii. 1860-61, p. 63.

3 Traite d'Anat. rath, tome iv. acne 1862, p. 684.

4 Revue Medicale, 1826. 8 Path. Anat by South, 1831, p. 258.
* Diseases of Heart, 1862, p. 357.

168 A 8Y8TEM 0* MEDICINE.

with the observations of Laennec and Cruveilhier. The different
writers who have alluded to this subject have agreed in asserting
that tuberculous affections of the heart are only met with in connection
with similar deposits in other parts of the body, and the cases which
have been recorded entirely confirm that view. The most frequent
co-existence is with tubercle in the bronchial glands, or in the lymphatic
glands of the mediastinum. In two of the cases which I have myself
seen, though occurring in persons twenty-eight and sixty-seven years
of age, there was tuberculous deposit only in the bronchial glands and
heart ; though the general rule is, as is well known, that, after early life,
if tubercle be found in any part of the body it also exists in the lungs.
In the third case, the subject of which was a girl thirteen years of age,
no tubercle was found anywhere else. In this instance there was alse
slight mitral valvular disease. In Sir G. Burrows' case the lungs, pleuTa,
bronchial glands, peritoneum, and spleen were tuberculous; and in
Dr. Baly's there were tubercles and ulcers in the intestines and lungs.
In. one of Dr. Bristowe's patients there was tuberculous perforation of
the intestines ; in a second, there was tubercle in the mediastinum ;
and in the third, in the brain, lungs, pleura, spleen, and mesentery.
The occasional occurrence of tuberculous deposits in the heart with
similar affections of the bronchial glands and mediastinum, and in
some cases when the lungs are entirely free, led Cruveilhier to
suggest that possibly the affection of the glands might be secondary
to that of the heart ; but this supposition is scarcely in accordance
with the advanced disease of the lungs which is reported to have
existed in other instances. Laennec supposed that the tubercles in
cases of this description were the result of the inflammation, and were
situated in the false membrane ; the latter is, however, certainly not
usually the seat of the deposit, and Sir G. Burrows is much more
probably correct in regarding the pericardiac affection as the effect
of the irritation set up by the deposit under the membrane. Indeed,
the first class of cases, in which the tubercles are situated deeply in the
substance of the heart or under the endocardium and assume the form
of separate tumours, cannot be regarded as essentially distinct from
the second, in which the tubercles are more superficial. The absence
of adhesions in some of the latter class of cases seems conclusively
to show that the inflammatory exudation is at least generally
secondary.

. The tuberculous deposits in the heart occur under the same
circumstances as those which attend similar affections in other parts
of the body; they may be found in both sexes, and at all ages, but
they are more common. in comparatively isarly life.

The age and sex of the subjects of some of the cases referred to
are as follows : —

ADVENTITIOUS PRODUCTS IN THE HEART.

169

Males 6} years.

»? 13 ,,

» 16 „

»» 1^ M

»» *1 »l

»» " II

» 34 ,,

» 36 ,,

„ 62 „

» 67 ,,

Females 14 years.

20 „

» 28 ,,

In several of the cases of tubercular pericarditis the evidences of
effusion in the pericardium had been observed during life. When
such signs arise in persons who are obviously tuberculous, and
especially if they assume the sub-acute form and are not attended
Toy any large amount of liquid effusion, they may be suspected to be
connected with tubercular deposits. It must however be borne in
mind that pericarditis, having no connection with tubercle, may occur
during the progress of phthisis. The inference as to the tubercular
origin of such cases is therefore by no means decisive.

CANCER

Cancerous deposits in the heart are of more common occurrence
than tubercle. Dr. Walshe,1 writing in 1846, says that he had readily
found twenty-five cases recorded ; and more recently, in a paper in the
Pathological Transactions,2 I collected the particulars of forty-five,
including in this number two which had fallen under my own notice.
The earliest published examples of the disease were, I believe, those
of Andral and Bayle in 1824.8

The cases of cancerous deposit in the heart may be classed into
four series: First, Cases of primary cancer, in which the disease
exists only in some part of the organ. These are of extremely rare
occurrence ; of the forty-five cases referred to, only two were expressly
stated to have been instances of the kind,4 though in the reports of
seven others, no mention was made of the existence of cancer in any
other part of the body.

Secondly, Cases in which the disease occurred coincidently and
probably simultaneously, in the heart and in different parts of the
body, and especially in parts adjacent to the heart. This form,
though still rare, is more common than the other.

Thirdly, Instances in which the disease first appears in parts
adjacent to the heart,- — the bronchial or mediastinal glands, the lungs,
or the glands around the larynx and in the neck, — and thence spreads
so as to involve the pericardium and the large vessels at the base of

1 Nature and Treatment of Cancer, p. 368. t Vol. xvi. p. 99, 1864, 1865.

8 Revue MeMicale, 1824, tome 1™, p. 268.

4 Ollivier, Traite de la Moelle Epiniere, 3m* edit., 1837, tome ii. p. 164 ; Segalas,
Rev. M£d. tome iv. 1$25, p.* 247. .

170 A SYSTEM OF MEDICINE.

the heart or the auricles. Cases of this kind are not uncommon,
though less frequent than those of the next series.

Fourthly, By far the largest proportion of cases of cancerous
disease of the heart occur secondarily to the deposit of cancer in some
distant organ. Of the forty-five cases, twenty-one were of this
description ; the primary disease being seated in different cases in the
eye, the cheek and bones of the face, the lower lip, the breast and
axillary glands, the ribs and pleura, the abdominal organs, the inguinal
glands, the uterus, vagina, labia, the penis and testes, and the upper
and lower extremities.

The heart may be affected by cancer in different forms. Thus, of
the cases collected seven are reported to have been cases of scirrhus,
four of melanosis, and twenty-five of encephaloid. The deposit also
may assume either the form of distinct masses or tubera> or it may be
infiltrated into the tissue, or occur on the surface.

The first form is the most common, especially when the deposits
are secondary. The ma&ses in different published cases are com-
pared in size to peas or beans, to almonds or chestnuts, or to hen's
eggs or oranges ; and they may be only one, two, or three in number,
or they may amount to a dozen or more 1 and in one very remarkable
case it is stated that they were so numerous that the examiner ceased
counting them after enumerating six hundred.2 The most frequent seat
of the disease seems to be the right auricle and ventricle, though the
tumours may also occur, either alone or otherwise, in other parts of the
organ. Generally they are situated beneath the attached pericardium ;
more rarely beneath the endocardium ; and still more rarely in the
substance of the auricles and ventricles or in the septa. The deposits
may only slightly project above the adjacent surface, or they may form
distinct and nearly separate tumours, the mass being only attached to
the part from which it projects by a narrow pedicle. In the Museum
of St Thomas's Hospital there is a specimen of medullary growth from
the left auricle, which is almost entirely detached from the lining
membrane. In some cases the masses are reported to have pressed
upon the cardiac cavities or apertures, so as to interfere with the
transmission of the blood or with the action of the valves.

More rarely the disease assumes the form of infiltration, and when
this is the case, the structure of the heart may be only slightly affected,
or it may be extensively and completely destroyed. In one instance it
is stated that not more than a twelfth of the organ was free from the
deposit.8

In the third form of disease the heart is found enveloped in a

1 Exposition d'un cas remarkable de Maladie Cancereuse (Paris, 1825), quoted by Dr.
Churchill in London Med. and Phys. Journal, vol. lvii. (N.S. vol. ii.), 1827, p. 280.

1 Case of Dupuytren, quoted by Cruveilhier in Essai sur l'Anat. Path. Paris, 181-6,
vol. i. pp. 86-87.

8 Killiet ; Bullet, de la Soc. dc Mud. 1813, No. 5, tome iii. p. 857. A very marked
case of cancerous infiltration with masses in the mediastinum, which occurred in a
patient of Dr. Barker's, at St. Thomas's Hospital, is described by Dr. Bristowe in the
Path. Reports, vol. vii. The specimen is preserved in the Museum, x. 67.

ADVENTITIOUS PRODUCTS IN THE HEART. 171

cancerous mass, which produces entire adhesion of all parts of the
pericardium. This is, I believe, of very unfrequent occurrence. A
case of the kind has, however, been described and figured by Dr.
Bright in the Medico-Chirurgical Transactions.1 A second is related
by Dr. Kilgour,* in the " London and Edinburgh Journal of Medical
Science ;" and a third was described by myself in the paper in the
Pathological Transactions before referred to.8

In only two or three of the recorded cases is the cancer stated to
have been softened or ulcerated, and the nature of one of them may
be doubted. In one instance, however, a cancerous mass situated near
the origin of the anterior coronary artery had softened and caused
perforation of the arterial coats and the escape of blood into the cavity
of the pericardium.4

Cancerous deposits in the heart do not appear to be generally pro-
ductive of any special symptoms by which their presence can be
detected during lite. In some cases, when there was disease of the
adjacent organs, there were signs of pressure on the large vessels and
of interference with the circulation of the blood ; and in three or four
other instances the formation of the deposits on the surface of the
heart occasioned inflammation of the pericardium which was recog-
nised by the usual signs during life. Of this I have myself seen two
instances. Most usually, however, there are no symptoms by which
the affection of the heart is indicated, and the condition is only de-
tected on post-mortem examination. In the case under my own care
which has been mentioned — notwithstanding that the existence of a
tumour in the chest was ascertained a considerable time before the
patient's death, and that the patient's father was said to have died of
cancer of the heart, and thus attention was particularly directed to the
state of the organ — no symptoms indicating the heart to have been
involved were detected.

SIMPLE AND OTHER CYSTS.

Lancisi mentions having seen a cyst containing thick matter (meli-
ceris) in the substance of the heart, and other writers describe the occa-
sional occurrence of cysts of different kinds in the heart or pericar-
dium. Thus Cruveilhier refers to hjematoid cysts as occurring in the
pericardium and other serous surfaces, but does not detail any in-
stance of the kind ; and I do not know any recorded case except that
reported by Dr. Ogle in the Pathological Transactions for 1857 and
1858.* In this instance a large cyst was found beneath the peri-
cardium covering the posterior surface of the right ventricle. It had
■firm and thick walls, and contained laminated coagulum with brownish

1 Vol. xxii. 1839, p. 15. * Vol. iv. 1844, p. 828.

3 Vol. xvi. 1864-1865, p. 100, Case 1. The specimen is preserved in the Victoria
Park Hospital Museum.

4 M. Broca, Bullet, de la Soc. Anat. 25s" , annle, 1850, p. 253.
• Vol. ix. p. 165.

172 A SYSTEM OF MEDICINE.

granular material The layers of pericardium were adherent, and
there were old and thick adhesions of the right pleura, with some
similar coagulum in its sac. No connection could anywhere be
traced between any of the cavities of the heart and the cyst; and
Dr. Ogle supposes that probably the blood had escaped from one of
the branches of a coronary artery ; and that having first lodged in
the pericardium, it had subsequently ruptured into the pleura. The
cavities of the heart were rather large, the lining membrane of the
right auricle was thickened and opaque, and the coronary arteries
were in various places rigid. The specimen was removed from a
man fifty-five years of age, who died with symptoms of cardiac
disease and dropsy, and who had been ill for two years ; but no
decided history of any attack to which the condition of the heart could
be ascribed appears to have been obtained. The condition of the
coronary arteries is in favour of Dr. Ogle's supposition, but it may
be open to question whether the cysts might not have originated in
acute hemorrhagic inflammation of the pericardium and right pleura.
Certainly in some cases the appearance of a cyst is produced by
the remains of a pericarditic effusion ; the two layers of serous mem-
brane becoming adherent, except in one portion, where a cavity
containing pus or serum still exists. A specimen of this kind was
exhibited at one of the meetings of the Pathological Society.

ENTOZOA

In the works of the earlier writers on morbid anatomy, cases are re-
ferred to in which the heart is stated to have contained worms. Such
reports are, however, generally entitled to little credit, though of late
years hydatid cysts, have, in various cases, been found in different parts
of the heart. Probably the earliest recorded instance of the kind is that
mentioned by Morgagni,1 of a man seventy-four years of age, who died
in the hospital at Padua ; but of whose previous state no further history
was obtained than that he had not suffered from any of the usual symp-
toms of cardiac disease. A tumour about the size of a cherry was found
at the posterior surface of the heart near the apex. It was half em-
bedded in the substance of the organ, and " on puncturing it a small
quantity of clear fluid escaped, but a more turbid humour remained,
and was only evacuated on laying it open. In so doing a small piece
of membrane escaped. This displayed white, and, as it were, mucous
particles, and a particle of tendinous hardness." The whole was in-
cluded in a dense sheath. Dupuytren,2 at the beginning of the pre-
sent century, placed a similar case on record. It occurred in a female
forty- years of age, who died in one of the Paris hospices, whose
body was dissected in the anatomical school. No history of the

1 Alexander's Translations, vol. i. p. 583. Letter xxi. Art. 4. See also Letter ill.
Art. 26, p. 60, where it is said a white membrane protruded like a hydatid.

2 Journal de Corvisart et Leroux, tome v. annee xi. p. 139.

ADVENTITIOUS PRODUCTS IN THE HEART. 173

case during life was obtained. The right auricle was very greatly
dilated, and on its inner surface, under a smooth membrane, were found
numerous cysts which nearly filled the cavity. About the same
time a third case was related by Dr. Trotter ; l it occurred in a boy
fourteen years of age, on board one of her Majesty's ships, who
had been very livid and subject to dyspnoea and palpitation : a large
cyst, containing several loose hydatids, was found in the right auricle,
and two similar bodies were also contained in the ventricle. Two
cases of the kind are contained in the Transactions of the Medical and
Chirurgical Society ; one of these, which was published in 1821,
occurred in a boy of ten, who died suddenly without having been pre-
viously ill, and the case is imperfectly related by Mr. David Price.2
The other was communicated by Mr. Evans8 in 1832. The subject of
the disease was a delicate female, forty years of age, who was sud-
denly seized with pain in the praecordia and difficulty of breathing,
and died in a few days. The pericardium displayed an effusion of
lymph and serum ; and a considerable tumour was situated at the apex
of the heart and projected into the right ventricle, filling a fourth of the
cavity. The tumour proved to be a cyst containing numerous hyda-
tids, varying in size from a pea to a pigeon's egg. A plate is given of
the specimen, which is stated to be preserved in the Museum of St.
Bartholomew's Hospital. In 1838, Mr. Smith of Bristol published a
somewhat similar case, which occurred in the practice of a surgeon at
Warminster. The subject of the disease was a female, whose age is not
stated, and who died after an illness of three hours. A large hydatid
was found in the right ventricle, and must have obstructed the
entrance of the blood into the pulmonary artery.

The more recent writers on cardiac diseases and on pathological
anatomy very generally refer to cases of hydatid cysts found in some
portion of the heart. Andral 6 says that he has seen three instances
of the kind. In one a tumour, the size of a walnut, was embedded
in the substance of the left ventricle ; in another a cyst, as laige as a
nut, was attached by a small pedicle to the lining membrane of the
right ventricle ; and in the third, three cysts, the size of nuts, were
embedded in the substance of the heart. The cysts were transparent
except at one point which was white and could be made to protrude
like a head from the centre, and he was thus led to regard them
as cysticerci. Rokitansky* relates the case of a woman, twenty-
three years of age, who died suddenly, and a tumour the size of a
hen's egg was found at the upper part of the interventricular septum,
and protruded into both ventricles. On the right side the cyst had
burst, and the contained hydatid had become impacted in the conus
arteriosus, so as to obstruct the entrance into the pulmonary artery.
In another instance, in a soldier thirty-five years of age, who also

1 Medical and Chemical Essays, 1795, p. 123. Case of a Blue Boy.

* Vol. xi. p. 274. a Vol. xvii. p. 507. 4 Lancet, vol. ii. p. 628.

5 Path. Anat. by Townsend and West, vol. ii. p. 848.

6 Path. Anat., Sydenham Society's Trans, vol. iv. p. 208.

174 A SYSTEM OF MEDICINE.

•

died suddenly, a tumour of the size of a duck's egg was found in the
upper part of the septum and corresponding portion of the left ven-
tricle behind. The sac contained fibrinous coagula mixed with portions
of acephalocyst. The surfaces of pericardium were adherent in the
seat of the tumour. M. Aran,1 in a paper on these and other forms
of tumour of the auricles, published in 1846, relates a case which
occurred to M. Dupaul, in a female twenty-three years of age, who
died suddenly after her confinement, and on examination a hydatid cyst
in the left auricle was found to have ruptured on both sides, so as to
allow of the escape of blood from the auricle into the pericardiac
cavity. It was evident that the tumour had been developed under the
endocardium of the auricle. Mr, H. Coote, in 1854,* found a large
cyst in the walls of the left ventricle of a subject under dissection
at St Bartholomew's Hospital, and he refers to a second specimen
as existing in the museum, doubtless the case of Mr. Evans before
referred to. In addition to the cases now mentioned several will
be found reported in the Pathological Transactions by Dr. Budd,8
Dr. Wilks,4 Dr. Habershon,6 &c., and one which occurred in a patient
of my own at St. Thomas's Hospital, is related by Dr. Hicks and
myself6 I have also had the opportunity of examining a specimen
exhibited by the late Mr. Ward, at one of the earlier meetings of
the society.7 In Mr. Ward's case the subject of the disease was
a man, twenty-two years of age, who died shortly after having
sustained an accident: the cyst was about the size of a French
walnut, and was situated at the posterior and upper part of the left
ventricle, beneath the superficial muscular fibres. My own patient was
a boy of eighteen, who died after an illness of about thirteen months :
the cyst, about the size of a walnut, was partially embedded in the
muscular substance of the right ventricle, but did not project into
the cavity. In the sixth volume of the Transactions,8 there is a
description of a case in which a patient at the Colney Hatch Asylum
died suddenly when under excitement, and after death two cysts, one
of which had ruptured, were found beneath the attached pericardium.
The precise nature of the cyst in some of the above cases is not clear.
The description given of that related by Morgagni is supposed by
Laennec conclusively to indicate the hydatid to have been a cysti-
cercus; and both Andral and Rokitansky speak of having met with
cysticerci in the substance of the heart. Most generally, however,
the cysts appear to be those of the echinococcus. Such is stated to

1 Arch. Ge*n. de M6d. 4m* sene, tome xi. p. 187.

* Med. Times and Gazette, xxix. p. 156. * Vol. z. p. SO.

* Vol. xi. p. 71. 8 Vol vi p. 108. • VoL xv. p. 247.

7 Vol. i. p. 225. Dr. Walshe mentions in nis work on Diseases of the Heart, Ac.
(3rd. edit. 1862, p. 65), that a specimen is figured in one of Dr. CarsweU's drawings,
and that a hydatid, the size of a pigeon's egg, situated in the interventricular septum,
is contained in University College Museum. In the Museum of St. Thomas's Hospital
there is in addition to the specimen described by Dr. Hicks and myself (x. 68) another
(x. 64) in which the cyst, as large as a duck's egg, is situated at the apex.

8 P. 114. See Report on the case by Dr. Wilks.

ADVENTITIOUS PRODUCTS IN THE HEART. 175

have been the case in the instances related in the Pathological Trans-
actions, though the bodies were not always met with. The Trichina,
on the other hand, is usually considered not to be found in the
heart. This is, however, denied by Dr. Cobbold,1 who says that
all the different forms of larvae occur in the heart, but they do not
stay there, the firmness of the muscular texture interfering ap-
parently with the development of the worm in that situation. The
same writer gives some calculations of the relative frequency with
which the echinococcus is found in the heart and in other organs. Thus
he states that Droaim, of 373 cases in which these cysts were found in
some part of the body, met with them in the heart in ten cases ; and
Dr. Cobbold, of 136 cases, found echinococci in the heart or peri-
cardium in nine instances. The most common situations for the cysts
appear to be the right auricle and ventricle, but no part of the organ
is free from them ; cases being recorded in which the walls of the left
ventricle were affected ; and, it will be observed also, the interven-
tricular septum. The cysts may be developed beneath the peri-
cardium or endocardium, or in the substance of the muscla Accord-
ing to the situation which they occupy is their tendency to grow, so as
to protude externally or internally ; and they may ultimately rupture
into the pericardium or into one of the cavities of the heart. In the
former situation they may give rise to acute pericarditis, or to adhe-
sion of the surfaces of the membrane covering the projecting portion.
In the latter the loose hydatids may escape into the cavity and pro-
duce fatal obstruction to the circulation of the blood. In one case, it
will be observed that a cyst ruptured both externally and internally,
and so allowed of haemorrhage into the cavity of the pericardium.

The hydatids in the heart appear frequently to be solitary, not
occurring in any other structure of the body. Such seems to have
been the case in the instances related by Morgagni, Dupuytren, Dr.
Trotter, Mr. Smith, and Mr. Coote, in one of those by Kokitansky,
and in the cases described in the Pathological Transactions by Dr.
Budd and Dr. Habershon, and probably also in that of Mr. Ward.
On the other hand, in the second case of Kokitansky there were
three separate cysts in the liver. In the case of Dr. Wilks, there was
also a cyst in the liver ; and in my own case, in addition to the cyst
in the right ventricle, there were numerous hydatids in the liver,
spleen, omentum, right kidney, and lungs ; and portions of cysts were
expectorated during life.

It will be seen that in the cases referred to the hydatids occurred in
persons of both sexes and of all ages. It may also be observed
that there are no certain signs by which their presence in the heart
can be detected during life. In some cases they have been found
without having been preceded by any indications of defect in the
circulatory organs; in other instances they have occurred in persons
who have died after longer or shorter illnesses, with symptoms clearly
pointing to some cardiac disease. In cases of the latter description,

1 Entozoa, 1864, p. 275.

176 A SYSTEM OF MEDICINE.

if there were evidences of hydatids in some other part of the system
the suspicion might be entertained that the cardiac symptoms were
due to the development of hydatid cysts in some part of the heart
In my own case there was nothing observed during life which at
all indicated that the heart was the seat of disease.

FIBRINOUS DEPOSITS ; SYPHILITIC AFFECTIONS OF

THE HEART.

The substance of the heart is not unfrequently the seat of fibrinous
deposits. These may occur either as the result of acute inflamma-
tion of the muscular structure, myocarditis, with or without peri-
and endo-carditis ; or they may be connected with an altered con-
dition of the blood, leading to the effusion of fibrine into the muscular
structure, in the same way as such effusions occur in other
organs, the spleen or kidneys, or as the blood coagulates in the vessels
themselves. When deposited the fibrinous material may soften and
allow of the partial destruction of the walls of the heart, so as to
constitute a false lateral or partial aneurism ; or it may undergo an
imperfect organization being converted into fibroid tissue, and this,
being less resistant than the natural muscle, may yield to the
pressure of the blood, and a true partial aneurism be formed. Closely
allied to these deposits are those which occur in the substance
of the heart in connection with constitutional syphilis. Corvisart,
struck with the remarkable resemblance sometimes presented by
vegetations on the valves of the heart to syphilitic warty growths
on the external organs of generation, suggested that in some
such cases the vegetations might have a syphilitic origin; and he
detailed several cases which he regarded as supporting this idea. His
views have not, however, been generally adopted ; and Laennec in
particular, considering the frequency of venereal affections and the
comparative rarity of such vegetations, expressed his decided dissent
from the supposition. More recently, however, writers have
attached more importance to the suggestions of Corvisart. Dr. Julia,
of Cazeres,1 has published several cases in which vegetations on the
endocardium were found in persons who were known to have recently
had syphilis and presented other indications of the disease ; and in two
of these cases there were small patches of ulceration on the surface
or in the substance of the heart. He also refers to a case published
in 1778, which, though often quoted as an example of ulcerated cancer
of the heart, is doubtless an instance of syphilitic ulceration. The
case was reported by M. Carcassone to the Acadthnie de M&lecine, and
occurred in a female of dissipated habits, twenty-two years of age,
who was an inmate of the House of Refuge at Perpignan. Her
illness, which followed upon chancres, was characterized by weight

1 Gaz. Med. do Paris 1845, No. 52, p. 845.

ADVENTITIOUS PRODUCTS IN THE HEART. 17 7

and pain in the region of the heart, and rapidly proved fatal ; after
death a large nicer with indurated base was found on the anterior
surface of the heart. More recently cases have been recorded by
Ricord, Lebert, and especially by Virchow.1 The latter writer has
indeed made the syphilitic affections of the heart the subject of a
special memoir, of which a translation has been published as a sepa-
rate work in French.2 In this country several communications of a
similar kind have recently appeared in the Pathological Transactions,
chiefly by Dr. Wilks,

The syphilitic affections of the heart resemble the similar degenera-
tion of muscular structure in general. They consist of fibrinous
exudations into the connective tissue, ^hich may either soften and
suppurate, forming ulcers or small abscesses; or they may be converted
into masses of hardened fibroid tissue, causing a puckered appearance
resembling a cicatrix on the surface, and are generally combined with
thickening and induration of the covering and lining membranes.
In the first case described by Virchow, it is stated that a portion
of the organ near the base of the posterior fold of the mitral
valves, for the space of about an inch and a half, was occupied by
a whitish-coloured hard mass, and the intra-ventricular septum was
also similarly degenerated tp the depth of from a quarter to half
an inch. The endocardium was nearly cartilaginous, and tendinous
cords passed deeply into the substance of the heart; the muscular
structure had undergone the fatty degeneration, and the surface of the
ventricle was marked by callous tuberosities. Under the microscope
in the points of a white colour and tendinous structure, the muscular
fibres had disappeared and were replaped by fibrous tissue. At the
apex of the heart there was a slight dilatation, indicating the com-
mencement of an aneurism.

FIBRO-CARTILAG1NOUS AND OSSEOUS DEGENERATION.

Under these terms, authors have described changes which are
not of uncommon occurrence. Corvisart has related a case in which
he states that the walls of the left ventricle were at least an inch in
width, and much hardened. " At the apex, up to a certain point
and throughout its thickness, the muscular structure was cartila-
ginous. The fleshy bodies also had acquired a remarkable hardness,
approaching that of cartilage.,, 3 This occurred in a man sixty-four
years of age, who died after an illness of about two years' duration
characterized by dyspnoea, dropsy, and other pardiac symptoms. The
state of the pericardium is not mentioned, but the mitral valve wras

» Archiv. fur Pa.th. Auat. und Phys. etc. 1864, p. 468.

* Le Syphilis Constitutionelle, par M. Rudolphe Virchow, traduit de l'AUeraand par
lc docteur Paul Picard, Paris, 1860.
» 3"" *d. 1818, p. 171, qbs. 28.
VOL. IV. K

178 A SYSTEM OF MEDICINE.

also cartilaginous. The condition here described was alluded to by
Laennec, and has been more fully illustrated by Cruveilhier.1

The transformation may either be general or diffused, extending
over a considerable portion of the heart ; or it may be partial and
limited to a small part. The diffused or more general change is
chiefly seen in the parietes of the right ventricle, occurring in cases
where the orifice of the pulmonary artery, the pulmonic circulation, or
the left auriculo-ventricular aperture is obstructed, so as to subject the
affected part to long-continued distension. This condition, which is
well known to all pathologists, has recently been made the subject of
a paper by Sir W. Jenner.2

The other or partial form is seen in the walls of the left ventricle,
and especially at the apex or outer wall When existing to a marked
degree, it is generally combined with some dilatation of the cavity in
the seat of the transformation, and not unfrequently with bulging of
the walls ; and it has been regarded by Cruveilhier as the first step
towards the formation of the true lateral or partial aneurisms. A
view somewhat similar is also maintained by Rokitansky.

In the slighter forms of the degeneration, such as occur in cases
where the change is diffused, the structure of the heart is much
coarser than usual, the altered parts have a yellowish colour and
a peculiarly hard leathery feeling, and resist when cut by the knife.
The more advanced degrees of the transformation are only seen in
cases in which the disease is limited in extent, and under such cir-
cumstances the muscular structure may be almost entirely replaced
by dense white fibrous material. This, as before mentioned, is gene-
rally only found at the apex of the left ventricle, but it may occur over
a large portion of the outer wall, or in the interventricular septum
and fleshy bodies ; and Cruveilhier says that he has seen the change
affecting fully a third of the muscular substance of tHe organ.

The mode in which the transformation is effected probably varies
in different cases. Cruveilhier supposed that it was a slow change, by
which the cellular tissue in the muscular substance became thickened
and indurated, and replaced the atrophied contractile tissue. Eoki-
tansky refers the change to inflammation ; and there can be no doubt
that inflammatory action, affecting the peri- and endo-cardium or
both these membranes, and involving to a greater or less extent the
interjacent muscular substance, does in some cases give rise to the
alteration. This is shown by the very general occurrence of thicken-
ing and induration of the investing membranes, or of adhesion of the
visceral and reflected layers of the pericardium, in cases in which the
muscular structure is transformed. The relative thinness of the mus-
cular substance of the heart at the apex affords apparently the explana-
tion of the greater frequency of the change in that situation ; and the
proneness to endocarditis on the left side accounts for the more marked
changes being only found in the walls of the left ventricle.

1 Traits d'Anat. Path. Gen. tome iii. 1856, p. 601.
1 Med.«Chir. Trans, vol. xliii. I860, p. 199.

ADVENTITIOUS PRODUCTS IN TEE HEART. 179

In other cases the change is probably due, as pointed out by Sir W.
Jenner, to long-continued congestion of the substance of the heart,
causing slow hypertrophy and induration of the connective tissue and
secondary atrophy of the muscular fibres. This seems the mode in
which the diffused and general induration of the walls of the right ven-
tricle is produced, though there does not appear to be any adequate
reason why it should be so frequently confined to the right side. In yet
othet cases the transformation is probably the result of the imperfect
organization of fibrinous material, which, in connection with an altered
condition of the blood, is effused beneath the investing membranes or
in the substance of the heart. These effusions are not of unfrequent
occurrence and generally co-exist with similar depositions in the spleen,
kidneys, &c. Whatever be the mode in which the disease commences,
the subsequent changes correspond, the connective tissue becomes
greater in quantity and more solid, and by its contraction compresses
the muscular structure and so leads to its atrophy, and in some in-
stances to its entire disappearance. It is not, properly speaking, a
degeneration or transformation of the muscular substance, but the
replacement of the muscle by fibrous tissue.

The older writers frequently speak of the conversion of portions of
the heart into bone, or of bones being found in the substance of the
heart, and most pathologists have met with cases of the kind. When
such formations do not occur in connection with chronic pericarditis
or in old false membranes, and are not traceable to the calcification of
the fibrous structures around the orifices or in the valves, they take
place in portions of the muscular substance which have undergone
the changes now described. Such formations are not, however, to be
regarded as truly bony, though they may be very hard, thick, and of
large size. They consist indeed only of granules of calcareous matter,
deposited in the altered tissue, without any of the elements of true
bone. structure.

POLYPOID GKOWTHS.

Most writers on cardiac pathology mention polypoid growths as
occurring in the different cavities of the heart. There can, however,
be no doubt that many of the cases which have been described
as of thisf description were only instances in which decolorized
coagula were adherent to the lining membrane. Such may be
concluded to have been the nature of the bodies described by
Dr. Ryan2 and Mr. Stewart,8 which have been frequently referred
tc by authors. In other instances, however, it may be inferred
that the formations observed were new growths. Such apparently

1 Case of M. Reuauldin ; Corvisart, p 175.

s Med. Gaz. vol. Hi. 1829, p. 336.

* Ed. Med. and Surg. Jour. vol. xii 1317, p. 182.

N 2

180 A SYSTEM OF MEDICINE.

were the polypi described by Mr. Keeves, Mr. Mayo,1 and Mr.
Wilkinson King,2 and by MM. Puisaye,3 Dubreuil,4 Choisy,5 and
Bouillaud.6 Most of these cases have been collected by M. Aran,
in a memoir published in 184(j.7 Two other similar cases are
described by Dr. Wilks8 and Mr. Birkett,9 in the Pathological Trans-
actions, and one has fallen under my own notice.

The true polypoid growths appear generally to occur in the left
auricle, and to be most usually attached to the fibrous zone of the
auriculo-ventricular valves. Sometimes they are connected with
some other part of the walls of the cavity, or are found in the
right auricle or either ventricle. When in the former situation,
they frequently project through the auriculo-ventricular aperture
into the cavity of the left ventricle. They vary considerably in size
in different instances. Some have been compared to partridge's or
pigeon's eggs or to walnuts ; others to hen's eggs ; and yet others are
stated to have filled the cavity from which they sprang. Most
usually they assume a pyrifonn or cordate shape, and are attached to
the walls of the cavity by a more or less constricted pedicle. The
surface of the growths is sometimes smooth, sometimes nodulated or
studded with vegetations ; and most generally they are covered
wholly or in part by the endocardium, this, especially at the root,
being thickened and indurated. They may consist of a simple
growth, or, on the contrary, may be composed of different portions.
The precise nature of the bodies is not clear in the accounts of several
of the published cases. Mr. Burns says, in reference to that
which he has described, that it was dense, laminated and fully
organized, and closely resembled the polypi of the nose. Mr. Mayo
is in doubt whether the specimen he mentions was to be regarded as
a slowly growing polypus, or a medullary sarcomatous growth. Tn
the case which occurred at the Middlesex Hospital,10 the structure of
the tumour is compared to the spleen ; in that of M. Puisaye the
growth is stated to have been fungous, and to have had the aspect and
consistence of gelatine ; and in those of M. Dubreuil, the tumours are
called fibrous or albugineous. Dr. Wilks and the reporters on his
case described the tumour as fibrous, and Mr. Birkett regards the
specimen he exhibited as fibroid. The growths are included by
M. Aran under the general term of " Tumeurs fongeuses san-
guines." The specimen which fell under my own notice was about
the size of a walnut ; it was attached to the auricular surface of the
mitral valve, was of a rounded form with a short and thin pedicle, and

1 Outlines of Human Pathology, 1836, p. 472.
8 Lancet, 1842, vol. ij. p. 428.*
» Gaz. Med. dc Paris, 1843, p. 270.

4 Ibid. p. 512. Two cases, one of which is quoted by Bouillaud.

5 Revue Medical e, 1833, tome ii. p. 425, quoted by Aran, p. 278.
• Vol. ii. p. 170. Obs. 105.

7 Arch. Gen. de Med. 4me serie, tome xi. 1840, p. 274.

8 Vol. viii. p. 150. » Vol. i. p. 224.
10 Lond. Med. Gaz. vol. xv. (1834-35), vol. i. p. 671.

ADVENTITIOUS PRODUCTS IN THE HEART. 18 J

was studded on its upper surface with vegetations or granulations. It
was apparently covered by endocardium throughout, and was of a
pearly white colour and obviously fibrous structure. The subject of
the disease was a young woman who was insane and died of gangrene
of the extremities, but had not during life presented any symptoms
attracting attention to the heart.

The mode of origin of these growths probably varies in different
cases. In some instances they may be simply adherent clots which
have become organized; in others they probably originate in
inflammatory exudations in the subserous cellular tissue. Indeed,
this would appear to be the most usual mode of origin of the poly-
poid growths, for, as before stated, they generally spring from the
fibrous tissue of the left auriculo-ventricular aperture and valves,
and are usually covered by the endocardium. As might be expected,
the cavities in which these bodies are developed ere ordinarily
considerably dilated ; and similar effects are produced on other parte
of the heart to those which would result from obstructions of any
other kind in the same situation.

The polypoid growths have been met with at various ages and in
both sexes, and generally in persons, who, for a longer or shorter time,
have presented obvious symptoms of cardiac disease. When, as in
most of the cases on record, the bodies obstruct the orifices of the
heart or interfere with the action of the valves, they give rise to the
ordinarj' effects of valvular disease which manifest themselves, by the
usual signs. In one very interesting case, quoted by M. Aran from the
" Annali Universali " for 1844,1 a pulsating tumour was observed for
a considerable period before the death of the patient, on the left side
of the upper part of the sternum, between the cartilages of the second
and third ribs ; and this ultimately attained a considerable size. After
death a tumour was found to occupy the upper and anterior part of
the heart, and proved to be connected with the left auricle. The peri-
cardium was inflamed and covered with recent exudation. The precise
situation and character of the tumour is not clear from the description.
M. Aran 2 also quotes from Schmidt, a case in which a hollow body
was found filling the right auricle, passing through the auriculo-
ventricular aperture, and communicating with the cavity of the aorta
by an opening between the sigmoid valves.

1 Supra, Obs. x. p. 275. 2 Obs. xviii. p. 287.

182 4 SYSTEM OF MEDICINE.

PNEUMOPERICARDIUM.

BY J. WAKBURTON BEGBTE, M.D.

This is the term employed to designate the presence of air in the cavity
of the pericardium, and may be applied to that condition, whether or
not the signs of inflammatory action in the sac are present. There
exist three different ways in which an accumulation of air in the
pericardial sac may be determined: — 1st. Such may be the direct
product of the irritated membrane itself. It is admitted that occa-
sionally, air is produced in the cavities of the pleura and peritoneum,
when these are the seat of inflammatory action, and if this be the
case, there can be no reason why the same formation should not occur
within the pericardium. Dr. Stokes has recorded an instance of this
nature, in which, although recovery happilv occurred, and the diagnosis
must therefore be regarded as inferential rather than demonstrative,
the opinion expressed by him seems alone tenable. " I could form,"
he says, " no conclusion but that the pericardium contained air in
addition to an effusion of serum and coagulated lymph." * 2d. Air
may result from the decomposition of fluid in the pericardium.
Laennec and other observers have not only pointed out the physical
signs which in their opinion indicate the existence of this lesion, but
the former more particularly, has in all probability greatly ex-
aggerated the frequency of its occurrence. The effusion of fluid and
air into the pericardial sac, in the opinion of Laennec, is a pheno-
menon likely to occur in the last stages of all diseases, and its exist-
ence he believed himself able to recognise both by percussion and
auscultation. " L'^panehement liquide et aeriforme k la fois du
P^ricarde peut avoir lieu dans l'agonie de toutes les maladies. II
m'est arriv^ quelquefois de Tannoncer k une r^sonnance plus claire
du bas du sternum, survenue depuis peu de jours, ou a un bruit de
fluctuation determine par les battements du cceur et par les inspira-
tions fortes."2 In a case recorded by M. Bricheteau, to which refer-
ence is made in Bouillaud's work, " Traits des Maladies du Coeur", as
well as in a note by Andral to his edition of Laennec s Treatise, and
which is also alluded to by Dr. Stokes and Dr. Walshe, the diagnosis
of air as well as fluid existing in the sac of the pericardium was made
during the life of the patient, and depended chiefly on the presence

1 Diseases of the Heart and Aorta, p. 21.

8 Traite de 1' Auscultation mediate : Des MaJadies ehi Ceeur — I>h Pneumo-Pericardc,
chap, xxiii.

PNEUMOPERICARDIUM. 183

of a peculiar sound with the heart's action, a sound compared by
Bricheteau to that produced by a water-wheel (" l'eau agit^e par la roue
d un moulin "), while on examination after death the pericardium was
found to be occupied by a peculiar fluid of very fetid character, air
escaping with a whistling sound when the sac was opened. Acknow-
ledging, however, the occasional occurrence during life of Pneumo-
pericardium, as the result of decomposition in fluid occupying the sac,
it is manifest that this source of the lesion is of much greater fre-
quency as a post-mortem occurrence. Laennec, indeed, has acknow-
ledged this, for after alluding to Pneumopericardium as of common
existence in autopsies, he adds, " Et surtout de ceux (cadavres) qui ont
iti gardes pendant un certain temps/* 3rd. Air may reach the peri-
cardium from a distance) through perforation, and the establishment
of a communication between its cavity and that of any hollow organ
normally containing airfc Thus the sources of the air may be
various, and the event may further be the result of direct injury
or of disease. A very remarkable illustration is mentioned by Dr.
Walshe, in which a communication was established between the
oesophagus and pericardium, in an attempt to swallow a long blunt
instrument, a juggler's knife — the case terminated fatally.1 A case
of traumatic Pneumopericardium, unattended by inflammation and
resulting in complete recovery, is given by Dr. Austin Flint, to whom
it was related by Dr. Knapp of Louisville. " The patient was stabbed
with a knife, which penetrated the pleural cavity and perforated
slightly the pericardium. A splashing sound with the heart's action
was immediately heard, which continued for a few days and disap-
peared. The symptoms and signs, subsequently, did not denote
pericarditis> but the patient had pleurisy, which was followed by
considerable contraction of the left side. The splashing sound
in this case/' continues Dr. Flint, "was fairly attributable to the
presence of air and probably a little blood within the pericar-
dium.*2 Whether the inference that no inflammation of the Peri-
cardium succeeded the injury in this instance be correct or not,
there can be no doubt that the ordinary result of a perforation
of the sac, whether by wound or by communication established
between it and any organ containing air, is pericarditis. Dr.
Walshe observes in regard to the latter : — " Now Pneumo-pericar-
ditis must exist temporarily, be it for ever so few minutes, as the
sole result of perforative communication between the pericardial
sac and any hollow viscus containing gas ; but in this isolated state
it has never been observed, pericarditis having supervened before clinical
examination has been wads.

After the N operation of Paracentesis Pericardii and injections of
iodine into the sac> physical signs have been discovered precisely
similar in character to those met with in traumatic cases. Such

1 Diseases of the Heart. See pp. 46 and 271.

* A Practical Treatise on the Diagnosis, Pathology, and Treatment of Diseases of th*
Heart. By Austin Flint, M.D. See p. &57.

184 A SYSTEM OF MEDICINE.

resulted in the memorable instance recorded by the late M. Aran
under the title, "Pericardite avec epanchement, trait^e avec succes
par la ponction et Tinjection iod£e."

Of communication established between the Pericardium and neigh-
bouring organs throngh the progress of disease, and permitting the
entrance of air into the cavity of the former, several instances have
been recorded by different writers. Dr. Graves has furnished a
remarkable example of communication by fistulous opening between
the stomach and an hepatic abscess, on the one hand, and the pericar-
dium on the other.1 Dr. M'Dowel exhibited to the Pathological
Society of Dublin the morbid appearances in a case of communication
established between a cavity in the left lung and the pericardium.2
The writer has placed on record the history of a very interesting case,
in which disease of a cancerous nature primarily affecting the
oesophagus, subsequently involved adjacent organs, giving rise to
pericarditis with effusion, and ultimately by perforation led to
Pneumopericardium. When the close anatomical relationship of
oesophagus to the pericardium, the former lying in the posterior
mediastinum in contiguity with the posterior portion of the pericar-
dium for nearly two inches, is considered, it will be seen how, in
their conditions of disease likewise, the one is very apt to influence
the other. In the instance now specially referred to, a careful scrutiny
had led to the opinion that rupture of the oesophagus where in con-
tact with the pericardium, and affected by cancer, had taken place,
and, as a result of the perforation, that the passage of air into the
pericardial sac had occurred. Post-mortem examination, con-
firmed the correctness of the diagnosis. On opening the chest, the
pericardium, marked by the pressure of the ribs, bulged forwards, and
on being punctured air escaped. Several ounces of dark-brown fetid
fluid existed in the sac : lymph, recent in its deposition, and
of yellowish colour, coated the inner surface of the membrane.
Cancerous ulceration, and destruction to a considerable extent of the
wall of the cesophagua existed, corresponding to its usual point of
contact with the pericardium.3

In the diagnosis of Pneumopericardium, of Pneumo-hydropericar-
dium, and Pneumo-pericarditis, reliance may reasonably be placed on
the physical signs as determined by percussion and auscultation.
Laennec, who, as already observed, exaggerated the frequency of the
occurrence of air in the pericardial sac before death, speaks of three
signs to be expected when air and fluid exist in the pericardium,
1. Unusual resonance over the lower part of the sternum : 2. Fluc-
tuation sound (" bruit de fluctuation ") audible with the action of the
heart, and on deep inspiration. 3. This specially relating to the
diagnosis of simple Pneumopericardium, that is, without fluid

1 Clinical Lectures, edited by Dr. Neligan. Edition of 1864, page 616.
8 See Dr. Stokes's work, p. 23, also p. 35 ; and Dr. Walshe's work, p. 271.
• Observations in Clinical Medicine, by J. Warbnrton Begbie, M.D. Edinburgh
Medical Journal, 1862.

PNEUAtO-PERICARDIUM 185

effusion, or inflammatory product ; the heart's sounds being heard at
a distance from the chest. Upon this sign the distinguished inventor
of auscultation placed very great reliance. Dr. Stokes, whose entire
observations on the subject of Pneumo-pericarditis are most instruc-
tive, noticed the fact of the heart's sounds being heard at a distance
in a case which he has recorded ; he remarks, however, that this
indication did not exist in the instances of Dr. Graves and Dr.
M'Dowel, already alluded to. Auscultation over the region of the
heart, when practised by the writer in the case which fell under his
own observation, revealed the probable existence of air and fluid
in the pericardial sac, by the extraordinary guggling sound which
accompanied the heart's action — a sound which cannot, he thinks, be
better described than as a churning splash. Dr. Stokes gives the
following description of ^he sounds which he observed : — "They were
not the rasping sounds of indurated lymph, or the leather creak of
Collin, nor those proceeding from pericarditic with valvular murmurs,
but a mixture of various attrition murmurs with a large crepitating
and guggling sound, while to all these phenomena was added a
distinct metallic character. In the whole of my experience I never
met so extraordinary a combination of sounds. The stomach was not
distended by air, and the lung and pleura were unaffected, but the
region of the heart gave a tympanitic bruit de pot feU on percussion,
and I could form no other conclusion but that the pericardium con-
tained air in addition to an effusion of serum and ooagulable lymph."
The phenomena on auscultation and percussion thus graphically
described by Dr. Stokes, will receive a farther value as indicating the
existence of Pneumo-pericarditis, if in addition there be noticed, as
was done by Dr. Walshe in the singular case of traumatic communi-
cation between the cesophagus and pericardium, a dull or tympanitic
sound over the precordial region, according to the position assumed
by the patient. Even without this indication, and in default of a
metallic character attaching itself to the Cardiac sounds, as noticed by
Dr. Stokes, the diagnosis of Pneumo-pericarditis, or, to be still more
explicit, of Hydropneumo-pericafditis, may be made from observing a
guggling or churning splash sound with the heart's action limited to
the cardiac region, with which more or less of tympanitic precordial
resonance on percussion is associated. These signs will be still more
available, if the guggling sound has been noticed to succeed a distinct
friction sound, and the tympanitic has replaced a dull percussion
note.

It is satisfactory to note that the phenomena to which attention
has now been called, and which serve to indicate the existence of a
very serious lesion, are not necessarily of a fatal import. In Dr.
Stokes's case, as already noticed, recovery resulted, and in the instance
of Pneumopericardium, traumatic in origin, noticed by Dr. Knapp,
and recorded by Dr. Flint, the termination was equally gratifying.
We may indulge the hope that the records of medicine may yet
contain other exatn'ples of a similar nature.

186 A SYSTEM OF MEDICINE.

PERICARDITIS.
BY Francis Sibson, M.D.. F.R.S.

CLINICAL HISTORY OF PERICARDITIS A^ IT OCCURRED IN THE
AUTHOR'S PRACTICE IN ST. MARY'S HOSPITAL.

Inflammation of the surface of the heart and the lining of the peri-
cardial sac occurs so vefy rarely by itself, and is so generally one
of the attendant affections of a general disease, such as acute
rheumatism, Bright's disease, and pyaemia or the secondary inflam-
mations ; or of a local affection, such as aneurism of the aorta or
cancer ; or of a local injury ; that we cannot practically regard it as
a distinct disease. Pericarditis is indeed, with very rare exceptions,
one of the inflammations attendant upon those diseases or injuries.

Pericarditis occurs so much more frequently in acute rheumatism
than in any other disease, that I shall first consider the affection as
it exists in connexion with that disease; and in so doing shall
examine the proportion of my cases of acute rheumatism that were
affected with Pericarditis, and shall describe the progress of that
affection in those cases.

RHEUMATIC PERICARDITIS.

I possess notes of 326 cases of acute rheumatism that were ad-
mitted under my care into St. Mary's Hospital during the fifteen
years ending in the autumn of 1866. This number does not include
fourteen patients in whom it was doubtful whether the affection was
acute rheumatism or acute gout.

One-fifth of those cases 1 (63) were attacked with Pericarditis, which
was accompanied in all but nine instances (54) by endocarditis, and
fully one-third of them with simple endocarditis (108), while in only
one-fourth of them was there no evidence of either endocarditis or
pericarditis (79). There was, however, an intermediate group,
amounting nearly to one-fourth of the whole number (76), in which

1 In two of those cases (59, 61) the evidence of pericarditis was slight and perhaps
doubtful, but I am of opinion that in both of them the affection existed though in a
slight and transient form. The numbers thus given here and elsewhere refer to the in-
dividual cases of Pericarditis as they occur in my records, so that the reader may trace
for himself each of those cases as it appears from part to part of this analysis.

PERICARDITIS. 187

endocarditis, though not established, was either threatened or prob-
able, the signs of that affection being either transient or imperfect.
I think that we may class this intermediate group arbitrarily into
two divisions, and consider that in one-half of them there was
endocarditis, and that in the other half there was no endocarditis.

If we add the cases of pericarditis that were also affected with
endocarditis (54), and half of those in which endocarditis wraa
threatened or probable (38), to those in which simple endocarditis
was present (108), we shall find that in my patients inflammation of
the interior of the heart (200) was fully three times as frequent as
inflammation of the exterior of the heart (63).

This summary, otherwise stated, stands thus : —

Cases of acute rheumatism with Pericarditis . . 63
Cases in which the Pericarditis was accom-
panied by endocarditis 54

Cases of simple endocarditis 108

Cases of threatened or probable endocarditis . . 76
Cases in which there was no sign of endocarditis 79

Total number of cases of acute rheumatism . 326

I.— Sex, Age, and Occupation in Acute Rheumatism in especial

BELATION fO PERICARDITIS.

Sex. — Acute rheumatism affected the female sex somewhat more
frequently than the male sex in the proportion of 168 to 158.

Pericarditis attacked 35 male and 28 female patients, so that
nearly one in four of the former (35 in 154), and only one in six of
the latter (28 in 166) were affected by it. Endocarditis was also
present in 31 of the male and 23 of the female patients affected with
pericarditis.

Simple endocarditis, on the other hand, attacked 47 male and 61
female patients, while, in addition, endocarditis was threatened or
probable in 32 male and 41 female patients.

The cause of the greater proportional frequency of Pericarditis,
usually accompanied by endocarditis, in the male sex, and of simple
endocarditis in the female sex in these cases, will, I think, be in part
explained hy the influence of age and occupation on acute rheumatism
and its complications.

Age. — One-half of the male (17 in 34)1 aud more than one-half of
the female patients (17 in 27) * affected with Pericarditis, wrere below
the age of 21: while two^fifths of the male (13 in 34) and only
one-seventh of the female patients (4 in 27) were above the age of 25.

If we group these two classes of cases separately in relation to age,

1 The age of one of the 35 "male patients and that of one of the 28 female patients
was not stated.

189

A SYSTEM OF MEDICINE.

and compare them with each other, we find that acute rheumatism
attacked 70 male and 77 female patients below the age of 21. and
that of these 17 of each 8ex were affected with Pericarditis, com-
biued with endocarditis in all but one or two cases, and 25 of the males
and 32 of the females with simple endocarditis; that in 12 of the
males and 20 of the females endocarditis was threatened or probable,
and that in 15 of the males and in only 8 of the females there was
no sign of inflammation of the heart, within or without.

On the other hand, we find that acute rheumatism affected 53 men
and 53 women above Ike age of 25, and that of these 13 men (13 in
53 or one fourth) and only 4 women (4 in 53 or one-thirteenth) were
affected with Pericarditis which was usually accompanied by endocar-
ditis, and 13 men and 17 women with simple endocarditis; that in 11
men and 11 women endocarditis was threatened or probable ; and
that the residue, or 16 men and 21 women, gave no sign of inflam- -
mation of the heart.

The accompanying Table shows the proportion in which endocarditis
and Pericarditis were absent or present in the coses of acute rheu-
matism, and the influence of age and sex in the proportionate pro-
duction of those affections of the heart in that disease.

M i.npwil.ls

Total.

Kale .
Female

Endomrditls

Threatened.

Probable. .

Total.

S}»

6,1B

fflW

S}»

1«8|SW

AgM.

■1

4
1

■3
m

■a
1

-1

*| 4

i'l !'.!-,!;

','

;;;

91 and -

•

i I

{

■

TuUI .

■M U ! 78

1,1 ■„.!,

■

l«

:■:<■■

We thus see that in these Cases of acute rheumatism, inflammation
of the heart, grouping together those in which it attacked the interior
and the exterior of the organ, affected the young below 21 (91 in 147)
more frequently than the adult above 25 (47 in 106) ; that the heart
was more frequently free from signs of inflammation in the adult above
25 (37 in 105), and especially in women (21 in 53), than in the young
below 21 (24 in 147), and especially in girls (8 in 77) ; that endocar-
ditis was threatened or probable as often in the young below 21 (32
in 147) as in the adult above 25 (22 in 106) ; and, this being the
point to which I would especially call attention, that Pericarditis —

PERICARDITIS. 189

while it affected the two sexes in nearly equal proportions below
the age of 21, the male patients (17 in 70) a little more frequently
than the female patients (17 in 77) — attacked men above the age of
25 (13 in 53) three times more frequently than women above that
age (5 in 53).

Occupation. — The study of the influence of occupation on the
occurrence of acute rheumatism and on the production of inflamma-
tion of the heart, both outside and in, throws light in two directions,
one on the influence of sex, the other on that of age in producing
those affections.

The accompanying Tables show (I. pages 190-3) the influence of
occupation in acute rheumatism in relation to age ; the presence or
absence of endocarditis and Pericarditis ; the degree of the affection
of the joints, and that of the heart : and (IJ. pages 194-7), for the sake
of comparison, of ages (1) of 1,000 patients, taken consecutively, with
an occasional break, from my hospital books, affected with all other
internal diseases besides acute rheumatism and acute gout, and (2)
of 326 cases of acute rheumatism with its attendant Pericarditis
and Endocarditis, in relation to occupation.

I take female domestic servants first, since they formed nearly
one-third (101 in 326) of the whole number of those of both sexes,
and nearly three-fifths of those of the female sex (101 in 168) who
were affected with acute rheumatism. Among those patients affected
with other diseases than acute rheumatism, female servants formed
one-fifth of the whole number (2U4 in 1,000) and two-fifths of the
female patients (204 in 453). Nearly two-thirds of the female
patients affected with acute rheumatism were below the age of 21
(57 in 100), while of those affected with other diseases, only one-third
were below that age (64 in 1 95, or 33 per cent) Table II. p. 12.

The influence of that employment in causing Pericarditis and endo-
carditis in acute rheumatism, especially below the age of 21, is
remarkable. Of the whole number of 101 servants only 13 — one-
eighth — presented no sign of inflammation of the heart, while one-
fifth of them (19) were attacked with Pericarditis, accompanied
in all but one instance with endocarditis also, and two-fifths of them
(43) with simple endocarditis, while in the remaining fourth part
(26) endocarditis was either threatened or probable. Servants formed
fully two-thirds of the whole of the female patients affected with
Pericarditis complicated usually with endocarditis (19 in 28), and
with simple endocarditis (42 in 60) ; and three-fifths of those in
whom endocarditis was threatened or probable (26 in 42) : while
they formed only one-third of those who gave no sign of affection
of the heart (13 in 37).

The influence of age in inducing inflammation of the heart in
servants affected with acute rheumatism is still more remarkable.
Of the whole number of servants (101) attacked with that disease, 57
were below the age of 21. In only 3 of these was there no mark
of affection of the heart, but one-fourth of them (14) were attacked

ACUTE

TIBIAL, Sap.lti.— OCCUPATION IN RELATION TO AOE, THE DBGRBB

„.„,„,.„.

Puiin

There was no Indication of

KndocsrdltK

Number. Yets, j Joint afleetiuu.

EDducirdltly vu ThnatvniMl or

probable.

KuDjl.-r. Years. Joint affection

Out-of-duor Enplnt/me 'it*.

Engaged in taboriovt etuphymtnU

in On 0|ir« air, Inclinliin; 111 ■

ara(] 7). garden..' [-('.), l.riikl'iy.i,
brick maker, aawyer (In twine),
inaion, duntnian, miWp, )■!»»■
tarer, loamau. andth* (4),
hutchen (ft), carpenter! (4) . .

[J-|

i r

f Sad. SO

la*

Engaged Id rMplutmrnU rMifin
iHirn (1), inilkun-u (■ . h»»k.-[,

1 Cm wtoii

.1 S ,. IK „ 10

V.:S

1 1 '.'.tl "

—

Employed n-.ili komianii in >'■'■
htti, Including groomi (ft), iM-

li::S

:? +

ToTiLot those employed In
the above laborious ovf-
o/-oWeo>ployn.nnU . .

"j I „ Srj „ at 1 a o +

Ei :; « ;: « i j

I 7 „ M „ M

20! 7 ., SI „ Si

1 a .. » .. »
l 3 „ « „ ss

'!i +

Painters (3), plumber, ipm-nttm

"1 i"..'s*

\7.i

>ii:S

-— —

baaMMD.

J I„1«U.1S

izt

l!:S.«

Jn -dwr KmntoyncpiU.
Including HtvanU (12). bakur. SI
paperliaBSiT.frenrh-i'olLi.lMj-1 11.
hoot and nho*niaker»(»X "aWf
man," gTeentToenr, drapers (<(,
rliFCM-rmiugrr. slop cutler, tai-
lor, teacher. •Uvrrsiiiith. . -Ii.-iii
maker, bath-ntlendanl, mid 'J

•'I 1 not staled

,Rch.-oIh.pj»(--.) .

...

1 -

Had no WftofBwBl, bdOdlKn

uliediai'luitgeil Irolulhe Navy (J"

i>TUpaii.,n nut stated

MATISM.

; APPECT10X AND THAT OF HEART AFFECTION.

PtTlIVTS IN WHOM TUUI WAS

■*"

.,,,. 1 FeriiMittlltfi, usually w
Jnt-olll. Similar. Tun. JL^iffi-

th Ea- 1
>■ ! Total
HHirt-iHT. .Vumutr. T*M«.

Joint nffcotlon

! j lit. 17 to 18

io+ ln>i-gMJ

1 1":S"M

;j +

1 C^3 ,12*1.17 li. 211

4 .try .wore + +
SI seven +
17 rMbnrwvere- +
a not severe n +

■

io +

fl „ IP,, 14

3 nnvere +

3 not severe o +
8 alight —
1 doubtful 1

s - +' 1 .. H
1,0 +

•♦

, I a !! ii " lis

1 rilghT"* - + |
1 doubtful !

i „ u

w - +.„/ J » g » g

,2'0 +l 1 S|; SI ", 3!

, U „ 43

4 + +

5± +

j§Ij"|B:jj:!

... 1 ...»

.? :sl!;:»■■,,

! 2X."™* } +

... 1 ....

9 ' 1 .. IB

■ »,„

» ,. 30

-■° +; I I :: SI i - +

4 - + : M\ 7 ., 27 ,. 30

.'. not severe O. +
i (light -

».. 13

1 o +|

io+ - ■• " - ,5

l o +

!SSE"J{

...»

>.%! *..,...,.

ItDgM

1 ,1 M

*w;i-+i,liKl*Lw

1 — + 1 S >»t lUted

.-w— +|

Table I. cont., ACUTE

„.„.„,.„.„.

Pat,**™

There wm no

Endoca

K umber. Yean.

indication of
rdltla.
Joint affee lion

Eiuliii'inliiis wli lhff»t*neil or
Iirobatilr.

•»MP.

( 3ieU0t<>2O

yt! * .. « ., as.

lot

f lrt.15

1 1 not listed

H — (■

eot

Cooks (H), charwomen (2), nnrw.
(&). lanndrense. <»), »uh»r.

/ !**. 20 to SB

1 - +

lOt

f S „ 10 ., Srt
J * ., 11 „ M

11:8

.I+- +

Rubnfflry In-door Knjilninnenh.
Needlewomen (8), nflfeM tlrom.
imkerir:!), Liilo«iu,iliiii'bimlM,

•!"s

1.,

._*

,„.,

1 +

Harried MM without tne-
rlal wrvipatlnn, Jnrltittitig two

I 3 " 9tt „ 40

!Ot

( 1 aotiitatcd

2 +

3 - +

Of no sccu|*tlon

f SrtWtoU
5 1 ..10
I 1 „ »

1 - +
I O +
1 —

3I 1 - «

-I i „ i»

!i +

Occnpatinii not atateri . .

lBtW

...

Mali Patiibts. TOTAL .

I r.M. 10 to in
*si s " h '.', an

5 „ SI m 40
1 S „ 41 „ M

« - +
s O +

•fill:!

* 1 not stated

1,0 +

FlUHMJ PATTKT.TO TOTAL

.Set. 13 to IS
( 5 „ 10 „ 20

3T'l3 „ 20 „ 80
' 1 .'.' 6* "

li— +
12, o +

[is ,. la „ so
J » „ ss „ as

1 a not ttnted

10 +

0,0 +

GRAND TOTAL if the Male

ud Female Pntionta . . .

( Sirt. 1 0 to IS

18, O +

t 4 at. ntoi4
I 3 not Hated

1 + *

RHEUMATISM

— (continued).

193

F*TI«KM IV WHOM THIE

■ W41

Simple Enducu
dumber. Year*.

ditbj.

Perii'inlitis nsonlly wiUi En-

Jin.-ardltii (54 In 68).

K muter. taa.] Jt-Jitt , Heart air

Total.
Number. Yews.

Joint affection.

[ll „ 10 „ 20
„ho ,. SI .. 35
™1 4 ,. 3« „ ao

U;;»",u

19 +

70 +

t lKt-15

1 1 ',', So "

1 0 +

8 +

1,0 +

JOwtlSlolS

|aa L' 21 " ss

) 1 not ilite'd

8 very KTtre + +

S3 nther latere — +
18 not.evere O +
1 .light -

«:!..

|j:S

6 1 „ 38
1 „«o
\ 1 not jUted

» — +

1 1

1 +
1 — +

10 +

S3' 5 „ 31 „ 40
IS „ 43 „ SO

[1 'notitited

1 doubtful I

•(i::if„»

10 +

( ! „ 18 „ 30

Bi a ;; si ., as

\ 1 „ 44 ,. 48

2 notMiere O +

...

»♦

<l:B

,„» +

*l 1 „ 40

1 - +

4i:S

l — +

1 +

17j « !! S4 " 40

T HthQT tblftt — +

(S „ IS „ IS
H 1 „ IB

( 1 oat Rated

8 +

1 o +

a „ is „ u

l +

:± +

pi „ e „ is

J 3 ., la ., so

"l 1 „ 38
t. 1 not lUtcd

3 not «T*ra O +
1 slight -

.. | .

.,.=.

1 rather He Tera — +

1 > „ 18 „ So

4T 3 ',', 36 ". SO
4 ,. 31 „ 38

I I „ 41

I I out total

• o +

ii „ io „ so s + +

4 „ 22 „ Sill +
BS( S „ ST ., 48,11 - +■

8 „ 31 „ SB] 4 O +

o + +

13 +
11 — +
9 Q +

fi» let 8 to IB

\*1 .. 18 .. 20

32 „ si „ -a
158'Sfl „ so ,, so

121 „ SI „ 40
0 .. 41 .. M
[ 3 Dot lUted

00 «iera +
68 nther wrore — +
IT not ieTcre O +
6 night —
1 doubtful t

pa„'io .. 3D
Jii „ 21 „ ss

ttT5 „ H .. SO

\1 Donated

3 + +
9,0 +

1 r

1 1 ,. 90 It

4 h

* O +

60 ,',' 10 ',', 10

"B:|:|

Is ", S3 ", 60

39 not lerere O +
2 illght —
2 doubtful 1

IP''"

1 1 3 not iuk-

1 + +

48 +

«- +
15,0 +

1 £«t. 11 tol&l

ss „ lo „ 2012 + +

10 „ 21 „ 35;S» +

m,)t „ 28 „ SO 18 h

03 | 8 „ SI „ 40 fl C +

' 2not»UtedJ

4 O
IS + +
21 +

• O +

1 I

I+OetStolS

107,. 1B„S0

66 „ It, ,3*

S38 SI „ 20. ,30

\ t not aUtod

1! (fry KTore + +

120 rather mere 1-

46 not ««e« 0 +
8 alight —

' s orta*M cue* di«d (i fro.'n Bright') dunue).

194

TABJjE

Ages of 7.-1,000 Patients affected with all other Internal Diseases except Acute SkewmUism

Pericarditis and Endocarditis, and ///.— 58 Patients

Male Patibxts.

Laborious em-
ployments .

Worker* out of Other diseases except acute
door*. rheumatism and acute gout

/Acute rheumatism . . .

Ditto with pericarditis . .

Ditto with simple endocardit.

VAcutegout ......

/Other diseases except acute/
rheumatism and acute gout
Acute rheumatism . . .

Workers on foot

Pericarditis .

Endocarditis
Acute gout .

[Other diseases except acute)
rheumatism and acute gout)

i /Acute rheumatism . . .
Workers among/ I
horses . . . ! (Pericarditis

f 8, or 33 3 per cent, at that age.
1 3, or 37 "2 per cent, of whole.

hers

j {Endocarditis
v Acute gout

Other diseases besides acute) j . .

rheumatism and acute ooutJ ! 2, or 5 per cent.

2, or 40 per cent

Below the age of 21.

21, or 10 per cent, of those)
whose ages are stated. J

12, or 20 6 per cent.

[1, or 83 per cent, at that age. l
11, or 10 per cent, of whole,'
[0, or 50 percent, at that age.
1 6, or 40 per cent, of whole.
0

{
{

6, or 177 per cent.

0, or 64 per cent.

1, or 11 per cent, at that age.

1, or 50 per cent, of whole.
It, or 22 per cent, at that age.

2, or 66*7 of whole.
0

1, or 15 per cent
9, or 39 per cent
0

rheumatism and acute gout)

Painters, plum- ) /Acute rheumatism

I) Pericarditis . . .

1 ^Endocarditis . .

Acute gout . . .

In-door employ
ments .

rOther diseases besides acute}
rheumatism and acute gout)

Acute rheumatism

Waiters, bar-
men, and one
commercial
traveller .

►/f~~ — ' ' '

AlPerioarditis . . . - . . i

1 \Endocarditis

I i l&

VAcutegout o

Other diseases besides acute\
rheumatism and acute gout/

/Acute rheumatism . . .

J I

S< Pericarditis

[Endocarditis

Acute gout

0
0
0

20, or 16 3 per cent.

20, or 52 5 per cent

10, or 50 '6 per cent, at that age.
10, or 77 per cent, of whole.
1 5, or 25 per cent, at that aqe.
\5, or 55"2 per cent, of whole.

(Other diseases except acute!
rheumatism, Ac. J

!».»« ««- »vv /Acute rheumatism . . .

school. . .llp^ricoftfak

^Endocarditis

Other diseases except acute)
rheumatism and acute gout)

E cute rheumatism . . .
tricarditis
ndocarditie

Total of Male
Patients.

Acute gout

2, or 16*6 peT cent.

2, or 15 3 per cent.

1 1, or 50 per cent, at that age.
Ut or 50 per cent, of whole.

37, or 100 per cent.

10, or 100 per cent.

4, or 25 per cent, at that age.
9, or 50'0 per cent at that age.

89, or 17 per cent

70, or 45 per cent

17, or 24 3 j>«r cent, at that age.
17, or 61-5 per cent of whole.
26, or 357 per cent at that age.
25, or 54 3 per cent. #/ whole.

From 21 to 25 Years.

31, or 15 per cent.

10, or 22 2 per cent

1, or 10 per cent, at that age.
I, or 10 per cent, of whole.
4, or 40 per cent, at that age.
4, or 27 per cent, of whole.
2

4, or 11 *7 per cent

3, or 21 4 per cent

1, or 33 3 per cent at that age.
1, or 50 per cent, of whole.
1, or S3 3 per cent at that age.

1, or 33 '3 per cent, of whole.
0

4, or per cent

0, or 26 per cent

fl, or 16'6 per cent at that age.
\l, or 100 per cent, of whole,

2, or 30 9 per cent, at that age.
2, or 25 per cent, of whole.

or 22 per cent. ;

or 20 per cent

0
0

20,

or 16 -3 per cent

5, or 13 5 per cent

1, or 20 per cent, at that age.
1, or 7 7 percent, of whole.
1, or 20 per cent at that age.
1, or 11 per cent, of whole.
2

2, or 16 "6 per cent

7, or 54 1 per cent

0
0

70, or 13 4 per cent

32, or 20*8 per cent

4, or 12 per cent, at that age.
4, or 12 per cent, of whale.
8, or 24-2 per cent at that age.
8, or 17-4 per cent of whole.

\ Here and elsewhere in these columns add after " age " of those with acute rheumatism who were so aifceiti

-and who were engaged in the class of employments indicated in the column beaded "MaU Patients." ^ _^

* Here and elsewharc in these columns I'wVolt" applies to the whole number of an ages of those with tea*

>. 189).

ft Chut, and II.— 328 Patient* ajfuted with Aeult Ekeumatum, with it

\eith Acute Gout, in rthtlion to Occupation.

Lboti 1s YiaRS.

imtmOoemM

TOTAL.

1 per cent.
Sjm-cinf. at Outage.

1 percent, otthntaae.
Sptretot. ifvlutr.

Ajk not atnled 14

::: ::: }
::: ::: )

nrf40 4 per cci.t. of Ihe male.
'l221 per relit. ...f the whole.1
(29 per cent, of the majen
114 per cent of the whole.

rxK1 "jom" *"* """

i ]0r SS'3 ptr will, of thoK irilA

IK per cent.
t-s per cent.

::: ::: ]

2 1

: 1

n.ie-iJ per cent of the melee.
v'\i1 per cent of Ihe whole,

,,,'tf per rent <j( the mnlei.

i'v ii .... -...;. h 1 1.,... .■■,■», '.',:.„,
t rAcunattoa,

to per rent

5 per cent.

f per rent. n( (kit arte.
i"S JW cmf (>/ JAr w*"Ff.

::: ::: ]

1 ]

fl.nSli per cent of the male*.

id '.' per cent, of the whole.

,. 114 iptf ..(111 .'1 the majea.

vrt 7 1 V "nt. cf the whole.

... ; ■-,....,,; ,., :*„.„ „■::), „,,fH
1 r*eu maJfan.
(Or 35 per oral, of t\ou will! ncttfe

9 per cent.

0 per cent

::: :::

Or|0'S per cent of the males.
V'U 1 per cent, of the whole.

urU-;. per cent, of the whole.
OrSOprrwiir, of rtov irtl* oc. r».

7-4 per cent.
1 per cent, i
itftr ant. at OaiBgt,

i-S percent. ofw\oll

lIS^eenttfWtoE'

::: ::: !

,-,.(22*6 per cent of the male..
'll2I> i-i- cent, of the whole.
,,, liM-.j j.it cent, of the ui.le*.
L,|114 per cent. t,f the whole.
lOr 35 per cent o/IAsu lrifj ocvtt
1 rAramotkin.

\Or 24-3 per cent, of Oust irlrt
I acute rAevnwUm.

(.« per cent.
on.peree.ii.c./ifAc.V

ii:

0t/2 2 per cent of the mules.

. , - ■ -i ],;.,■ .,.ji ,-,f i.Iid mule).
WH per cent, ft the whole.
lOr fi'3 per cent, of thirst yclthrtcttti

I n,lll per cent of the molee.

U'|5J per Lent, of the whole.

. OrMpercenLn/tikoiewfliiK. rk.

| Or 53 per cent, ofrton wfrt ac. rh.

8-4 per cent.

Age not .toted 27

»T per cent + 1 occu-
lt not .tated.

»lj*r«*i . of whJs.'

a^r^.to/trlX

. ■■.'. (ii \ ..■'. . "ii not - la' ' .'.

[WAS.'"*}

,AfH (1) 1 + 1 KB

net itattJ
,jB.(l)on((-xr.™i
[ tfotell
f Aft (It — 3 Oct

fl55 + 8 MCtl
I not stated |
133 + 2 «c.|

i net rtUed |
,40 + 1 ecc.l

iam whoee *ga were stated, an J who were so affected, who wi

I in the column headed "Male FiUenta."

i and elsewhere is thin comma "whole" appllee to the whole

s engaged In Uie claaa of occnpetioni

194

TABLE

Ages of 7.-1,000 Patients affected with all other Internal Diseases except Acute EkeuwuUism

Pericarditis and Endocarditis, and III. — 58 Patients

Male Patibxts.

Laborious em-/
ployments *

Workers ovt of Other diseases except acute
doors. [ rheumatism and acute gout

/Acute rheumatism . . .

Ditto with pericarditis . .

Ditto with simple endocardit.

VAcutegout

Other diseases except acute/
rheumatism and acute gout
Acute rheumatism . . .

Workers on foot

Pericarditis .

Endocarditis
Acute gout .

[Other diseases except acute)
rheumatism and acute gout)

Workers among
horses . .

Painters, plum-
bers . . .

i /Acute rheumatism . . .

^Pericarditis

[Endocarditis

[ Acute gout ......

/Other diseases besides acute)
rheumatism and acute gout)

!' Acute rheumatism . . .
Pericarditis
. Endocarditis

I Acute gout

Bklow the age of 21.

21, or 10 per cent, of those)
whose ages are stated. j

12, or £6 0 per cent.

1, or 88 per cent at that age.
,1, or 10 per cent, of whole, *
6, or 50 per cent, at that age.
6, or 40 per cent, of whole.
0

6, or 177 per cent.

0, or 64 per cent

1, or 11 per cent, at that age.
1, or 60 per cent, of whole.
"2, or 22 per cent, at that age.
,2, or 66 7 of whole.

1.
0,

f8,

13,

0
0
0

or 1 5 per cent
or 30 per cent

or 33*3 per cent, at that age.
or 37*2 per cent, of whole.

or 5 per cent,
or 40 per cent.

In-door employ
tncnts » .

rOther diseases besides acute>
rheumatism and acute gontj

/Acute rheumatism . . .

Waiters, bar-
men, and one
commercial
traveller .

20,

Pericarditis ......

1 ^Endocarditis

VAcutegout

'Other diseases besides acute\
rheumatism and acute gout/

E rheumatism . . .
dilis
rditis

Acute gout

(Other diseases except acutel
rheumatism, &c. J

£~v.vu -~v* •» /Acute rheumatism . . .

school. . •\\pericardiH8.

\\Endocarditis

/Other diseases except acnte\
rheumatism and acute gout)

E cute rheumatism . . .
tricarditis
ndocarditiM

20,

10,
10,

5,
0

{

or 16*3 per cent.

or 52 5 per cent.

or 50 '6 per cent, at that age.
or 77 per cent of whole,
or 25 per cent, at that age.
or 65 '2 per cent, of whole.

Total of Male,
Patients.

Acote gout

2, or 16*6 per cent.

2, or 15*3 per cent.

1 1, or 50 per cent, at that age.
VI. or 50 per cent, of whole.

37, or 100 per cent.

16, or 100 per cent.

4, or 25 per cent, at that age.
9, or 66*6 per cent, at that age.

89, or 17 per cent.

70, or 45 per cent

17, or 24 -3 per cent, at that age.
17, or 61'5 per cent, of whole.
26, or 357 per cent at that age.
25, or 54 3 per cent #/ whole.

From 21 to 25 Years.

31, or 15 per cent.

10, or 22 2 peT cent

1, or 10 per cent, at that age.
I, or 10 per cent, of whole.
4, or 40 per cent, at that age.
4, or 27 per cent, of whole.
2

4, or 11 7 per cent

3, or 21 4 per cent

1, or 83*3 per cent at that age.
1, or 50 per cent, of whole.
1 , or 33*8 per cent at that age.

1, or 33*3 per cent, of who fa
0

4, or per cent

6, or 26 per cent

(1, or 16*6 per cent at that age.
\1, or 100 per cent of whole.

2, or 309 per cent, at that age.
2, or 25 per ceni. of whole.

9, or 22 per cent.

1, or 20 per cent

0
0
0

20, or 16 3 percent

5, or 13 "5 per cent

1, or 20 per cent, at that age.
1, or 77 pereenf. of whole.
1, or 20 per cent at that age.
1, or 1 1 per cent, of whole.

2, or 16*6 per cent

7, or 54 1 per cent

0
0

70, or 13 4 per cent

32, or 20*8 per cent

4, or 12 per cent, at that age.
4, or 12 per cent, of whole.
8, or 24*2 per cent at that age.
8, or 17-4 per cent of whole.

* Hers and elsewhere in these eohmms add after « age " of those with acute rheumatism who were so sJIeeted

and who were engaged in the class of employments indicated in the ootassa headed "Male Patients."
• Here and elsewhere in these columns * whole " applies to the whole umber of an ages of those with

acute

189).

195

!e Gout, and II. — 326 Patients affected with Acute Rheumatism, with its attendant
nth Acute Gout, in relation to Occupation.

bote 25 Years.

j Age and Occupa-
tion NOT 8TATED.

per cent.

per cent at that age.
per cent of whole.
per cent, at that age.
per cent, of whole.

•6 per cent.
•3 per cent.

Age not stated 14

• ••

3 per cent
per cent

per cent, at that age.
'b per cent of the whoh.

per cent.

percent, at thatogt.

4 per cent.

per cent. ]

■3 per cent, at that age.
3 per cent, of whole,
per cent, at that age.
3 per cent, of whole.

•6 per cent.

per cent, at thai age.
percent, of whole.
per cent, at that age.
9 per cent, of whole.

• ••

• • •

... 1

4 per cent.

•7 per cent + 1 occu-
not stated.
per cent, at that age.
*3 per cent, of whole,
per cent, at that age.
•2 per cent, of whole.

ttcnpation not stated.

{

Age not stated 27

Age (?) 1 + 2 occ

not stated
Age (?) 1 + 1 occ.

not stated
Age (!) and occ. not

stated I
Age (?) — 3 occ. \

not stated »

Total.

221

15
15

14
o

3
2

8
15

129

0
13

12
13

2 -
3

4
9

547

155 4- 3 oec.

not stated
i33 + 2 occ.
\ not stated
j4C + 1 occ.
I not stated

n f40 4 per cent of the males.
"rl22 1 per cent of the whole.3

1 29 per cent, of the males.
114 per cent, of the whole.

jOr 22 per cent, of those with acute
I rheumatism.

Or 33 3 per cent, of thou with
acute rheumatism.

{

0 [6*9 per cent of the males.
<8*8 per cent of the whole.

{

per
q<9 per cent of the males.

14 3 per cent of the whole.
Or 14 per cent of those with acute

rheumatism.
Or 21-4 per cent, of those with

acute rheumatism.

0 (12 6 per cent of the males.
v 1 6 -9 per cent, of the whole.
0J14*8 per cent of the males.

T, 71 per cent, of the whole.
[Or 4 3 per cent, of those with acute

1 rheumatism.

iOr 35 per cent of thou with acute
\ rheumatism.

0 [9 5 per cent of the males.

14 1 per cent of the whole.
0 (3 2 per cent of the males.

U'5 per cent, of the whole
Or 20 per cent, of those tcith ac. rh.

0 f23*6 per cent of the males.
vrU2-9 per cent, of the whole.
0 (24"5 per cent of the males.

\ll-4 per cent of the whole.
IOr 35 per cent, of those with acute

rheumatism,
\0r 24*3 per cent of those with

acute rheumatism.

0r f 2 2 per cent of the males.
w\l*2 per cent of the whole,
fv f8*4 per cent of tho males.
u U per cent, of the whole.
Or 8*3 per cent of those with acute
. rheumatism.

Or 16*6 per cent, of those with
rheumatism.

6*9 per cent of the males.

3 8 per cent of the whole.

1 1 per cent of the males.

5*3 per cent of the whole.

Or 24 per cent of those with ac. rh.

Or 58 per cent of thou with ae. rh.

Or
Or

m whose ages were stated, and who were so affected, who were engaged in the class of occupations

In the column headed " Hale Patients."

and elsewhere in this column •• whole" applies to the whole number of patients of both sexes.

o 2

Female Patiehte.

(other di«™«« eicept acuta
i-heumntjiim

SaWb..

/ Acute rkemnaMai ....

I itrfcardflii

Otlier dleeeMi eicept eeote'

fin

J Acute rheamAtlnn ....

{l4, or-3-J p€T anl.'of Ae whalt. '
ISS, or U ptr cent at All one.
|», or MS percent q/ wMt.

£'.iT!'".'l'«""»"' •

EmlManHfii ,

Other dimi
rheanutu
tScdenUij In- . . .

nwnti . . . firtnniili

1, or J 7 per cent

S, or Ml per cent

(Other dieeuei except tcuU
rhemn.tl.m
Acute *„___.
EndocanlKfc .

•cloof'

^l Acute.

I Endoeurdtht

I 67, or 100 per cent
j J, or 11 -4 per oentai

Total of fanule/ ,

or a-ijtrcat. DfOu w»o(e.
or 2S"S ptr cento/ Ini wAoIc.

tr dieeaMi except neatoi 215, or 195 per cent of tl
urutllDi and »cut« gout/, whole Witt «ge« lUted

terheuuiitunn . . . . 1(7 or M'T per cent.

1 Endocarditis

ijH or 53 per ant. at thai aft.

' [n, or Wo per cral. 0/ tkicfeofe.

r 32 2 per cent 0/ tkt icnoff
»r 83"3 per cent oEfnat acre.
>r IB-) per wnt of tti w*ok

wtthigaa itnted

ir 10 0 per ant. 0/ OewAob

irttSaJWoloo*.

)T 18 percent ofduv

• Ben end elnewhore In thcic column " whole " nppllei to the whole number of ill igee

'otthOH with wuti

71, or M-4 per rem.

61, or 86-1 per i
IS. or <H per cei

of the femulM.

t. of the whole

t of (he feimlen.
it. or Iha Kholo.
(Or las per ml. or (tow iritt

•r MS per ««(. o/ rftoee wltt
acute rheuMotltm.

OrfJ.f

Jf the fomelei.

IS JW «■!. 0/ IAok HJlCJt

1 38

i". or 825 percent.

Wgpffrtlll,^ wftoli
" 10if£r™..<"fir*ol(

jr 50 per cent.
srlMjwccnl. of flnl

or SI -g per cent

I- 1 occupation not at

1 I not eUtei

, («■( per cent of the fenielei.
WII'« per cent, or the whole,
i 164 per cent. oT the fcmmlei.
•"IBS Per cent. of the whole.

( atmtt AcHKiallm-
nJlo-S per cent of the femsJee.
Dr\ 74 per tent or the whole.
- (IB'2 per cent of the (erntlee..
"T. S-S per cent, of the whole.
(Or 118 per XM. 0/ 1*0* ttUA

)0'"l'lA per cent, 0] Hum leftt

. 13 * per cent of the fennJee.

"Us per cent of the whole.
__|1 -2 per cent of the femeJee.
"Ho-B per cent, or the whole.

. 6 -7 per cent or the whale.
- fa-fl per cent or the femnlos.
^{i per cent or the whole.
>11 iprrent aflhonvUkacrh.
>r« percent o/UioMWittoc. r*.

it X 3 per Ml. ri/Kho'i.

>■* per cent, of tht vrfo.tr.
or tS 1 tier em r. nt Mar<nw.
*rM4jcr<**t. </**«£

. jIAge (!) B + 3
!{J* ^rfLd

j Age end o

1,000 |

otitated }|
+ 2 MC.1

iciiitaKd (I
+ 1 oecl!

striated j

+ » occl!

otiUted j

IwHetted in the column '

■e aUted, end who were « affected, who w*

uled "Mele Patlente."

:hla column " whole " »rplf*» to the whole i

« eapiged In the alul of ocenpttioa
unber of petlenti of both nxei.

198 A SYSTEM OF MEDICINE.

with Pericarditis, all of whom had endocarditis also, and nearly one-
half of them (25) with simple endocarditis, while endocarditis was
either threatened or probable in the remaining 15. Three-fourths of
the servants attacked with Pericarditis and endocarditis (14 in 19),
and three-fifths of those with simple endocarditis (26 in 42!) were
below the age of 21, while only one-fourth of those who were quite
free from symptoms of heart affection were below that age (3 in 13).

Girls engaged in the hard labour of a servant, at work, at a tender
age, from morning to night, when attacked with this disease to which
they are so subject, are all but certain to have inflammation of the
heart without or within. Servant-girls below the age of 21, keeping
in view their time of life and constitution, are more exposed to the
causes of acute rheumatism and its attendant inflammation of the
heart than persons of any other class. They are growing, their frame
is not yet knit, they are sensitive to cold and wet, and they are
subject to palpitation. Before all, in these young women their joints
are not yet perfected, the ends of the bones forming them being still
united to their shafts by cartilage ; their growth is active so that the
blood circulates in them freely; their structures are sensitive; and
while they are supple, and their play is free and lively, they are
tender and do not bear undue pressure ; they are liable to strains, are
unequal to labour and fatigue, and are easily affected by draughts,
and by exposure to wet and cold, especially after undue and prolonged
exertion. Then the labour of these poor girls, especially in hard
places of service, is great and constant ; they carry weights up and
down stairs, often in lofty houses ; they are constantly on foot, stand-
ing rather than walking, so that full pressure is continuously made
on the joints; or what is worse, they are kneeling sometimes on
cold and even wet stone floors, hard at work, scrubbing and brushing.

The joint affection was, as a rule, more severe in servants suffering
from acute rheumatism than in the rest of those so affected, the joints
being attacked with severity in one-half of the servants (49 in 101),
and a little over one-third of the rest (91 in 225). Among those
servants who suffered from Pericarditis, the joint affection was severe
in fully three-fourths (15 in 19), and in a large proportion of these
(6) it was very severe. If we compare these cases with the rest of
the servants affected with atcute rheumatism, we find that the severity
of the joint affection rose in the scale in exact proportion to the
severity of the heart affection. The joint affection was severe in less
than, one-third (4 in 13) of those servants who presented no sign of
inflammation of the heart, while it was so in a little over a third (9
in 26) of those in whom endocarditis was threatened or probable, and
in one-half of those who were attacked with simple endocarditis (21
in 42) ; while, as I have just said, it was severe in three-fourths of
the cases with Pericarditis (15 in 19).

In the servants who were attacked with Pericarditis, the severity
of the joint affection bore a strict relation to the severity of the heart
affection in the great majority of the cases.

PSSICARDITia.

Id one-third of them (6 in 19) the joint affection was very
severe ; and in the whole of these the heart affection was very severe,
while in one of them it was fatal

In nearly one-half of these patients (9 in 19) the joint affection was
severe in the second degree, and in two-thirds of these (6 in 9) the
heart affection was severe ; in two cases it was rather severe ; and in
one it was slight. In three patients the joint affection was rather
severe, and of these the heart affection was severe in one, rather so
in a second, and not so in a third.

The last case is a notable exception to this rule. The attack in the
joints was slight, but the attack at the heart was very severe, and
proved fatal.

The accompanying Tables show (1) the proportion in which female
domestic servants affected with acute rheumatism were attacked by
endocarditis and Pericarditis, and the influence of age in the propor-
tionate production of those affections of the heart in that disease ; and
(2) the relation of the degree of the joint affection to the degree of the
heart affection in those cases.

1. Degree of the Joint Affection iu Scmtnta affected with Acute Mi
to Ago and Heart Affection.

KlL'J.'. .Ll'tjU*.

SSSt

*~m.

Total.

rolnt Affection.

• nl*

*\*- 1

^ -■'■

-,-ls

*S IS

Total.

k|:|l!l

i!li

i\i

ill

■T««vm + + .

;

.1. .

jjji i

P 0

11
i

10
r

0 0

1 \i

u ii

All

i
1»
11

0
1

11
1

!■
I

0
1

Total . . .

4 j 1 1 13

sjsji

11 4

Degree or the Heart Affection.

Total

the Joint
Affection.

Degneof tho
Joint Affection.

Fatal.

Btim.
+ +

Rather - Not

Slight

JJTWW++ ■ ■
tot ttTirt *+..'.

•

;

1 + +
9 +
3 — +

Heart Affection .

!F7.

0 + + | « +

■♦

'•

2001 A SYSTEM OF MEDICINE.

I will now briefly consider the occupations of the remaining female
patients who were attacked with acute rheumatism. I have thrown
into one group the cooks, charwomen, nurses, and laundresses, who
numbered altogether 22. Of these 5 had Pericarditis, 4 of whom had
endocarditis also, and 4 had simple endocarditis ; in 7 endocarditis
was threatened or probable ; and in 6 the heart gave no evidence of
being affected. Of the whole number less than a fifth were younger
than 21 (4 in 21 1). Of the five cases with Pericarditis, in one the
attack was severe but transient, and in that patient the joint affection
was severe. In two others the heart affection was rather severe, and
in the remaining two it was slight, while in none of these was the
joint affection severe.

Nine of the women followed sedentary employments, using chiefly
the needle ; and in none of these was there Pericarditis ; four. of them,
however, had endocarditis.

The married women numbered 17, and of these only two had Peri-
carditis and endocarditis, one severely, the other slightly. In both
the joint affection was rather severe. Of the remainder, 2 had simple
endocarditis, and 5 were threatened with it, while one-half (8) gave
no sign of heart affection. These patients were all older than 23.

Sixteen of the female patients had no occupation, only one of whom
was above the age of 20. Only two of them had Pericarditis, one
of whom had endocarditis also ; in one of these the heart affection was
fatal, in the other it was severe ; and in one of them the joint affec-
tion was severe, while in the other that ended fatally it was so only
to a moderate degree. Seven of these cases had simple endocarditis
and 2 were threatened with it; while 5 of them presented no
indication of endocarditis.

These cases, taken as a whole, show that those women who followed
at a mature age occupations as laborious as the young servants, were
affected in but a moderate proportion with Pericarditis, and that in a
comparatively mild form. They also show that those of tender age
who followed no occupation were not attacked with inflammation of
the heart with anything like the same frequency as young female
servants. We thus see, in brief, that in acute rheumatism affecting
the female sex, youth with labour is nearly always attacked or
threatened with endocarditis or Pericarditis, or both ; that youth with-
out labour is thus attacked with comparative infrequency ; and that
mature age with labour is attacked less frequently and much less
severely with inflammation of the heart than youth with labour.

The male patients give us two great illustrations. One of these is
supplied by those working in-do<yi% and they naturally run in the
same grooves as the female patients, who were, all but two, occupied
in-doors. The other is supplied by those following out-of-door occu-
pations ; and they stand completely apart in kind of labour, age, and
character of disease, as well as in sex, from the female patients, whose
cases have just been considered.

i In one of the 22 cases t>e?onging to this group the age of the patient is not stated.

PERICARDITIS. 201

I have brought the male patients working in-doors including ten
servants, into one group, numbering 37. In several features this-
group presents a remarkable agreement as regards age and the fre-
quency of heart affection, and especially of Pericarditis, with the
important and large analogous group of female servants. Thus in
each group more than half of the patients were below the age of 21
(of the male patients 19 in 37, of the female servants 57 in 100) j1 in
each, the proportion of cases with Pericarditis was great, amounting
among the males to one-third (13 in 37), among the female servants
to one-fifth (19 in 101) ; in each three-fourths of those thus affected
with Pericarditis were below the age of 21, (10 of the 13 male
patients, and 14 of the 19 female servants) ; in each the proportion
of those in whom the heart presented no sign of inflammation was
small, amounting to one-sixth of those male patients (6 in 37), and
one-eighth of the female servants (12 in 101) ; and in each few of the
patients whose hearts were thus unaffected were below the age of 21,
amounting to fully one-third of those male patients (3 in 7), and to
one-fourth of the female servants (3 in 13). Here, however, this
close parallel ends, since among the patients affected with acute
rheumatism above the age of 25, Pericarditis attacked the men
working in-doors more frequently (2 in 13) than the female servants
(1 in 22), and among those with Pericarditis, less than one-half of
the males (6 in 13), and almost as many as three-fourths of the
females (15 in 19) were attacked with severity ; while the proportion
of cases affected or threatened with simple endocarditis was much
smaller among the male patients (9 and 9 respectively in 37) than
the female servants (42 and 26 in 101).

Looking at these two sections of the patients in their larger and
more vital relations, it is evident that in both sexes the same causes
produce, under like conditions, the same effects ; and that a very large
proportion of the young persons who work on foot in-doors during
many hours daily, are attacked with inflammation of the heart when
affected with acute rheumatism, while a very small proportion are
thus attacked of the men and women of mature age who are engaged
in the same manner.

If we looked solely to the kind of employments just considered it
would be natural to infer that overwork in-doors in young people
of both sexes was the main cause of acute rheumatism and of its
attendant Pericarditis and endocarditis. While, however, as we have
just seen, the whole of the female patients with occupations were
engaged in-doors, save two poor women who each kept a stall, only
about one-fourth of the male patients worked in-doors.

The larger proportion of the male patients affected with acute
rheumatism, amounting nearly to three-fifths (82 in 154), excluding
those working with lead, worked out-of-doors. More than one-half
of these (45 in 84) were engaged in hard labour. Pericarditis attacked

1 In one of the 99 female servants affected with acnte rheumatism, the age of the
patient is not stated.

202 A SYSTEM OF MEDICINE.

nearly one-fourth of these patients (10 in 45). We here find, what
is at first sight an unexpected result, that of these laborious workers
out of doors thus attacked fcwith Pericarditis only one in ten was
below the age of 21 ; whereas of the male in-door workers thus
affected, fully three-fourths (10 in 13) were below that age. If we
look at those of older age, we find the scale exactly reversed ; since of
those labouring out of doors four-fifths (8 in 10) were above the age
of 25 ; while of those working in-doors only one-sixth (2 in 13)
were above that age. We here, I consider, find the explanation, that
I promised when considering age, of the twofold fact, that the male
cases of Pericarditis usually combined with endocarditis outnumber
the female cases by one-fifth (35 to 28) ; and that the number of the
men so affected above the age of 25 is three times as great as that of
the women so affected (men with Pericarditis 13 in 53, women 4 in
53). I think we may infer from these facts that excessive labour in
the open air in men of mature age is a frequent cause of acute
rheumatism having a strong tendency to Pericarditis.

Male patients with acute rheumatism, whose occupation was chiefly
on foot, such as watchmen and porters ; and those employed with
horses and in stables, whose habits make them liable to gout, in-
cluding coachmen, cabmen, and grooms ; did not suffer from Pericar-
ditis so frequently as those who were engaged in hard labour : since of
those working on foot only one-seventh (2 in 14) and of those employed
with horses only one-twenty-third (1 in 23), while of those whose
work was laborious, nearly one-fourth (10 in 45), were thus attacked.

These facts support the view that Pericarditis tends to attack men
of mature age affected with acute rheumatism when their work is
hard, but not when it is comparatively easy.

It remains to me to speak of two other classes of employments,
painters and plumbers on the one hand, and waiters and barmen on
the other, who tend to have gout much more frequently than acute
rheumatism. I find, however, that 11 waiters and barmen and 5 of
those working with lead were attacked with acute rheumatism. One
of each of those classes was attacked with Pericarditis, both of whom
were above 30 years of age. Seven of the waiters and barmen and
two of the workers in lead presented no sign of heart affection.
These were all but one below the age of 2i, and in none of them
was the great toe affected.

It would thus appear that when barmen, painters, or workers among
horses, whose employments tend to induce gout, are attacked with
acute rheumatism, especially when young, they do not tend to have
Pericarditis or endocarditis.

II. — The Affection of the Joints in Eheumatic Pebicarditis.

The inflammation of the joints and the inflammation of the heart
in acute rheumatism form one disease. We know that in a certain
proportion of the cases the heart shows no sign of being touched by

PERICARDITIS.

203

the disease, and here and there perhaps in a very rare instance the
heart is attacked with inflammation when the joints are free from it.
The unity of the two phases of the disease, the external phase, in the
joints, and the internal in the fibrous structures of the exterior and
the interior of the heart being established, we have to inquire
what was the relative intensity of the inflammation of the joints and
the inflammation of the heart in my cases of acute rheumatism, and
especially in those affected with Pericarditis.

We have just seen that in servants attacked with acute rheuma-
tism, the joint affection was, as a rule, only of moderate severity when
the heart gave no sign of being affected ; that the joint affection was
more severe when the heart was threatened or probably attacked with
endocarditis ; and that the severity of the joint affection increased in
a direct ratio with the increased certainty and severity of the heart
affection ; the joint affection being greater when simple endocarditis
was actually present than when it was threatened or probable, and
much greater when the heart was attacked with both endocarditis and
Pericarditis.

I find that the same rule applies to the whole body of the cases of
acute rheumatism ; as may be seen in the accompanying Table, show-
ing the degree of intensity of the joint affection in relation to the
absence or presence of endocarditis and Pericarditis in cases of acute
rheumatism.

Degree of intensity of the Joint Affection in relation to the absence or presence of
Endocarditis and Pericarditis in cases of Acute Rheumatism.

Joint Affection.

No Endo-
1 carditis.

Very severe .
Severe . . .
Katiier s°\*ere
Not severe
8Hgtat . . .
Doubtful . .

Total

34
18

4
1

Eudocar-

ditU

Endocar-

Pericar-

threatened'

ditis.

probable.

•>

•W

108

S3
fa »

» 0

O
P.

125

129

84
97

•»
i

326 - 101 = 225

Thus the joint affection was severe in one-fourth (22 in 78) l of
those patients in whom the heart gave no sign of inflammation ; in
two-fifths (32 in 76) of those in whom endocarditis was threatened
or probable ; in more than two-fifths (48 in 107)2 of those affected
with simple endocarditis, and in three-fifths (37 in 62) 8 of those who
were attacked with Pericarditis, all but 9 of whom (54) had endocar-
ditis also.

* The degree of the joint affection was not stated in one of the 79 cases belonging to
this group.

• The dei
this group.

» The d<
this group.

Legree of the joint affection was not stated in one of the 108 cases belonging to
egree of the joint atfection was not stated in one of the 63 cases belonging to

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PERICARDITIS. 205

The inflammation of the joints was very intense in 12 of the 37
patients with Pericarditis, usually coupled with endocarditis, in whom
the inflammation of the joints was severe, whereas in only 3 of the
184 patients in whom simple endocarditis was present or threatened,
and in none of the 79 in whom the heart gave no evidence of being
affected, was the joint affection of this great degree of intensity.

In the cases of Pericarditis, there was a close correspondence in
severity between the inflammation of the joints and the inflammation
of the heart. The accompanying Table [see opposite page] shows in
detail the degree of the joint affection in relation to the degree of the
heart affection in sixty-two cases of Rheumatic Pericarditis.1 The
joint affection was very severe in 12 cases, and in three-fifths of those
cases (7) the heart affection was very severe, being fatal in one ; in
one-fourth of them (3) it was severe ; and in only one-sixth of them
(2) was it of moderate severity. The joint affection was severe in 25
cases, and in one-third of those cases (9) the heart affection was
very severe; in less than one-half of them (11) it was severe,
and, in one-fifth of them (5) it was of moderate severity, or slight.
If we combine these two groups of cases, amounting to 37, that were
marked by the severity of the joint affection, we find that in four-
fifths of them (30) the affection of the heart was severe, while in one
fifth of them (7) it was not severe or only moderately so. Endocar-
ditis was present in all but two of the 30 cases in which the affection
both of the joints and the heart was severe ; while the signs of endo-
carditis were either absent or doubtful in 4 of the 7 cases in which the
affection of the joints was severe, while that of the heart was either
of moderate severity or slight.

If we examine those cases, amounting to 25, or two-fifths of the
whole number, in which the degree of the joint affection was below
the line of severity, we find that in 18 of them the affection of the
joints was only of moderate severity, while in 7 of them it was slight ;
and that in two-fifths of these (10) the heart affection wets severe,
while in three-fifths of them (15) it was either slight or of moderate
severity. We find, then, that in the 37 cases of Pericarditis in which
the joint affection was more severe, the heart affection was more severe
in four-fifths (30) and less severe in one-fifth (7) ; while in the 25
cases of Pericarditis in which the joint affection was less severe, the
heart affection was more severe in two-fifths (10) and less severe in
three-fifths (15).

III. — The Degree of the Joint Affection during the Acme of

the Effusion into the Pericardium.

When the exterior of the heart is attacked by inflammation in
cases of acute rheumatism, the distress and oppression in the region
of the heart and in the chest is often so great as to call the patient's

Mil one of the 63 ea^es of Pericarditis the joint affection was not described.

206 A SYSTEM OF MEDICINE.

attention away from the seat of suffering in the joints. At the same
time the physician or the clinical clerk is so much interested in the
state of the central organ that he readily overlooks that of the joints.
I find that in 12 of the 45 cases given in the accompanying plans (see
pages 190, 191), the condition of the joints was not reported during the
acme of the pericardial effusion, and in one other case the joint affec-
tion was not noted until the attack of Pericarditis had declared itself.

The state of the joints during the period of the acme of the inflam-
mation of the exterior of the heart, marked by the extent of fluid in
the pericardium being then at its height, is shown in 32 of the 45
patients under examination. These cases divide themselves naturally
into two groups ; in one of these, amounting to 12, the Pericarditis
was at its acme at the time of admission, or on the following day ;
while in the remaining 20 cases the effusion into the pericardium
reached its acme after the admission of the patient. In the latter set
of cases, the intensity of the joint affection had been, as a rule, modi-
fied and lessened by rest and soothing treatment, and, especially in four-
fifths of the cases, by opium given at repeated intervals ; while in the
former set of cases in which the pericarditis was at its height at the
time of admission, the joint affection had been, as a rule, somewhat
aggravated by the removal of the patient from home to the hospital.
The set of cases, therefore, that were admitted with pericarditis at its
height show the natural relation of the degree of the joint affection
to that of the heart affection during the period of the acme of the
disease, in a manner less affected by other influences than the set in
which the pericarditis came on and reached its height after admission.

The inflammation of the joints was severe at the time of admission
in more than one-half of the patients (7 in 12) who came in with
the Pericarditis at its height, and in six (16, 18, 12, 51, 55, 35,) of
these seven cases the joint affection was of about equal severity before
admission and at the time of the acme of the effusion into the peri-
cardium ; while in one of them (56) the joints were less severely
affected before than during the period of the height of the Peri-
carditis.

In two-fifths of this group of cases (5 in 12) the joint affection
was not severe when the Pericarditis was at its height, at the time of
admission or on the next day, and in three (6, 43, 40) and perhaps in
four (42) of these the inflammation of the joints was more severe be-
fore admission than after it and during the period of the acme of the
effusion into the pericardium. The remaining case (13) stands alone,
since in it, although the affection of the heart proved fatal, that of the
joints was but slight, both before and after admission.

The second group consists of twenty cases in which the effusion
into the pericardium reached its acme after admission ; and it will be
seen that the relation of the joint affection to the heart affection was
very different in this group from what it was in the former one in
which the patients came in when the Pericarditis was at its height.

The inflammation of the joints was more severe at the period of the

PERICARDITIS.

307

acme of the pericardial effusion than before that period in one-fifth
of these cases (4 in 20) (3, 4, 30, 49), and it was of equal severity
during the two periods in one other case (19).

The affection of the joints became less severe during the period of
the acme of Pericarditis than before that period in three-fourths of
these cases (15 in 20).1 Four-fifths of these patients (12 in 15) took
repeated doses of opium, with lessening joint affection during the
acme of Pericarditis, while only one of the four patients with increasing
joint affection during the acme was placed under the influence of
opium.

It is evident that if we looked only to the first group, or only to the
second group of these cases, we should arrive at opposite conclusions
with regard to the relation of the degree of the joint affection to that
of the heart affection during the acme of Pericarditis- Thus the
joint affection lessened during the acme of the disease in one-third of
the first group (4 in 13) and in three-fourths of the second group
(15 in 20). The influence of repeated doses of opium evidently told
on the second group of cases, and the movement of the patients from
their homes to the hospital, on the first group of cases, to modify the
relation of the joint affection to the heart affection.

I think that we may safely draw an inference midway between
these two extreme illustrations, and consider that in about one-half
of the cases of Pericarditis the joint affection was of equal severity
during the period of the acme of the disease, and before that period ;
and that in about one-half of them the joint affection became less
severe when the Pericarditis was at its height. The general conclusion
may be drawn from this inference, that the joint affection tends to
lessen in severity when Pericarditis is at its height in about one-half
of the cases.

IV. Time in the Hospital.

The accompanying Table shows the average time that the patients
remained in the hospital in relation to the absence or presence of
endocarditis or pericarditis in acute rheumatism : —

Time in the Hospital in relation to the absence or presence of Endocarditis
and Pericarditis in cases of Acute Rheumatism.

Is the Hospital

No Endo-
carditis.

Endocarditis
threatened

or
probable.

Endocar-
ditis.

Pericarditis.

Total

„ 21 „ 80 „ '.

x\n uncertain numkr of days . .

22 i 14

21 ! 31

21 ! 37

8 i 21

2 | 3

00 I

Total

70 . 74* 1 100*

310*

* Since this Table was drawn tip, seven cases have been added, making the total number 326.
1 8, 15, 20-22, 24, 26, 28, 31, 38, 34, 86, 44a, 50, 54.

208

A SYSTEM OF MEDICINE.

The time that the patient remained in the wards measures the
duration and severity of the disease. Two-fifths of the patients in
whom the heart gave no sign of being affected, left the hospital before
the end of the third week (33 in 76), three-fourths of them during
the first month (56 in 76), and one-fourth of them after the first
month (20 in 76). Those who had Pericarditis usually accompanied
by endocarditis remained in the wards for a much longer period,
since only one-ninth of them (7 in 63) left the hospital before the
end of the third week, and one-fourth of tliem (15 in 63) during the
first month, while three-fourths of them remained in the hospital
longer than a month (48 in 63), and one-half of them more than fifty
days. Those with simple endocarditis remained in the house much
longer than those whose hearts were healthy, but not nearly so long
as those with Pericarditis usually combined with endocarditis.

v. — occcrbknce or non-occurrence of one or more previous

Attacks op Acute Eheumatism.

The accompanying Table shows the proportion in which the patients
affected with acute rheumatism had been previously attacked by that
disease in fully three-fourths of the patients (243 in 319 cases). Less
than one-third of those who gave no sign of endocarditis (23 in 76)
and nearly one-half of those who were affected with endocarditis (48
in 106,) had suffered from one or more previous attacks of acute
rheumatism ; so that in my cases the occurrence of a previous attack
evidently favoured the presence of endocarditis. This did not,
however, appear to be the case with pericarditis, for only one-third of
the cases with that affection had been previously attacked by acute
rheumatism. The previous occurrence of acute rheumatism implies
in a certain proportion of the cases the presence of valvular disease
of the heart, a condition that promotes the occurrence of endocarditis
in acute rheumatism. It is open to inquiry why valvular disease
should have more frequently influenced the production of endocarditis
than of pericarditis in my cases.

Occurrence or Non-Occurrence of Previous Attacks of Acute Rheumatism in relation to
the Absence or Presence of Endocarditis and Pericarditis.

Joint Affection-

No Endo-
carditis.

Endocarditis
threatened

or
probable.

Endocar-
ditis.

Pericarditis.

Total

No previous attack

No note of previous attack . .

One previous attack '

More previous attacks than one .

23
17
24
10

31
27
35
13

117
76
91
35

Total

74*

10(5*

319*

* Since this Table was drawn up, seven cases have been added, making the total number 326.

PERICARDITIS. 209

VI. — The Time of the First Observation of Friction Sound and

OF THE BEGINNING OF EHEUMATIC PERICARDITIS IN IiELATION TO
THE BEGINNING OR RELAPSE OF THE AFFECTION OP THE JOINTS.

In a large proportion of the cases of acute rheumatism affected
with Pericarditis, friction sound was heard over the heart either at the
time of admission or very soon after it. Thus in more than one-tliird
of the total number of the cases, the rubbing noise was noticed on the
day that they entered the hospital (22 in 63) ; in all but one-half of
them (29 in 63) it was heard on that or the following day ; and in
fully two-thirds of them (41 in 63) it was observed either at the time
of admission or during the three days following it. In nine-tenths
of the whole number of cases affected with Pericarditis (55 in 63) the
frottement was distinguished during the first nine days of the patient's
residence in the hospital.

These facts do not, however, point out how soon Pericarditis
occurred after the commencement of the attack of acute rheumatism.
To ascertain this, we must add the number of days from the com-
mencement of the attack to the time of admission, to the number of
days from that time to the period at which the to-and-fro sound was
heard. This plan answers with those cases in which the friction
sound was observed on or after the third day from the date of admis-
sion, since in all but four of them the heart had been previously ex-
amined. It does not, however, apply to those patients in whom the
frottement was detected during the day of admission or on the next
day, since in those cases we do not know how long the rubbing
sound may have been in existence before the patient came in. This
applies to one-half of the patients affected with rheumatic Pericarditis,
since they had suffered from acute rheumatism for a period varying
from two days to three weeks before entering the wards. These
cases are, however, of use in showing how early in the disease, and
how late, Pericarditis may declare itself by friction sound in full
play. Thus out of the twenty-nine cases in which frottement was
heard during the first two days, more than one-fourth (8 in 29) had
been affected with acute rheumatism for a period of from two to four
days ; while on the other hand one-fifth of them (6 in 29) had been
ill for from two to three weeks before admission.

If we bring together the whole of the 63 cases of Pericarditis, we
find that in one-sixth of them (10 in 63) the rubbing sound was
audible as early as from the third to the sixth day after the com-
mencement of the disease ; while in one-half of them (30 in 63) that
sound was audible on or before the eleventh day of the illness.

In only seven of the cases did the heart affection show itself so late
as the twenty-fifth day and from that to the sixty-third after the
onset of the acute rheumatism.

These facts point, I think, to the conclusion that in a certain small

VOL. IV. v

210 A SYSTEM OF MEDICINE.

proportion of the cases, amounting perhaps to one-eighth (8 in 63)
the onset of the inflammation both of the exterior and the interior of
the heart took place at the very commencement of the disease, and at
the same time with the onset of the inflammation of the joints.

It is scarcely needful to say that the first appearance of the rubbing
sound is later than the beginning of the inflammation of the surface
of the heart. In this respect, the inflammation of the outside of that
organ corresponds with the inflammation of the joints, since, as in
inflammation of the joints, pain and tenderness precede exudation and
swelling, so in Pericarditis, in at least some instances to which I shalt
. now refer, pain and exquisite sensitiveness over the heart preceded
the notable increase of effusion into the pericardium and the existence
of a rubbing sound.

In five of the cases in which friction sound was heard on the day
of admission (13, 15, 44a, 53, 61), pain had existed over the region
of the heart, or in the left side, or in the chest, for one or more days
before the patient entered the hospital. In one of these cases (44a)
pain wTas present over the heart from about the beginning of the
illness, the precise time of which is not stated.

In nearly one-half of the patients in whom the frottement was
heard for the first time from one to fifty-three days after admission
(16 in 39), there was pain over the region of the heart or in the
chest from one to seven days before the rubbing noise was observed.
In seven (51, 8, 26, 28, 50, 29, 5) of them the pain was noticed one
day ; in three (57, 56, 23), two days ; in one, three days (14) ; in two,
four days (55, 36); in two, six days (123,30); and in one, seven
days (20) before the first observation of the friction sound.

The patient (24), in whom friction sound was heard on the fifty-
third day after admission, presented a chain of symptoms interesting
in two points of view, one, that the attack of Pericarditis was im-
mediately preceded by a relapse of the joint affection ; the other,
that pain over the heart preceded the frottement. The patient was a
labourer, aged 27, and had almost passed through a severe attack of
acute rheumatism with endocarditis, resulting in permanent injury to
the mitral and aortic valves. On the 36th day, he being stronger
and of better colour, was allowed to get up. On the 42nd his general
health w.as good, his pains were diminished, and he walked about.
On the 45th he felt stiffness in the right hip-joint on walking, that
joint having been affected for eight months previously ; and on the
48th the pain in the hip was worse, though he was otherwise free
from complaint, and his appetite was good. On the 50th day, how-
ever, his neck was stiff, and he had flying pains about the knees ; and
on the next day his face was flushed, he perspired copiously, and
complained of great pain over the region of the heart and palpitation.
On the 52nd he suffered from a terrible pain in the neck and head,
the wrists were swollen and painful, and the heart's action was so
loud that the mitral and aortic murmurs were inaudible ; and on the
following day a loud and harsh double friction sound was heard over

PERICARDITIS. 811

the heart Here the attack of Pericarditis immediately followed the
relapse in the joint affection, and the pain over the heart preceded
the rubbing sound by two days.

In four other cases in which the friction sound appeared some time
after admission, the Pericarditis followed closely upon a relapse of the
joint affection. In one of these (36), a woman, aged 20, who was
motionless on admission from the affection of the joints, the pain was
worse on the 6th day, she was still powerless on the 7th from the
pain in the joints, and on the 8th a harsh grating frottement, chiefly
systolic, was heard over the apex of the heart In another patient (3),
a man, aged 26, who was re-admitted with a severe relapse of the
affection of the joints six days after leaving the hospital, the hands
and hips were better on the 5th day after his Teadmission, but on the
8th there was again pain in the hip, and on the 9th there was excessive
pain and tenderness in the fascia of the thigh. On the next day (the
10th) there was pain, and increased dulness on percussion over the
heart, and a double friction brush was audible at the apex. In a
third case (30), a man, aged 31, all the joints were swollen and painful
when he came in, but were so much better on the 8th day that they
only pained him when he moved. The pain in the joints returned,
however, on the 9th, being better next day, when a harsh doable
friction sound was audible over the heart.

In the last case of this group (17), a female servant, aged 20, the
joints were painful and swollen on admission, they were less so on
the 4th day, and on the 7th they were almost of the natural size.
On the 9th a little pain returned in the joints and there was oppression
over the heart On the 13th the pain had increased and she suffered
much in the chest, the first sound being rough and prolonged. On
the 1 6th there was a murmur all over the heart, which was the seat
of pain ; and on the 17th a soft double friction sound was established
over the region of the pericardium.

To these cases must be added one of a series that were treated by
rest during the years 1866-68. In this patient, a man, aged 20, the
pain in the joints, which was considerable on admission and which
lessened on the 4th day, again increased in the arms and neck on
the 5th, when a pain, beginning at the lower portion of the breast
bone, shot through the region of the heart to the back. This symptom
and pain in the region of the apex were relieved by leeches. The
joints also improved, but on the 10th, after he had been using his
hand, pain returned in the finger, and on the 14th, the next report,
Pericarditis had fully declared itself.

P 2

212 A SYSTEM OF MEDICINE.

VII. — The Presence or Absence of Endocarditis in Rheumatic

Pericarditis.

Cases where Endocarditis was lYresent. — There was evidence of
inflammation in the interior of the heart in all the cases excepting
nine (54 in 63).

The heart was healthy at the time of the attack in 46 of the cases
with endocarditis, and the mitral, or mitral and aortic valves were
crippled by previous disease in the remaining 8 cases, including one
just alluded to (24) in which Pericarditis followed a relapse of the
affection of the joints, the aortic and mitral valves having become
affected during the earlier part of the attack of acute rheumatism.

A tricuspid murmur was alone present in three of the 46 cases
of endocarditis : in two of these cases that murmur was persistent,
and in One of them it disappeared. These cases were comparatively
free from serious symptoms, the heart affection being severe in only
one instance, and the inflammation of the joints being very severe in
another. The proportion of cases of this class with simple tricuspid
murmur, was much smaller in these cases of combined endocarditis
and Pericarditis than in those of simple endocarditis; 1 in 18 of
the former, as we have just seen (3 in 54), and 1 in 8 of the latter
(13 in 108) being thus affected.

The mitral valve was affected in 42 of the 46 patients with Peri-
carditis in whom endocarditis attacked the heart when previously
healthy, in 6 of whom the aortic valve was affected as well as the
mitral. The aortic valve was attacked in one other case in which the
mitral valve was not involved.

I have divided these 43 cases with mitral (36), aortic (1), and
mitral and aortic (6) incompetence into three groups; in the first
group, containing 16 cases (11 mitral, 5 mitral and aortic incompe-
tence), valvular disease was finally established, or, in two instances,
the disease proved fatal when the murmur was in full play ; in the
second group, which numbered 8 cases with mitral regurgitation, the
murmur was lessening when the patients were discharged ; while in
the third group, amounting to 19 (17 mitral, 1 aortic, and 1 mitral
and aortic incompetence), the murmurs disappeared on the recovery of
the patients from acute rheumatism, and the heart was restored to a
healthy condition.

The accompanying Table shows the relation of the degree of the
affection of the joints and that of the affection of the heait to the
occurrence and degree of endocarditis in cases of acute rheumatism
affected with Pericarditis.

If we compare the cases of endocarditis thus combined with Peri-
carditis, with the cases of uncomplicated or simple endocarditis, we
find that valvular disease was finally established, that the murnuir
lessened in intensity, and that the murmur finally disappeared in
nearly the same proportion in the two sets of cases. Thus in 70 cases

PERICARDITIS. 213

of simple endocarditis, either mitral (53), aortic (10), or mitral and
aortic (7) incompetence was present. If we divide these cases, like
those with Pericarditis and endocarditis, into three groups, we find
that in the first group containing 28 cases (16 mitral, 5 aortic, and 5
mitral and aortic incompetence), valvular disease was finally estab-
lished, or, in two instances, the disease proved fatal ; in the second
group, which numbered 11 cases (11 mitral incompetence), the
murmur was lessening when the patients were examined for the
last time ; while in the third group, amounting to 31 cases (24
mitral, 5 aortic, and 2 mitral and aortic incompetence), the murmur
had disappeared on the recovery of the patients from acute rheu-
matism, and the heart became again healthy. A tricuspid murmur
was alone audible in 13 additional cases of simple endocarditis : in
7 of these the murmur disappeared, but in 6 of them it was still
audible when the heart was listened to for the last time.

I am of opinion, notwithstanding the remarkable correspondence in
the effects of the inflammation of the valves in the three parallel
groups of each of these two sets of cases, that when inflammation
attacks the interior of the heart alone, it is less likely to induce per-
manent valvular disease, than when the heart is inflamed both
without and within. This, I think, is d priori self-evident, and it is
supported by two pieces of clinical evidence that I shall now adduce.
(1) Disease of both the mitral and aortic valves, which is the most
extensive form of valvular disease, was established in 5 of the 43
cases affected with both endocarditis and Pericarditis, and in 5 only
of the 70 cases affected with simple endocarditis. (2) Simple endo-
carditis was present in 28 out of 74 cases of acute rheumatism that
were treated by me in St. Mary's Hospital on a careful and rigid
system of rest. Valvular disease of old standing existed in 7 of those
patients, and a recent mitral murmur, accompanied in one instance by
aortic incompetence, affected the remaining 21 cases. The heart re-
gained its healthy condition in 14 of these patients, the murmur was
lessening or doubtful in 4 of them on their recovery from acute rheu-
matism, and valvular disease was established in 3 only of the whole
series of 21 cases.

The inflammation both of the joints and the heart was more often
-severe in those cases in which the valves became permanently dis-
eased, than in those in which the recovery of their function was com-
plete. The heart affection was severe in 12 of the 16 cases in which
the valves were permanently disabled, being fatal in two and very
severe in six of them; while it was severe in 13 of the 19 in which
the valves were restored to health, being very severe in four of them.
The relative intensity of the joint affection was even greater than
that of the heart affection; since, in the former class of cases, it was
severe in 12 of the 16 in which the organ became diseased, and in
only 10 of the 19 in which its recovery was perfect.

There was mitral regurgitation in the whole of the group of cases,
amounting to 8, in which there was previous valvular disease, in three

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216 A SYSTEM OF MEDICINE.

of which the aortic valves were also incompetent. The heart affection
was severe in the whole of these cases save one, and the joint affection
was so in five of them. The all but universal presence of inflamma-
tion within the heart in patients of this class, supports the inference
that in acute rheumatism, old standing valvular disease, by throw-
ing additional labour on the organ, tends to produce endocarditis and
pericarditis, and to increase the severity of the inflammation of the
heart, both within and without

II. Cases in which Endocarditis was absent or doubtful, — The signs
of endocarditis were absent or uncertain in only 9 of the 63 cases of
Pericarditis. In five of these patients no murmur was audible ; in
one there is no note that a murmur could be heard, and in the
remaining three the existence of a murmur was doubtful. One of
these cases proved fatal, and the affection of the heart was severe in
two and of moderate severity or slight in the remaining six patients.
The joint affection was severe in six of these cases.

Classification of the cases of Pericarditis. — I have classified the cases
according to the presence or absence of endocarditis, and subdivided
those with endocarditis into the groups which have just been described
and which are specified in the following scheme :

I. Cases of Pericarditis in which Endocarditis was present 5 (

A. — Cases with Endocarditis attacking the healthy heart ... 46

1. — Cases with tricuspid regurgitation <- 8

a. — Cases in which the regurgitation became permanent ) «- ~
after recovery from acute- rheumatism. ... j «-

r.— Cases in which the regurgitation disappeared on re- j «- -
oovery j «-o *■

2. — Cases with mitral (36 ->), aortic (I 1), and mitral-aortic

(1 *-*) regurgitation 43

a. — Cases in which the regurgitation became pcrmancEt
after recovery from acute rheumatism (mitral 11,^,
mitral-aortic 1 -*!-►)

h. — Cases in which the regurgitation lesscnod after recovery

(mitral 8^) 8

e. — Cases in which the regurgitation disappeared after recovery

(mitral 17 ^ aortic 111, mitral-aortic 1 1°-*) 10

B. — Cases with Endocarditis attacking a heart already affected with

mitral (5 *£>), or. mitral-aortic (3 >iy«>>), valve-disease . . 8

II. —Cases of Pericarditis in which Endocarditis was absent (6) or doubtful (3) 9

Total number of cases of Pericarditis 63

PERICARDITIS. M

VIII. — Sketch of the Progressive Changes that take place in the
Heart and Pericardium during the progress of Pericarditis.

We cannot rightly understand the symptoms and signs of Peri-
carditis unless we keep in the mind's eye the changes that are going
on in the heart and pericardium, and the surrounding organs during
the periods of the beginning, increase, and acme, the decline and end-
ing of the disease. I shall, therefore, before discussing the symptoms
and signs of the disease that were present in my cases, give here a
slight sketch of the more important morbid changes, in so far as they
make themselves appreciated during life, and shall afterwards describe
some of those changes more fully when the consideration of the
symptoms and signs of the affection seems to call for it.

When the surface of the heart becomes inflamed, a blush of fine
vessels, consisting of a velvety network, appears on the surface of the
organ, and especially over the larger coronary vessels at the base and
septum of the ventricles. The inner surface of the pericardial sac,
wherever it rests upon the inflamed heart, kindles also into a blush
of fine vessels. The inflammation caught from the heart on the inner
lining of the sac, spreads rapidly to the fibrous structure of the peri-
cardium, and through it may even often extend to the surface of the
pleura covering the sac. The inflammation of those parts tells upon
the nerves distributed to them. The surfaces of the heart and sac,
instead of being smooth and glistening, become dull and velvety;
and fluid is poured out and lymph exudes from the inflamed surfaces.
The liquid in the pericardium increases rapidly. At first it falls
into the back part of the sac, but as it increases in quantity it makes a
space for itself between the floor of the pericardium, which it depresses,
and the lower surface of the heart, which it elevates, and it gradually
distends the pouch in every direction, displacing the lungs to each side
in front, pushing the central tendon of the diaphragm, the stomach,
and the liver downwards, and pressing backwards, when the distension
from the fluid becomes great, upon the bifurcation of the trachea, the
left bronchus, the oesophagus, and the aorta. The fluid at the same
time re-acts upon the heart so as to compress the auricles, the venae
cavse, the pulmonary veins, and the ascending aorta ; and to displace
the apex and body of the organ and its great arteries upwards and
forwards, owing to the extensive interposition of the fluid between the
lower surface of the heart and the floor of the pericardium.

The lymph is poured out upon the surfaces of the heart and the
sac. Where those two surfaces touch each other, the soft lymph is
drawn into threads and little pointed ridges and prominences, and
wrought into a network, so that when ridges or prominences are
present on the heart, ridges or prominences are present on the inner
surface of the pouch lying upon it, and when a network of lymph
covers the heart, a network of lymph lines the corresponding sac,
The constant play of expansion and contraction of the heart alter*

218 A SYSTEM OF MEDICINE.

nately stretches and relaxes its coating of lymph, so that its surface
resembles a honeycomb in structure.

The heart, elevated by the fluid between the under surface of the
ventricles and the base of the pericardium to a degree proportioned
to the amount of the fluid, leaves the broader part of the chest below,
and ascends into the narrower part of the chest above. The lungs,
and especially the left lung, are consequently displaced from before
the swollen sac and the heart, and the front of the right and left ven-
tricles, including the apex and the great arteries, beat with some force
against the higher costal cartilages and intercostal spaces, and the
adjoining portion of the sternum, with which they come into close
contact. Owing to the narrowing compass of the portion of the chest
in which the heart i3 then situated, and the withdrawal of the lung
from before the organ, its impulse is both elevated and widened out-
wards, so that it is felt beating strongly in the second and third,
or third and fourth left spaces, according to the amount of the effu-
sion, the apex-beat being felt above, and beyond the nipple ; instead
of the impulse, as in health, being felt gently in the fourth and fifth
spaces, the apex-beat being within the nipple line. When the peri-
cardium is distended to the utmost, its sac becomes pyramided or
pear-shaped, the apex or narrowest part of the pyramid pointing up-
wards, behind the lower portion of the manubrium and to the left of
it, the base of the pyramid bearing downwards and extending across
the ensiform cartilage from the sixth right costal cartilage to the
lower border of the sixth left cartilage at its attachment to the rib.
The fluid rapidly fills the sac, and often reaches its acme in two,
three, or four days ; but it soon begins to lessen, and in from four
to six additional days it usually returns to its healthy amount. At
the same time the heart descends and comes again in contact with
the lower end of the sternum and the top of the ensiform cartilage,
the fifth space, the sixth costal cartilage, and the diaphragm. In
most instances slight threads of adhesion form between the sac and
portions of the right auricle, and often also between the sac and the
"apex and interventricular septum, that being the portion of the front
of the heart that presents the least movement during the action of
the ventricles. These soft threads of adhesion are generally drawn
out, by the oscillating movements of the heart, until they at length
yield, and break away, but sometimes permanent adhesions form,
which may be partial or universal.

IX. — Over-Action of the Heart in Acute Eheumatism as a
Cause of Endocarditis and Pericarditis; and (in illustra-
tion), Over- Action of the Limbs, Local Injury, and other
Influences, as Causes of Acute Eheumatism with Affection
of the Heart.

In a small number of my cases of rheumatic Pericarditis the
inflammation of the heart commenced soon after laborious, or violent,
action of the organ. t

PERICARDITIS. 219

A woman (12), aged 26, a servant, was attacked, seven days before
admission, with great pain in the soles of her feet. On the following
day the pain continued, and proceeded up the legs to the knees and
hips, so as to confine her to bed. On the third day she was seized
with violent palpitation of the heart, and pain below the lower part of
the sternum. On admission her countenance was flushed and anxious,
the pulse was 160, and there was pain on pressure over the region of
the heart, which was beating with great force. A friction sound was
perceptible at the apex with each beat, but indistinctly, owing to the
violent action of the organ. The breathing was hurried. Eight
leeches were applied over the region of pain, and next day her aspect
was better, the action of the heart was natural, the area of dulness on
percussion over the region of the pericardium was greatly enlarged,
reaching as high as the second cartilage, and friction sound was
audible over the whole front of the heart, where the pain was
only slight. After this the heart's action became feeble, irregular,
and intermittent, but it regained its regularity in eighteen days. The
friction sound lasted for about three weeks, and a mitral murmur
became permanently established.

Another patient (24), already referred to, a labourer, aged 27, came in
with acute rheumatism and endocarditis, presenting first mitral and
then aortic regurgitation, both of which became established. He was
allowed to get up on the 36th day. On the 48th he looked well, but
pain in the hip, a trouble of old standing, had increased in severity.
On the 50th the right side of his face was swollen and flushed, and
he complained much of stiffness in the muscles of the neck, and next
day of great precordial pain and palpitation, the heart acting strongly
and rapidly. On the 52nd he was seized with terrible pain in the
neck and head, and the heart's action was so loud that the endocardial
murmurs were rendered inaudible, and on the 53rd he suffered from
acute pain about the pnecordia, the left cartilages were arched, pre-
cordial dulness extended up to the third space, and a loud and harsh
double friction-sound was heard over the front of the heart. His attack
was of unusual severity, but the rubbing sound had disappeared on the
68th day after his admission, and on the 83rd he was walking about.

A third case (17), a servant girl, aged 20, who was affected with per-
manent mitral disease owing to a previous attack, was admitted on the
fifth day of her illness with severe joint affection, the heart being
rapid and its sounds loud. Next day its action was very tumultuous,
its impulse was strong, and its sounds were ill-defined, loud, and
harsh. Leeches were applied to the chest, and the bleeding from one
of the bites could not be restrained. On the 3rd the sounds of the
heart were softer ; on the 13th the first sound was more rough, on
the 16th the impulse was very much diffused, and a murmur was
audible over the front of the heart, and next day friction sound was
heard over that region and Pericarditis in a severe form was fully
established. After this the heart's action became irregular and inter-
mittent, and she looked and felt anxious and depressed. A long,

2i>() A SYSTEM OF MEDIC [NE.

severe and varying illness followed. On the 55th day she seemed to be
sinking, though she thought herself better. On the 58th day she kept
nothing on her stomach, but on the 59th she felt better and looked
much brighter. Small-pox, however, then in the wards, declared itself
on the 62nd day, and on the 63rd she died.

In the first and second of these cases the heart continued to act
with increased force during the period of the onset of the Peri-
carditis ; but in the first of them this condition gave way after the
application of leeches to irregular action of the heart, which lasted
for eighteen days. In seven or eight other cases the impulse of the
heart was strong during the early period of the inflammation of the
exterior of the heart. As a ride, however, the impulse of the heart
was feeble when first observed during the attack of Pericarditis.
The condition of the impulse of the heart during Pericarditis will,
however, be considered under its proper heading.

If we look at these cases, and especially the first and second of them ;
combine with them the six others already given in which Pericarditis
followed closely upon a relapse in the joint affection, brought on often
by getting up too soon ; and add to these the relation that existed in my
cases of acute rheumatism, between the severity of the joint affection
and the presence, character, and severity of the heart affection, the
joint affection being slight in the majority of cases without signs
of endocarditis, severe in the majority of cases with simple endo-
carditis, and still more severe in the great majority of cases with
Pericarditis and endocarditis ; the severity of the heart affection
corresponding, as a rule, with the severity of the joint affection ; we
must, I consider, conclude that we have here not a mere lifeless chain
of passive links, but a living succession of active events, one giving
birth to the other. Exposure to cold and wet, combined with undue
labour or exertion, give the first impulse, — the start, to the affection
of the joints. When the joint affection is severe, it may call forth
excessive labour or even tumultuous action of the heart. In acute
rheumatism, inflammation attacks the fibrous structures, especially if
those structures are unduly strained, and the increased action of the
heart may therefore, I consider, induce inflammation of the fibrous
tissues of that organ, such inflammation being proportioned in severity
to the augmented action of the heart.

This interesting subject derives larger illustration from the influence,
already considered, of sex, age, and occupation in the production of
acute rheumatism, accompanied, in proportion to the severity of the
affection of the joints, by inflammation of the heart within and without
I need only here again refer to the large number of young female
servants, in whom the ends and shafts of the bone are as yet only
united by cartilage, who are attacked by acute rheumatism in a
severe form ; and the very large proportion in which those cases have
endocarditis or Pericarditis, or both, the heart being subject, in those
overworked young women, to undue action and palpitation.

PERICARDITIS. 221

In illustration of the influence of over-action of the heart in pro-
ducing inflammation of the interior and the exterior of that organ, I
shall give here a brief summary of the influence of local injury,
scarlet fever, chorea, abscess, and general illness in the production of
acute rheumatism with endocarditis and Pericarditis, including those
cases of acute rheumatism in which a relapse of the joint affection,
followed by Pericarditis, was induced by the too early use of the
limbs, when the recovery was almost but not quite perfect.

Two influences usually combine to produce acute rheumatism ; one,
exposure to wet and cold ; the other, the over-use of certain limbs and
joints. The part immediately in use is usually the part first attacked,
while the joints that take the greatest share in the permanent
labour of the patient are generally those visited by the disease with
the greatest severity and duration. Thus, among the coachmen
admitted under my care, one was first attacked in the right thumb,
the knees being afterwards affected ; another was seized badly in the
right arm, and then in the left ; a third in the wrist and hands ; and
u fourth in the hands, and especially the middle finger, the arms, and
then the knees, the affection of the fingers being obstinate ; in a fifth
the back and hips were the seat of pain ; and in the sixth the ankles,
knees, hands, and hips were all involved. If we take the carpenters,
we find that one of them was attacked in the arms, wrists, and
elbows ; another, who was in search of work, in the arms, back,
ankles, and knees ; and a third was seized, when walking, with pain in
the knees, the ankles, shoulders and arms being afterwards affected.
Young female servants, for to them I must here again refer, who
usually work too hard, whose joints are not yet perfect, being still
in a state of active growth, are for the most Dart first attacked in
the feet and ankles, that is to say, the parts that more immediately
tread the ground. The knees usually then surfer, or perhaps earlier,
at the same time as the feet and ankles ; and afterwards the wrists,
hands, arms and shoulders, in succession, share in the affection. The
knees, which generally bear not only the internal pressure of standing,
but also the external pressure of kneeling when at work, are, as a
rule, more constantly and deeply affected, and for a longer period,
than any other joint. The effect of past labour is, so to speak,
stored up in the knees, which are therefore in these cases more affected
in acute rheumatism than any other joint.

Under the combiued influence, then, of exposure and overwork,
rheumatic inflammation is set up in the joints, and under the com-
bined influence of the disease thus established, and overwork of the
heart, rheumatic inflammation is established in that organ.

In a small but important group of my cases, acute rheumatism
followed local injury. The' first of these, a stonemason, fell from a
scaffold on his back. He had pain in his back and legs, and could
not stand. On the 5th day he had a profuse sour perspiration, and
his finger and elbow-joints were red, swollen, and paiuful. The hips,
knees, and shoulders were afterwards attacked, and he probably had

222 A SYSTEM OF MEDICINE.

endocarditis, the first sound being prolonged, while the second was
followed by a soft murmur. The second patient was admitted under
Mr. Lane's care for a slight injury, and was attacked on the fourth
day with pain in the chest and inflammation of the wrist and ankles.
On the 7th he was transferred to my charge with acute rheuma-
tism, mitral murmur, and Pericarditis. A third patient, a dustman,
hurt his back by carrying a sack of flour. The pain in the back was in-
creased by his getting wet ; and this was followed by acute rheumatism.
A fourth patient was attacked with the disease in the wrists 32 days
after breaking his leg. A fifth came in with acute rheumatism five
days after leaving the surgical ward ; and a sixth, who was admitted
with endocarditis and transient Pericarditis, had received a kick in the
groin five weeks previously, and since then had been subject to pain
in the loins. In some of these cases the disease appeared to be
directly, and in others to be indirectly, caused by local injury.

These cases and others given below are allied to those previously
given, in which the too early use of a limb, during the period of
convalescence from acute rheumatism, produced inflammation in
the used joint, a relapse of the affection in the other joints, endocarditis
and Pericarditis, ending in permanent crippling of the valves of
the heart. The whole of these results, the latter of them so perma-
nently injurious, started from the renewed focus of the disease in
the single joint thus affected for the second time.

Through what means is this diffusion and transmission of the
disease effected ? Is it by a blood poison ? Is it by a change in the
fibrous structures of the limbs and the heart ? Or is it by reflex
influences, transmitted through the afferent nerves, locally acted upon
in the inflamed joint or injured part, and sent back through the vaso-
motor or other nerves distributed to the fibrous structures of the
joints and the heart ? The local character of the injury inducing this
general effect, and the quickness with which the effect is induced,
would appear to forbid the material agency of either blood poison or
change in the tissues ; and would tend to throw us upon the trans-
missioii of influences through the nerves for an explanation of these
remarkable effects, — effects not less remarkable, but rather more so,
that they are open to daily observation ; or must we look for some
other explanation than any of these here suggested ?

We cannot, however, limit ourselves to the points of view just
sketched in our inquiry into that many-sided disease, acute rheuma-
tism, with its attendant inflammation of the heart ; and I would
here briefly state the other influences that have been apparently at
work in the origin of the disease, besides overwork and exposure on
the one hand, and local injury on the other.

In three of my patients the disease was associated with scarlet
fever, one of whom had Pericarditis in the hospital, one out of it.
The latter was the son of a medical friend, who detected symptoms of
acute rheumatism just as the scarlet fever was declaring itself, and by
which the acute rheumatism was suspended. When, however, the

PEBICARBITIS. 223

eruption had ceased and desquamation was going on, endocarditis and
Pericarditis, the offspring of the original rheumatism, declared them-
selves. This case did well, and though a mitral murmur existed for
some time, it at length disappeared. In the two other cases, acute
rheumatism followed a chill caught by too early exposure after the
scarlet fever had disappeared.

In several of my cases, chorea has given place to acute rheumatism
or the reverse. In one patient, a girl, acute rheumatism passed into
ehorea, for -yhich she was admitted. After a time the choreal move-
ments were for a period suspended by the renewal of acute rheumatism.
I do not here speak of that terrible complication, the occurrence of
serious local choreal and tetaniform symptoms in connection with
rheumatic endocarditis and Pericarditis, complications to which I
shall soon refer.

In three patients the acute rheumatism was preceded by recent
abscess, in one of them in the axilla, in another in the perineum, and
in a third in the tonsil ; and in a fourth case, abscess in the neck
existed sometime before the supervention of the rheumatism.

Sore throat appeared for from one day to three weeks before the
occurrence of acute rheumatism in tliirteen cases, including the
case of abscess in the tonsil just quoted. Two of these patients had
Pericarditis ; three had simple endocarditis ; in three endocarditis was
threatened ; and live gave no sign of heart affection.

In eleven patients, pain in the chest, sometimes accompanied by
cough, existed for from one day to two or even three weeks before the
developement of acute rheumatism.

I refrain from pursuing this important collateral subject farther in
this place.

X.— Pain.

I.— Pain over the Region of the Heart and Pericardium.

Pain over the region of the heart and pericardium showed itself in
six different ways : 1. Over the front of the organ ; 2. On pressure
at the same place ; 3. In the Epigastrium, chiefly on pressure ;
4. Over the back of the heart, when it was excited by swallowing
and by eructation ; 5. After eating ; and, 6. Pain shooting through
the heart, evidently anginal in character.

1. The pain over the front of the heart extended usually from the
right of the sternum at its lower two-thirds to the left nipple ; it was
more or less continuous, and was complained of in three-fourths of
the cases (48 in 63). This pain came on in one-fourth of the patients
affected wTith it (9) before the friction sound was heard, and in a
greater number (16, including 5 in which the pain and the friction
sound were both present on the day of admission) at the time that
the sound was first audible. In a few instances (7) it was felt
soon after the appearance of the rubbing sound. It was either
relieved, suspended, or removed by the application of leeches. It

224 A SYSTEM OF MEDICINE.

was complained of in about one-fourth of the cases (8) at the
time the effusion was at its height, but usually relief, which was per-
manent, came at that time. In two instances (15, 51) of relapse,
the second, and in one (44a) even a third, wave of increase of peri-
cardial effusion was preceded by a second, and in one even a third
attack of pain over the heart ; but in three cases the pain came late
in the period of the relapse, and when the effusion was declining. In
scarcely any instance did the pain over the heart continue during the
whole period of the duration of the friction sound, and in only two
or three of the cases did it last over the first half of that period.
When the pain comes on with the first blush of the inflammation on
the surface of the heart, before it has spread to the inner surface of
the pericardial sac, and before friction sound is audible, it may be
inferred that it is seated in the sentient nerves distributed to the
surface of the heart When, however, the pain strikes over the heart
at the same time as the appearance of the friction sound, and still
more when it comes on at a later period, it is generally, I believe,
seated in the pericardial sac, and especially in the pleura covering
the sac.

The accompanying table gives a resume of the period of the occur-
rence of pain over the region of the heart in relation to the time of
the appearance of friction sound in the cases of Pericarditis (see
page 225).

2. If the pain over the heart is increased or excited by pressure
over the region of the organ, it may, with an approach to certainty,
be attributed to inflammation of the pleura, especially if the pain on
pressure is complained of, not before, but at the time of or after the
first presence of friction sound.

Pain on pressure over the heart occurred in one-fourth (14 in 63) of
the whole number of cases affected with acute rheumatism, and in
one-third of those who suffered from continuous pain in the region
of the heart (11 in 38). In two only of these cases was the pain
excited by pressure before the friction sound was audible, and in
these the pain was probably excited over the surface of the inflamed
heart. In one-half of the patients the pain on pressure and the rub-
bing sound appeared on the same day, and in the rest the pain was
preceded by the friction sound. In most or all of these cases, the pleura
covering the pericardial sac, or the fibrous structure of the sac itself,
was the probable seat of the suffering (see Tables, pages 225, 226).

In one-half of those patients (7 in 14) the skin over the region
of the pericardium was tender and sensitive, so much so indeed, in
some instances, as to forbid the slightest manipulation over the chest,
and to make a proper examination of the heart impossible until this
exquisite sensibility was subdued by the application of leeches or
of belladonna liniment with chloroform.

In the majority of the cases the pain was deeper than the skin, and
was not excited unless actual pressure was made. In three of the
patients the pain was only felt when pressure was made over the

PSRlCAMJITfH, 2»

region of the heart; but in all the others continuous pain already
uxUted over that region, and was intensified by the pressure. In one
or two instances the suffering and distress over the lieait were so
great as to drown all other complaints ; but in three others, as I have
just said, the pain was only brought into play when pressure was
exerted. Between these two opposite extremes, there was every
shade in the extent, variety, and constancy of the pain.

Period of Ou occurrence of Pain
to the time of the appearaat

over the region of At Heart tmd Pericardium in relat
of Friction Sound in cane* of Rheumatic PnicardUit.

** ' H

aaartsiiraasa

" hm,TeJ

\\3*

Pain over heart o and friction sound oil

Appearing lie fore
flic t ton sound .

day of admission

■ 1 '

P*in Over epigastrium and friction J
sound od day of (in one day alter) |

Appearing same

time as friction

admission, included nliove . . !

sound ....

Pain over heart Q before admission, )

Appearing after
first indication

friction Round on admission . . (

Paiu over heart O before appearance 1

of friction sound

Appearing after
friction sound

Pain over epigastrium before api>ear' i

ance of friction sound, included/

Pain over heart cj and friction sound 1

! J"

-i

1 14

occurring on same da; .... J
Pain over epigastrium, and friction 1

sound occurring an same day, not >

included abovo 1

Pain over heart V coming on after j

friction sound had bean observed j

Pain over epigastrium coming on i

after friction sound had been, oil- ■

served, not included above . . \

Ditto, included nboro . . . .

Paiu over heart 9 appearing shortly 1

before relapse (renewed increase off
fluid in the pericardium) not in- (

1 Explanation if Symbol*.

Paiu over epigastrium liefore relapse .
Paiu over heart t? late in period of j

1.
1

'-» mltiat regurgitation.
; X sortie regurgitation.

relajue, not included above . . j

_ 1 pnltial-aartlc tiKurglU-

Pain over heart Pat the time of acme i

„

at Pfcricarditi* \

Pain over heart 0 shortly before time )

of acme of Pericarditis . . . \

Pain or epigastrium at time of acme 1

of Pericarditis f

Ditto before mum of Pericarditis1 .' .

Ditto after acme of Pericarditis . .

826 A SYSTEM OF MEDICINE.

Tablt shoving the proportion in which Pain teas present over the region of I

Heart ej, in the Side, and in the Chest, in 326 cases of Acute Rheumatism.

(This table ia continued on tins following two pages.)

CASF.S WITH pKHICAJiWTIR.

Explanation of Symbols.
<— tricuspid regurgitation.
-* mltnl regurgitation.
J, sortio regurgitation
-*^ mltral-sortic resurgltstion.

•»)""

Psln on pressure owi thel'ncluded

l»art Winch

Pain thooling through the heart, inclu
P.ln in the Piiigiiilric *|-!H'e [in-tll.lfii :
(Faineeitrd llL |.Hk-nli!iiji:il|,.,,, ;,, .],.,

Piin Id the abdomen. Fatal ,„,
not uotatl In epigastrium ./""

Pain it hick of pericardium,! , . , ,
from twsiiuHlng . . . _ j-'in-iu-iL-Li

pn.^'r!\?'^rici^BnMinduded

Piill in back of pfrii'nHiiiii

Tot.l cum with pain in thereiiion oftbe heart Q
»nd pericardium, including lli« SUhMsMBr

Painof.Uls ,in,tu.l,,,,w,

I not included si

u .. right elde Id .

■ i „ both tn right >nd left tic

■■ ,. or uncertain situation

Pnln of -heit i 'BL'lllded abon

Leeches to region nf heart, i included obovi

without note of pain . -(ncHncludsdsboi
Tightncw of chat, without i imludednbovo

■\xol Included sbo<

OR and TOTAL

it I

g
I

: - --

S" i

-;i^

3 Flit

PERICARDITIS. 827

mtinned from p. 226) showing the proportion in tckieh Pain wai praent over the

ttrt \iuil Included ■!>

mclud~! a\

III. :■.;■(■.! ill

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PERICARDITIS.

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230 A SYSTEM OF MEDICINE.

3. Pain was present over the epigastric region, frequently increased
and sometimes induced by pressure, in one-fourth of the patients with
rheumatic pericarditis (16 in 63), and in nearly two-fifths of those
who suffered from pain over the region of the heart (14 in 38). It
would appear curious, at first sight, that pain ovei the pit of the
stomach should be a marked feature in so many cases of pericarditis.
When, however, we consider that in health the lower boundary of the
heart is situated behind the upper third of the ensiform cartilage, and
that the pericardial sac, when distended with fluid in Pericarditis,
dips downwards so that its lower boundary may be on a level with
the point of that cartilage, or perhaps even below it, we see how
natural it is that pain should be excited by pressure over the epi-
gastric region (see Tables, pages 225-229).

This epigastric pain appeared in only two cases before the super-
vention of friction sound. Those two patients, however, suffered from
a renewal of the pain after the commencement of the rubbing sound,
consequently in every case the suffering over the pit of the stomach
was complained of either at the time of the first observation of the
friction sound (7 in 16, including 4 in which the pain and the fric-
tion sound were both present on the day of admission), or from one
to several days later (9 in 16).

In one-third of the cases (6) the epigastric pain appeared at
the time when the effusion into the pericardium was at its height,
and when the sac bulged downwards into the epigastric space ; and in
four of them it was complained of before, and in four of them after,
the effusion had reached its acme.

In all these cases the disease had reached a stage in which the
heart was separated by the intervention of fluid from the floor
of the pericardial sac, which is formed by the central tendon of the
diaphragm. The pain in the epigastric region in these cases, espe-
cially when it is increased or excited by pressure, is therefore seated
not in the surface of the heart, but in the lower portion of the peri-
cardial sac. It is natural to suppose that the branches of the phrenic
nerve must be the immediate seat of the pain, but the exact
anatomical distribution of the phrenic nerve has not yet been ascer-
tained. These questions suggest themselves : is this pain seated in
the fibrous tissue, the pericardial surface, or the peritoneal surface
of the affected diaphragmatic portion of the sac ?

Peritonitis affecting the central tendon of the diaphragm has been
noticed in few or no fatal cases of Pericarditis, but indirect evidence
of its existence has been supplied in rare instances by the dis-
covery of partial adhesions of the spleen and liver to the diaphragm
in cases with adherent pericardium. We may, however, 1 think, fairly
infer that the pain on pressure below or at the side of the ensiform carti-
lage is in these cases due, not to peritonitis, but to inflammation of the
fibrous structure and pericardial or inner surface of the central tendon
of the diaphragm, where it forms the floor of the pericardial sac, and
the lower and anterior portion of that sac.

PERICARDITIS. 231

The distribution of the nerves to the pericardium, like that of the
phrenic nerve, has not yet been ascertained, and this interesting
clinical question therefore invites the attention of the physiologist.

4. In three of the patients affected with rheumatic Pericarditis
deep pain was felt between the shoulder-blades, and in one of them
this pain was increased by the act of swallowing. Pain in the chest
was excited in three cases by swallowing, and in two others it was
complained of there after eating. Another patient complained that
the ascent of wind from the stomach gave much pain over the pos-
terior region of the heart. In all these instances, amounting to nine,
the suffering must have been seated in the back of the inflameid
pericardium, being either constant or induced by local pressure, due
to swallowing or eructation. In several other cases it is stated that
pain was seated in the back, but it is impossible to say, from this
description, whether the pain was situated in or near the pericardium
or lower down.

5. Pain and fulness after eating was complained of by one patient,
and I think it likely that the suffering in this instance was excited by
the pressure made by the distended stomach over the lower and back
part of the pericardium.

We thus see that in a large proportion of my cases affected with
rheumatic Pericarditis, pain was felt over the heart, frequently in
front of the pericardial sac, and occasionally behind and below it,
the pain being usually fixed, sometimes increased by pressure, and
less often excited by it.

6. The heart itself was attacked with a shooting pain, more or less
violent, associated either with faintness or failure in the action of
the organ, and evidently anginal in character, in four of my patients
affected with rheumatic Pericarditis.

In two of these cases the heart, already crippled by valvular
disease, was attacked with inflammation within and without, but in
the others the Pericarditis and endocarditis seized upon the virgin
heart, the valves being previously healthy ; one of these two cases
proved fatal, and in the other valvular disease became established.

In the fatal case (4). a man, aged 27, a carpenter, a darting pain
passed now and then from the heart to the right side on the day of
his admission. This pain was relieved by leeches, the application
of which was followed by faintness. On the 3rd his limbs started
when he fell asleep ; on the 6th he was seized with delirium and
trembling ; and on the 7th, the day of his death, he was noisy and
restless, and was continually moving his lower jaw.

Another patient (15), a servant girl, suddenly became very faint
on the evening of the 10th day, when she was suffering from a re-
lapse of Pericarditis, and was attacked with great pain over the heart
This pain returned on the evening of the 12th, when it was also
felt between the shoulders.

One (3) of the two remaining patients had old standing aortic and
mitral disease, and suffered from pain over the region of the heart on

«232 A SYSTEM OF MEDICINE.

the 10th day, when friction-sound appeared. On the 16th day, when
the Pericarditis was at its height, when I was examining him, he cried
out as if from pain, beginning over the stomach, and begged to be
raised up, the dyspnoea becoming extreme, the face being flushed,
the perspiration pouring off it, the lips somewhat livid, and his
countenance being expressive of extreme anxiety. He was imme-
diately raised up, and, having a towel placed behind him, was as it
were slung in it, when he took a little port wine and fell asleep.

The other patient (17), a young woman, affected with old mitral
disease, was attacked on the 17th day, when the Pericarditis was at
its acme, with great pain over the sternum and the whole front of the
chest, the pain passing through to the back. She ultimately died on
the 63rd day, with small-pox, which attacked her when in a state of
extreme exhaustion.

If we add to the cases in which there was continuous pain over the
region of the heart (38), those others not so affected in which a, there
was pain on pressure over the heart (3) ; 6, pain over the epigastric
region (2) ; and c, pain at the back of the pericardium on eructation (1);
we find that in 44 of the 63 cases of Pericarditis, or in 70 per cent.,
there was pain over the heart or pericardium.

II.— pLKi'KiTir Pain in tub Side.

Pain in the side was complained of in one-half of the cases of
rheumatic Pericarditis (31 in 63). Pain was present over the region
of the heart and pericardium also in all but 4 of these patients.
The pain was limited to the left side in 19 cases, and to the right in
only 5, while it attacked both sides in 6 instances. There were,
besides the pain, other symptoms or physical signs of pleurisy in
all but seven of the patients thus affected.

Pleuritic friction sound was heard in nearly one-half of those
cases (15 in 31) and in five others there was tenderness on per-
cussion over the seat of pain. In a large proportion of the cases the
pain was increased or excited by a deep breath (18 in 31j, and in
four of these it was catching. The pain was induced by coughin<
or laughing, stooping or moving in fourteen instances, and in thre<
it was " pleuritic " or cutting.

The first complaint of pain in the side was made after the appear-
ance of the friction sound in 19 of the 31 cases that suffered in this
manner ; the pain and the friction sound appeared together in seven
patients; and the pain occurred before the friction sound in five. In
one, of the five, and three of the seven patients just spoken of. the
pain affected both sides, having appeared at a late period in one side,
and at a period actually or comparatively early in the other.

The pleurisy that induced the pain in the side which came into

PERICARDITIS. 233

play either with or after the friction sound, was due to two causes ;
one the extension of the inflammation through the fibrous structure
of the pericardium to the pleura covering it; the other, the occurrence
of pulmonary apoplexy with its attendant pleurisy.

The more frequent appearance of the pain, and the greater spread
of the pleurisy on the left side of the chest than the right, is, 1 con-
ceive, due in many instances to the greater extent to which the
inflamed pericardium occupies the left side of the chest than the
right, and the great displacement backward of the left lung, and
especially its lower lobe, by the distension of the pericardial sac.
Perhaps the pressure of the distended pericardium on the left bronchus
increases the tendency of the left lung to inflammation.

In one of the five patients that were seized with pain in the side
before the supervention of the friction sound, the pain came on at
the first onset of the disease, and at the same time as the affection of
the joints three days before admission. I think it likely that this
case was attacked with pleurisy and acute rheumatism affecting the
joints at the same time , the pleurisy being, however, rheumatic in
its nature, like the joint affection in this instance, and like the Peri-
carditis in the other cases. We may have, in short, in these cases,
rheumatic pleurisy, just as we may have rheumatic Pericarditis.

In another of these cases (20), the patient, a married woman, aged 24,
was attacked with pain in the joints the day after being wet through,
and a week before admission. She came in with very severe pain in
the left side, which had. existed for some days, and which was some-
what reduced by leeching. On the 6th day after admission she suffered
much in the left side, and a pleuritic friction sound was audible
just below the seat of pain. Friction sound from Pericarditis was
heard over the region of the heart for the first time on the same day.
In this case the pleurisy preceded the Pericarditis by ten days.

Pain in the side was, in proportion, twice as frequent in Pericarditis
usually accompanied with endocarditis as in simple endocarditis ;
one-fourth of the latter (26 in 108), and as we have just seen,
one-half of the former (31 in 63) being thus affected. A similar pro-
portion of such cases existed among the patients who were threat-
ened with endocarditis, of whom rather more than one-fourth were
affected with pain in the side (17 in 63). None of the thirteen cases
classed under the heading of "probable endocarditis" suffered from pain
in the side, and only three of those who were attacked with acute rheu-
matism and had no endocarditis, complained of pain in that region
(3 in 71). The pain more frequently attacked the left side than the
right in the cases of endocarditis in the proportion of 14 to 6 ; but
among those threatened with endocarditis, the two 3ides were affected
in nearly equal numbers, the right side being rather more often attacked
than the left in the proportion of 7 to 6.

234 A SYSTEM OF MEDICINE

III. — "Pain in the Chest."

"Pain in the chest" was present in 30 of the 63 cases of rheumatic
Pericarditis. The pain thus described is so indefinite in situation —
that it may be seated either at the centre of the chest or at its sides,
either over the pericardium or the pleura. Fortunately, to guide us
to the actual seat of suffering, the " pain in the chest " was attended
in all but two instances with other pain, either over the heart, or in
the side, or in both regions. Thus in all but four of the thirty
cases, pain was present over the region of the heart or the epigastrium ;
in all but nine, in the side ; and in one-half of them (16 in 30)
it was situated both over the heart and in the side.

In fully one-half of the cases (17 in 30) the pain in the chest was
itself associated with symptoms of pleurisy, in the way of being in-
creased or caused by deep breathing, or coughing, or moving, or it was
a cutting pain, or it was accompanied, in two instances only, by
pleuritic friction sound. There were symptoms of pleurisy in eight of
the nine cases in which pain of the chest was not associated with
pain of the side, and I think those eight cases may be added to the
31 in which pain in the side was actually present, thus bringing their
number up to 39 in 63 cases of rheumatic Pericarditis. On the other
hand, there were four cases with pain in the chest in which there was
no notice of pain in the heart, and I think that these four cases may
probably be added to those in which the presence of cardiac pain is
stated ; thus bringing the total number so affected up from 44 to
48 in 63.

Eleven patients suffered from pain in the chest, either previously to
admission or before friction sound was audible. In the greater
number of these I think that the pain was seated over the region of
the heart, and was not due to pleurisy. And I find, giving strength
to this view, that in all of these but two, pain was described as being
present over the heart.

It would be futile to compare the relative frequency of pain in the
chest in Pericarditis, and in the other various groups of cases in acute
rheumatism, since to do so would be to compare unlike conditions
under the same name. But it will be instructive to compare the
proportion of cases attacked with pain over the heart, in the side
and in the chest, combined together, with those in which there was
no such pain, in cases of acute rheumatism with Pericarditis and
endocarditis, and with and without simple endocarditis. The accom-
panying table, and graphic scheme, will show this comparison, the one
by study, the other at a glance (see pages 225—229).

In those affected with Pericarditis, most of whom had endocarditis
also, four-fifths had pain in the heart, chest, or side, and one-fifth
had no such pain ; in those with endocarditis nearly six-tenths had
such pain and over four-tenths had none ; in those threatened with
endocarditis, less than one-half had pain, and more than one-half had

PERICARDITIS. 235

none ; and in those who gave no sign of endocarditis only one-tenth
suffered from this kind of pain, and nine-tenths had no internal
pain, thus nearly reversing the proportion that we find in cases
affected with Pericarditis.

XL Irbegularity axd Failure of the Action of the Heart.

Faintness.

We have already seen that in two of the patients, in whom the
action of the heart, which was powerful and tumultuous before the
occurrence of Pericarditis, became at a later period feeble, irregular,
and intermittent, this state being accompanied by a look of great anxiety
and depression. We have also seen that the four patients who were
attacked with pain shooting through the heart, experienced faintness or
failure in the action of the organ (p. 231).

In the following case (13) death took place from syncope. A female
servant, aged 25, came in on the 7th day of her illness, with difficult,
hurried breathing, which was relieved when she was raised, great pain
in her chest, cough, which had continued from the 2nd day of the
attack, mucous rattle, slightly rusty phlegm, a sensation of choking,
difficulty in swallowing, and great anxiety. The joint affection was
slight, and apparently limited to the shoulder. Pericarditis, with friction
sound and great effusion, was at its height. She was very ill throughout,
perspiration being profuse, the voice husky, the face flushed and
anxious, and breathing laborious. Her face was brighter, and she
breathed with ease from the 7th day to the 13th, when her appetite
was improving ; but at two hours after midnight, in the early morning
of the 14th, when attempting to turn on her side, she became quite
pulseless, her face turned livid, and she frothed at the mouth. After
taking some wine she gradually recovered. An hour later the sounds
of the heart were murlled, and the rubbing noise, which had been
harsh, loud and dry on the previous day, could not be detected. In
another hour she had a similar attack, in which she died. There were
18 ounces of fluid in the pericardium, the heart was covered with
honeycomb lymph, and there were patches of pulmonary apoplexy
in the left upper lobe.

Faintness occurred as a symptom in several of the cases, but in
none, besides those alluded to and that just given, did it appear in a
threatening form.

Although, as we have already seen, in a few cases the action of the
heart was unusually strong during the early period of Pericarditis, yet
even then, or rather when the attack was first observed, the impulse
of the heart was more frequently feeble than strong, and this was
especially the case during the remaining course of the affection.

Feebleness, irregularity, and even failure of the heart's action,may evi-
dently be induced in these cases by several influences working separately
or together, and by the exhaustion of the nervous and general forces

236 A SYSTEM OF MEDICINE.

induced by the accumulated effect of those influences, all tending to
lower and exhaust the power of the heart, and even, as in the case just
told, to arrest its action. Among such influences are, the pain and
inflammation "of the joints when severe, extensive, and prolonged ; the
paiu in the heart and pericardium, the side, and the chest ; the ex-
istence of endocarditis with its immediate and remote consequences ;
the presence of previous valvular disease ; the grave influences exerted
by great distension of the pericardium, which, — by compressing the
venae cavae, the pulmonary veins, both auricles, and the aorta, impedes
the supply of blood through the venae cavae and pulmonary veins to
both sides of the heart, and through the aorta to the system, and
causes the accumulation of blood in the lungs, — by pressing upon the
bifurcation of the trachea and the left bronchus, and by lessening the
size of the lungs, seriously embarrasses respiration — and by compress-
ing the oesophagus, renders deglutition difficult ; and the existence of
congestion of the lungs, of pulmonary apoplexy and pleurisy, due to
one or more of the causes just named.

Besides these, there are two important influences that may induce
feebleness, irregularity, and perhaps even failure of the action of the
heart ; one, the inflammation of the superficial muscular fibres of the
heart ; the other, the inflammation of the nerves situated at the sur-
face of the heart and great vessels. Inflammation of the superficial
muscular fibres of the heart, which sometimes occurs in pericarditis,
paralyses the affected fibres. This paralysis of the inflamed fibres must
in itself embarrass the action of the heart, especially when we consider
that those superficial fibres turn inwards by a double entrance at the
apex, to become the innermost fibres of the left ventricle, where they
end in the papillary muscles of the mitral valve. But this influence
cannot be limited to those fibres, but must extend in a varying degree
to the other muscular structures of the organ so as to interfere with the
exercise of their power ; just as inflammation of certain limited fibres
of a voluntary muscle, say the biceps, while it paralyses those fibres,
interferes with the exercise of the whole muscle.

The many and important nerves situated at the surface of the
heart and great vessels may be more or less involved in the inflamma-
tion affecting those parts in Pericarditis. That accurate physiologist,
Dr. Burdon Sanderson, remarks, " that nothing is known either as to
the anatomical distribution of nervous elements in the hearts of mam-
malia, or as to the functions which they perform." l When, however, we
consider that electrical or other excitation of the vagus retards the con-
tractions of the heart, and if it is strong enough, arrests the organ in
diastole, and in the dog, lessens arterial pressure, while division of the
vagi produces acceleration of the contractions of the heart, and in
the dog, increased arterial pressure ; that the lower cervical ganglion
of the sympathetic exercises an accelerating influence, not always in
action, on the contractions of the heart ; and that in the frog, the
ganglion cells contained in the heart are the springs of its automatic

1 Handbook for the Physiological Laboratory, ]>. 26U.

PERICARDITIS. 237

movement ; and that the surface of the heart is rich in nerves con-
nected with the vagi, the sympathetic and the intrinsic ganglia of
the heart, and that those nerves are therefore locally affected by the
inflammation in Pericarditis ; we must, I consider, conclude that this
affection exercises in such cases an important influence, either to
stimulate or to injure those nerves and so to accelerate or retard the
contractions of the heart, to excite or, more frequently, depress the
powers of the organ, and to increase or diminish arterial pressure.
It is for the physiologist to ascertain, by direct experiment, the effect
of the inflammation or irritation of those nerves on the functions of
the heart.

It is right that I should mention another depressing influence on
the action of the heart in Pericarditis, accidentally due, in the case
about to be referred to, to treatment. In one case (17) already given
at page 219, the loss of blood due to irrepressible haemorrhage from
a leech-bite seemed to produce serious irregularity of the action of
the heart.

XII. Difficult and Quickened Respiration.

Kespiration was disturbed to a marked degree in 49 of the 63 patients
affected with rheumatic Pericarditis ; it was slightly or not at all
affected in 3, and in 1 1 its character was not recorded. The Pericar-
ditis was severe in 2 only of the 11 cases in which the state of the
respiration was not noticed, and in none of the 3 in which the breathing
was but slightly affected ; but the attack was severe in 37 of the 49
patients in whom the respiration was markedly disturbed.

The respiration was rendered difficult and quick by three or four
local causes: first,. in order of time, the inflammation of the heart,
without and within, and of the pericardial sac, including the central
tendon of the diaphragm, and the accompanying pain in the heart,
the sac, and the diaphragm, with the consequent restraint imposed
upon the movements of the latter ; after this, the distension of the
pericardial sac with fluid, which greatly enhanced the severity of the
symptoms ; and, at a later period, the supervention of pleurisy with
its attendant permanent pain and stitch in the side, or of pulmonary
apoplexy, often accompanied by pleurisy. The breathing is hurried,
and rendered laborious by distension of the pericardium, often so as
to demand a raised posture, owing to two causes, one, the encroach-
ment of the swollen sac upon both lungs, and especially upon the
lower lobe of the left one ; the other, the direct pressure, backwards
and upwards, exerted by the fluid in the tense pericardium on the
trachea at its bifurcation, and on the left bronchus, a pressure that is
materially relieved by the erect posture, and still more by the forward
attitude which throws the volume of the liquid forwards and downwards
towards the diaphragm and away from the trachea.

There was great distress, difficulty, and rapidity of respiration in
24 of the cases of rheumatic Pericarditis, ami in one-half of them it

238 A SYSTEM OF MEDICINE.

. is recorded that the patient was raised or propped up. The attack
was fatal in 4 of those patients, and severe in 18, being very severe
in 11.

One of those cases (3), a sawyer, aged 26, who had aortic and mitral
valve-disease of old standing, came in feeling low and anxious, and
was delirious at night. On the 5th day he was better, the respirations
being 20 in the minute; but on the 10th he had pain and friction
sound over the heart, and the respirations rose to 30 in the minute.
The dulness over the pericardium increased, and reached its acme on
the 19th. ~*On the 16th he was seized with extreme and urgent
dyspnoea, which was relieved when he was raised. The respirations
were 70 during the attack, and fell after it to 35 ; on the 18th they
varied from 36 to 44, and on the 21st, when the pericardial dulness
had greatly lessened, they had fallen to 28 in the minute.

A man (24), whose case I have already given, had Pericarditis with
rubbing sound, on the 53rd day, the pericardial effusion being at its
height on the 57th. On the 55th the respirations were 44 in the
minute, and he had extreme difficulty in breathing, which was relieved
by the upright posture. On the 58th the pericardial effusion had
lessened, the respirations had fallen to 24, and he breathed easily in
the recumbent posture.

Another patient (36), a servant girl, breathed 32 times in a minute on
admission, as well as on the 7th day when leeches were applied over the
region of the heart On the 8th friction sound appeared, and the
effusion was at its height next day, when the respirations were 52,
and on the 10th her head and shoulders were propped up. On the
11th the effusion had lessened, and her breathings numbered 40. On
the 14th there was pleuritic pain, followed by friction sound, and
the respirations rose to 48 ; but on the 20th, when there was no
pain in the chest, they had fallen to 24.

In the following case (38), a female servant, the breathing rose in fre-
quency a second time during a second wave of increased pericardial
effusion. On the Cth the respirations were 28 in the minute ; on the
7th they were 40 ; on the 9th friction sound was heard over the heart,
and on the 10th the pericardial dulness was at its height. On the
12th the effusion had lessened ; she was in a raised position breathing
more freely, 40 times in a minute; but on the 17th the fluid in the
pericardium had again attained to the full; she had pulmonary
apoplexy and pleurisy, and the respirations mounted up to 66 ; but
next day, with a renewed diminution of the fluid, there was a renewed
lowering of the respirations to 44.

I would gladly illustrate this point by additional cases, but shall
limit myself to one more instance (55) that shows the effect on
the breathing of pulmonary apoplexy and pleurisy in cases of rheu-
matic Pericarditis. A young man was admitted with pain in the
chest and shortness of breath. On the second day friction sound
was heard, and pericardial effusion had already reached its acme;
leeches gave relief, and the breathing was more free; but on the

PERICARDITIS. 239

6th he had a stitch in the side, and the respirations numbered 60
in the minute ; on the 8th, when he was easier, they were 46 ; but on
the 13th pulmonary apoplexy was established, and they had risen to
72. On the 17th he had diphtheria, the respirations being 50 ; on
the 28th this was nearly well, and he raised little phlegm, the respi-
rations being 36, and on the 35th they were 28.

We thus see that with pain over the heart and pericardium, the
breathing is hurried and distressed, while it is slackened and relieved
with the relief of the suffering ; that with the rise and fall of Peri-
carditis, with the increase, the acme, and the decline of peri-
cardial effusion, we have an increase, an acme, and a decline in the
number of the respirations ; that a second wave of increase in the
amount of pericardial effusion, leads to a second wave of increase in
the number of the respirations; and that the respirations are also
again accelerated, if, in the later progress of the case, pleurisy should
spring up from the spreading of the pericardial inflammation ; or if
pulmonary apoplexy should declare itself, especially if combined, as it
usually is, with notable pleurisy.

XIII. Difficulty in Swallowing.

There was difficulty or pain in swallowing in 13 of my cases of
rheumatic Pericarditis.

I have already spoken of cases in which the act of deglutition
caused pain over the back of the inflamed pericardium, generally
complained of, however, in the chest* by the pressure of the morsel
of food upon the inflamed structures during its descent along the
oesophagus, where it passes behind the affected region.

The difficulty in swallowing, of which I now speak, occurs when
the pericardial sac is distended to the full with fluid, and is caused by
the compression of the oesophagus between the swollen sac and
the spinal column. When the effused fluid lessens, the pressure
diminishes, and swallowing becomes easy; but it becomes again
difficult when a relapse takes place and the effusion again in-
creases.

When the patient lies flat, the weight of the fluid in the pericar-
dium falls backwards with full pressure upon the oesophagus, and
deglutition becomes more difficult; when, however, he is raised into
the sitting posture, and especially if he leans forwards, the volume of
the liquid tends forwards and downwards, and swallowing is more easy.

A servant girl (15), aged 16, who had been ill about 3 weeks, came in
suffering much both in the joints -and the chest. Her breathing was
laborious and very rapid ; she looked anxious ; dulness was increased
over the pericardial region, and a soft friction sound was audible over
the heart on pressure. On the 3rd day the amount of effusion in
the pericardium had reached to its acme ; swallowing was difficult,
breathing was accelerated, her face was livid and anxious, she had

240 A SYSTEM OF MEDICINE.

pain in the epigastrium increased by pressure, and the veins of the
neck were full. On the 5th she still had much difficulty in deglu-
tition, but on the 8th the pericardial dulness had lessened all round,
and she swallowed much more easily. On the 9th she was more
bright and lively, the pericardial dulness had lessened much, but pain
came in catches over the heart. On the evening of the 10th she had
a relapse, she became suddenly faint, her lips turned blue and dusky,
and she had great pain over the heart, which was soon relieved, but diffi-
culty in swallowing returned. Next day the dulness over the pericar-
dium had again increased, and the difficulty in swallowing was very
great. On the 12th she was still very ill, but she could swallow more
easily, and on the 15th the effusion into the pericardium had again
lessened, and she was better. The friction sound was audible until
the 17th day. She improved daily and gained strength.

The poor female servant (13), who died from sudden failure in the
action of the heart, whose case I have just related, on the day of
her admission, when the amount of effusion into the pericardium was
great, swallowed more easily when the shoulders were raised than
when she was lying flat.

One patient (44 a), a female servant, had a four-fold attack of difficulty
of swallowing ; on the second day after admission, from great disten-
sion of the pericardium, the effect being heightened by shortness of
breath; on the 4th from diphtheria; on the 7th from a renewed
increase in the effusion owing to a relapse, there being great distress
in the chest; and on the 11th to a slighter degree from a second
relapse with increase of the pericardial effusion. This case recovered
perfectly without valvular mischief, after passing through an attack
of pneumonia or rather pulmonary apoplexy and pleurisy.

Each patient presents some peculiarity in the way in which deglu-
tition is affected ; but I shall only allude here specially to two more
cases ; one of them (40), a youth, could not swallow solids readily, but
could drink freely ; the other (50), a coachman, aged 22, sometimes
when drinking had a spasm which stopped his breath before he could
swallow.

The possibility that diphtheria may be the cause of the difficulty
of swallowing must not be overlooked. It was, as we have seen, the
intervening cause, in my case (44 a), with double relapse, and it was
the cause of dysphagia in another patient (55), a young man of 18, a
commercial traveller, who had diphtheria on the 6th day after the
cessation of friction sound, and the 16th after admission.

XIV. Loss of Voice.

In the case fatal from syncope (13), a female servant, to whom I
have several times alluded, on the 5th day after admission the voice
was husky, and she spoke in a whisper, but she could, with a great
effort, speak aloud. She was less husky on the 5th, and on the 8th

PERICARDITIS. 241

her voice was more natural. This case tends to support the view that
the left laryngeal recurrent nerve may become so affected by the
contiguous inflammation as to paralyze the larynx.

XV. Effects on the Pulse of Eheumatic Pericarditis.

The pulse obeys the same law as the respiration under the in-
fluence of the disease; it rises in number, like the respirations,
as the disease rises in intensity, is at its greatest rapidity when
the disease is at its acme, and falls in number as the disease
declines. The increase in the rate of the pulse is not as a rule in
proportion to the increase in the number of the respirations. During
the early stage of the inflammation of the heart, when pain is generally
felt and friction sound is audible over the organ, the pulse usually
mounts up to 90, 100, or even 120, while the respirations increase to
from 30 to 40 in the minute, so that at this early period the ratio of
the pulse to the breathing is in number as about three to one, instead
of maintaining the healthy standard of about four to one.

When the amount of the effusion into the pericardium reaches its
height, the pulse is usually quicker than it is during the early stages,
and on rare occasions it becomes very much quickened, reaching even
to 160, More often, however, the pulse is not more rapid at this the
stage of the acme of the disease than it is during its early period.
The breathing, as we have just seen, is almost always more quickened
and laborious at the time the fluid in the pericardium has reached to
its height than at any previous period, so that then the ratio in number
of the pulse to the respiration is often two or two and a half to one,
instead of maintaining the healthy ratio of four to one.

At a later period, when the effusion is lessening, and the inflamma-
tion of the pericardium is coming to an end, the pulse, like the respira-
tion, falls in number. At this stage, however, in severe oases, one or
other, or even both of the two secondary affections, pleurisy and pul-
monary apoplexy, that quicken the respirations quicken also the pulse,
when the numbers of both, and the proportion that they bear to each
other, are as a rule nearly the same that they were during the early
period of the attack, the ratio of pulse to respiration being usually
three to one.

In considering the effects of rheumatic pericarditis on the pulse and
respiration, I have separated from each other the advance, the acme,
and the decline of the disease, and the two secondary influences,
pleurisy and pulmonary apoplexy. In nature, however, those stages
melt into each other, and those various causes combine and operate
together to produce the hurry and distress of breathing and tie
quickening of the pulse of which I have just spoken.

VOL. IV. R

242 A SYSTEM OF MEDICINE.

XVI. Fulness of the Veins of the Neck from Distension of

the Pericardial Sac.

In several of the cases of rheumatic pericarditis there was fulness
of the veins of the neck, sometimes with pulsation, during the period
that the effusion into the pericardium was at its height, and the sac
was distended to the utmost.

The fulness of the veins of the neck present at this period must, I
consider, be mainly due to the resistance offered to the return of the
blood through the venae cavae into the right auricle, owing to the
yielding inwards of the thin walls of that cavity before the pressure
of the fluid contained in the swollen pericardium. The fluid exerts
also direct pressure upon the thin walls of the descending vena cava,
which carries on the latter part of its course for the extent of an
inch within the pericardial sac. The ascending cava on the other
hand sustains this pressure to a considerable extent by being short
and very large, and by possessing walls thickened by fibrous struc-
ture derived from the central tendon of the diaphragm. We may,
indeed, measure the degree of the distension of the pericardial sac by
the degree of the distension of the veins of the neck. This compres-
sion inwards of the right auricle must be looked upon as one of the
most serious consequences of pericardial distension, for it materially
lessens, or in extreme cases may almost tend even to cut off the
supply of blood to the right side of the heart, the lungs, the left side
of the heart and the system. The walls of the left auricle, being
thicker, do not yield so readily as those of the right, but the com-
pression of the left auricle and of the pulmonary veins by the fluid
in the distended pericardium produces its own special mischief by im-
peding the flow of blood from the lung, thus often inducing pulmonary
apoplexy. From this joint compression of the sister auricles flows a
succession of consequences to which I need not here allude in detail,
but which in their turn tend to produce weakening and intermission
of the heart, a feeble irregular pulse, and even death from syncope. I
shall have occasion by-and-by to speak of the support that the thin
walls of the auricles and veins derive from the coating of lymph with
which they are covered, and which enables them to bear much of
the pressure to which they are then subjected.

One patient (16), a servant girl, after being ill for a week and affected
severely in the joints for two days, came in breathing hurriedly, suffer-
ing from pain over the region of the heart, and in great distress.
There was dulness over the pericardium from the second space to the
sixth, and a loud, harsh friction sound was heard over all that
region. The left jugular vein was distended and did not empty during
inspiration ; next day the amount of effusion had lessened, she
improved rapidly, and the friction sound ceased on the ninth day,
when a mitral murmur declared itself.

PERICARDITIS. 243

In another servant (13), whose case, already referred to, proved fatal,
the veins on the right side of the neck pulsated strongly, while those on
its left side did so to a less extent, as they did not fill or empty them-
selves so completely. She died in a fit of syncope on the 14th day.
Eighteen ounces of fluid were found in the pericardium, and several
patches of pulmonary apoplexy were diffused through the upper lobe
of the left lung.

Another fatal case (4), a carpenter, who died delirious on the eighth
day, presented pulsation in the neck on the second day after admission,
when the pericardial effusion had reached its acme. This pulsation was
partly in the carotids but was chiefly venous and was more marked on
the right side of the neck, the veins on that side being fuller than
those on the left. On the third day the upper boundary of the region
of pericardial dulness was lower, having descended from the third to
the fourth costal cartilage, and the venous pulsation was not so
perceptible. I will name two other cases of this class : one (29), a man
who came in with an anxious expression of face : on the fifth day friction
sound was heard over the heart, and on the seventh he presented
extensive double venous pulsation in the neck: the other (15), already
related, a girl who came in with rheumatic pericarditis, and in whon*
the veins of the neck were full during expiration on the third day
when the pericardial effusion was at its height and deglutition wa
difficult.

There was visible pulsation of the jugular veins in three of the
patients who had been affected with valvular disease of some standing
before being attacked with rheumatic pericarditis. In these cases, the
venous pulsation was evidently due to the valvular affection.

XVII. Appearance and Expression op the Face during the

course or Pericarditis.

The face was flushed, dusky or very pallid, or its expression was
one of anxiety or depression, in 43 of the 63 patients affected
with rheumatic pericarditis. In six other cases it is stated
that the aspect had improved, although there is no previous descrip-
tion of the face. There was thus a marked change in the appearance
of the patient in four-fifths of the cases (49 in 63). The face is not
mentioned in the remaining thirteen cases, and in one only of these
was the attack severe, while it was so in thirty-six of the patients
in whom its appearance was notably altered. The face was similarly
affected in three-fifths of the patients attacked by endocarditis
(60 in 108\ in less than one-half of those who were threatened with
endocarditis (27 in 59), and in one-fourth only of those who pre-
sented no sign or symptom of endocarditis. The appearance of the
face was less and less profoundly altered in these patients, as the class
to which they belonged became less and less affected in the heart, and

r 2

244 A SYSTEM OF MEDICINE.

still less in the class made up of those who gave no evidence of
affection of that organ.

The face was flushed in 19 of the 63 cases of rheumatic
pericarditis. Perspiration was copious in all but three of these, the
perspiration often standing in beads upon the face. The flush, instead
of being limited to the cheeks, was diffused over those parts that are
usually white even in persons of the most rosy hue, the forehead,
namely, the eyelids, the nose, the white skin of both lips, and the
chin. I never noticed the colour spread at the first blush from
feature to feature, but it seemed to tint them all at once. Thus the
face was pallid on the day of admission in a fatal case already quoted
by me, and on the following day it was flushed all over. But the
flush which at first seemed to suffuse the whole face usually vanished
step by step ; the pink skin of the upper and lower lips first becoming
white, then the nostrils and, in succession, the eyelids, the chin, the
brow, and the cheeks in several of my cases.

The face was pale during the period of the friction sound in nine
cases. One of these (13), a female servant, was very pallid and
sallow, the features being pinched, when admitted with pericarditis ;
while on the following day, the face was rather flushed, and the fever
seemed to be greater. Another case, (44a) a servant girl, aged 20,
admitted with pericarditis, was flushed on the second day, but on the
third, when the fluid in the pericardium had reached its acme, de-
glutition was difficult, and she was depressed, pallid, and weak. The
lace was twice as often flushed (19 times), as pale (9 times), during
the attack of pericarditis. I have been unable to discover clinical
reasons for the difference in these cases of the hue and colour of the
face. The clinical history of the pallor of the face induced by
rheumatic pericarditis is illustrated by a case, the physical features of
which I published in 1844 j1 a youth, aged 16, was admitted into the
General Hospital near Nottingham, on the 17th of November, 1842,
under the care of Dr. Williams, suffering from acute rheumatism, with
pericarditis. His countenance was pale, and his surface generally
was also pale. On the third day after admission, the general symptoms
were milder, although the extent of pericardial dulness had not
lessened, and the face was less pallid, the lips being red. On the sixth,
the following is my report : " The gums are slightly tender, his
general appearance improves, the hue of the skin is clear, and rather
red; the reflex influence of disease in contracting the capillaries
being removed. " He made a complete and rapid recovery. In this
case, the general surface was pale as well as the face; but in the
cases under analysis, my notes do not, as a rule, describe the hue of
the body.

The aspect was dusky, muddy, or glazed in sixteen, and the ex-
pression of the face was anxious or depressed in thirty-five of the
patients affected with pericarditis.

1 Pror. Med. Trans., rol. xii., 1844, p. 588.

PERICARDITIS. 245

I would here briefly compare these numbers with the numbers of
those thus affected in the other cases of acute rheumatism.

The face was notably flushed in one-fifth of the cases with simple
endocarditis (19 in 108), one-eighth of those threatened with en-
docarditis (8 in 63), and in one-twentieth of those giving no sign of
endocarditis (4 in 79). The aspect was dusky or muddy in one-tenth
of those with simple endocarditis (10 in 108), in one of those threatened
with endocarditis (1 in 63), and in one of those who gave no evidence
of endocarditis (1 in 79). The expression was anxious or depressed in
one-fourth of those with simple endocarditis (25 in 108), in one-sixth of
those threatened with that affection (10 in 63), and in one-twelfth of
those who presented no sign of inflammation of the heart (6 in 79).

I have drawn up these numbers from a careful examination of my
case books, and they present an accurate return of the symptoms there
recorded. These cases are however necessarily reported with varying
degrees of minuteness, and the more severe cases, attracting the
greatest interest, are naturally observed and related with greater care
than those that present no unusual features. These must therefore
be taken not as the actual, but the approximate numbers.

Keeping this in view, it must be felt, from what I have said, that
rheumatic pericarditis with endocarditis, and to a less degree
simple endocarditis, produce a remarkable change on the complexion,
aspect, and expression of the face. The attention is at once drawn to
the heart by the altered countenance. When the inflammation of the
heart is established, the varying hue and expression of the face tell,
with remarkable accuracy, the varying state of the powers of the
heart, and of the double inflammation with which the organ is
affected.

When the tide of the effusion into the pericardium has reached its
height, as I shall illustrate in the next section, the hue of the face is
usually more dusky and livid, and its expression more anxious than
at any other time ; but when the tide has fairly turned, and, the
effusion having lessened, the inflammation ceases to be active, the
face becomes often quite suddenly cheerful, while its hue becomes
clear ; the eye at the same time, instead of being heavy and charged
with blood vessels, becomes blight and clear. After this, if there is
no relapse, the powers rally with remarkable quickness and freedom,
and the appetite returns. This state is very different from the con-
valescence of fever, which passes through its period of improvement
slowly and with scarcely perceptible steps.

In a patient, to whom I have already alluded, whose heart acted
strongly and rapidly at the time of the first onset of the inflamma-
tion, the right side of the face was swollen and flushed, evidently
under the influence of the attack of pericarditis.

What are the causes of this remarkable influence of inflammation
of the exterior and interior of the heart on the face ?

There are probably more causes than one at work to produce the
flushing or pallor present in pericarditis. The moderate elevation of

246 A SYSTEM OF MEDICINE.

temperature present in all cases of inflammation is probably connected
with flushing of the face, either as a cause, or rather as a common
effect. The question must here be put, what is the cause of the
moderate elevation of temperature in cases of inflammation ? Is it
from general relaxation of the arteries, with elevation of temperature,
owing to the influence of the inflammation on the afferent nerves of the
part affected ? such influence being conveyed to the vaso-motor centre
in a manner analogous to that in which relaxation of arteries and
elevation of temperature is produced on one side of the head and
face by the division of the sympathetic on that side of the neck, or
by the pressure of that nerve by an aneurism of the arch of the aorta.
This influence would, of course, only account for the moderate rise of
temperature in local inflammation, and does not touch the question of
the cause of the increased heat in fevers or in cases of acute rheu-
matism with delirium.

Putting this cause aside, which applies to every case of inflamma-
tion, I would suggest that one great cause of the flushing or pallor of
the face in pericarditis is the influence of the inflammation on the
afferent nerves at the surface of the heart and great vessels, which,
being depressed or stimulated, may induce reflex dilatation of the
arteries of the head, with flushing of the face, or reflex contraction of
the arteries of the head with pallor of the face. I suggested this
in principle as the cause of the pallor in the Nottingham case in my
note-book in 1842, and am still disposed to do so. In aneurism of
the arch of the aorta, pressure on the branches of the sympathetic
of one side causes relaxation of the arteries and elevation of tem-
perature on the corresponding side of the head and face. I consider
that a parallel effect would result from the excitation or the injury of
the sympathetic and sensory nerves, and perhaps of other nerves
having, say, a vaso-inhibitory property distributed to the seat of the
inflammation of the heart and great vessels in pericarditis ; contraction
of the arteries of the head and face with pallor being produced on the
one hand, and relaxation of those arteries with flushing and perspira-
tion on the other. In one case only, just referred to, was there
flushing and perspiration notably limited to one side of the face. It
is natural, however, to expect that as the inflammation affects the
nerves of both sides in pericarditis, both sides of the face should be
equally affected, as it was indeed in all but one of my cases of peri-
carditis affected with pallor or flushing of the face.

I would here remark that as the reflex contraction or dila-
tation of the arteries with pallor or flushing, from excitation or
injury of the sympathetic or sensory nerves is continuous, it differs
essentially from the reflex movements of the muscles caused by the
excitation of an afferent nerve, such movements being necessarily short
and intermittent, the withdrawal and renewal of the stimulus to the
afferent nerve being needful for their reproduction. In short, the
reflex vaso-motor current is continuous, while the reflex excito-motor
current (of the muscle) is interrupted.

PERICARDITIS. 247

The increased contraction of the arteries caused by the excita-
tion of a sensory or sympathetic nerve appears to be due to the
increased discharge of nervous force directly from the vaso-motor
centre when that centre is thus stimulated by the excitation of those
nerves. That centre would indeed seem to require, for the exercise of
its proper functions, to be reinforced and stimulated through the
sympathetic nervous system, and probably by the blood circulating in
the arteries, when we consider that the division of the left splanchnic
in the rabbit may lower the arterial pressure from 90 millimetres to
41, that excitation of the divided nerve may raise the pressure to
115 millimetres, and that division of the other splanchnic may further
lower it to 31 millimetres.1

I would here remark that similar effects are produced by analogous
causes in pneumonia, and especially in pneumonia of the upper lobe,
when the face, besides being congested, presents a dusky hue and a
powerless expression that speak of the profound influence exercised
upon it by the disease. In this disease also, as in pericarditis, with
the turn of the tide of the inflammation and with the removal of its
products, the veil is as it were lifted away from the countenance ; and
a patient, one day, under the weight of the inflammation, with an
aspect dark depressed and anxious, presents on the next day, with the
removal of the exudation from the affected air cells, and the renewal
of their respiration, a face clear, and clean, and an expression bright
and cheerful.

The eye is every now and then reported to have been dull, and
heavy in appearance during the attack of pericarditis, its minute
vessels being congested; but it is more frequently described as
becoming bright and clear when the effusion into the pericardium
was lessening, and the inflammation was becoming inactive and only
present in the shape of its results. I had not, until quite recently,
made any close observation of this organ, but in one of the last cases
of acute rheumatism with endocarditis treated by me in St. Mary's
Hospital, I found that during the acme of the disease, when the
face was flushed, dusky and anxious, the conjunctiva was crowded
with small vessels which ended a very short distance from the cornea,
so that round the clear of the eye there was a white zone or ring
edged by fine converging vessels. When the inflammation ceased to
be active, and the face, in keeping with this improvement, became
clear and cheerful, the eye became bright, and the vessels crowding
the conjunctiva lessened in number, so that the ball of the eye
became again white. This organ requires careful observation in cases
of rheumatic pericarditis and endocarditis.

1 Ludwig and Cyon, quoted by Dr. Burdon Sanderson : Handbook for the Physio-
logical Laboratory," p. 249.

248 A SYSTEM OF MEDICINE.

XVIII. Condition of the Face when the Pericardial Distension

was at its Height.

When the pericardium is distended to the full with fluid, under the
three-fold influence of (1) what may be termed the " fluid" pressure,
induced by the distension of the sac bearing with varying force, out-
wards upon the oesophagus and trachea, the left bronchus, the lungs,
especially the left, and the diaphragm ; and inwards on the descending
vena cava, the right and left auricles, and the pulmonary veins ;
(2) inflammation involving the nerves distributed to the surface of
the heart and the great vessels; and (3) inflammation of the superficial
muscular fibres of the heart itself ; as we have seen, point by point,
pain may be present around and within the heart, over the pericardial
sac and the pleura ; swallowing may be difficult ; the voice may be
hoarse or reduced to a whisper ; the action of the heart, which at the
beginning of the attack is often forcible, may become feeble and in-
termitting, or even altogether fail ; the respirations may be hurried and
laborious, often so as to compel the raised and forward posture; the pulse
may be rendered weak and irregular and be quickened, though not in
the same proportion, as the breathing, the ratio of the pulse to respira-
tions being two or three and a half to one, instead of, as in health,
four to one ; and the veins of the neck may be swollen and pulsating.
The last effect of the over distension of the pericardium that I shall
illustrate is that upon the circulation of the head and face.

A female servant whose case (15) has already been alluded to was
admitted with acute rheumatism and pericarditis of great severity. On
the third day, I found that the pericardium was distended to the
full, she complained of a sensation of choking, swallowing was
difficult, the countenance was anxious, the face was livid and
perspiring profusely, and the veins of the neck were full. On the
sixth day the pericardial dulness had lessened all round, her face was
less dusky, and her aspect had improved. On the tenth, in the
evening, she suddenly came over faint, the lips being blue, and the face
dusky ; but in a few hours the face, though still anxious, lost its dark
hue and the lips became again red. Next day it was found that the
pericardial effusion had again increased. The fluid, however, soon
again diminished. On the twelfth her aspect had again improved, on
the fifteenth her face was flushed, and on the sixteenth it was of good
colour, and its expression was no longer anxious. Here, twice over,
the effusion in the pericardium reached its acme, and under the in-
fluence of its pressure and the inflammation of the organ, the heart
faltered, the venous blood was delayed in its passage, the arterial
blood was with difficulty supplied, the face and neck became charged
with venous blood, and the lips became livid ; and here, twice over, the
pressure was removed by the lessening of the fluid, when the colour
returned to the face and the expression of anxiety disappeared.

PERICARDITIS. 249

XVII. Affections of the Nervous System in Rheumatic Pericarditis.

Dr. Davis, of Bath, in the year 1808 x published three cases of
acute rheumatism, two of them being affected with pericarditis, and
one with endocarditis. One of the cases of pericarditis, which was
observed in 1785 by Dr. Haygarth — who curiously does not mention this
important case in his " Clinical History of the Acute .Rheumatism,"
published in 1806 — was affected with moaning, restlessness, and
delirium ending in death. The other case of pericarditis, a young
lady, who was under the care of Dr. Davis, had great heats, with
perspiration, screaming, and the most violent jactitation of the body,
" occasioned by the extreme anguish which she felt in the region
of the heart." She was perfectly sensible throughout, and died after
the disease had lasted twenty-six days. The patient with endocar-
ditis was affected with want of sleep and violent delirium, for nine
days, at the end of which time she died.

In a series of important clinical contributions, Corvisart, Mr.
Stanley, Dr. Abercrombie, Dr. Macleod, Andral, Dr. Latham, Dr.
Bright, Dr. Mackintosh, M. Bouillaud, Sir Thomas Watson, Sir
George Burrows, and Dr. Kirkes,2 have described cases of pericarditis,
some connected with acute rheumatism, but many not so, in which
delirium, coma, convulsions, temporary insanity, chorea and chorei-
form movements, or tetaniform symptoms and rigidity, and even actual
tetanus were present.

These observations suggested to several of those authors, including
Andral and Dr. Bright, a close connection amounting even to cause
and effect, between pericarditis and the affections of the nervous
system associated with it.

The affections of the nervous system in cases of rheumatic pericar-
ditis, and acute rheumatism are always serious, often fatal, and com-
paratively rare. Recent observations have shown in many of those
cases the presence of a very high temperature, delirium and coma,
ending in death. I shall therefore, in inquiring into the clinical history
of those associated affections, examine those cases admitted into St
Maiy's Hospital under my care during the twenty years that I have
held office, and all the published cases that I can find of this class.

I have brought together from various sources, 180 cases of acute
rheumatism with affections of the nervous system, more than one
half of which had pericarditis (92 in 180). The temperature of the
body was recorded in one-third of the total number of cases (61 in
1 80) ; and although these cases were observed at a much more recent
period than those in which the temperature was not recorded, I shall
examine the more recent series of cases first, for they throw light
upon the older series of cases. (See tables on the following pages.)

1 ' 'An Inquiry into the Symptoms and Treatment of Carditis, ' ' by John Ford Davis, M.D.

* For references to these authors, see the note riven in the appendix to the table at
pages 250-253, of cases of acute rheumatism with affection of the nervous system, in
which the temperature of the body was not observed.

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2M A SYSTEM OF MEDICINE.

Cases of Acute Rheumatism with Affections of the Nervous
System, in which the Temperature of the Body was Observed.

Dr. Sydney Ringer, published in the year 1867, three cases of acute
rheumatism with pericarditis, in which the temperature rose before
death respectively to 1092°, 110*8°, and 110-00.1 These three patients
had delirium, followed by coma and death, and one of them was
under the care of Dr. Reynolds as early as May 1862.

Dr. Kreuser related in 1866 2 three fatal cases, of acute rheumatism
in which the temperature rose respectively to 109*4°, 110*2°, and
110*4°, and these three patients were affected with delirium, and one
of them with coma also.

More recently an important series of cases of this class have been
communicated by Dr. Hermann Weber in an important paper, Dr.
Murchison, Dr. Burdon Sanderson, Dr. Greenhow, Dr. Southey, Dr.
Henry Thompson, Dr. Meding, Mr. Anderson, Dr. Wilson Fox, whose
work on the treatment of hyperpyrexia is of great value, and Dr.
Andrews.8

I have brought together from these and other sources, sixty-one
cases of acute rheumatism, affected with coma, delirium, chorea,
or convulsive choreiform, or tetaniform symptoms, in which the
temperature was observed during the progress of the illness. See
table, pp. 250—253.

Of the sixty-one cases in which the nervous system was affected,
and the temperature was ascertained — I. twenty-seven had peri-
carditis; II. thirteen had simple endocarditis; and, III. twenty-one
were free from pericarditis, endocarditis being absent or doubtfaL

I. — Cases with Pebicarditis in which the Nervous System was

AFFECTED, AND THE TEMPERATURE, GENERALLY VERY HIGH, WAS
OBSERVED.

SUMMARY.

A1 Had coma without delirium, maximum temp. 110° . . 1

A* Had delirium followed by coma, temp. 110*8° — 104*6° . 11

A4 Had delirium followed by stupor, temp. 106°*— 103° . . 1

Had delirium and convulsive movements, temp. 107° — 110*2° 1

B1 Had uncomplicated delirium, temp. 110*4° — 103° ... 9

Had delirium with general stiffness, temp. 103*2° — 102*2° 1

Had temporary or partial coma, temp. 101*8°— 99*3° . . 2

C1 Had chorea, temp. 101*5° 1

Total ... 27

i "Medical Times and Gazette," 1867, IT. 378.

* "Medicinisches Correspondenz-Blatt des Wiirttembergischen artzlichen Vexeins,"

band xxxvi. p. 105.

8 For references to these authors, see the note given in the appendix to the table, at
pages 250-258, of cases of acute rheumatism with affection of the nerrous system, in
which the temperature of the body was observed.

PERICARDITIS. 265

The temperature of the body was observed in twenty-seven cases
of rheumatic pericarditis with affection of the nervous system, and
was very high in three-fifths of them (15 in 27), their highest tem-
perature varying respectively from 106*8° to 115.8°. Five of these
cases were placed in a cooling bath, when their temperature, then at
the highest, was ascending rapidly, with the effect of arresting its
rise, cooling the body, and, in four instances, leading to the recovery
of the patient. The bath was employed also in two cases in which
the temperature was 105° and 105*5° respectively, with the effect of
cooling the body ; but as the ascent of the thermometer was neither
rapid nor very high, those cases can scarcely be included with those
of hyperpyrexia. The temperature was 104*6° and 105*3° respec-
tively in two cases during the period of delirium, but was not observed
during that of coma, and I therefore think that both those cases
may be included with those of hyperpyrexia — which bring their
number up to seventeen, or two-thirds of the total number of cases
with pericarditis.

Seven of the remaining ten cases, or one-fourth of the total number,
had a high, but not very high, temperature, varying from 103° to 106°,
so that these cases would rank, as regards the heat of the body, with
fever or pyrexia. The temperature was only moderately high in the
three remaining cases, or one-eighth of the total number, varying
from 993° to 101-8°.

A1 Profound coma, without delirium, was present in one case ;
As, 4, delirium that passed into coma in eleven cases, into stupor
in one case, and into convulsive movements in one case; B, un-
complicated delirium was present in nine cases, one of which had
Blight's disease ; and delirium with stiffness of jaws, neck and limbs
occurred in one case. Temporary coma occurred in one case, and
semi-consciousness in another, both with albumen in the urine ; and
C1 chorea and slight continuous contraction of certain muscles existed
in one case.

A1 The case of coma without delirium, a woman, was under the care
of Dr. Wilson Fox,1 with acute rheumatism and pericarditis. The
temperature was about 102° on the morning of the fourteenth day of
illness, and had risen to 108*4° at 9.15 p.m., when she became entirely
unconscious, and to 1091° at 9.50 p.m., when she was put into a bath
at 96°, and ice was applied to her body. She was unconscious, pulse-
less and cyanotic, her respirations were irregular, gasping and
stertorous, and she appeared to be dying. In half-an-hour, her tem-
perature had fallen to 106*2°, when the pulse became perceptible,
and she showed signs of consciousness. In ten more minutes, the
temperature was 103*6°, and she. was taken out of the bath, and
twenty minutes later it had fallen to 100*1°, when she could speak, and
had imperfect consciousness. After various oscillations, this patient
recovered. I relate this case here briefly not to illustrate the treat-
ment, but to show that profound coma became established when the

1 " Treatment of Hyperpyrexia," by Dr. "Wilson Fox, p. 2.

256 A SYSTEM OF MEDICINE.

temperature was excessively high, and that consciousness was re-
stored when the body was cooled.

A*. Ten cases, in which delirium was followed by coma, and in
which the bath was not used, proved fatal, but one such case recovered
after the employment of the bath.

Delirium appeared at a temperature of from 103° to 104*8° in eight
of the eleven cases in which coma was preceded by delirium, the tem-
perature in six of these being at or above 104° when the disturbed state
of mind was first noticed. In three of these cases delirium was still
present when the thermometer was as high as from 107° to 108°, and
in one of them when it was as low as 99*6°.

Profound coma declared itself when the temperature had risen
from 109° to 109-4° in five of the eleven cases in which complete
unconsciousness followed delirium, when the thermometer stood at
108-4° in one of them, at 106-8° in another, and at 106*6° to 107'6°
in another, in which the coma, not profound, was transient.

In several of these cases it was noticed that the temperature rose
between the supervention of coma and death.

The delirium was violent in five of those eleven patients who
passed from delirium into coma, two of whom got out of bed ; was
active in three of them ; and resembled delirium tremens in two, while
in another the manner was strange and excited, and the sentences were
disconnected and incoherent.

The transition from a state of violent or active delirium to coma
was usually gradual Muttering replaced active delirium in three in-
stances, the muttering delirium being accompanied by restlessness in
two of them. A state of semi-consciousness, accompanied by moaning
in one and by restlessness in the other, intervened in two cases
between the period of delirium and that of coma ; and two other cases
passed from delirium to a state almost of unconsciousness, and from
that to coma. Violent delirium ceased abruptly after venesection
in one patient, who was quiet for a short time, but soon passed into
a state of perfect unconsciousness.

The duration of the delirium was very various in the different cases,
lasting in one case about three-quarters of an hour, and in another,
eight days. The delirium was more frequent by night than by day,
and lasted from one to four nights in four cases in which it was
scarcely observed during the day.

The period of coma varied much less than that of the delirium,
lasting from a quarter of an hour to seven hours in nine of the eleven
cases with delirium and coma. In one of the remaining cases, the
duration of the coma was prolonged, death being delayed, and in
another of them consciousness was restored, and recovery was es-
tablished, by the use of the bath.

The two cases were fatal in which delirium preceded semi-ster-
torous breathing, with violent spasmodic movements of the whole
body in one instance, and profound stupor in the other. The teni~
perature in the former case rose to 110-2° before death, but in the

PERICARDITIS. 257

latter"! it was never higher than 106°. Dr. Murchison favoured me
with the leading features of that case.

Bl Delirium without coma or other important modifications
affected nine cases of acute rheumatism with pericarditis. These
cases divide themselves naturally into two groups ; in the first group,
consisting of four, the delirium was of the usual character, and the
temperature was very high, varying from 107*3° to 110*5°, and was
kept in check in two of them by the cooling bath; while in the
second group, containing four cases, the temperature was not so very
high, varying from 103*3° to 105*3°. The delirium was accompanied
by tremor, and usually by hallucinations, and a general condition
resembling delirium tremens. The remaining case of delirium belongs
to neither of these groups, since the delirium was slight, and gave
way to general emaciation, ending in death.

Delirium was present throughout in one of the four cases with very
high temperature, and in that patient it ranged from 103° to 105*6°,
and ascended to 107*4° during the last ten hours. Death was sudden.
The second case, a coachman who had lived well, was under the care
of Dr. Wilson Fox.1 His temperature was 107°, his pulse 100 — 108,
respiration 44 — 45. At 2 A.M. he was put for twenty-five minutes into
a bath at 89° to 86°, when his temperature fell from 107° to 103*1°,
and he became perfectly conscious. Fifteen minutes after the bath
his temperature had fallen to 98°, when his pulse was 84, respiration
20, and he was perfectly rational and conscious. The pericarditis in
this case was of unusual duration and severity. The bath, the wet-
pack, or the ice-bag was employed during the next six days to keep
down the temperature, which had a strong tendency to rise. This
patient recovered. In another case, a man, the temperature was
lowered by the bath from 108*2°, when he was delirious, to 103*8°,
when he could answer questions rationally. A second bath lowered
his temperature from 105° to 102°, and thirty-five minutes after his
removal from it, to 98*7°, when he was quiet. He recovered slowly.2

One of the four patients with tremor, hallucinations, a state re-
sembling delirium tremens, and a temperature not excessively high,
who was under the care of Dr. Southey, was an intellectual, nervous
man, and a drinker of beer. His tongue and hands were at a tem-
perature of 105° ; he was placed in a bath at 71° for ten minutes,
when he felt cold, talked rationally, and thought it the queerest
treatment for rheumatism. He was wet-sheeted whenever his tem-
perature rose to 104°, when he was always delirious. He died with
bronchial symptoms. Sir William Gull saw the case, and suggested
that it indicated the association of acute rheumatism with delirium
tremens.3

The next case resembling delirium tremens was a poorly nourished,
pale man. The bath lowered his temperature on the first occasion

1 " Treatment of Hyperpyrexia," p. 10.

2 Dr. Andrews, " St. Bartholomew's Hospital Reports," x. 338.

3 Lancet, 1872, ii. 562.

VOL. IV. S

258 A SYSTEM OF MEDICINE.

from 104-3° to 998°, and on the second from 105*3° to 101*6°, when he
was rational, and after the second bath he had risus sardontcns, his
limbs were tremulous, and he remained delirious until the fourteenth
day (temp. 103*4° to 100*2°). After this he steadily improved.1 Dr.
Southey favoured me with the notes of another case of this class, a
poorly nourished, anaemic man, a coachmaker, who had been ill ten
days. When admitted (temp. 103°), his tongue was tremulous, and he
perspired profusely. On the fifth day he had pericarditis ; on the
seventh night, constant muttering delirium ; and next day an abrupt
manner. On the ninth, after a delirious night, his hands were tremu-
lous. On the seventeenth day his skin was hot and dry, temp. 103*8° ;
and the activity of his mind resembled what is observed in delirium
tremens, but he had no horrors. The ice-bag was applied to his head
on the eighteenth, and as he was sleepless, he had 30 grains of
chloral, after which he slept for four hours. On the following day
he was conscious, had pain in the knees and shoulders, perspired less,
and looked better, but still had some tremulousness and jactitation. His
respiration and temperature steadily fell, and he gradually recovered.

The fourth case was a constable, who ten years before had been
unconscious after a kick. His highest temperature was 103*3°, but it
rarely exceeded 102°. In the course of his illness he had delirious
nights, choreal movements of the left hand, on one occasion tremor
of the right hand, hallucinations, and frequent rolling of his head
from side to side. He improved slowly, but remained for some days
incoherent, and childish in manner.2

B* Delirium with stiffness of jaws, neck, back and limbs, occurred
in a patient of Dr. Bristowe's, a bargeman, aged 21, with slight acute
rheumatism, pericarditis, and endocarditis.8

Two cases, one affected with temporary unconsciousness, the
other with stridor and semi-consciousness, were under my care in
St Mary's Hospital. Thejr had albumen in the urine, and were both
fatal. The tirst case had previous aortic and mitral valvular disease.
The second had a presystolic murmur, and mitral and tricuspid
systolic murmurs, and the inspection after death showed pericarditis,
button-hole contraction of the mitral valve, and acute Bright's disease
of the kidneys.

C1 Choreal and continuous contraction of some muscles occurred
in the following case, a delicate, excitable girl, aged eleven, for
observing which I am indebted to Mr. Saunders. When I first saw
her, about the tenth day of her illness, a loud pericardial friction
sound prevailed over the whole front of the chest, extinguishing all
other heart-sounds. Ten days later, temp. 101*5°, she took little
notice, bent and extended her right arm and hand irregularly, but
bent the hand backwards on the fore-arm, flexed the fingers, and
pointed the right great toe downwards, by the continuous, but not

1 Dr. Andrews, " St. Bartholomew's Hospital Reports," x. 350.

2 Dr. Greenhow, Clin. Soc. Trans, vii. 172. * Path. Trans, xxiv. p.

PERICARDITIS. 259

constant, contraction respectively of the flexors and extensors of
the fore-arm and the muscles of the calf. The face was still, the
tongue protruded itself steadily and for long ; her body was quiet,
and speech was limited. During the night she alarmed her mother
by screaming violently, throwing herself about the bed, and tossing
her head from side to side. After about twenty minutes she became
quiet and fell asleep. Four days later she had a return of pain
and swelling in the right knee, friction sound was barely audible
over the heart, and the movements of the right arm had lessened
and were more simply those of ordinary chorea.

The ciffection of the joints during the early period of the attack of
acute rheumatism was severe in three-fifths (15 in 27), and of moderate
severity in one-third of the patients (8 in 27), not severe in two in-
stances, and in one, the condition of the joints was not described.
The affection of the joints disappeared,, or was much lessened in
severity at the time of the delirium, coma or chorea in all those
cases (20 in 27) in which the condition of the joints is described.
In thirteen cases the affection of the joints was well at the period
in question ; in four it was slight, and in three it was not severe.

The invariable subsidence of the inflammation of the joints in these
cases, when affection of the nervous system takes place, shows that
there is some connection between the appearance of the one affection
and the disappearance of the other. The improvement of the in-
flammation of the joints generally coincides with improvement of the
general symptoms, unless the heart is inflamed. We may therefore,
I think, infer that the presence of trouble in the nervous system,
whether accompanied or not by a very excessive rise in temperature,
has a distinct association with the lessening of the affection of the joints.

The perspiration, before the nervous system was affected, in these
cases was noted in ten of the fourteen cases with coma, stupor or
convulsions preceded in all but one instance by delirium, and during
that early period it was profuse in seven, and moderate or slight
in three of those ten cases. The perspiration was observed in
eleven of the fourteen cases just noticed during the period of
delirium or coma, when it was absent in three, slight in four,
moderate or considerable in two, and profuse in two of these eleven
cases.

The perspiration was noted both before and during the period of
the delirium or coma in nine of those fourteen cases. In eight of
those nine patients, the temperature was excessively high at the
time of the delirium or coma, and perspiration was then absent
or lessened. In one case with delirium, the highest temperature
observed was only 103*8°, and perspiration, previously moderate, was
then profuse.

The perspiration was observed during both periods in four of the
nine cases in which delirium was present without coma or stupor,
and was profuse in those four cases during the early period of the
disease. One of those patients had on previous days perspired

s 2

260 A SYSTEM OF MEDICINE.

freely, but the skin became dry when the temperature rose to
107*3°. In another of them, the skin previously perspiring, felt
hot and dry when delirium appeared at a temperature of 103 '8°. The
perspiration remained profuse in two cases during the period of delirium
with hallucinations and tremor, the temperature being then respec-
tively 105° and 102°. Both of those patients were predisposed to
affections of the nervous system. Dr. Wilson Fox justly regards the
cessation of perspiration while the temperature is still high as a
symptom of very great gravity. It would appear from what I have
just stated, that the cooling influence of the perspiration may have
kept down the temperature in the three latter cases, while in the
ten former cases the want of that cooling influence may have allowed
the temperature to rise unchecked when heat was supplied from
within by the rapid combustion of the tissues of the body during the
disease.

The presence of a miliary eruption or sudamina was noticed in
nearly one-half of the cases (12 in 26).

The Pericarditis was of average intensity or severe in eleven and
slight in three of the fourteen cases with coma, stupor, or convulsions,
in all of which but one the more grave affection of the nervous
system was preceded by delirium. In seven of the nine cases with
uncomplicated delirium, the pericarditis was of average severity, and
in two of them it was slight. The pericarditis was of average
severity in the remaining three patients, in none of whom was the
temperature above 101-5°, one of them having transient coma, one of
them coma, and the other choreal symptoms.

We shall be better able to consider whether the presence of pericar-
ditis had any influence in producing the excessive rise of temperature
in cases with " hyperpyrexia " when we have inquired into the whole
chain of cases, those namely without as well as those with that
affection.

Endocarditis was present in nearly one-half of these cases, with
pericarditis and affection of the nervous system (11 in 26), was ab-
sent in almost as many (9 in 26), and was doubtful or not noted in
the few remaining cases (5 in 26).

Convulsive, Choreiform and Tctaniform- Movements. — Movements
of a convulsive, choreiform or tetaniform kind affected nine of
the twenty-four patients with acute rheumatism and pericarditis
in whom the temperature was observed, including the case just
related, in which choreal symptoms were present without delirium.
Besides these, two patients affected with delirium had distinct risiw
sardonicus.

One of these patients, a shopman in a cigar shop, aged 28, had in
the morning muttering delirium, and a temperature of 107°. In the
afternoon he had violent spasmodic movements of the whole body,
his respirations were semistertorous, his temperature was 110-2°,
and an hour later he died.1 Another of them, a female servant,

1 Dr. Mnrchison, Clin. Soc. Trans, i. 32.

PERICARDITIS. 201

being violently delirious, temp. 107*8° F., was bled, and became, as
I have already stated, abruptly unconscious. Then succeeded a
peculiar series of irregular muscular movements of the hands and
arms, with chattering and grinding of the teeth, and convulsive
movements of the jaw, or trismus. Fully two hours later, after
being in the bath, when she had cooled down to 104°, she had an
attack of clonic spasms of the muscles of the arms, lasting some
minutes.1 There were muscular twitchings of the limbs in three
patients when in a state of unconsciousness.

One patient, a police-constable, aged 23, who, ten years previously,
had been unconscious from a kick in the mouth, after little sleep, had
wandering, much jactitation, constant movement of the fingers of the
left hand, tremors of the right hand, and subsultus. Two days later
there was also frequent rolling of the head from side to side. His
temperature was not above 102°.2 Another patient, a woman aged
29, also rolled her head from side to side, contracted her brows, and
distorted her face into various grimaces. Her temperature was 107*8°.3
One patient, a man aged 23, on the evening before he died, temp.
105'4°, was very delirious, and rolled violently about the bed, so
that he required to be held down. This violence quickly passed away,
and he then lay half unconscious and moaning loudly.

Symptoms of a more or less tetaniform character, that is to say,
with continuous rigidity or contraction of muscles, appeared in five of
the cases.

Dr. Wilson Fox's patient, already sketched at page 257, after the
bath, temp. 1006°, had at times spasms of rigidity of the muscles
of the lips and neck, but not of the limbs. Another patient, a
gardener, seven hours before death, became incoherent, and within
ten minutes, unconscious; his lips pouted and rubbed incessantly
over the teeth, and his whole voluntary muscles twitched constantly.4
The third is that of Dr. Wilson Fox just referred to, with chatter-
ing and grinding of the teeth, and convulsive movements of
the jaw, or " trismus." 6 The fourth case is Dr. Greenhow's,
already noticed, with choreal movements of the left hand. When that
hand was turned on to its back,6 there were constant twitching move-
ments of the hand and fingers, and the forefinger became flexed
towards the palm. The fifth case is my own, already related at page
258, with choreiform movements of the right arm. Her right hand
was bent backwards, her right fingers were flexed, and her right toe
pointed downwards, owing to the continuous contraction of the
corresponding sets of muscles, which offered steady resistance when
put on the stretch. These five cases seem to suggest a combination
of convulsive, choreiform and tetaniform movements.

The question naturally arises, were the cases presenting choreiform

1 Dr. Fox. " Treatment of Hyperpyrexia," 44.

* Dr. Greenhow, Clin. Soc. Trans, vii. 175.

* Br. Sydney Ringer, Medical Timts and Gazette, 1867, ii. 380.

4 Mr. Anderson, British Medical Journal, 1871, i. 529.

5 Loc. cit. p. 48. 8 Loc. cit. p. 174.

262 A SYSTEM OF MEDICINE.

movements associated with endocarditis? The answer to that is,
however, as regards these cases, definitely in the negative, for en-
docarditis was absent, or not observed, in those cases, excepting to
a slight and doubtful degree in one of those with muscular twitching.
Endocarditis was, however, present in Dr. Wilson Fox's case with
spasms of rigidity of the muscles of the lips and neck. I shall again
briefly consider these cases when I return to the important question
of the association of pericarditis with tetaniform and choreiform
movements.

Tremor was present in seven of the cases, all of which have been
already alluded to.

II.^-Cases with Simple Endocarditis in which the Nervous
System was affected and the Temperature, generally very
high, was observed.

SUMMARY.

Az Had delirium followed by coma, temp. 104*4° — 110*2° . 4

A- Had delirium and convulsive movements, temp. 111-6° . 1
JB1 Had uncomplicated delirium in three, temp. 108'5° —

111-4° ; in two, temp. 102*8°— 103*9° 5

B2 Had delirium, cerebral embolism and hemiplegia, t. 103° 1
2?3 Had delirium and chorea (minute cerebral embolism)

temp 1

Had high temperature without notice of delirium, temp.

105-8° (ice-bag) 1

Total .... 13

The nervous system was affected in thirteen cases of simple endo-
carditis in which the temperature was observed. The majority of
these cases, like that of those affected with pericarditis, presented an
excessively high temperature ; and in three of the whole number the
temperature, when undergoing a rapid ascent, was arrested in its
rise, lowered, and kept down by the use of the cooling bath or the
external application of the wet sheet and ice. The temperature was
as high as from 108*5° to 111-6° in three-fifths of the cases (7 in 13) ;
and in the one of those cases in which the temperature was the lowest,
108-5°, the vigorous use of ice-cold water within and without arrested
the rise of temperature and induced its permanent lowering, followed
by the recovery of the patient. In one patient the temperature
was checked at 105*8°, and brought down by the bath; and in
another the thermometer was at 104*4° during the period of delirium,
but was not employed during that of coma. In four of the cases
the temperature was only of a moderate height, being from 103*9°
to 102*3° ; and we may therefore infer that fully two-thirds of the

PBMGARDHm 263

cases with simple endocarditis (9 in 13) in which the nervous system
was affected, had " hyperpyrexia."

A2* Twelve of the thirteen cases had delirium, which passed into
coma in four instances, ended in convulsive movements in one, B1
was without complication in five, was associated with J52 cerebral
embolism and hemiplegia in one patient, and with .B3 minute cerebral
embolism and chorea in another. In one instance, in which the
temperature was high (105*8°), there was no note of delirium.

A* One of the four cases in which delirium passed into coma was
a delicate, ailing woman. On the seventh day her temperature in
the morning was 102°, but it rose in the evening to 109-5°, when
she was comatose. For want of a bath, she was taken downstairs,
placed, doubled up, in a washing-tub containing water at 80° cooled
to 62°, and cold water was ladled over her body. Spasms soon came
on, which were more and more continuous until she was taken
out of the bath in one of them after being there for forty-five minutes,
while her temperature had fallen to 100*3°. Towards midnight she
was much convulsed, the teeth closing firmly on the lower lip and
drawing blood. On the tenth day the temperature rose to 105*1°,
she was again put into the tub for fifty- eight minutes, and at the end
of that time was taken out in a state of well-marked opisthotonos,
which passed off gradually in about two hours. She died on the
twelfth day.1

BL Three of the four cases with delirium without coma had high tem-
peratures, 111*4° — 108*5°; while in two the temperature was com-
paratively low, 103*9° — 102*8°. One of the patients with delirium
and high temperature was a female servant, aged 22. On the eighth
day of treatment, temp. 108*5°, her sensorium was much disturbed,
and her skin, which hitherto had been moist and sometimes covered
with sweat, was dry. Cold was used energetically. Ice-cold water
and cloths were applied freely to the body, and ice-water enemata
were given every half-hour. In an hour's time she breathed more
freely, her head was relieved, and the pulse fell At half-past
six in the evening her temperature was 98*6°, skin perspiring, mind
clear, and she felt like a new-born person. Two days later she
sat up in bed, and took food with appetite.2

In the two cases with comparatively low temperature the delirium
was only present during the night. The temperature was 103*9° in
the daytime in one of these patients, and 100*4° in the other.
Convulsive movements affected four of the thirteen patients belong-
ing to this group with endocarditis.

The affection of tJic joints was severe in eight and was rather
severe in one of the tliirteen cases with simple endocarditis before
the period of delirium or coma; while it was absent in two and
not severe in three ; and its condition was doubtful in four of those
cases during that period.

1 Dr. Andrews, " Bartholomew's Hospital Reports" x. 346.

2 Dr. Meding, Archiv der Heilkunde, xL 4(57.

264 A SYSTEM OF MEDICINE.

Perspiration was profuse in five and absent in one of the cases of
simple endocarditis before delirium set in ; and it was absent in two,
slight in one, probably profuse in one, and doubtful in two of those
cases after the appearance of delirium, while it was profuse in another
patient who was delirious when admitted and whose temperature never
rose above 102-8°.

III. — Cases in which theke was no Pericarditis, Endocarditis

BEING ABSENT OR DOUBTFUL, IN WHICH THE NERVOUS SYSTEM
WAS AFFECTED, AND THE TEMPERATURE, GENERALLY VERY HIGH,
WAS OBSERVED.

SUMMARY.

A* Had delirium followed by coma, temp, lll'l0 — 105*8° . 6

Ak Had delirium followed by somnolence, temp. 106° ... 2

J51 Had delirium uncomplicated, temp. 110° to 100*4°. . . 10

Very high temperature without delirium, temp. 1 10*8° — 106*3° 2

Twitching of limbs, temp. 102° 1

Total .... 21

Twenty-one cases had no pericarditis, endocarditis being absent or
doubtful; and the majority of these cases, like that of those with
pericarditis and with simple endocarditis, presented an excessively
high temperature ; and in five of the whole number the temperature,
when undergoing a rapid ascent, was arrested in its rise, lowered, and
kept down by the use of the cooling bath, the wet sheet, or ice. The
temperature was as high as from 106° to 111*2° in three-fifths of the
cases (12 in 21), being kept down in the one of those in which it
was the least high by the use of the cooling bath. In one-fifth of
the cases (4 in 21), the highest ascertained temperature varied from
106° to 103*4°, and in these the cooling bath was not employed. In
one-fourth of the cases (5 in 21), the highest temperature varied
from 102° to 100*4°. From this summary it would appear that three-
fifths of these cases of acute rheumatism without pericarditis, endo-
cardititis being absent or doubtful, in which the nervous system was
seriously affected, had hyperpyrexia.

Pericarditis was absent and endocarditis was absent or doubtful, as
we have just seen, in twenty-one cases of acute rheumatism in which
there was affection of the nervous system and the temperature was
ascertained. A8 In six of those cases delirium gave place to coma, and
in one of these the delirium reappeared : A4 in two delirium passed into
somnolence. Bl Delirium without coma was present in ten cases. Two
patients had very high temperature without delirium, one of whom was
restless and talked when asleep, and the other had vomiting and
dyspnoea ; and in one there was twitching of the limbs and body
without delirium, the temperature not rising above 102°.

PERICARDITIS. 265

Az The whole of the six cases in which delirium passed into coma
were fatal. The delirium was present in these patients when the
temperature varied from 102*2° to 108*4°, and coma replaced the
delirium in five of them at fca temperature ranging respectively from
108° to 110°. The highest temperatures observed in these cases
towards or at the time of death was from 109*5° to 111*1°; In a case
in which delirium gave place to coma and that again to delirium,
the temperature about the period of coma was 104°, but eight hours
before death it was 105*8°. *

The delirium was violent or active in four of these six patients,
three of whom got out of bed or tried to do so ; and in two of them
it was muttering or quiet.

The duration of the delirium varied much in these cases. In one
patient the delirium continued for four days, in another two ; in one
it lasted four hours, and in another, the most interesting of the series,
after it was slight for one day, it became muttering for half an hour.
The duration of the coma was more constant. It lasted for from an
hour to an hour and a half in four cases, and in one for four hours,
while in one there was alternate delirium and coma for two days.

A* In two cases delirium passed into drowsiness. One of these, a
dull, corpulent woman, aged 32, was strange in manner (temp. 103*4°)
on the eighth day after admission, and had low muttering delirium.
At 2 A.M. on the following night (temp. 105*3°) she awoke restless ;
and at 5 a.m. (temp. 106°) she was dull and somnolent. She was put
for twenty minutes into a bath at 90° to 81°. When in the bath she
felt comfortable, but at length she complained of cold (temp. 102°).
After this her temperature never rose above 104*7°, she had bronchitis
and pneumonia for some days, and finally recovered.

I was favoured by Dr. Murchison with notes of the other case of
this class. A lady, aged 35, stout, was attacked with acute rheu-
matism. At the end of ten days her joints were better, but she
became sleepless and delirious. Opium, chloral, and bromide of
potassium only made her worse. Her pulse was 108, weak ; temp.
102*5°. She gave no signs of peri- or endo-carditis, and had head-
ache. The following is the report of her case ten days later : — " The
temperature has been as high as 106°, but is now only 101°. She is
heavy and drowsy, but has been very noisy and delirious. Eespira-
tion is quick and irregular — cerebral. She swallows well. Pulse 64.
Heart seems still sound. Urine is made in bed. There are bed-
sores, and she has some pains in the joints." She died next day.

B1 There was delirium without coma in ten cases. In three of these
the temperature was very high, being 110° in a fatal case; and 108*2°
and 107° respectively in two that recovered after the use of the cool-
ing bath ; in one of these the temperature, rarely above 104*6°, once
rose to 105°, and this case died in spite of the repeated use of the
bath ; while the remaining six cases had the comparatively low
maximum temperatures respectively of 104*5°, 103*4°, 101*2°, 101*1°,

1 Lebert, " Klinik des acuten Gelenkrheunintismus," p. 55. A

266 A SYSTEM OF MEDICINE.

1011°, and 100-4° ; and of these the first case (temp. 104-5°) and that
in which the temperature was the lowest (100#4°), a case with Bright's
disease, died, while the four others recovered.

The duration of the delirium was very various in different cases,
having ended in death in one instance in two hours and a half, and
being prolonged with interruptions in another for twenty-nine days,
the high temperature being kept down and lowered and the delirium
from time to time suspended by the cooling effects of a succession of
twenty baths.

As I have just said, in two of the three cases with delirium and
very high temperature, the temperature was kept in check by the
cooling bath. One of these cases, a youth, on the morning of the
fourth day of treatment, muttered to himself but could be roused,
temp. 107*8°, and at 7.45 temp. 108-2°. After being half an hour in
a bath at 76°, his temperature was 101°, and half an hour later 98*8°,
when he fell asleep, and awoke in a perfectly conscious state. In the
evening, a second bath again lowered the temperature from 105*8° to
98°, when he perspired freely and slept. After this the temperature
never rose above 99*8°, and he recovered.1 The second case, a woman,
with a temperature of 107°, was put into a bath at 90° cooled to 42°.
Her temperature was lowered to 97*5°, and her mind became clear.2

One patient, a man, who had been a free liver, presented throughout
from time to time profuse sweating, variable delirium, tremor of
hands, subsultus, and twitchings of the face, and a temperature
varying from 104*4° to 106'4°. The use of the cooling bath invari-
ably lowered the temperature, restored the patient from a state of
delirium to one of consciousness, and caused a subsidence of the
other nerve-symptoms, tremor, subsultus, and facial spasms. This
condition lasted for twenty-nine days, during which time twenty
baths were employed, five of them in one day for a combined period
of over five hours, and the patient finally died, the temperature at
the instant of death being 104'2°.3

Among the six cases with delirium in which the temperature was not
very high, varying from 104'5° to 1004°, two died and four recovered.

One of these cases, with a temperature of 103'5°, was a great beer-
drinker. His hands were tremulous, he wandered during the day,
was very noisy towards the evening, when he screamed out much, con-
tinued in a state of variable delirium for fourteen days, and finally
recovered.4

The highest temperature observed in the four remaining cases with
delirium was 101#4° and 100*4° respectively. Two of them had albu-
men in the urine, and the other one had obstinate diarrhoea, and was
delirious when the diarrhcea was checked.

There were three cases of hyperpyrexia in which there was no

1 Dt. Weber, Clin. Soc. Trans, v. 186.
* Sir WiUiam Gull, Lancet, 1872, il 662.

3 Dr. Greenhow, Clin. iSoc. Trans, vi. 7.

4 Dr. Johnson, Lancet, 1867, i.

PERICARDITIS. 267

delirium. One of these was a man whose temperature rose to 106'3°.
He had previously been deaf and very restless. Under the influence
of a cooling bath his temperature fell to 101'8°, and later to 99*8°.
After the bath his deafness left him, and he did welL1 Another case,
a woman aged 24, was suddenly seized with dyspnoea and vomiting,
which continued until death; a short time before which event her
temperature was 110*8°.2

Convulsive, Choreiform and Tetaniform Movements. — Twitchings
were present in four of the twenty-one cases that form this gronp, in
which there was no pericarditis and endocarditis was absent or
doubtful. The twitchings affected the body in one instance, the limbs
and features in another, the muscles of the face for a long period
in another, whenever the temperature rose ; and in a fourth, the
features occasionally twitched with a sardonic grin. In one case the
patient was restless and moved his arms about; bnt, perhaps with
this exception, there were no notable choreiform or tetaniform move-
ments in any of the cases. In two cases there was tremor — in one,
of the trunk and limbs, in the other, of the hands.

Twitching movements were present in four of the twenty-six cases
with pericarditis, in one of the eleven cases with simple endocarditis,
and as we have just seen, in four of the twenty-one cases in which
there was no pericarditis and endocarditis was absent or doubtful.
Twitching movements were therefore distributed in nearly equal pro-
portion in those three groups of cases, and were therefore not due to
pericarditis. Twitchings were present in eight cases with hyper-
pyrexia, and it is therefore probable that they were associated with the
very high temperature. This is borne out by a case of Dr. Greenhow's,
in which twitchings came on, and were again and again renewed when
the temperature became very high, and were again and again almost
or quite suspended by the cooling bath.

In the remaining case with twitchings, a man who was under my
care, the temperature was never above 102°. On the fifth day, temp.
100*2°, he hacl muscular twitchings all over the body, which continued
for several days, and reappeared on the twenty-eighth day. There
was albumen in the urine on both occasions when the twitchings
were present. His recovery was slow.

There were choreiform or tetaniform symptoms — or both — in seven
of the twenty-four cases with pericarditis, but in only one of the
eleven cases with simple endocarditis, and in none of the twenty cases
in which there was no pericarditis, endocarditis being absent or doubt-
ful. The question how far the choreiform and tetaniform movements
observed in these cases was connected with pericarditis will be con-
sidered when we review the larger series of cases of acute rheumatism
with and without pericarditis in which the temperature was not
observed.

The affection of the joints during the early period of the disease

1 Dr. II. Thompson, Medical Times and Gazette, 1873, i. 269.

2 Dr. Ogle, Lancet, 1870, ii. 154.

268 A SYSTEM OF MEDICINE.

was severe in ten, and moderately so in five of the twenty-one cases
in which there was no pericarditis and endocarditis was absent or
doubtful. The affection of the joints was more severe before than
during the delirium or other affection of the nervous system, in
all but three cases, in which the joint-affection was equally severe
during the two periods. In two of these three exceptional cases the
temperature never rose above 102°, in one of these the delirium was
only present during the night, and in the other there was no delirium,
but twitchings were present for a short time during the early days
of the illness.

Perspiration. — The state of the skin is described in one-half of the
cases belonging to this group (10 in 21), and all of these had profuse
perspiration before the nervous system became affected. In seven of
those cases there was either no perspiration, or it was much lessened
during the period of delirium. In that case, perspiration was equally
copious during the two periods. In three of these cases the skin,
winch had been perspiring profusely before the excessive rise of tem-
perature, and the occurrence of delirium, was hot and dry when the
temperature was 110° to 111/1°; coma was present, and death ap-
proached. These clinical facts correspond with those which, as we
have already seen, occurred in the analogous cases affected with peri-
carditis. One of the cases in which there was no affection of the
heart was observed by Mr. Anderson night and day. This patient, of
a nervous, excitable temperament, a labourer, aged 29, had a hot, dry
skin, and rambled during the night for four succeeding nights ; but
during the three intervening days his skin was covered with a profuse
acid perspiration, and his mind was unaffected. On the morning of
the fourth day his manner was wild and excitable, not unlike that of
a patient in the early stage of delirium tremens, and his skin was hot
and dry, and covered with a miliary eruption. After a bath, he sprang
out of bed, ran into the grounds, and struggled violently. His tem-
perature at that time was 107°, and later in the evening, ten minutes
before his death, it was 110*3°.

Dr. Greenhow's case, already referred to at page 261, offers a contrast
in some respects, but not in others, to Mr. Anderson's case. In this
man, perspiration was absent with delirium at a temperature of 104*8°,
and was absent without delirium after the bath at 100*2°, and was
present afterwards with obscured intellect and intermediate tem-
peratures.

Perspiration, which is not present at ordinary temperatures, is in-
deed an index of the internal production of great heat, and a safety-
valve for carrying away a large portion of that heat. When per-
spiration takes place from an exposed skin in a dry air — in motion
— its evaporation tends to keep down the heat. In these patients,
however, lying, as they do, in their own perspiration, covered by bed-
clothes, in a still air saturated with moisture, evaporation can do com-
paratively little towards cooling the body.

We must look, then, to some other influence than evaporation to

PERICARDITIS. 269

account for the cooling effect of perspiration in acute rheumatism.
Such an influence we find in the welling out of hot liquid from every
part of the body — a liquid charged with a portion of the surplus heat
generated hy the rapid combustion or disintegration of the internal
structures in that disease. It is self-evident, that if the temperature
of the body be 103° or 104°, the fluid poured out from the body must
likewise have a temperature of 103° or 104°, and that this fluid during
its steady universal expulsion must carry away with it a corresponding
proportion of the heat generated within, and so tend to keep down
the temperature of the whole of the structures that compose the body.

If, on the other hand, the skin is dry, the chemical heat generated
in the rapidly-changing tissues tends not to escape, and may be stored
up in accumulating quantities in the blood and the tissues, with the
effect of producing an excessively high temperature, or " hypeTpyrexia.,,

Respiration. — I have not made an analysis of the rate of respira-
tion in cases of acute rheumatism with affection of the nervous
system, with and without high temperature. One well-observed and
well-treated case of hyperpyrexia is sufficient for our present purpose,
which is to illustrate the influence of an excessively high temperature
of the body on the one hand, and of the cooling of that body on the
other, on the frequency of respiration. In Dr. Wilson Fox's case,
already related at page 257, when the temperature of the body was
107°, the patient was delirious, and the respiration was 45 in the minute,
but when the patient's body had been cooled down by the bath to
98°, the mind was clear, and the respiration was 20 in the minute.

It is evident, therefore, that during hyperpyrexia, the cooling effect
of respiration is stimulated to its highest degree by the excessive
heat of the body, but that this cooling effect is quite inadequate to
keep down the temperature of the body below that of hyperpyrexia.

There were some conditions common to the three sets of cases —
those namely with : 1, pericarditis ; 2, simple endocarditis; 3, without
pericarditis, endocarditis being absent or doubtful — and I shall now
briefly notice those conditions.

Restlessness affected a considerable proportion of the patients before
the occurrence of delirium. Six of the twenty-seven cases with pericar-
ditis ; three of the thirteen cases with simple endocarditis ; and ten of
the twenty-one cases that had no pericarditis, endocarditis being
absent or doubtful, were thus affected with restlessness.

A miliary eruption or sudamind appeared in a considerable number
< >f the cases, being noticed in twelve of the twenty-seven cases with peri-
carditis ; in three of the thirteen cases with simple endocarditis ; and
in eight of the twenty-one cases in which there was no pericarditis
and endocarditis was either absent or doubtful.

An abundant secretion of urine took place in a few of the cases, at
the time of the great rise in temperature. The urine was very abun-
dant under those circumstances in three of the twenty-seven cases
with pericarditis ; in three of the thirteen cases with simple endocar-

270 A SYSTEM OF MEDICINE.

clitis ; and in two of the twenty-one cases in which there was no
pericarditis, endocarditis being either absent or doubtfuL

DiarrJuea, sometimes profuse and offensive, was present when the
temperature was very high in seven of the twenty-seven cases with
pericarditis ; in four of the thirteen cases with simple endocarditis ;
and in five of the twenty-one cases in which there was no pericar-
ditis, and endocarditis was either absent or doubtful.

Excessively high temperature or " hyperpyrexia " in acute rheumatism
with and without pericarditis. We have just seen that in sixty-
one cases of acute rheumatism in which the temperature of the patient
was observed, the nervous system was affected, and we shall now
enquire how many of them presented an excessively high temperature,
and what was the influence of pericarditis in those cases of hyper-
pyrexia. The temperature was excessively high, ranging from 106*8°
to lll'l0 in thirty-one of those sixty-one cases, and was arrested
during its rise when it was at from 105° to 106*3° by the use of the
cooling bath, or cold externally, in six cases. In three of those six
cases, the tendency of the temperature to rise was great, but in three
of them it was not so. The temperature was not observed during the
period of coma or the last hours of life in three fatal cases in which
the temperature was 104*6°, 104*8°, and 105-8° respectively at the
time of the last observation, and I consider that these three cases and
three of the six in which the high temperature was kept in check by
the bath, ought to be added to the thirty-one cases in which the
temperature was very high, thus bringing up the number of those
with " hyperpyrexia," to thirty-seven of the total number of sixty-one
cases. Thus estimated, we find that seventeen of the twenty-seven
cases with pericarditis, nine of the thirteen with simple endocarditis,
and eleven of the twenty-one without pericarditis, endocarditis being
absent or doubtful, either had, or were threatened with, "hyper-
pyrexia." Among these thirty-seven cases of hyperpyrexia, one had
coma without delirium, twenty-one, delirium followed by coma, or, in
one instance, stupor, two, delirium with convulsive movements, ten,
uncomplicated delirium, and three had neither coma nor delirium.

The case of simple coma, and all but one of the twenty-one cases
in which delirium passed into coma, were affected with actual (18) or
threatened (3) hyperpyrexia. The temperature observed soon rose
above 100° in three cases with delirium and stupor, but in one of
these it was kept down and lowered by the cooling bath, while in
both the cases which ended fatally with convulsive movements, the
temperature was very high. Of the twenty-four cases with uncom-
plicated delirium, only two-fifths had hyperpyrexia (10 in 26).

Coma preceded by delirium is, as we have just seen, the typical
effect of rheumatic hyperpyrexia, and one-half of those with hyper-
pyrexia and coma preceded by delirium, had pericarditis (10 in 20).
From these clinical facts it would appear that hyperpyrexia attacked
cases of acute rheumatism almost as frequently when they had peri-

PERICARDITIS. 271

carditis, as when they were not so affected (17 in 27 with pericarditis,
20 in 37 without pericarditis). When we consider that pericarditis
usually attacks only one in every five or six cases of acute rheuma-
tism, we must multiply the cases of pericarditis with hyperpyrexia
by five or six if we would make a parallel comparison between those
cases with pericarditis and those without it. It would appear from
this that the presence of pericarditis in a case of acute rheumatism
increases the chance of the occurrence of hyperpyrexia with delirium
and coma, in the proportion of four or five to one. An important
case successfully treated by Dr. Wilson Fox by the cold bath had
pericarditis in its worst form. The dulness or percussion over the
region of the pericardium filled the whole left front of the chest from
apex to base. In that case the tendency to the renewed excessive rise
of temperature after it had been brought down again and again by
the cold bath, the ice-bag, or the wet-pack, continued until the seventh
day ; when the pericardial dulness fell to the first rib mid-sternum, and
the tendency to the increase of temperature lessened. It is a clinical
fact that here the renewed rise of temperature continued so long as
the pericarditis was severe, and gave way when the pericarditis gave
way, and it is probable that the continued severity of the pericarditis
had an influence in keeping up the tendency to the rise of tempera-
ture. It must however not be lost sight of that as a rule, cases of
acute rheumatism with pericarditis are in all respects worse than
those without it, and that, not only at the time of the pericardial in-
flammation, but usually also before it. It becomes therefore a question
whether or not the same severity of the acute rheumatism itself that
brought the pericarditis into existence, brought also the excessively
high temperature, with its attendant delirium and coma into existence,
the two affections being affiliated, and due to a common cause.

The occurrence of a high temperature of the body in cases of acute
rheumatism, corresponds in essential features with the high tempera-
ture observed in sun-stroke, in certain exceptional cases of tetanus,
and in injuries to the cervical portion of the spinal marrow. In sun-
stroke the temperature varies from 112° to 105'5°, the skin is hot and
dry, coma supervenes, preceded occasionally by delirium, and death
tends to ensue unless the temperature of the body is lowered by
cold.1

The temperature in tetanus, though variable, does not as a rule rise
to a very great height Wiinderlich, however, gives a case in which
it attained to 44*75° C. (112-55° F.) before death.2 This instance
resembled in all its main features the cases of hyperpyrexia in acute
rheumatism. The patient, before the time of the fatal rise of heat,
was very restless ; had profuse perspiration and an abundant miliary
rash ; then came on delirium, night trembling, contracted pupils, and

1 Dr. Levick, " Pennsylvania Hospital Reports," 1868, p. 371 ; Dr. Gee/Gulstonian
Lectures on Pyrexia, Brit. Med. Journal, 1871, I. 802 ; Dr. ^Maclean on Sunstroke,
Reynolds' "System of Medicine," II. 128.

* Wiinderlich, Arckiv der Heilkunde, II.

272 A SYSTEM OF MEDICINE.

death. Wiinderlich, without giving any reason for it, gives the name
of rheumatic tetanus to another but less extreme case of the same
kind.

Injury of the spinal cord from the fourth to the sixth cervical
vertebra from fracture or caries of the spinal column has induced an
excessively high temperature in several cases published since the
first observation to that effect by Sir Benjamin Brodie.1 The symptoms
in these cases closely resemble those of hyperpyrexia in acute rheu-
matism, but in only one of them was it stated that the final and fatal
coma was preceded by delirium. One of Dr. Hermann Weber's two cases
was a youth, who could walk supported, but like a drunken man, and
could move his arms twenty minutes after the accident, which caused
fracture and incomplete dislocation of the third, fourth, and fifth cervi-
cal vertebrae. He voided urine frequently and in great quantities. An
hour after admission his temperature was 100*4°. Two hours and
a-half after the accident he passed liquid motions unconsciously, had
occasional convulsive twitches in the arms and legs, his skin was
slightly moist and hot, and his temperature was 109*58°. Four. and
a-half hours after the accident there was complete coma, and his
temperature was 1110, and it was 111*2° at the time of death, eight
hours after the accident.2

Dr. Burdon Sanderson, who has favoured me with the use of the
manuscript notes of his lectures delivered at Manchester, gives an
account of experiments made by him in which the cervical portion
of the spinal cord was injured. He found that there was no increase
of temperature for two hours after the injury to the cord, but that at
the end of that time it began to rise and to rise rapidly, attaining
a very great elevation, 42° C. or 107*6° F., or higher than that of fever.
Dr. Burdon Sanderson considers that this experiment shows conclusive-
ly that the process of which the higher temperature is the outcome,
must consist in a gradual modification of those processes on which
heat production depends, must have as wide a localisation as they,
and cannot therefore be attributed to any sudden interruption of the
relation between the centre and the periphery of the nervous system.
These experiments correspond remarkably with Dr. Hermann Weber's
case just reported.

Cases in which the temperature of the body was below that of hyper-
pyrexia.— We have just seen that of the sixty-one cases of acute rheu-
matism associated with affection of the nervous system in which the
temperature was observed, in thirty-seven there was actual (31) or
threatened (6) " hyperpyrexia." In the remaining twenty-four cases,
the maximum temperature of the body observed in the different
instances varied from 99*3° to 106*3° temp. Ten of the twenty-seven
cases with pericarditis, four of the thirteen with simple endocarditis,
and ten of the twenty-one without pericarditis, and in which entlo-

1 Sir Benjamin Brodie, Med. Chir. Trans, xx. 118 ; Roineke, Berliner Klinisrhe
Worterbuch, 1869, 113, 301 ; Billroth, Archiv fur Klin. Chirargie Langenbeck, ii. 482.

2 Dr. Hermann Weber, Clin. Soc. Trans. I. 108.

PERICARDITIS. 273

carditis was absent or doubtful, belong to this group in which the
temperature was not excessively high. In twelve of these twenty-
one cases, the maximum temperature varied in the different cases from
103° to 106°, and in nine of them from 99*3° to 1028°.

A considerable proportion of those who were attacked with delirium
at comparatively low temperatures were either habitual drinkers, or
of a nervous temperament, or had been subject to anxieties and priva-
tion, or to lowering diseases, or had received injuries affecting the
nervous system, and in several of those cases the affection was closely
allied to delirium tremens ; several such cases occurred among those
affected with pericarditis. This was so in Dr. Southey's two cases
with pericarditis, referred to at pages 257, 258, in Dr. Greenhow's
case, given at page 258, in Dr. Murchison's two patients, quoted at
page 265, and in a patient of my own.

To these must be added the case with which Dr. Southey favoured
me since the above was written, given at page 258, and two of Dr.
Andrew's cases.

Most of these cases had pericarditis.

Cases of Acute Rheumatism with Affections of the Nervous
System in which the Temperature of the Body was not observed.

There were 119 cases of acute rheumatism with affections of the
nervous system in which the temperature was not observed. Of these
65 had pericarditis ; 16 had simple endocarditis ; and 38 were free
from pericarditis, endocarditis being absent or doubtful.

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PERICARDITIS.

281

SUMMARY OF CASES OF ACUTE RHEUMATISM, WITH AFFECTIONS OF
THE NERVOUS SYSTEM, IN WHICH THE TEMPERATURE WAS NOT
OBSERVED.

A1 — Coma without delirium or convulsions

A* — ,, with convulsions

A3 — ,, preceded by delirium ....
A* — Stupor preceded by delirium ....
A — Had Coma or Stupor. Total . . .

Had Semi- consciousness

B1 — Delirium, uncomplicated

B*—

»»

passing into temporary in-
sanity

with chorea or choreiform
or tetaniform symptoms

Total ....*..

B3 — Delirium, with chorea and choreiform
movements, not including those
with temporary insanity . . .

B* — Delirium with tetaniform movements,
not including those with temporary
insanity

B — Delirium without Coma. Total . ,

Delirium. Totals (including those with )
coma) j

C1 — Chorea without delirium

C* — Choreiform movements (jactitation), )

without delirium {

C3 — Tetaniform symptoms, without deli- j

rium |

/)-Had slight at. .

E— Had Embolism, hemiplegia ....

F — Had Paraplegia

O — Had agitation and prostration . . .
Total

With
Pericar-
ditis.

II
5

2
5
0

Simple
Endocar-
ditis.

0
1
0
0

5
o

2 o
13

•!

2! -

No Perlc,
Endocard. T
absent or 10TAI^
doubtful.

2
2
8
2

2
1

77
92

7
2

1
1
2
1
119

I. — Cases affected with Pericarditis.

There were sixty-five cases of acute rheumatism with pericarditis,
in which the nervous system was affected. (A.) Ten of these had
coma, of which (A1,) three had uncomplicated coma; (A2,) two had
coma with convulsions ; and (A3,) in five the coma was preceded
by delirium. (B.) Forty-three cases had delirium without coma ;
of these (B1,) twenty-one had uncomplicated delirium, one of which
had " symptoms of inflammation of the brain," and one apparently
had pyaemia ; (B2,) sixteen, of which five had choreal or tetaniform
symptoms, had temporary insanity, lasting from two weeks to three

282 A SYSTEM OF MEDICINE.

months, or, in three instances, insanity was cut short by death ; (B8,)
four had chorea or choreiform movements, and (B4,) two had tetani-
form symptoms without temporary insanity. (C1.) Eight of the cases
had chorea or choreiform movements, and (C2,) two had tetaniform
symptoms without delirium. (D.) One of them had a slight fit with
ptosis.

II.— Cases affected with Simple Endocarditis.

There were sixteen cases of acute rheumatism with simple endo-
carditis, in which the nervous system was affected, excluding cases of
ordinary chorea, but including cases of chorea rapidly fatal, or with
delirium.

(A2.) One of these cases had coma with convulsions, associated with
acute Bright's disease from embolism. (A8.) One had delirium end-
ing in coma, with embolism of the minute cerebral arteries. (B.)
Twelve of them had delirium without coma, of these (B1,) seven had
uncomplicated delirium; and (B2,) five passed into a state of tem-
porary insanity, lasting from three weeks to four months. (C1.) One
had chorea ending rapidly in death. (E.) One had embolism with
hemiplegia.

III. — Cases in which there was no Pericarditis and Endocarditis

WAS ABSENT OR DOUBTFUL.

There were thirty-eight cases of acute rheumatism without peri-
carditis, endocarditis being absent or doubtful, in which the nervous
system was affected, exclusive of cases of ordinary chorea. (A.) Twelve
of these had coma or stupor, of which, (A1,) two had uncomplicated
coma, (A2,) two had coma with convulsions, (A8,) in eight the coma
was preceded by delirium ; and there were also (A4,) two Cases in
which delirium passed into stupor. (B.) Twenty of the cases had
delirium including two with "cerebral rheumatism," and one that
had pus in the pia mater ; of these (B1,) fourteen had uncompli-
cated delirium; (B2,) five passed into temporary insanity, two ot
which had chorea also; (B8,) one had chorea; and (B4,) one had
tetanic spasms. (F.) Two of the cases had paraplegia. (G.) One of
the cases had agitation and prostration ending in rapid death.

A. — Coma.

I. — Cases with Pericarditis. A1. — Uncomplicated Coma. — Three
cases with Pericarditis had coma without convulsions or delirium,
all of which proved fataL

A2. — Coma with Convulsions. — In the two cases of coma with
convulsions, death was speedy.

A8. — Coma preceded by Delirium. — Four of the five cases in which
delirium passed into coma, died ; and one recovered. One of the
cases passed rather into stupor than coma. The duration of the

PERICARDITIS. 283

coma in these cases was variable and uncertain, and that of the
delirium lasted for from one or two nights to nine or ten days.

II. — Cases with Simple Endocarditis. A2. — Coma with Convul-
sions.— One fatal case of coma preceded by convulsions had simple
endocarditis with embolism of the spleen and kidneys, the coma
and convulsions being evidently associated with acute Bright's
disease.1

III. — Cases witlwut Pericarditis, Endocarditis being absent or doubtful.
Ah 2. — Coma without and with Convulsions. — There were four fatal
cases of coma without delirium among the cases without perioarditis,
endocarditis being absent or doubtful, two of them having convulsions.
In three of them death was very rapid, and in one coma, coming on
after convulsions, lasted for twelve hours before death.

These cases did not differ materially in character and history from
those with coma and pericarditis.

A3. — Coma and Delirium. — Coma was preceded by delirium in
eight fatal cases that presented no sign of affection of the heart.

The delirium was more frequent by night than by day, being pre-
sent in three of the cases from two to five or six nights, while it was
absent in the daytime, and it lasted in the other five cases from two
to four or five days.

The coma, as a rule, soon ended in death. In one half of the cases,
or four, the delirium became violent, and in the other half, its character
was not described.

These cases do not differ materially in essential character from
those with pericarditis that were affected with delirium and coma.
There were, however, nervous symptoms in the form of agitation,
twitchings, and choreiform and tetaniform movements in a much greater
proportion of those with pericarditis than of those not so affected.

A4. — Delirium and Stupor. — One of the two cases in which deli-
rium preceded stupor recovered after the employment of the wet
sheet, and the other died.

B.— Delirium.

B1. — Uncomplicated Delirium. — 1. Cases with Pericarditis. — Twenty-
one of the sixty-five cases with rheumatic pericarditis had uncompli-
cated delirium, including one with u symptoms of inflammation of the
brain," and one with probable pyaemia. Eleven of these cases died and
ten recovered.

The duration of the delirium varied much. The delirium was more
active by night than by day, and in five cases was present from one
to three or four nights, but was absent during the day. In the
rest of the cases it lasted from for a few hours to four or five days.
The delirium was noisy or violent in eleven instances, moderate in
four, and slight in five cases.

1 Freriohs, "On the Diseases of the Liver," New Sydenham Soe. Edition, vol. i. p. 16*.

284 A SYSTEM OF MEDICINE.

One case, a female servant, felt much better at the evening visit,
but a quarter of an hour later became delirious, with loud continuous
cries. A varied treatment, including wet packing, was employed, and
she recovered.

Another case, a workman in Messrs. Guinness's Brewery, drank
largely of their XX porter besides whisky. He had pericarditis,
and " delirium tremens," and recovered after taking opium.1

2. Cases with Simple Endocarditis. — Seven of the sixteen cases
with simple rheumatic endocarditis had uncomplicated delirium.
Three of these cases died and four recovered.

The duration of the delirium varied from, for a single night in one
patient, to at least nine days in another. It was present more often,
and, as a rule, with greater violence by night than by day. In four of
the cases the delirium was active or violent, in one the delirium was
wandering, and in another, it was accompanied by somnambulism.

One of these cases was observed by Dr. Boisragon and Mr. Tudor,
and reported by Dr. Davis, and is, so far as I have discovered, the
first case in which endocarditis was well described.

Three of the cases of endocarditis with delirium were under my
own care, and of these, one died and two recovered.

3. Cases without Pericarditis, Endocarditis being absent or doubtful. —
Fourteen of the thirty-eight cases without pericarditis, endocarditis
being absent or doubtful, had uncomplicated delirium. Ten of the
fourteen cases died, and four recovered.

The duration of the delirium varied much in the different cases.
It prevailed more during the night than the day. In three instances
it was only present during the night for from one to three nights. In
one case the delirium was only present for a quarter of an hour before
death, in four cases it existed for one day, and in four others from two
to five or six days. The delirium was violent or lively in five of the
cases, and five were simply " delirious."

These cases corresponded in essential features with those that had
delirium with pericarditis.

" Hyperpyrexia " in cases of acute rheumatism without and vfUh Peri-
carditis in which the temperature was not observed. — The ten fatal cases
belonging to the last group of fourteen with delirium, the twelve with
coma and the two with stupor, all of which had neither pericarditis
nor endocarditis, evidently belong to the important group of cases of
acute rheumatism with hyperpyrexia. All of those twenty-four cases
except one with stupor, died, and that patient recovered after the
external use of the wet sheet. The ten cases with coma, and the
eleven fatal cases and one case that recovered under the use of wet
packing that had uncomplicated delirium among the patients with
pericarditis, and three fatal cases of delirium with simple endocarditis,
may also be ranked among the cases of hyperpyrexia. According to this

1 Dr. Graven, " Clinical Lectures on the Practice of Medicine," vol. i. p. 531.

PERICARDITIS. 285

estimate, twenty-two of the sixty- five cases with pericarditis, three of
the sixteen with simple endocarditis, and twenty-four of the thirty-
eight without pericarditis or notable endocarditis, in which the tem-
perature was not observed, were affected with " hyperpyrexia."

These forty-nine cases corresponded in their broad features as
regards coma, delirium, and death with those cases of" hyperpyrexia"
in which the temperature was observed. As in those also so in these, in
the few cases where these conditions were observed, the affection of the
joints ceased when the delirium appeared, and the perspiration, copious
during the earlier stages, was absent or much lessened during the
stage of delirium or coma, when the skin was usually dry and hot.

Convulsive, choreiform, and tetaniform movements in the cases with
hyperpyrexia.^— There was an important difference in the two sets of
cases with and without pericarditis, as regards the presence of con-
vulsive, choreiform, and tetaniform symptoms in combination with the
far more important symptoms of " hyperpyrexia."

Convulsive movements, jactitation, agitation, choreiform movements
without actual chorea, and tetaniform symptoms, appeared more fre-
quently in the cases of coma or delirium with pericarditis, than in
those without pericarditis. Involuntary movements of the muscles
occurred in one, and general agitation in three of the twenty-five
cases of hyperpyrexia that had neither pericarditis nor notable endo-
carditis. A convulsive fit occurred in one, jactitation of the limbs
or body in two, tetaniform symptoms in two, and great general
agitation in three, of the twenty-two cases with hyperpyrexia that had
pericarditis. Besides these eight instances of convulsive, choreiform
or tetaniform affections among the fatal cases of coma and delirium
with pericarditis, there were two with jactitation, and one with
twitchings of the muscles of the face, among the cases of delirium
with pericarditis that were not fatal. Four of the eleven cases with
pericarditis thus affected with convulsive, choreiform, or tetaniforni
movements had endocarditis, three had no endocarditis, and in four
the presence of endocarditis was doubtful.

We have already seen that among the cases of " hyperpyrexia," iu
which the temperature was observed, choreal and tetaniform symptoms
occurred much more frequently among those with, than among those
without, pericarditis ; while on the other hand twitching movements
were as frequent among those without, as among those with, peri-
carditis.

Delirium resembling Delirium Tremens.— Among the cases of deli-
rium in acute rheumatism without pericarditis or evident endocar-
ditis as among those previously analysed with pericarditis, there are
several that present symptoms partly allying them to delirium
tremens — partly to the delirium of rheumatic hyperpyrexia, and that
are associated with previous habits of drinking, or with some affection
of the nervous system. One of these patients, a hard drinker, com-
plained of being unable to see, called out " thief," rushed out of bed
and fell down. After this he struggled with two attendants, and then

286 A SYSTEM OF MEDICINE.

dropping back, died. All this took place in less than a quarter of an
hour.1

Two of my own patients belong to this class, one of whom recovered,
the other died. One was a stout florid waiter, aged 40, who perspired
profusely, slept but little, and became very violent. On the seventh
night he slept with an opiate. He recovered rapidly.

The patient who died was a barman, aged 23, who was rather rest-
less, and hurried in speech on the day after admission, became more
restless on the third day, and died suddenly.

B 2. — Temporary Insanity with Taciturn Melancholy and

Hallucinations.

B2. I. — Cases with Pericarditis. — The series of cases that I have now
to consider present a remarkable succession of symptoms. In eleven
cases of acute rheumatism with pericarditis, delirium, usually
desponding and taciturn, often with hallucinations, came on when the
heart was inflamed ; but instead of passing away quickly, this sombre
delirium lasted for from two or three weeks to three months. Of
these eleven cases of temporary insanity, ten recovered, and one died ;
eight of those cases were females, six being below the age of twenty,
and three were males. All but one of these patients were affected
with endocarditis as well as pericarditis.

The duration of the insanity varied considerably, and the return to
a healthy state of mind was gradual, and never sharp. The temporary-
insanity lasted for above a fortnight in three cases ; for about a month
in three ; for two months in one ; for ten wreeks in one patient, whose
mind was not yet clear at the end of that time ; and one died with her
intellect still confused at the end of two months.

The prevailing feature of the delirium was a state of taciturn
melancholy. Only one patient, a young woman, the fatal case, was
at times in wild delirium, at times taciturn and almost idiotic, and
at times quiet and rational.2 Eight of the patients were taciturn, and
two others were confused in mind or speech. Four of them had
hallucinations ; one saw her mother at her side ; one a knife and
poison ; one was followed and insulted, and then reached out his
hand as to an old friend ; and one complained of vermin. Another
patient had delusions.

Two of my patients belong to this series of cases. One of these, a
potman, aged 21, on the seventeenth night after his admission was
in a state of partial stupor and delirium. On the following day he
answered no questions, and as he would not take food, stimulants
were given by enemata. On the twenty-sixth day he again took food,
but he continued to be taciturn. On the thirty-ninth day he recovered
the powers of nature, was up on the forty-seventh, and left on the
seventy- fifth day, his heart-sounds being healthy.

1 Trousseau, " Lectures on Clinical Medicine," (New Sydenham Soc.) vol. i. p. 613.
1 Sir Thomas Wataon, loc. cit. ii. 307.

PERICARDITIS. 287

The other case, a labourer, with endo-pericarditis, had a vacant,
torpid, and wandering mind for three weeks, which followed an attack
of hemiplegia from embolism affecting the right side, with loss of
speech, which was apparently a mixture of aphasia and a taciturn
character of mind. On the tenth day his face was paralysed on the
right side, and the pupils were irregular. On the thirteenth he would
not or could not speak, but muttered slightly, and tried to get out of
bed. He improved daily and his speech returned, but his expressions
were incoherent. On the thirty-eighth day he had more command over
his articulation, and on the forty-second had almost regained the
use of his right side. He improved steadily, and on the seventy-
second day he went out well, the heart-sounds being healthy.

Besides the eleven cases just spoken of with temporary insanity
of a taciturn melancholic type, there were five others in which a
similar condition was associated with chorea or choreiform movements
(in 4) or with tetaniform symptoms (in 1). Three of these cases
were fatal, and two of them recovered. The whole of the five cases
were below the age of twenty-one, and two of them were male and
three were female patients. All of them had endocarditis as well
as pericarditis. The affection lasted in one of the two that recovered
about a month, and in the other for a shorter period. The three
fatal cases died respectively in about twenty-three, sixteen, and nine
days after the beginning of the mental trouble. One of those patients
was taciturn, then delirious, and finally had the most violent chorei-
form movements, ending in death. Another fatal case had difficult
utterance, incoherence, tossing of the head from side to side, and
choreiform spasms which put on the character of the most violent
convulsions. A third case spoke loud and low, after, in succession,
being excited and stubborn, weeping, seeing a dead man, and grimacing
as in chorea : death took place an hour after an attack of universal
convulsions. One of the two cases that recovered had a rather childish
appearance ; her answers were sometimes irrelevant, sometimes rational,
and she had choreal movements of the right arm and leg.

The last case had delirium with tetanic spasms ; at first he had
an excited manner, with wild rolling of his eyes, then furious delirium,
followed by firm clenching of the hands, sleep, and a more tranquil
state. After this he was idiotic and violent by turns, until the twenty-
eighth day after the first disturbance of the mind, when he became
tranquil.

These sixteen cases with taciturn melancholy, often with hallucina-
tions, lasting for from three weeks to three months, and then usually
getting well, present a group of conditions that seems to separate
them from the twenty-one cases of delirium that were not followed
by coma, and the five that were so. In those cases the delirium was
often violent, generally active, sometimes muttering ; in these it was
melancholic and taciturn. In those cases the delirium was often ex-
clusively by night and was then almost always most noisy ; in these
it was present day and night, though it was usually more active by

288 A SYSTEM OF MEDICINE.

night. In those cases the delirium lasted for from one or more hours
to five or six nights and five days ; in these it lasted for from three
weeks to three months. In those cases perspiration was generally
profuse before the appearance of the delirium, the skin usually be-
coming hot and dry as the temperature rose to the fatal height ; in
these perspiration was only noted as being profuse in two cases, and
slight in one. In those cases death was the natural result ; in these,
all but one of the eleven without chorea recovered, while three of the
five with chorea died. In those endocarditis was absent in three-
fifths of the cases (11 in 32) with coma and delirium, but three more
of those cases probably had endocarditis ; in these endocarditis was
present in all but one.

We saw that in the two sets of cases, in one of which the
temperature was, and in the other, was not observed, delirium pre-
sented itself in two forms : (1) one, and the leading form, of delirium
with hyperpyrexia, ending in death ; (2) the other, the secondary
form, with a less high temperature in which a condition resembling
delirium tremens associated itself with and modified the delirium of
hyperpyrexia, often occurring in persons who had been intemperate,
anxious, nervous, or in want, and ending generally in recovery.

In these cases of temporary insanity with taciturn melancholy
we have clinical evidence of a third kind of delirium, differing
from the two other kinds of which we have just spoken.

These cases resemble in some of their symptoms, cases of insanity
with settled taciturn melancholy ; but from those they differ in this
essential point, that while in those the insanity is obstinate, often
indeed for life ; in these the insanity comes definitely to an end in
from two or three weeks to three or even four months.

The features, then, that characterize these cases of temporary
insanity are youth and previous good health ; or in a few casea in-
temperate habits ; the absence of hyperpyrexia ; the existence of endo-
carditis ; the settled though varying and even intermittent character
of the taciturn delirium, which is present, though modified, by day as
well as by night; and the dying out of the affection in a limited
period. These conditions point, not to a rapidly progressive and
varying cause, which marks hyperpyrexia, which is kept in check or
suspended by a perspiring skin, or the external use of cold, and is pro-
moted by a hot dry skin ; but to a continuous cause, that is excited
during the height of the disease, but that varies in operation for
from two weeks to three months after the acute rheumatism and the
acute stage of the endocarditis have passed away. In one of my own
cases there was embolism, evidenced by the loss of power in the right
side, and taciturn aphasia, in combination with endocarditis ; and
it appears to me that in embolism of the minute cerebral arteries of
the convolutions, we have a series of conditions that correspond with
those occurring in the whole of these remarkable cases. Embolism of
the cerebral arteries comes on with endocarditis, and arrests for a
time the circulation of the blood through the parts of the brain sup-

PERICARDITIS. 289

plied by the affected vessels ; its effects remain after the acute stage of
the originating endocarditis has passed away ; and, if death does not
cut short the clinical history of the case, those effects usually gradually
lessen and disappear in from two or three weeks to several months,
unless the extent of the plugging of the vessels be such as to cause
extensive softening of the part of the brain supplied by those vessels.
I therefore consider that to embolism we may have to look for the
explanation of these cases. We shall find other instances of a like
nature among the cases without pericarditis, in which endocarditis
was present, and in those also in which it was doubtful or absent.

B2. — II. Cases with Simple Endocarditis. — Five of the sixteen cases
that had endocarditis without pericarditis were affected with delirium
of a desponding type with taciturn melancholy. Two of these died
and three recovered. In addition to these five cases with taciturn
melancholy, there was another analogous case of embolism of the
basilar artery, with headache and agitation, and in the evening
apoplectic symptoms, right hemiplegia, and difficulty of speech.1 As
this case did not survive the first great attack, I shall not add it to
the rest. The length of time that the mind was disturbed varied in the
different cases from three weeks to four months ; one of the fatal cases
lasted twenty-three days, and another two months ; while those that
recovered were affected for one, two, and four months respectively.
Four of them were restless ; three were taciturn, especially during the
night; another answered slowly; and the fifth case in a low voice ; three
had hallucinations, including one of those that were also taciturn, and
two would get out of bed. Three of them were desponding or melan-
choly ; one was apathetic ; and the remaining one, a fatal case, was
for ten days in a state of quiet delirium, and afterwards preserved a
dogged silence. Two of them were confused ; and one of them was
violent. If we compare these five cases of temporary insanity, with
simple endocarditis ; with the sixteen cases of the same class with
pericarditis and endocarditis, we find that the two sets of cases
correspond in their main features. Both had disorder of mind, by
day as well as by night, though with greater accentuation at night
in those with simple endocarditis; in both early restlessness, obstinate
silence, melancholy, apathy, and hallucinations prevailed ; and in both
the affection of the intellect commenced during the attack of acute
rheumatism, and of the accompanying endocarditis, and lasted for a vari-
able period after the acute affections had ceased.

As we have just seen, five out of the sixteen cases, or one-third, with
•simple endocarditis, not including the fatal case of embolism, difficult
speech, and right hemiplegia, and another case with embolism of the
minute cerebral arteries and delirium that died on the eleventh day; and
sixteen of the sixty-five with pericarditis, all but one of them having
endocarditis also, or one-sixth, were thus affected with taciturn melan-
choly lasting for a limited period after the cessation of the acute

1 Bouillaud, " Maladies da cc&nr," vol i. p. 405.
VOL. IV. U

290 A SYSTEM OF MEDICINE.

affection. We may, I think, consider that the existence of endocarditis
in so large a proportion of such cases adds to the probability of em-
bolism being the cause of the temporary insanity.

Since the above was written Dr. Broadbent has favoured me with
his notes of an important case of acute rheumatism and endocarditis,
with chorea and delirium, in which there was capillary cerebral em-
bolism. I have also met with a case observed by Dr. Dickinson of
acute, rheumatism aud endocarditis with delirium and minute cerebral
embolism, and red softening of some of the convolutions ; and with
another case of chorea and endocarditis with delirium and minute cere-
bral embolism. These three cases afford direct evidence of the asso-
ciation of embolism of the minute arteries of the convolutions of the
brain with delirium.

Dr. Broadbent's patient, a laundryman, aged 17, when attacked,
had severe affection of the joints, and was light-headed ; two days
later his right limbs twitched and jumped, and he was delirious. On
admission, after being ill a week, he seemed stupid, had to be
spoken to loudly, liis answers were confused, his articulation was in-
distinct, and his limbs still twitched, but especially on the right side.
T. 103°. During the two following nights he had no sleep, was very
delirious, talked, screamed, and jumped out of bed. He slept after a
dose of chloral, but was soon pale and prostrate, and died on the fourth
day after his admission. Eecent loose clots were found in the minutest
arteries and capillaries of the corpora striata and of some of the con-
volutions.

B2. — III. Cases vntlwv.t "Pericarditis, Endocarditis being absent
or doubtful. — Five of the thirty-eight cases in which there was
no pericarditis, and endocarditis was absent or doubtful, or one in
eight of the whole number, became delirious during the acute stage
of the disease, and remained of unsound mind for two months and
a half in one, and for about a month in four instances. Two of
these patients were also affected with choreiform movements. Four
of these wrere men, and one was a girl, aged 16. Two of the men
had been at one time drunkards, one of them had suffered in health
from losses and excesses, and the other man was a servant, and pro-
bably lived generously. The speech was affected in all of them. One
stammered, one answered slowly, one was taciturn, one refused to
answer, and the girl did not reply to the question put to her, but spoke
of something else. Two of them had hallucinations ; one was despon-
dent ; another, after being noisy, became sulky ; one was morose by day,
and had lively delirium. One, with choreal movements, after being
confused and delirious in paroxysms, became so continuously; and the
fifth, also having chorea, was strange in manner.

In none of these five cases was there any notable sign of endocar-
ditis, and the disturbed state of mind and speech could not therefore
be attributed to embolism.

B2. Temporary Insanity — General Summary. — There were alto-
gether twenty-one cases of acute rheumatism with temporary in-

PERICARDITIS. 291

sanity ; and six of delirium, usually of the low melancholy type, in
wliich the insanity was cut short by death. Of these twenty-seven
cases, sixteen had pericarditis, six simple endocarditis, and five had
apparently neither pericarditis nor endocarditis.

Four-fifths of the cases had endocarditis (21 in 27), and one-fifth
of them gave no evidence of endocarditis (6 in 27).

I have already given clinical reasons for thinking that the tem-
porary insanity may have been due to embolism of the minute cere-
bral arteries in those cases with endocarditis, and direct evidence that
in two cases that condition coincided with delirium.

In six of those cases with endocarditis the temporary insanity
delirium, or melancholy was associated with chorea, and their cli-
nical history would seem to suggest that in those cases the temporary
insanity and the chorea were due to a common cause acting perhaps
on different parts of the nervous centre. This view is strengthened by
Dr. TuckwelTs important remarks on Muscular Chorea and its pro-
bable connection with Embolism. This memoir is illustrated by a
case l in which there were two large patches of red softening affecting
the cortex, and in one of them the white substance also, of the right
hemisphere of the brain. The arterial branches leading to one if not both
of these softened patches were occluded by coagula, and very fine
granular particles were dotted along the small bloodvessels in the
softened cerebral grey matter. This patient, a boy, was attacked with
chorea nine days before admission, and became delirious during the first
night after it. On the third day he had wild maniacal delirium, and
furious choreic movements. This wdld state soon quieted itself, but
was renewed on the eighth night, and on the ninth day he became
comatose and died.

More than one-half of the cases were below the age of twenty-one
(14 in 27) and of these all but one had endocarditis, while one-third
of them were above the age of twenty-five (9 in 27) and of these nearly
one-half (4 in 9) presented no sign of endocarditis.

Although the majority of these cases, and especially those "with
endocarditis, were young people of previously good health, yet a small
but definite group of the cases form an important exception to this
typical series. Six of the cases, all men, were either known to be of
habits of intemperance, or were of occupations in which such habits
are possible. Three of those male patients were drunkards or given
to excess, and of the rest, one was a policeman, one a man-servant, and
the sixth was a postboy. Four of these patients, all of whom recovered,
presented no sign of endocarditis, and the two others had endocarditis.

The question arises here, whether the temporary insanity in these
four men who had not endocarditis, one of whom had chorea
also, may have been due to thrombosis or the spontaneous
collection of fibrine in the minute arteries of the convolutions ? I
simply put this as a question, but in support of the possibility of

1 British and Foreign Mcdico-Chirurgical Review, xl. p. 506.

u 2

292 A SYSTEM OF MEDICINE.

this condition I find an important case that was closely observed by Dn
Charlton Bastian during life and after death. The patient was a strong
man, a gate porter, who had been accustomed to drink a great deal
of late, and was attacked with erysipelas of the head and face follow-
ing a fall, when he cut his head on the kerb-stone. He became vio-
lently delirious, was then quieter, became comatose at night, and died
early on the following morning. The heart was healthy ; the pia
mater and brain were abnormally vascular ; the consistence of the brain
was good. Minute embolic masses were present in the small arteries
and capillaries of the brain in every specimen looked at.1

B* & C \ 2, 3. — Chorea and Choreiform and Tetaniform Move-
ments, WITH AND WITHOUT DELIRIUM, IN CASES OF ACUTE EHEU-
MATISM, WITH ESPECIAL REFERENCE TO PERICARDITIS.

The occurrence of chorea without delirium in cases of acute rheu-
matism when connected with endocarditis will be considered when
we enquire into that affection. The present enquiry will be limited
to (J) cases of chorea and of choreiform movements with delirium, or
ending in sudden death, occurring in acute rheumatism with or with-
out pericarditis ; and (2) cases of chorea and choreiform movements
without delirium, occurring in acute rheumatism with pericarditis;
and in inquiring into these cases, I shall briefly include the cases
of combined chorea and temporary insanity that have already been
considered.

B2 & C1,2. — I. Cases with Pericarditis. — Chorea occurred as a definite
accompanying affection in six instances with delirium, and in seven
without delirium ; and choreiform movements not amounting to definite
chorea occurred in two instances with delirium and in one instance
without delirium among the sixty-five cases of acute rheumatism affected
with pericarditis now under examination. In addition to these cases so
affected, there were six patients with pericarditis who had delirium, or
coma, or both, as the principal affections, and who had choreiform
movements as a subsidiary affection. There were thus twenty-two
cases of rheumatic pericarditis with chorea or choreiform movements,
not including several who had also tetaniform symptoms.

The thirteen cases with chorea, and two of the three with limited
choreiform movements, were below the age of twenty- one, nine of these
being girls and six youths. The remaining case with limited choreiform
movements was a man aged 22. Nine of these sixteen choreal cases
died and seven recovered.

Thirteen of these cases, including the whole of those with delirium,
had endocarditis as well as pericarditis ; in two cases endocarditis was
probable, and in one it was absent or doubtful.

In eight of the cases the chorea appeared after the commencement
of the pericarditis; in seven of them the two affections probably

1 Path. Trans, xx. 8.

PERICARDITIS. 293

came into existence about the same time ; and in one exceptional
case, recorded by Dr. Ormerod, the chorea appeared first, then the
pericarditis, and finally the affection of the joints, thus reversing the
usual order of succession of those affections.

The chorea appears to have continued up to the time of death in
most of the fatal cases when the pericarditis was active ; but the
reports of several of them are, in this respect, imperfect.

The relation of the termination of the chorea to that of the peri-
carditis varied much in the cases that recovered. In one case the
choreic movements were violent on the day that the frottement
diminished, and were absent four days later. In another case the
chorea improved with the improvement of the state of the heart.1 A
patient of my own made objectless movements with his hands when the
pericarditis was at its acme; and two days later those movements ceased.
In a boy with pericarditis, violent chorea appeared when the rheumatic
and cardiac affections rather suddenly disappeared. Six days later
with return of pain in the joints the chorea ceased.2 In another
patient, a girl, chorea appeared four days after the disappearance of
friction sound.3

Partial choreiform movements, usually of short duration, appeared
in six of the cases that were affected with delirium with and without
coma, and in all of them the movements appeared when pericarditis
was present.

The character of the choreiform movements was peculiar in some of
the cases. Two of the patients rolled the head from side to side ; one
smacked his lips, another pursed his mouth, a third snapped, grimaced,
and cried out ; two moved the left hand and arm constantly ; and in
five the spasmodic movements of the body were very violent, so that
in three of them personal restraint was demanded. In one of those five
patients, on the second and third days, the spasms put on the character
of the most violent convulsions. The cases of chorea with delirium
presented considerable variety; and several of them, as we have already
seen, had temporary insanity.

Five of the eight cases with delirium were fatal, and three recovered.
The duration of the cases varied considerably. The five fatal cases
died at various periods from the fourth to the sixteenth day of the
delirium. Of the three that recovered, one had delirium for a month,
one had chorea for three weeks, and in one, a man under my care,
quick and needless movements of the hands, and occasional muttering,
lasted two or three days.

B 3. — II. Cases with Simple Endocarditis. — No case of chorea with
delirium, and only one with rapid death, occurred among the cases of
acute rheumatism with endocarditis.

B3. — III. Cases without Pericarditis, Endocarditis being absent or
doubtful — I have already given two cases of this class with chorea

1 Guy's Hospital Reports, vi. 1841, pp. 420, 421.

* Mr. Land, Lancet, 1873, i. 38.

3 Dr. Kirkes, Trans, of the Abernethian Society, 1850, p. 57.

294 A SYSTEM OF MEDICINE.

and delirium that were affected with taciturn melancholy of limited
duration. The third case, a girl, aged 14, also had chorea and
delirium.1

B8. Cases with Clwreiform Movements in which those movements
were partial and of secondary importance, and occurred in patients
already included among those with delirium or coma. B8. — I. Cases
with Pericarditis, — Six cases with delirium, one of which had coma
also, among the sixty-five cases of rheumatic pericarditis had move-
ments of a choreiform character for a single day in the course of the
disease. Three of these patients died and three recovered. Four of
them were male and two were female patients, and of these, five were
above the age of twenty-five, and only one below that of twenty-one.

B4, C3. — Cases with Tetaniform Movements sometimes associated with
Choreiform Movements. — I. Cases with Pericarditis. — In a small but
important group of cases tetaniform symptoms occurred in connection
with rheumatic pericarditis. Seven of the sixty-five cases of peri-
carditis had tetaniform movements, or continuous contraction or
rigidity of muscles, of greater or less intensity. Some of these affec-
tions approached in their severity and characteristic form to tetanus,
others could only be indistinctly associated with that disease.

The first case was an excitable man, aged 19, a gardener, who had,
when first seen, twitching of the muscles, and of the right side of the face,
increased by speaking. He had increasing agitation, indistinct articu-
lation, and a difficulty in opening his mouth, which he closed with a
snap. After this he threw his head from one side of the bed to the
other, his convulsions resembled tetanus and opisthotonos, and his
distress in swallowing was like that in hydrophobia. Four days later
he rolled his eyes, ground his teeth, and smacked his lips ; and he
died exhausted by laborious spasm and probably by want of susten-
ance. His brain was vascular, and there was questionable softening
around a vascular spot in the spinal cord opposite the first dorsal
vertebra. There was pericarditis and endocarditis.2 The next case,
an over- worked girl, aged 19, at a late period of its history, seemed
to plunge almost at once into the tetaniform condition. She rolled
her eyes wildly, had furious delirium, and violent tetanic spasms with
firm clenching of the fingers. After a week the delirium subsided,
but she talked incessantly and incoherently, and was half maniacal,
half idiotic up to the forty-sixth day, but from that time her progress
to recovery was steady.3 The third case, a youth, had pericarditis, but
no endocarditis, inflammation of the kidney, occasional delirium, and
slight opisthotonos ; and on the eleventh day he died.4

The two following cases, both of which were fatal, were under my
own care. The more important case was a youth aged 17. On
the eighteenth day, the left side and the tongue were affected with

1 Tungd, loc. cit. 1860, p. 125.

* Dr. Yonge ; Dr. Bright, Guy's Hospital Reports v. (1840) p. 276.

8 Dr. Fuller, loc. cit. 201. * Dr. Fuller, loc. cit. 289.

PERICARDITIS. 295

choreiform movements, which extended, with stiffness, to both arms.
On the thirty-eighth the left arm, which still jerked and shook about,
was rigid, the fore-arm being bent on the arm, the hand on the fore-
arm. On the forty-seventh day, stiffness of the neck appeared, and he
moved his arm with difficulty ; and on the following day he died. He
had both pericarditis and endocarditis. In this case the rigidity of
the limb points to an affection of the nervous centre, probably due to
embolism.

The other case, a man aged 27, a carpenter, came in with pericarditis
at its acme, and endocarditis. On the third day he frequently slum-
bered and, as the eyes were half-closing, the arms and legs started.
On the evening of the seventh day he was restless, and not quite
rational, trembled, and kept moving his lower jaw and biting his lips.
Half an hour later he was more noisy, and knocked about, still shaking
his jaw. His pupils were dilated and very sluggish, and at eleven
o'clock he died. I can find no notes of his post mortem examination.

The two remaining cases with tetaniform symptoms belong to the
group of cases of endo-pericarditis with delirium and coma. One of
these, a young man, had pain in his right temple, followed by
wild delirium. During the night general convulsions came on in
occasional spasms of a tetanic character, and in the intervals he lay in
a state of coma. He remained in this condition for three more days,
wrhen he died.1 The remaining case, a young woman, became restless
and flighty on the sixth day of her illness, and next day pericarditis
and endocarditis declared themselves. She then became very violent.
The right arm and leg were never still ; at times, however, this state
became aggravated into one of general convulsions of a tetanic cha-
racter. She continued thus for nine days, the convulsions being
incessant. On the twelfth day she became comatose, after jumping
up and falling out of bed with her forehead on the floor. She finally
recovered.

Pericarditis— neither Rheumatic nor from Bright's Disease —
accompanied by affections of the nervous system.

An important series of cases of pericarditis in which there was
neither acute rheumatism nor, so far as was directly ascertained,
Bright's disease, have been published from time to time by Rostan,
Dr. Abercrombie, Dr. Bright, Bouillaud, Andral, and Sir George
Burrows.

The cases of this class that I have gathered together from the
records of various observers, and from the note-books of St. Mary's
Hospital amount to twenty-six. See Analytical Table at page 280.

These cases present examples of the whole series of affections of the
nervous system that have been observed in cases of rheumatic peri-

1 Sir Thomas Watson, loc. cit. ii. 306.

296 A SYSTEM OF MEDICINE.

carditis, with the exception of those with temporary insanity, and
these were possibly represented by one fatal case that had obstinate
taciturnity.

Among these twenty-six cases, (A1) one had coma without deli-
rium ; (A3) four had delirium and coma, the delirium in two of them
preceding, and in two of them following the coma ; one had delirium
and convulsions ; (B1) eleven had uncomplicated delirium which was
slight and of short duration in seven of them ; and of those without
delirium, (C1, 2) three had chorea or choreiform movements ; (C 3)
two had tetanus, and (D) one had slight convulsions. The affections
of the nervous system in these cases of pericarditis, instead of being
similar in character were thus very various.

A1. Coma. — The patient with coma was a woman who was sud-
denly seized with complete loss of consciousness, remained in this
state four days, and died. Pericarditis was the only appreciable
lesion.

A8. Coma ivith Delirium. — Among the four cases with coma asso-
ciated with delirium, in two instances the delirium, as usual, preceded
the coma, while in two the delirium followed the coma. One of the
former class, a boy, aged 12, affected with pyaemia, was delirious, and
after a night without sleep, became unconscious and died in the after-
noon. Pericarditis was associated with small deposits of pus in the
walls of the heart, the fibres of which were soft and almost black.1
The other case in which delirium was followed by coma, presented
tetaniform symptoms. A woman aged 26, was admitted soon after
a false conception in a state of delirium and obstinate taciturnity.
After this she frequently reversed her head backwards, had convulsive
movements of the face, and the arms presented from time to time a
rigidity almost tetanic. On the fifth day the arms when raised fell as
if paralysed, she became comatose, and died in the evening. Peri-
carditis was the only morbid state discovered after death.2

Three of these cases may have been affected with " hyperpyrexia."
There is, however, no indication that their temperature was raised.

In the other patient, a house-painter, in whom the coma preceded
the delirium, I think that Bright's disease, not noticed after death,
when the kidneys were not examined, was the probable cause of the
fatal conditions spoken of.3

The patient with delirium and convulsions was a schoolboy with
evident pyaemia, who had, in the opinion of all who saw him, severe
inflammation of the brain. His brain was healthy, but his pericar-
dium was inflamed, and innumerable small patches of pus oozed from
among the muscular fibres of the heart.4 The case with convulsions
without delirium was also a boy, aged 7, who had pain in the left
side and the epigastrium, and on awaking next morning was seized

1 Mr. Stanley, Med. Chir. Trans, vii. 322.

1 Andral, Chniquc Medical, i. 25.

' Bouilland, loc. cit. i. 319.

4 Dr. Latham, London Medical Gazette, iii. 1829, p. 209.

PERICARDITIS. 297

with slight convulsions, sank into a low exhausted state, and died in
half an hour. There was universal pericarditis, and when the heart
was cleared from its soft gelatinous envelope, it was covered with
small irregular granulations.1

B1. Delirium without coma or other complications was present in
eleven cases of pericarditis not occurring in acute rheumatism or
Bright's disease.

The most important of these cases was a man aged 36, under the
care of Sir James Alderson. Three and a quarter pounds of dark
amber-coloured fluid were found in his pericardium, the heart being
covered and the sac lined with a thick honeycombed layer of new
membrane. The supra-renal capsules, especially the right one, were
enlarged with tubercular deposit. He had excessive distress and
pain over the heart, the whole front of the chest was dull on per-
cussion, and the impulse and sounds of the heart were absent. From
the presence of these signs Sir James Alderson concluded that his
patient was affected with pericarditis. On the twenty-second day
after admission he became delirious, and on the twenty-fifth he was
maniacal, and died.

Another case of this class was a shoe-black, aged 67, who had delirium,
with great loquacity. He raised himself suddenly, went to the window
to breathe, returned to bed, lay down and soon died. There was ex-
tensive pleurisy on the left side, spreading to the pericardium, which
contained a pound of purulent liquid ; the walls of the heart being
soft and its fleshy substance yellow.2 A third case, a man, had peri-
carditis associated with pyaemia, following an operation for stricture.

Seven of the remaining cases of this series presented only slight
delirium and may be conveniently grouped together. One, who had
pleuro-pneumonia and pericarditis, recovered.8 Another had slight
delirium and fever, and pericarditis. One, had empyema and peri-
carditis. Two cases under my care were delirious the day before
death. One had pytumia, and puruleut dots were scattered through
the fleshy substance of the heart ; the other had empyema of the left
side, and pericarditis. In the two remaining cases the delirium ap-
peared a short time before death ; one had extensive phthisis of the
right lung and a vast cavity, the other had empyema of the left side,
the pericardium being inflamed and thickened. In all these cases
the delirium appeared to be quite as much connected with the disease
upon which the pericarditis had grafted itself as upon the pericarditis
itself, and in most of them it was little more than the wandering of
mind incident to illness of so lowering and fatal a character.

The remaining patient of this group, a coachman, aged 51, and a
drunkard, who was under the care of Dr. Chambers, presented a con-
dition resembling delirium tremens. He had extensive pleuro-pneu-
monia of the left lung, and pericarditis. Two of these cases with

1 Dr. Abercrombie, Trans. Edin. Med. Chir. Soc. i. 1821-4.

1 Corvisart, lac. cit p. 239. * Bouillaud, loc. cit L 867.

298 A SYSTEM OF MEDICINE.

brief delirium, were under the care of Sir James Alderson, and two
under that of Dr. Chambers.

C1, 2. Clwrca and Choreiform Movements. — Two cases of non-rheu-
matic pericarditis had chorea, and four presented movements of a
choreiform character.

C1. Chorea. — One of the cases, a well-grown girl of 15, had chorea
for six weeks before admission, and on the twenty-seventh day after
it, was suddenly seized with obstructed respiration followed by a con-
vulsive fit, and died. There was pericarditis, and the mitral valve was
somewhat thickened, but the presence of endocarditis was not noted.
The other case, a little girl, was under my own cara She was brought
to the hospital in her mother's arms, in great distress. She presented
prominence over the region of the pericardium, dulness on percussion
extending up to the clavicle, and a pericardial friction sound. There
was evidence also of pleurisy of the left side. Choreal symptoms
appeared in the face, beginning in the corrugator supercilii, on the third
day after admission, and chorea was established on the fifth day. On
the ninth day she was much quieter ; her face was pale, her lips were
blue, and the veins of the neck pulsated, being full during expiration
and during the ventricular systole ; and a loud mitral murmur was
audible at the apex. She died on that day, but I have found no
notes of the examination after death.

C2. Choreiform Movements. — Four cases of non-rheumatic pericarditis
presented in the course of their illness movements of a choreiform
character. These cases hold an intermediate place between those with
well-developed chorea, and those with regularly repeated local con-
vulsive movements. The most important case ought perhaps to
be included among those with chorea, but it developed certain cha-
racteristic symptoms of the choreiform type that are rarely or never
present in uncomplicated chorea. This patient, a young lady, after a
fortnight of extreme restlessness, and a good deal of delirium, fell
into a state resembling chorea with convulsive agitation of the limbs,
constant motion of the head, and wild rolling of the eyes. Cold
was applied to the head, her symptoms subsided in a few days, and
she gradually recovered. Three months and a half after the commence-
ment of her illness she took cold, became suddenly worse, and died on
the seventh day. The pericardium was universally adherent to the
heart by lymph, and a deposit of lymph covered its outer surface.1

The other three cases, all fatal, of non-rheumatic pericarditis
were reported by Corvisart, and the most remarkable symptom was
a state of extreme agitation amounting to jactitation. They all had
pleurisy as well as pericarditis, and one had pneumonia also. One of
them had delirium, in another the mind was affected, and in the third
disturbance of the intellect was not noted.

C8. Tetaniform Symptoms and Tetanus. — Two of the cases of non-
rheumatic pericarditis were affected with tetanform movements, or

1 Dr. Abercrombie, Trans, of Med. Chir. Soc of Edin. i. 1.

PERICARDITIS. 299

rather with actual tetanus, some of the symptoms of which were
unusual. One of these cases was a boy who when admitted had
cramps, and a threat of suffocation. His fingers, arms and forearms,
his legs and feet were strongly bent, and the muscles of his limbs
and abdomen and his masseters were so hard that they felt like touch-
ing a stone, especially during the paroxysms. A warm bath and cold
affusion gave great relief, and the paroxysms of suffocation ceased
half-an-hour later. After this the jaws were slightly closed, he
had a return of the suffocation, especially when he drank, and occa-
sional cramps. On the fifth day he had a cold bath by accident, and
was seized with cramp when in the bath. He had spasmodic contrac-
tions of great intensity on the following day, and died in a paroxysm
of suffocation. There were two ounces of pus in the pericardium,
the surface of which was injected.1

The other patient with tetanus was a gentleman of middle age who,
when first seen, was suffering from a violent spasmodic contraction
of his limbs. On the fifth day he had cramps of his extremities
and occasional spasmodic rigidity of the whole body, which wTas
sometimes bent backwards, being supported by the occiput and the
heels in a state of complete opisthotonos. During the night his
spasms were so severe that he could scarcely be kept in bed, and he
died suddenly on the following day. He had pericarditis, and the
brain and spinal cord were healthy.2

I have ranked these cases with those of tetanus because they pre-
sented universal rigidity of the limbs and body ; which, in the first
case, extended to the masseters ; and in the second, caused, during
the paroxysms, complete opisthotonos. There were, however, certain
conditions in which they both differed from ordinary tetanus. In neither
of them did the affection commence with trismus, and in the second
case its presence is not mentioned. In both of them at the outset of
the attack the muscles of the extremities were involved ; and in the
first of them, besides cramps of the legs, the fingers, arms and forearms
were strongly bent. In tetanus I need scarcely say that the reverse
conditions prevail, for trismus is usually the earliest symptom, and
the affection of the limbs is comparatively late, while that of the
hands and arms is usually slight, the extensor muscles being more
affected than the flexors. In tetanus the advance of the disease is
steadily progressive, but there was a suspension of the spasmodic
contraction of the limbs in both of these cases.

Dr. Bright describes a case of tetanus occurring in a man affected
with inflammation of the pleural surface of the right side of the peri-
cardium, involving the phrenic nerve, in which there was no pericar-
ditis. In this instance the tetanus advanced rapidly through its
usual progressive course. On the first evening he complained of
difficulty in opening his mouth, and swallowed with a convulsive
catch. During that night his teeth were completely closed, and

1 Bouillaud, loc. cit. i. 333. 2 Dr. Mackintosh, Practice of Physic, ii. 25.

300 A SYSTEM OF MEDICINE.

next morning he could get nothing into his mouth, and could not
even swallow his saliva. There were slight indications of opistho-
tonos, and spasmodic action of the muscles of the back. In the
afternoon there was no relaxation of the spasm; he had several
epileptiform seizures, during which his face was purple, his eyes
stared, and his whole body was convulsed. He rambled occasionally,
and died twenty-fours hours after the first seizure of dysphagia.
Dr. Bright suggests that in this case tetanus may have been caused
by the phrenic nerve being involved in the seat of the inflammation.1

Convulsive Movements, Chorea, and Choreiform and Tetaniform Symp-
toms in Cases of Acute Rheumatism with and without Pericarditis, and
in cases of Non-Rheumatic Pericarditis, in which BrigMs Disease was
Absent. Summary. Convulsive Movements. — I do not consider here
cases of coma with convulsions, of which there were five, three with
and two without pericarditis, one with and three without endocarditis,
which was probably present in the remaining instance ; nor those
with convulsions associated with albuminous urine, of which there
was but one patient, affected with both pericarditis and endocarditis.

There were altogether nineteen patients with convulsive movements
among the whole series of 180 cases of acute rheumatism with
affection of the nervous system; twelve of whom had pericarditis
and seven had no pericarditis, while eight or perhaps nine of them
had endocarditis. Fourteen of these cases had twitchings of the
limbs or face, and of these, eight had pericarditis, and five endocarditis.

From this resume it is evident that although these convulsive
movements are probably influenced, and may in some instances have
been caused by the co-existence of pericarditis or endocarditis; yet
they may, and often do occur quite independently of either of those
aflections, and in the absence of both of them.

Hyperpyrexia (actual in seven cases, inferred in four), was present
in eleven of the nineteen cases with convulsive movements or
twitchings. In Dr. Greenhow's important case, given at page 266,
twitchings of the face were generally present when the temperature
ranged from 1021° to 106*2°, but they were suspended by the cooling
bath, and returned after removal from the bath.

The general affection of the nervous system varied in the different
cases with convulsive movements and twitchings. In one patient
a convulsive fit preceded coma without delirium. In seven cases
there was delirium followed by coma. In four of these, twitch-
ings occurred during the delirium ; while in two of them, twitch-
ings, and in one, convulsive movements, accompanied the coma.
Convulsive movements of the whole body in one instance, and of the
face in another, followed delirium and preceded death. There were
general convulsive movements in one, and twitchings of the face in
two cases of uncomplicated delirium,

1 Med. Chir. T rans. xxi. 4.

PERICARDITIS. 301

There were twitching movements in four cases with chorea and
delirium, in one of which there was also a state resembling tetanus
and opisthotonos. In these four cases the twitchings were probably
choreiform in character.

In one of the two remaining cases, a slight fit with ptosis preceded
death by a few hours ; and in the other twitching was present with
albuminuria.

Convulsions were present in three, and convulsive agitation of
the limbs in one, and of the lips or face in two of the twenty-six
cases of non-rheumatic pericarditis, in which there was no Bright's
disease.

Chorea, and Choreiform, and Tetaniform Symptoms. Chorea. —
Twenty-one of the 180 cases of acute rheumatism with affections
of the nervous system had chorea. Fifteen of those patients with
chorea had pericarditis, six had no pericarditis; while fourteen of
them had endocarditis ; three had no endocarditis ; and in three of
them, endocarditis was probable or doubtful. Pericarditis and endo-
carditis attacked three-fifths of these patients conjointly (13 in
21). It would appear from this, at first sight, as if pericarditis
favoured or influenced the production of chorea, thus apparently
supporting the view of Dr. Bright that the more frequent cause of
chorea in conjunction with rheumatism is inflammation of the
pericardium, the irritation being probably communicated thence to the
spine through the phrenic nerve.1 This view is apparently strength-
ened by the history of several of the cases in which the chorea and
the pericarditis appeared, improved, and disappeared simultaneously.
On the other hand, in one case, chorea preceded pericarditis, and
in at least two others it came into play when the pericarditis was
vanishing. The united presence of inflammation without and within
the heart in so many of these cases, complicates the question as to
the influence of pericarditis on the production of chorea ; and these
clinical statistics favour the view that endocarditis may be the cause
of the chorea, quite as much as that pericarditis may be its cause.
I will not pursue this question in this place farther, excepting to repeat
that in Dr. Broadbent's and Dr. Tuckwell's important cases of
chorea and delirium, there was embolism of the most minute cerebral
arteries, associated with endocarditis. These two cases seem to
show that it is possible that in some of the above cases also,
chorea may have been associated with minute cerebral embolism due
to endocarditis. I have already illustrated the possible or probable
connection of temporary insanity in cases of acute rheumatism with
endocarditis and minute cerebral embolism, or with minute cerebral
thrombosis, the convolutions being affected ; and five of these cases
of chorea had also temporary insanity, in three of which there was
endocarditis, while in two there was no endocarditis.

Chorea was present in two cases of non-rheumatic pericarditis

1 Med. Chir. Trans, xxii. 15.

302 A SYSTEM OF MEDICINE.

without Bright's disease. In one of these the onset of the chorea
preceded, and in the other followed, that of the pericarditis. In one
of those cases endocarditis was also present, and in the other it was
doubtfuL

Choreiform Movements. Jactitation. — Chorea, as we have just seen,
affected twenty-one of the 180 cases of acute rheumatism with affec-
tion of the nervous system. Besides these there were fourteen cases
that had choreiform movements without definite chorea. One patient
moved automatically, as in chorea, and another made objectless
movements with his hands. Both of these cases had endo-pericarditis.
Eight patients were affected with jactitation, which was general in six
instances, and limited to the right or left side in two. The whole of
these patients had pericarditis, while endocarditis was present in three
of them, was absent in one, and probably absent in four.

There was extreme jactitation of the whole body in three cases of
non-rheumatic pericarditis, probably without endocarditis, observed
by Corvisart ; two of these had pleurisy, and the other one pleuro-
pneumonia ; those affections in two of the cases being the probable
cause of the pericarditis.

The invariable presence of pericarditis and the frequent apparent
absence of endocarditis in these cases of general jactitation, would
appear to point to pericarditis as a possible cause of that condition,
and perhaps by inducing reflex movements.

Agitation. — Fourteen of the cases with affection of the nervous
system in which the temperature was not observed had agitation,
which is a condition allied to general jactitation, which was also pre-
sent in two of them. I find no express mention of agitation in the
sixty-one cases in which the temperature was observed. Five of the
fourteen cases with agitation had pericarditis ; eight of them had
endocarditis ; while five of those cases had neither endocarditis
nor pericarditis.

Ten of the cases with agitation died and four recovered.

Boiling of the Head from side to side. — A peculiar, regularly
repeated rolling of the head from side to side occurred in eight of the
180 cases of acute rheumatism with affection of the nervous system.
Five of these cases had well-developed chorea, and two others had
limited choreiform movements. Six of these cases had pericarditis,
while five of them had endocarditis, and in one its presence was
doubtful. All of them had either endocarditis or pericarditis. This
peculiar oscillating movement of the head, though generally connected
in these cases with chorea or choreiform movements, is not, so far
as I know, ever present in ordinary chorea, and it forms, therefore,
a feature of difference between those cases and these. One patient,
who had endo-pericarditis, delirium, and coma, rolled violently about
the bed so that he required to be held down.

Choreiform movements were present in four cases of non-rheumatic
pericarditis without Bright's disease. In one of these the state
resembled chorea, there being convulsive agitation of the limbs and

PERICARDITIS. 303

constant motion of the head, with delirium ; in another patient there
was slight convulsive agitation of the face ; and in two other cases
there was violent general jactitation.

Tetaniform Symptoms and Tetanus. — Thirteen, or if the presence
of "risus sardonicus" alone be included, fifteen cases presented
symptoms of a tetaniform nature.

In eight of those cases the tetaniform symptoms were general.
Some of these had also chorea, or choreiform movements. In one such
case the chorea! convulsions put on a character resembling tetanus
and opisthotonos, and the distress in swallowing was not unlike that
in hydrophobia. Another case had opisthotonos and tetanic spams ;
and a third had slight opisthotonos. Three other cases had spasms
or convulsions of a tetanic character, which were accompanied in one
instance by firm clenching of the hands. One patient under my care
had stiffness of the neck ; and rigid jerking and shaking about of the
left arm ; the forearm, at a later period, being bent on the arm, the
hand on the forearm. The eighth case, a woman, had a temperature
of 1095, and after being put into a tub of cold water was attacked
with tonic spasms. Two cases had spasms of rigidity of the muscles
of the neck, in one after being cooled in the bath from t. 109°
to 1036°, and two had stiffness of the neck, one of which has
been already alluded to.

One patient who was violently delirious at a temperature of 10780
to 109°, after being bled, immediately passed into a state of uncon-
sciousness, and was attacked with trismus, and convulsive movements
of the jaws, hands and arms. Two cases were affected with stiffness
of the jaw; which was accompanied in one of them by swelling
of the temporo-maxillary articulation ; this being the patient just
spoken of who was seized with tonic spasms after the bath ; and
who closed her teeth firmly over her lips, drawing blood. Another
patient, a man, was continually moving his lower jaw and biting his
lip ; and another, also a man, kept incessantly pouting his lips and
rubbing them over his teeth. One patient, spoken of above, with
spasms of rigidity of the neck after the bath, had also spasms of
rigidity of the lips. Another case with opisthotonos and tetanic
convulsions, closed the lips in snaps before, and smacked the lips
after having convjilsions.

" Risus sardonicus " was observed in five cases, in three of which
there were, and in two there were not, other tetaniform symp-
toms.

Of the above thirteen cases with tetaniform symptoms, not including
the two with simple " risus sardonicus," ten had endo-pericarditis, one
had pericarditis, endocarditis being absent, in one both of those
affections were doubtful, and in one they were both absent. These
clinical facts make it probable that pericarditis or endocarditis, or
both, may sometimes be concerned in the production of tetaniform
symptoms. Other influences were, however, at work connected with
hyperpyrexia in some of the cases. Thus trismus appeared in one

304 A SYSTEM OF MEDICINE.

patient just alluded to who became unconscious after being bled, the
temperature rising from 107*8° to 109° ; and in three cases the tetani-
form symptoms came into play after the excessive temperature had
been cooled down by the bath.

We have already seen that in one case of non-rheumatic pericarditis
ending in coma, the arms presented occasionally a rigidity as of
tetanus ; and that in two other cases of the same kind, there was
actual tetanus of a peculiar type. These three fatal cases had no
endocarditis.

Andral, in commenting on the first of these cases, or that with
occasional rigidity of the arm, and delirium ending in coma, asks
whether the cause of the affection of the nervous system in these cases
is not in the inflammation of the pericardium itself? We have
already seen that Dr. Bright looks to the communication of an
influence from the inflamed pericardium, through the phrenic nerve
to the spine, as a cause of choreal and tetaniform affections. I would
here remark that tetanus may be caused by a wound and by exposure
to cold, and there is nothing therefore inconsistent, so far as I can
see, in the idea that it may be caused also by an internal inflammation
affecting local nerves, and through their channel acting on the
spinal marrow.

Tetanus is not, so to speak, an intermittent contraction of the
muscles of the reflex type, but a continuous contraction of the
muscles, due to the direct continuous action of the spinal cord. In
tetanus, as Dr. Lockhart Clarke has shown, there are areas of dis-
integration in the spinal cord. In traumatic tetanus, the cause of the
affection is the injury to the nerve, and in these cases the nerve must
carry from its periphery to its centre an influence that sets into action
the disintegration of the cord. If the inflammation of the peripheral
ends of the nerves of the pericardium excites tetanus, it would perhaps
do so in some such manner as that just suggested. The cases of
tetanus and tetaniform affection associated with pericarditis, though
striking are very rare, and we may fairly ask whether in those
cases in which the two affections coincided, some other cause may
not have been at work to induce the tetanus. I know of no instance
in which tetanus was induced by any other internal inflammation,
and if this be so, it is not easy to see why pericarditis or pleurisy
affecting the phrenic nerve should be the only internal inflammations
capable of inducing that affection in its typical or modified form.

THE PHYSICAL SIGNS OF RHEUMATIC PERICARDITIS.

In every case of rheumatic pericarditis there is an increase in tho
amount of fluid in the pericardium, and a layer of ridged, roughened,
or honeycombed lymph is spread over the opposing surfaces of the
heart and the pericardial sac. The amount of the fluid poured into
the sac is made known by the extent of dulness on percussion, the

FERICARDITIS. 305

prominence of the sternum ami costal cartilages, ami the widening
of the intercostal spaces over the region of the pericardium, and by
the position of the impulse ; while the presence of lymph covering
the heart and lining the sac is told by a friction sound.

Effusion of Fluid into the Pericardium in Rheumatic Pericarditis. —
Although in the prescribed order, the examination of the chest by the

eye and the application of the hand rightly precede that by percussion
l" shall here reverse this order, aud begin with percussion, for by it
we really judge of the extent of the fluid in the sac.

The pericardium of an adult man with a healthy heart is capable
of holding from fourteen to twenty -two ounces of fluid, and that of a

VOL. iv. X

306 A SYSTEM OF MEDICINE.

boy of from 6 to 9 years old, about six ounces, when the sac is
distended to the full by injecting water into it by a syringe, through
an opening made in the anterior wall of the pericardium.

The effect of this artificial distension of the pericardium on the
size, form, and position of the sac and on the situation of the
surrounding parts is shown in the accompanying figures (33, 34).
The pericardium, thus distended, is pyramidal or pear-shaped. It
is formed, so to speak, of a larger and a smaller sphere, the smaller
one resting on the top of the larger. The larger and lower sphere
contains the heart, the ascending vena cava, and the pulmonary
veins; and the smaller sphere holds the great vessels. The dis-
tended sac occupies the whole centre of the chest, filling up the space
between the sternum in front and the spinal column behind; and
extending across the chest from a little within the right nipple to
a little beyond the left nipple. The whole sac is lengthened; its smaller
end reaches upwards almost to the top of the sternum ; and its floor,
being formed by the central tendon of the diaphragm, presents a
large spherical prominence that bulges downwards into the ab-
domen, occupies the epigastrium, and reaches as low as the tip of
the ensiform cartilage and the lower edge of ttie sixth costal cartilage.
The enlarged and swollen sac displaces all the organs and parts
surrounding it. In front it separates the two lungs from each other,
so as to uncover the pericardium in front of the heart and great
arteries. It pushes forwards the two lower thirds of the sternum,
the ensiform cartilage, and the adjoining costal cartilages, especially
the left, from the third to the sixth; and by counter-pressure
backwards it compresses the oesophagus, the descending aorta, the
bifurcation of the trachea, and the left bronchus between itself and
the bodies of the vertebra upon which those parts rest. It displaces
the lungs to either side and backwards ; and the central tendon of the
diaphragm where it forms the floor of the pericardium, the stomach,
and the left lobe of the liver downwards.

The artificial distension of the pericardium closely corresponds in
general form with its natural distension from pericarditis, when the
amount of the effusion has reached its acme. I have already sketched
at page 217 what I believe to be the usual course of the increase of
the effusion from the beginning of an attack of pericarditis to the
period of its acme. When, however, the inflammation of the pericar-
dium has existed for some time, the walls of the sac, so thin, tough, and
firm in health, become comparatively thick, soft, and yielding ; and as
the sac cannot expand to a material degree either upwards towards the
neck, or downwards towards the abdomen, it yields sideways and back-
wards, and widens to the right and especially to the left, so as to en-
croach on both lungs, but more seriously on the left lung; as may be seen
in the accompanying figure, which is taken from a case of chronic
pericarditis of long standing, in which the sac contained three pounds
and a quarter of fluid (fig. 35). When thus distended, the sac seems to
occupy the whole front of the chest ; and it completely conceals the left

PERICARDITIS. 307

lung, which is pushed backwards and compressed by it so that compara-
tively little air is admitted into that lung at its lower and posterior
part ; this effect being increased by the compression of the left
bronchus.

There is another effect of this distension of the pericardium to
■which I have already alluded, its inferred effect namely upon the
heart itself. The muscular walls of the ventricles arc so thick,
and their action is so powerful, that the direct effect of the fluid
pressure upon them cannot be very
great. But the pressure of the fluid
tells inwards upon the weak and
unresisting walls of the auricles,
the vena cava descendens within
the pericardium, and the pulmonary
veins, so as to compress and lessen
those vessels and the auricles, and
to resist and impede the currents
of blood, on the one liand from the
system along the cava, and on the
other from the lungs along the pul-
monary veins. This partial blocking
of the double stream from the sys-
tem and the lungs to the het.rt
lessens the contents of the organ,
and tends to diminish the size of
its cavities. At the same time
the supply of blood to the aorta is
lessened, and the ascending aorta
is therefore also compressed by the
fluid. The pulmonary artery, how-
ever, owing to the obstacle to the
flow of blood through the lungs,
tends to resist the pressure of the
fluid in the swollen sac, and to re-
main distended.

While, however, this influence on fI(,. 35— Caw irf nericanKti* in which
the part of the fluid pressure of °nc ««: ™ntniii«l 8| llw. of fluid. The
the distended pericardium is at Jg«^ "*»«•«»«* Br Jm»
work compressing the auricles and

veins ; a second influence is at work, also set up by the inflammation,
to counteract the first influence, and to shield to some extent the
weaker parts of the heart. The auricular appendices shrink at an
early stage, and the walls of the auricles and veins are thickened and
somewhat protected from the pressure of the effused fluid by a
leathery coat of mail in the shape of the roughened and honeycombed
coating of lymph that clothes and strengthens the feeble natural walls
of those parts. Thus the double march of the inflammation supplies at
the same time a compressing fluid, and a sustaining covering of lym ph

306 A SYSTEM OF MEDICINE.

boy of from 6 to 9 years old, about six ounces, when the sac is
distended to the full by injecting water into it by a syringe, through
an opening made in the anterior wall of the pericardium.

The effect of this artificial distension of the pericardium on the
size, form, and position of the sac and on the situation of the
surrounding parts is shown in the accompanying figures (33, 34).
The pericardium, thus distended, is pyramidal or pear-shaped. It
is formed, so to speak, of a larger and a smaller sphere, the smaller
one resting on the top of the larger. The larger and lower sphere
contains the heart, the ascending vena cava, and the pulmonary
veins ; and the smaller sphere holds the great vessels. The dis-
tended sac occupies the whole centre of the chest, filling up the space
between the sternum in front and the spinal column behind; and
extending across the chest from a little within the right nipple to
a little beyond the left nipple. The whole sac is lengthened; its smaller
end reaches upwards almost to the top of the sternum ; and its floor,
being formed by the central tendon of the diaphragm, presents a
large spherical prominence that bulges downwards into the ab-
domen, occupies the epigastrium, and reaches as low as the tip of
the ensiform cartilage and the lower edge of tne sixth costal cartilage.
The enlarged and swollen sac displaces all the organs and parts
surrounding it. In front it separates the two lungs from each other,
so as to uncover the pericardium in front of the heart and great
arteries. It pushes forwards the two lower thirds of the sternum,
the ensiform cartilage, and the adjoining costal cartilages, especially
the left, from the third to the sixth; and by counter-pressure
backwards it compresses the oesophagus, the descending aorta, the
bifurcation of the trachea, and the left bronchus between itself and
the bodies of the vertebrae upon which those parts rest It displaces
the lungs to either side and backwards ; and the central tendon of the
diaphragm where it forms the floor of the pericardium, the stomach,
and the left lobe of the liver downwards.

PERICARDITIS. So-

iling, wliicli is pushed backwards and compressed by it so that compara-
tively little air is Admitted into that lung at its lower and posterior
part ; this effect being increased by the compression of the left
bronchus.

There is another effect of this distension of the pericardium to
■which I have already alluded, its inferred effect namely upon the
heart itself. The muscular walls of the ventricles are so thick,
and their action is so powerful, that the direct effect of the fluid
pressure upon them cannot be very
great. But the pressure of the fluid
tells inwards upon the weak and
unresisting walls of the auricles,
the vena cava descendens within
the pericardium, and the pulmonary
veins, so as to compress and lessen
those vessels and the auricles, and
to resist and impede the currents
of blood, on the one hand from the
system along the cava, and on the
other from the lungs along the pul-
monary veins. This partial blocking
of the double stream from the sys-
tem and the lungs to the liej.it
lessens the contents of the organ,
and tends to diminish the size of
its cavities. At the same time
the supply of blood to the aorta is
lessened, and the ascending aorta
is therefore also compressed by the
fluid. The pulmonary artery, how-
ever, owing to the obstacle to the
flow of blood through the lungs,
tends to resist the pressure of the
fluid in the swollen sac, and to re-
main distended.

While, however, this influence on f,0. a&— tim.- or iwrinnUtbi in which
the part of the fluid pressure of one •*> ™ntnin<«[ s} ll». of fluid. The
the distended pericardium is at £■£££" ■"hr tl,on,reof Sir J»mea
work compressing the auricles and

308 A SYSTEM OF MEDICINE.

The distension of the pericardium with fluid produces two other
effects on the heart. 1. The heart is heavier than the fluid in which
it plays, and its ventricles consequently tend to sink backwards so
that the left ventricle rests upon the posterior wall of the pericardium,
just as the liver sinks backwards when the abdomen is distended
with fluid in cases of ascites. 2. The other effect of pericardial
distension on the heart is the lifting or tilting upwards of the organ
within the sac. The heart is attached by its great vessels to the
posterior and upper parts of the sac, and the whole organ, therefore,
tends to shrink upwards and gravitate backwards towards its points ot
attachment At the same time the accumulating fluid which occupies
in volume the space between the lower surface of the heart and the
central tendon of the diaphragm, displaces the organ upwards into
the higher part of the pericardium.

The natural effect of this gravitation, shrinking, and upward dis-
placement of the heart, owing to the great accumulation of fluid in
the sac, would be, I conceive, if not modified by other agencies, to
cause a layer of fluid to be interposed between the front of the heart
and the anterior walls of the chest. Practically however we find that
this is not usually the case over the mass of the ventricles ; for with
one or two rare exceptions we can always feel the impulse of the
heart beating sometimes with force, sometimes with a thrill, in the
second and third, or third and fourth left spaces, extending from the
edge of the sternum to above and beyond the nipple. A layer of
fluid is, however, evidently interposed between the lower portion of
the front of the heart and the anterior walls of the chest.

The reasons for the presence and pulsation of the heart in the upper
intercostal spaces when the pericardium is distended, I believe to be,
firstly, the distension of the pulmonary artery, and to a less extent, of
the right ventricle, owing to the difficulty with which the blood flows
through the lungs ; and, secondly, the raised position of the heart,
which having left the broader space of the chest below, where it
enjoyed free play, occupies its narrower space above, where the heart
and pericardium are as it were grasped between the walls of the chest in
front and the bodies of the vertebrae behind. The result is that under
the combined influence of the elevation of the heart ; the distension
of the pericardium ; and the contracted area of the upper part of the
chest in which the heart is lodged, the left lung is displaced from
before the organ and the right and left ventricles, and the apex and
the great arteries beat against the higher intercostal spaces with which
they come into direct contact. In consequence of the withdrawal of
the lung from before the heart, and the narrowing compass of the
portion of the chest in which the organ is situated, its impulse
besides being raised, is also widened outwards, so that the apex beats
against the third or fourth space, at or above the level of the left
nipple, where it extends beyond the nipple line.

Although the upper portion of the right ventricle is in immediate
contact with the walls of the chest, I am satisfied that a portion of

PERICARDITIS. 309

the fluid effused into the sac is interposed between those walls and
the lower portion of the right ventricle over its anterior surface.

We shall afterwards see that the impulse is raised in position when
the fluid in the pericardium increases, and is lowered in position when
that fluid diminishes, so that under these circumstances the varying
amount of the fluid is told by the varying position of the impulse.

Cases, included in the following tables, that form the subject of this
inquiry- into tlie physical signs of pericarditis. — I possess notes of 44
of my 63 cases of rheumatic pericarditis, of the increase, acme, and
diminution of the quantity of fluid in the pericardium, as shown by
the enlarging and lessening area of the dulness on percussion over that
region ; the progressive changes in the position of the impulse ; and
the variations in the tone, intensity, and area of the friction sound ;
all of which signs are at once the effects and the witnesses of the
advance and decline of the inflammation. I have arranged these 44
cases in columns in the accompanying tables (see pages 313 — 327), so
that day by day each of those parallel effects of the disease may be
seen either singly or in comparison with each other ; and have com-
bined with them the co-existing endocardial murmurs, the presence of
pain over the region of the heart and elsewhere in the chest, and the
affection of the joints ; and I shall now briefly analyse point by point,
these parallel effects in those cases.

Percussion.

The enlarged Area of Dulness on Percussion over t/tc Pericardium,
caused by the Increase of Fluid in the Sac. — In 22 of the 44 cases under
examination, the increased amount of fluid in the pericardium, as
indicated by the extended area of dulness over that region, had
already at the time of its first observation reached its acme, and
from that time, the amount of fluid with its area of dulness steadily
declined. One of these cases had a relapse and proved fatal on the
14th day. In the remaining 22 cases the period of the greatest dis-
tension of the sac was preceded by a gradual increase, and was followed
by a more gradual decrease, in the amount of the fluid ; the periods
of increase, acme, and decrease of the amount of fluid, being shown
by the corresponding gradual enlargement, greatest area, and lessening
of the region of dulness on percussion over the pericardium. In 11 of
these 22 cases there was a single rise and fall of the tide of the
effusion; but in the 11 remaining cases there was a relapse, and
the amount of effusion, after lessening considerably, again increased
and attained to a second acme. In five of those cases, indeed, there
was a second relapse, so that the fluid in the pericardium presented
a third, and in one of them even a fourth wave of increase.

The duration of the whole period of increase of dulness on percus-
sion over the region of the pericardium varied much in different

310 A SYSTEM OF MEDICINE.

patients. Of the 22 cases in which the region of dulness had attained
to its greatest area at the time of the first observation, the average
duration of the increased dulness from the effusion into the pericardium
was eight days, the extreme duration varying from three days on the
one hand, to seventeen on the other. The average duration of the
period of increased dulness in the 11 cases in which there was a
gradual increase, single acme, and a decrease in the amount of fluid
effused into the pericardium, amounted to fully eight days, the
extreme variation ranging from four to thirteen days. The average
duration of the whole period of increased pericardial dulness was
more than twice as long in the 11 cases of relapse, as in the cases
with a single acme, since in them it amounted to eighteen days, the
extremes varying from fourteen to twenty-four days.

The increase of fluid in the early stage was usually rapid. In one
half of the cases in which this increase was watched, the area of
dulness had reached its maximum on the second or third day after
the first observation (11 in 22), and in all but two or perhaps three
of the remainder, on the fourth or fifth day. The early advance of
the dulness was, as a rule, more slow in those patients who suffered
from a relapse than in those who did not do so.

The time during which the effusion into the pericardium remained
at its height was, as a rule, very short. In 39 of the 44 cases the
region of dulness extended over its greatest area for about a single
day. It may have lasted longer, but on the next examination, made
usually on the following day, but sometimes later, the tide had
turned and the extent of dulness had lessened. The acme of the
pericardial dulness lasted two days in three of the remaining cases,
and three days in two of them.

The period of the decrease of the effusion in the pericardium was much
longer than that of its increase, its average duration having been, as
we have already seen, eight days in the 22 oases in which the effusion
was at its acme on the first examination.

We thus see that the period of the advance of the effusion, dating
from the time of its first observation in the early stage, usually
lasted about three days ; that the period of the acme of the effusion
was usually observed during only one day ; and that the period of the
decline of the effusion generally lasted about eight days.

The fluid in the pericardium begins to increase on the first day of
the inflammation ; but, as it necessarily gravitates backwards during
the early stages, the effusion does not appear in front until it has
accumulated so as to occupy the natural hollow at the back of the
sac, and the space between the lower surface of the heart and the
floor of the pericardium. Dulness on percussion over the region of the
pericardium therefore does not declare itself until the inflammation has
lasted for a day or two. I have no exact indications telling how soon
the fluid advances to the front of the heart in sufficient quantity
to push aside the lungs. That it must, however, have been rapid
in certain cases is I think shown by the following instances ; —

PRR1CABDITIS.

Fio. 37.

Figure 36, Tram a youth aged 17, afflicted with rheumatic pericarditis, who recovered
in uinu days from the time of his admission.

Period of the rapid increase of the effusion into the pericardium, just be/are tile occurrence
of it* acme. The effusion completely distended the sac

Day of admission.

The pericardial effusion distends, lengthens, and widens the sac, to the same extent
and with the same effect as when the healthy pericardial sac is artificially distended with
fluid (see figs. 33, 34, p. 305). The swollen pericardium is pyramidal or shaped like a
pear, as in figure 34. Its smaller and higher portion (I, 1,} contains the great arteries ;
and ita 'larger portion is occupied above (2,2,} by the heart, and below (3, 3,) by the great
volume of Bald which accumulates between the under surface of the heart and the floor

s the auricles ; and that io the lower portion of the sac, between the under surface of
the heart and the floor of the pericardium, elevates the heart Owing to the displacement
of the luugs from before the pericardium, the whole of the anterior surface of the heart
and great arteries is exposed, including the right auricle and ventricle, the apex and front
of the left ventricle, the ascending aorta within the pericardium and the pulmonary
artery ; and, owing to the elevation of the heart by the fluid, that organ presses and rubs
with increased force against the walls of the chest in front of it ; the anterior surface of
the heart at its lower portion is, however, separated from the sternum and cartilages by
a thin layer of interposed fluid.

This explanation, and that which follows, given once for all, will apply to figures 37 ,'
40, r>. 338 ; 42, p. 342 ; 45, p. S5H ; and 48, p. 3BS, which lepresent, each of them, the
single, or first or second seme of the pericardial effusion.

There is prominence over the region of the pericardium, the left costal cartilages and
ribs from the third to the eighth being raised and moved outwards.

The region of dulness on percussion over the distended pericardium, ("pericardial
dulness," see the black space,} indicates the extent of the pericardial effusion ; has the

Cyramidal or pear-shaped form of the distended sac ; and extends from a little above the
iwer end of the manubrium, where it displaces the lungs, down almost to the tip of the
enairorm cartilage, where it intrudes on the epigastrium. The lower and larger portion
of the region of pericardial dulness over the heart and the great body of the effusion is
more than twice the width of ils upper and smaller portion over the arteries. This
narrow upper portion forms therefore a peak which gives to the region of pericardial
dulness its pear-shaped form, aud which rises high behind the sternum, and occupies the

312 A SYSTEM OF MEDICINE.

lower portion of the manubrium. The wider portion of the region of pericardial dulness
bears chiefly to the left ; and its upper border, starting from the foot of its narrower por-
tion, is on a level with one of the higher left costal cartilages or spaces. The upper and
left boundary of the region of pericardial dulness is therefore indented ; and its upper
border is much higher behind the manubrium, than behind the adjoining left costal carti-
lage or space that may form its higher limit The higher and narrower region of peri-
cardial dulness (1,1,) over the ascending aorta and pulmonary artery, is about two
inches in width, and is situated behind the sternum, on a level with the first and second
spaces, and for about half an inch to the left of it in those spaces. The lower,
larger and wider region of pericardial dulness that extends over the heart itself (2, 2)
and over the accumulated fluid that occupies the depending portion of the sac below
the heart, and that bulges downwards into the epigastric space (3, 3,), extends from the
upper edge of the third left costal cartilage, and the corresponding portion, of the
sternum, down to the lower edge of the sixth left cartilage, and almost to the tip of the
ensiform cartilage ; and from about an inch to the right of the lower half of the sternum,
to half an inch or more to the left of the nipple. The lower border of the fifth cartilage,
and a line running thence across the sternum to the fourth light space, probably forms
the lower boundary of the heart (2, 2), and the upper boundary of the depending space
(3, 3,) occupied by the volume of the fluid distending the pericardial sac.

The impulse of the heart occupies the third and fourth left spaces, (see the curved
lines in those spaces,) and extends in the latter space to just beyond the nipple ; and
the pulsation of the pulmonary artery is felt in the first and second spaces to the left of
the sternum ; where the first impulse is followed by a sharp second stroke, which is
synchronous with the loud second sound of the pulmonary artery, and which gives the
effect of a double impulse, one systolic and gradual, the other diastolic and sharp.

Figure 37, from the same patient as figure 36.

Period of the acme of pericardial effusion.

Third and fourth days after admission.

The explanation of pericardial effusion and dulness given with figure 36, applies also
to this figure.

The pericardial effusion, which distended the sac on the day of admission (see fig. 36, )
has steadily increased in quantity since then, so that the whole pericardium has become
enlarged, and has yielded sideways, and especially to the left ; but it has not lengthened
from above downwards. In this patient, therefore, the region of pericardial dulness (see
the black space) during the acme is unusually wide, and especially along its left border ;
this increased width being fully as great above'over the great vessels (1, 1), as lower down
over and below the heart (2, 2, 8, 3). The left boundary of the region of pericardial dul-
ness over the great arteries (1, 1), extends about an inch to the left of the sternum, in
the first and second spaces ; while the left boundary of the large region of pericardial
dulness over and below the heart, extends fully half an inch to the left of the mammary
line (2, 2, 3, 3). In all other respects, except the increase of the dulness to the left,
the region of pericardial dulness corresponds with figure 36, taken on the day of
admission. The apex of the left ventricle seems in this case to be behind the fourth left rib
or space, and the lower boundary of the heart probably extends along the upper edge of
the fifth left cartilage, and across the corresponding portion of the sternum ; the heart hav-
ing been much elevated by the increase of the fluid, which interposes itself between the
anterior surface of the heart at its lower border and the walls of the chest.

The prominence over tfie region of the pericardium has increased.

The impulse is peculiar ; it is felt beating (4th day) from the first to the third left
costal cartilages, while the third and fourth spaces are retracted during the systole (see
the curved and straight lines in those spaces). These movements give to the impulse
the appearance of an undulation. The interposition of the fluid between the apex and
lower border of the front of the heart and the walla of the chest has combined with the
elevation of the organ to raise the impulse.

For later views o? this case see figures 38, 39, p. 335.

The effusion had reached its acme in one patient three days after the
beginning of the attack of acute rheumatism ; aud the increased cardiac
dulness was observed for the first time on the fifth or from that to
the seventh day after the beginning of the illness in nine cases.
Pain attacked the heart in three cases the day before, and in one

PBRICJJW1T18.

CASES OF RHEUMATIC PERICARDITIS.

Xiri.lKAfTOH.

i* upper boondiir of tbe region of pericardial di
1-t formed the upper limit of the dulneeo.

tl* apace 01 cartilage tint ,. ..

1— nww mm the upper or lower boundArr, acoonling
friction »onnd oier Use iltnuim, and I. plaaad on a ton I wl
limit of the region of friction tooutl. The whole apace between 1
lij tlw fihitlna —nil

a.— «• maun tbe upper or lower boimdnrj, u-oordlna: to Id poettkn, of the region of pericardial

friction acond orer tbe ewtml cartOagia and tbelripecoa, and la i— "-- ■'■'■ " — ■"■-—

the limit of tbe friction aonnd. Tba whole apace between ther
bj tbe rriotlon aonnd.

i m Uui portion gf (;,n bslrt'a lntpuhw, and la on

■a felt.

poaHion, of tba region of pericardial
-part of tba itenuua thai forma tba
pper and lower bonndarlea 1* occupied

in a line with tbe epaoe or cartilage forming
* upper and lower boundaiiaa I) oompied

a level with the epaoe where tba tmpulaa

mitral a

eyatollc murmur; ^, pulmonic murmur; o-* m
The thin line* mereljr connect tbe auoceealii

lion a* to the point In qneetlon wa* made on ■■
U., Mak I FT, female.

1 murmur ; 1 . aortle regurgitant uvnrmur ; t ■ aortic
latlone with each other, and ihow that no Tirtmln-

A SYSTEM OF MEDICINE.

Kriaff Ml sew (ronlfJlUHf).

iTIimt

1 2nd .'nrtU.

ft
... ari tuts,

... «b urtll.

■ iiitil

71h CHrtll.

■ (Wv.-,',]

, lOMi

i Third

i titcuriil. C
I

I iii-l . nvtil

Srd ppico

« 19 II 12

Hi. M.niuni.

m | 2nd cwtil.
j f Middle Jjmlcartll.
(Tbird .. Lth artll.

fmtni .J#th .■.«[]. i0'

"I Joint. } ■

i ii ifl 17 is IB a

-Eft)

PBRICJRDTTTS.

Cam wllk a Urill (mUimraO (Ik-Can *U* a frattw frietim nnl <UHiv <*« «

(

°"

)

Sternum

Left acuta!

Bpan.

a— *- i-i* *_.

cartihurre

el tillage).

■

11 11

i»

Mnou-1

itcirtll

letipace

(brim,, 5

Sndeuti]

™.

•n

2nd ipuo

Muldle ...

tod carta

Third ...

tthnrUL

Lower ...

Bth eirtlL

Gthipue

„

1 bird .,

! .-,■.:;■■:,. 1.
MltU. j

TUicnrtll.

nth miict

™

sen

""«,[

*lhr„rtil

Murmur

FUn ~

•*

::. a

AITmUoh 1 (SEC «ve«
of Joint. } - Jg^f ^ ...

Hh pp. M*. s». h3< 3m-

(8.J— Cttu riO, a Ann* Amik/rfcHm wind daring On atm<. (Sm pp. 9St, :■■;.:.

—

mmm

Spacer.

DW".

Bt.rr.am.

eirtll*gct

■..rliW-s

• s

JM.uo.,

umm.

1 brituii

2nde*rtll

indip.ee

,:6

jMiddh-..

irdtwUl.

Srd .p.«

.,,..

„

—

(Third ..

Ith BOtiL

tth rfaca

*«

::;■

hin..[ ..

5tli oar-Ill

Eniirnnu

Mh >p*ce

Humor

■

[Vwj MKm...

AffcrtloD i iBevsn

of Joint* J ' j Hither Kver*

Isiight

Bw p. as*.

Sternum.

UftwUl

Spaee.

^_ D*^

ntna*.

'■1[lll:i;-.'-

llMiddlr. ..

aid ami
Jrd cutll.

Mt^l

....

:.;:

iVTliIrd ..

(Ui otrU

":':

( Lower ..

Mh ravtO.

t.th«pa«

Third ..

iEiuifonn
cirUl. |

rthcartil.

■r-

—

Murmur

-t

-»

-*J

o-.

Affection 1 J Severe

of Joint* f ~ ilUOwriioTOre

A SYSTEM OF MEDICINE.

tor Xrplanatlan •« p. 111.
■ *(tt a hnk rimMi /rlrf*™ «wl dnrt»» a» oau (amttonnf).

■ bet men
cartilage*

I briuin l
(Middle ...
trhlnl ...

iThirt ...

" ,lf...T,l|

(VBTBTBn...

1 lejetere ... ...

f - 'l Rather »vera

(Slight

«pp.Sll..Kti.

IL— CASES IN WHICH NO THRILL WAH ■iHSKHYKN nlhlll 1 1 1 37: IIKi'rluN OP THE HE
THE ACHE OF I'liKli. u;ln M. Ki-Ti sliJN". (See pp. S,V>-S61.)
Il \-C <r!t\ m ifrmMrij friction »ik< taring Ifca «W (So pp. S55-1W.]

*t. Sltrauoi. I'

. i Mmuj- i
. \ brium I SnJ

.to .Jsrd eutll. "
I

(Tiint _.<th carta.

flower ...J6th «artlL

(TMkI ...jath oartll.

artlLiga. a

i 2nd cartH.
... 3rd carta
.. 4th euttl.
... 6th airtll.
... ttUi carta.

~ Ir.

8 * A 8 T S

PBBIVAHDITIH.

-"ti]M«a- rutllignt. ' 1 » A 5 II T I I U 11 U 11 11 U It IT M U tt

:lr.! .-art-1.

«he»rtil

(Third

Affection 1
of Joint* I

|V«y«Y«. _

a s t a o t

, Middle .
tThlrd .

\Thlrd .

{Out K-ri* m *>•»!« <■«•.}

rt. Slflmom.

I I te I

I I brmm f

I Middle™
Ilhtnl

enrtfl.

llhclrUL
ttliwUL

flee pp. MS. Ml.

T I I 10 11 11 19 14 IS 10 IT

I \\\\\

A SY8TJSM OF MEDICINE.
For EipluuUon k* p. lis.

.{SSI

iMUldlo

Iriiinl

andartil.

ettta.
1th cartil.

SUlOUtB.

... fltb eirtll.

D i Isbymo ...

* 1 - IRatberKTt

iNMKHit

S * 5 6 T 8 »

1 1 t 9 6 I M id II

(Middl* ..
'Third ..

(third ..

outfl.

MhnrUL

; vlth a gratUq friclOm M

s g 10 iilia uitu

(Third ... jfth eutll.
Idw« ...!ftUie«tlL
TbltU ...ieihmrtll.

SfdlpftCQ

4ff«ctloii > jS#Tere ... ■

PUBITJ RVITJS.

For Expluiillon He p. 31!

0 11 11 II || 14 Ifi lb 17 1H 19

( M»dU-

[ttMb ■

(Third .

(Third ...I

K,;.,i,.r:.M

cmriii. (;;

in wlntk Ulrri via ifJlKiU toKbltfi ir lion found, WHallf fcarui, ilarlnf !** II
<7«k> v™ u*fcJi Merit irni a crenWun frittio* iiwiut o» jreiaxe.

, Ul«*I S2 ,' ",?'-JlM _

''""«■«"■ purtiy™,. 1 « 3 4 I t T l.» » 11 l!l!ll

a pp. 347-31*.)

pun .'....,... 1"?'-^—

HlSlft 1 * 3 « * * T g. 1 10 11 l'i IS M U 17 IB 30 SI il

!flllitd>...iSrdcirt11.

jlTbknl ...lithnrtii.

\u*m ...SthMHil.

llTkird ...Wheirttl.
Ennifoim I
(•Mtll. fTtkBUMl

Itntn ... ...

rirtib*.. «g*

10 II It 10 M SI «

Third ,
'Third .

Jill 'ilrtil

sth e«rtll
'm enrtfl.

«■— H

,1).-.

- I

*■«•.«,«> P. W° ; Igi. 44, «. f. nit "4 H **• V w*

A SYSTEM OF MEDICINE.

PERICARDITIS.

Fut Brplmatlon «m p.

A SY8T£M OF MBDICIKE.

P ERICA JtDJTTff.

A srSTEM OF 11SDICINS.

Cnaaj «tfa ■ ttrttt— Com

Fo
vita a

Explanation Ha p. III.
aarah donate /rfcrton nwl (farta* Oa o

«u (anJiawd).

M
¥.

n
iv.

Sternum.

.I'd i-.wi«i
entllagea.

Space.

1 „.,»„.,!

cartilage..

aTa.™**

4 1

M 11

i« ■

fc>

H
i',

Kami- |
. briuin 1

Middle ...

Third ...

Third ...
carta. ]

a ... '.

■ad carttl.
SidcntiL

IthCMtll

5th carta

-th«rtil.
«h carta.

2nd ip.ce

<th apace
9th .pace.

■

■ ■

la
3

~ =

i?=

ADectlon j -JBann „ ...

or Joint* I "' ' 1 lUtlier mm

ISIight

il.-CAMKS IS WHICH NO TllHtl.i, ».V, nHsKKVKII i>VHIt TliE UK N Of Tilt: IIEAIIT DUIlINt:

THE ACMr. •'!■' I'UUl IKI'IM. EFfTWIOS. l&M pp. UB-J61.)
(1.)— Caw nrfrt a cretHni, friction tounii rfurinp <•• MM. (Sm pp. 3M-1M.)

F.
a*.
M,

Btarnnm.

Space.

...... ^

ii, ;.i ;, ■■

riniU--,-,

1 *

e n-

-■

ii 17

S 1H -j

■

■:.

1 Mug- 1|

I brlutn f|2nd carta

{Middle J 3rd tuUl,

(r«frd „l4th«nu.

{timer ... Bib eartil.

5th .pace

tei

■

"":

7th emtll.

nnonr

Ho _.

dth .pace

^■,'S

oiJoinU/ - 1 Rather mum
^Not ■■ i ■■! ■■ ...

-™»

URmW

Bpra

Am, I1""

■■..,!ll:i.,,H

m-i:,..'-.

-1

■■■

'JO .'.

1 Mann-
t briuin

(Middle..

(Third ..

(Third ..
nation I

JndeartlL
Brd carta
«h cutll.
6th until,
ath carta.

m IBM

3rd .pace
1th apace

;;-

••-

PBRWARDITIHt.

Left™.Ul &Z

onrtilogtu. pirtJE^J, i I i a |~4 U|*Tt j 8 I il I loj ll I li llsl U lis I lSJ HJltllt |»

(Middle.
(Third ,

(Third .
Mrtll.

leuta.
hwML

lonl (Severe ... -

nOf ■" Ifauher severe

gee pp. *lfl. 3S6.

i i t & s 1 s

™\»

| 2nd aril!.
■dMrtlL
:h eutil.

(Third ...St

(Com vilk ■ Amtfe ac«.)

A SYSTEM OF MEDICINE.
For Expkniiioa «* p. sis.

I Mann- 1
■| brinin j

dMfft

3rd carta
MrUL

Sth carta
ewtU.

7th .'•nil

Itfeveie ... ,

,rr:.:;,

OMMu

'Third ■

4 S A 7 * ■

113 345 a T8« 10 1

a irlrt ■ rrall-v/Helion wiiirf dvriitir l*c m

5 e t * * » n i

I briom jiSnd cirtli
,lllddis...3rd««rtll.
(Third ...4lhMrtiI.

(Third ...iOUim

PERICARDITIS.

For ExpUiulton vit p. 313

14'

l.-fT .-■■■;l.i

ruUlagri

.1111 in i:<':.

Jan* D*"'

1 ft

■*>

f Mum- \

fSi*il(...»n1p»rtl].
tThird ...«h«rtJL
[Ijiwar ...ISlh p.rtll.
[Third ...iMhcutl].
ortll. ||7thr»rtfL

in.l -iifli'.'
Ml tpac

9th tan*

Ira

■Mr.

pnufi

Sat aa.

1S7-SM.)

[

Palm ...

(9.1-Cui 1. ■»«» tlurr ™.i daft

BWiw

>]4

ii,

Irj

i!-:

i Hun- l]

1 hrium find cartil

jWddlr ...:Srd etrti].

Stlnpace

(

■ ■

t™

■":

'■

IfThmt ...lath mtul

iEn«iforml

cwtil. /Ttbrartll.

Pais >_

•X

of Joint* ( '• iMkuamm
(eligbt ... ...

■0

.■il'.'

H
Pa

......

Space.

1*Jar* r*4em J"*»ow

onrtilsKM

■firtiljW.,

•

9 10

Mrwi). 1
brfiun 1

Mlddlx ..

Third ..

!*-«..

Third ..

:n-it..ri-.

lolnul -

ardcartil
tthcutl!.

Sih euta

eth eutlL

71 h «rti).

sth-inll

1th fj)|M

Sth.ti»w

-,;-

.:,

...

■

■4 \'\: MS

mh, m.j

77-S7».

- •*• Ifj. *4, it, p. »»; Em. m, «, a. *77-, tod. *«.».»,¥- *»%

A SYSTEM OF MBDlCiNR.

PERICARDITIS.

A HYOritU Of MBD1C1NK.

pHk.

'Third

(Third

l!'i- if..!:'.

t-itrtil.

2nd aiJU-'p

^Middle
(Thlid ..

mpmt

D I |S«Tert ..

a ) - J Ratbor »

I Slight ..

, Bnnces

1 Wlv,.-.,,

) 2nd curHL

ft
... 3rd curtf]

... 5th cnrtil.
... Sti cnrtil

PERICARDITIS.

For ElplimmUi.il we p. 113.
(Cam with a a'mUi new. I

(8K!

i Middle,

cutil.

2ni
lid cutU.

Sri
UhurtiL

H
Mn cartll.

.. 6th carta. |

7 Tth carta. I

■SflB

lijulisl 20|5l|iali*[l*

VThird

(■|l!!!-l

] -Mi'] vartil

. arf oatfla,

. 4th eartil.

i carta.

:: BUM

•i SSS2

™ between ,

?nd apace
3ni apacn

Sthipaw

4" w

oT JoinUj ■" Buthei

Verj Miere .

■■Wmii win'

might ... .

5 ' 10 ! 11 U 13 U JS ID U 18 19 SO

pilddle ...
irard -

(Third -.t

Kiisir-mi
cartiL 1 1

Fain ...

Adection
of Joint*

a sraTXM or uxdioixb.

For BiplmmUon m p. AID.
i/wWl/ridioi »HHut,tul
(Can with a InMi a

,„™

Jlllil-I^'L.

BpKal 1 Mb* BW^M*-. J-J*

■artLlOKfi

-i

su' s

•

i.'

■jo

-*;

A
of

■_>.-..

( Itiim- 1
. lirluw |

Middle ...

Thlnl ...

Third ...

lidcattU.
ItboartlL
SUmntttl.
nth eiTtil.

Ind apace

■th epnoe

rtejWdita

■1

dD-

51
li,

f, di-,i

•

«•;

-.:■
-•

{

«d

—

«lbn

tmrtli. f

■ ...
Vrtlou I

.. 'ii'.Vi,'.

a in vhUi

'."

•da

Stenram.

■:i)t[J.L^i::.

SSMM

A-» D-*6

-.Ulilll^h 1.

•

•■■

.-.

l-i

| M.uu- 1
[ brinin |

[Middle ..

[Tnird ..

iThlri ..

n ...
lection)

2nd C«W.

irdurtlL
tthcutll.

BthwrtiL
Mh rortll.

2nd ipun
3rd (pace
MfctpMt

'ilh ipsen

£•

■:.■

Btcrnwii

Bp™.

rfo» "W«-

i-ll](il!!Mi'S

■■LL lM.l-<'h

■

•■•

If.

1 Mun-
| brluin

/Middle..

llhlrd ..

tTWnl ..
In '..'.' .

SndiwtlL
BrdelrtlL
«hc»rtil
Mb cacti L
Mb ottil

[Bstli

41k iptce
5 th >pli>*
fltli ipece

■

PERICARDITIS.

Slrraum.

Lift postal
lartltage..

■iirtilK;.'.. s

?-£^ D»^ i&CL I™

]■•

l:t

.■4

■

M,..,-i- 1
brlain 1

Middle...

Third „

Third ...

Sndcirtil.
4thartlL
dtb curtil.

-th ctrtB,

4th tftCC

ithipoce
8th ipnce

—

C: » >r

•$

' ■

Murmur ... .„

Fmin _. ... „ .„ „

(Verr«Ter« ...
ABfccUon 1 iBevuni ... ...

of Joint* f '" lluthcr (even

UUght _ ._

-i

-t

....

(Cm *tth n fotrfiM km)

F.
i.r.
Hi

HWmnm.

«U

«U™ r-w1"**' «w «-M™

curtiligri.

'iu-uliit;i'H

■

".'-!

.10

ISS)

(Third ..
1 Third ..

!.,,.„|.l:,i

crntiL

2nd cull).

4thcutB.
5th curtil.

nwW

"Hi unrtil.

4th ipnee
Mhip»ce

i^-

Pnln -. " ~ ~ "
Affrctkin J iVeryKMrfl ...
of Julnti f - iseven

Cttt in K\tck the friction ■

:;!

pro

r-i

IX.

Sternum.

Bp^ ! *<™ D^"'

MM*.

hei*«n

curtlliges. . 15

i;i

III

£i

.'9

:ii

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A SYSTEM Of MBDWTNE.

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388 A 8Y8TBM OF MBDWINB.

INFLUENCE OF PRESSURE IN (I.) EXCITING AND (II.) INTENSIFYING A
FRICTION SOUND WHEN APPLIED WITH THE STETHOSCOPE OVER THE
BEGION OF THE HEART IN CASES OF RHEUMATIC PERICARDITIS.
I.— Injtumt* o/Preuure over the Region of Uu Heart in Exciting a friction Sound mAm not
prevumtty audible.
(For the explanation or ihia part of tire Tabic, nee peg* m.)

lo the preceding

Tablee, tee pp. S19-S17. TLe repetilfun of the
Igmeano^lhat the algnwaa again r-JI"

ByetoUefri
Boo We Mi

Time or rhythm of Motion »

Byitolle Motion eound

Double friction, or to and fro aound
Time or rhythm of Motion aonnd D

OhUm or rntteo wawr—
Byitolle otealnng friction n

!} ! "•"** t "

_1_

Id, 40, 47, SO, M, 50.
54, Si, 4T, 47, 1ft
JS, SO, SO, as.

1«, 19 (feint Motion eoni

o, 11, 68

«.

US, -SO, 'SO, 13.
S,-3S,W,44,4*,48.
|s, -M, SS, BO, 44.

IS (grating).

— Influence of Pressure over Ute Segion of the Heart in Intensifying a Friction Sound
already oraent.
(For the explanation of tbla pan of the TahLe. aae page AM.)

iven In the preceding tables (*ee pp. SIS-SIT). The amall flgurae abow tba
ft on which the obaervetlon waa made.

i, Incnaied by pnaauie, 86 2nd day after admlsalon.

" ™, 80, lHth day. ■

dered louder by preeeare, 90, 8Mb day.
[Feeble murmur, replaced, onpneeure, by double friction murmur, M, 1Kb day.
| Mitral mnrmur to right of, ur above, nipple (-»; replaced, on preaaure, by a

friction aoond, SB. nth day ■ IT, Both (.*£>..
I Double endocardial murmur, begU

1 mnrmur, not beginning with t , __, _. . . ....

| rictionmurmur,^ul*nainedl.ypr™ure.4. Ttta day ; fl, 6th ; M, Wtb.

Frletlon raunuur modlhod by

Friction aonnd resembling a
murmur, changed by pros-

au™ to definite friction

...... Mutton

beginning witn ao "" " '

Duruiurilnlenalne-^ , „ . „

BjTtolic Motion murmur : on jicreBUre, a donble friction mumiur, 6, 7th.
Byitollc friction mnrmur: nplaood, on preaaure, by a to-and-fro Mctlon aonnd

H, Slat: M. 8th.
Donble friction murmur : tntenaiflad by preaaore, B4, Mth ; 83, Sl.t ; 88, lVt* ;

SB, IStb i 49. 11 th-Htth,
Donble friction uununr : converted hy preaanre Into a double Motion aoond, M,

"th ; 98, 11th : U. Srd : H, 1Mb.
Friction aound, like a bellows murmur : much handier on preaaure, 88, 4th day.
Friction enuniifof murmuring ebaravter: rendered grating by preaanre, 41 lSlh.
Friction aound, almoat a murmur ; changed, by pressure, to a lianh double friction

aonnd, M, lSu.
Frletlon aonnd, ecarcely audible ; on preaanre, a hanh duuble friction aonnd, 96. 17th
BjatoUc friction aound ; intenalBed by preaaure, B. let : 81. Oth ; 40. 7th ; 40, 18th.
Systolic frletlon aound : followed, on preaaure. by a dlaatollc murmur, 81, 1th.
Byito'lc friction aonnd : changed, by preaaure, to a double friction aound, la, 6th

89, isth; 41. 16th; 44.10th-
ttmootb, BofL or grulng double friction aound ; Inteneifled by preaanre, 4. Srddu;

4. 17tfa: ft, 4th; 86, 5th; 18 5th ; 88. *ih ; 81. Wh ; 81, »sth ; 89, 17th.

40. 14th r«. <tb ; 47. Hth : 44, ith ; 08, ai.t.
Sin»ith [>r«oft '-friction •oond" probably double, inteuallled by preeeure, 4 , Srd

86. lit; BftlSh ; 89, 14th.
a~i- ■>: il- 1 inl< hMd-l ur altered to. character by preaanre, 8, Hat day;

0. 1«; 7.*i1k 8 ■■■'■'■■ 8- 1 111.; 8. I6ih ; 11, lit; 18, 6th j 18, eth; lB.Brd;

30. lltli;2». ■■ ■• H.:.-.' M."h: 88. and : 89. 7th ; 41, 1th ; IS, dtt;

(0. .tli j fit klLMl S6-l*th;iB,»Ui:fl8,l5uL
" fiii tl.'ii ■ . 1 = : ■ ■ 1 . 1. 1 1 .'.... 1. 1 v.l. 11 i. ,. ; lutenalnod or altered tn chanctar by preaaure,

T.otl. -M: 20. ■ ... 24. ■>■').: 88. 5th; IB. otb;S9. l»h;44, loth: 44,

ml. ; 46. »«' ; 44. I7tli ; 46. l»th ; 84, 7th : 56, .nd : H. Sr'
ilu-i: .'L l . ■■ ■!■ ■■■ ind ; harsher on i.rettiure, 7, 5t

■Hi; 11. bin: 88.14th: 82 . -"h ; 8*. »"; 89. l~v- "" ""
l.'lli; 42. II!!' . M. :.■! : SB. Mb : 89, «b-
[!:,i-' ,.,v i....::ii " F , 1.1 ; - ■ 1 , ■ . . j 1 ,i, prohahly double, tntenalned by pt enure, 19,

lOtli : 81, Olii ; 33. 13th.

In. <:.... ■ 1 ...,. 1. 1 v . .ii. III.:... siting on preaaure, 48, »th.

h,,![!.|,. in... ,.,1, ....in,. 1 : .j,].-!., 'dmI grating by pteaaure, 49, 1!
[i„nLk lii.-lii.ni mm\'i ; ti'inlvri'i' ~"' — v ~" *" """ " "a

, 86, Ith;

«.ure™,'itli ; IS, 5th : 19,

i: SB, 8th; 40, 6th; 43,

PERICARDITIS. 329

three days before the first appearance of increased dulness over the
pericardium ; and from one to four days, before the effusion had
reached its acme in eight other cases.

Friction sound, like increased pericardial dulness, is not present at
the first blush of pericarditis, and in my cases the two signs usually
appeared at the same time. Thus they did so in 16 of the 22
cases in which the dulness on percussion was detected in the early
stage ; while in only one of those cases did the first brush of the fric-
tion sound precede, and in the remaining five it followed the onset
of the increased pericardial dulness.

The upper boundary of the pericardial dulness when first observed,
was limited by the space between the third and fourth left cartilages
in 11 out of 22 cases, by the fourth cartilage in three cases, and by the
third cartilage in seven cases. In one patient only did the dulness
on its first observation reach as high as the second space.

The increase of the region of dulness over the pericardium
was sometimes gradual, sometimes rapid. In rare instances the gradual
ascent was slow and irregular. As a rule, however, the ascent was
rapid.

The contour of the area of dulness on percussion over the pericar-
dium when swollen with fluid in acute rheumatism corresponds very
closely with the outline of the sac when distended with water after
death. (See figures 33, 34?, p. 305.) In a paper in the Provincial
Medical Transactions I gave illustrations of the area of pericardial
dulness in which the boundary lines of the effusion were ascertained
with care, and I here give figures of those cases (figs. 36, 37, p. 311 ;
38, 39, p. 335 ; 40, 41, p. 338 ; 42, 43, p. 340) ; and elsewhere, views
taken from a case of pericarditis in St. Mary's Hospital, which
show the same point during various stages of the affection. (See
figures 44, 45, p. 356 ; 46, 47, p. 394 ; 48, p. 395.)

The form of the region of pericardial dulness changes as its area
increases, its upper boundary being then on a higher level over the
sternum than over the costal cartilages, instead of being, as in health,
on the same level. The pericardial dulness, at the same time, ex-
tends further downwards in the manner shown in the figures just re-
ferred to, so as to intrude on the abdomen, and to replace the liver
and stomach to a degree proportionate to the amount of the effused fluid.

When the increase of fluid in the pericardium reaches its height,
and the sac is completely distended, the area of dulness over the
affected region is pyramidal, or, more exactly, pear-shaped, and it
extends over and beyond the heart, and in front of the great vessels.
The inner borders of the right and left lungs are pushed to each side by
the distended sac, so as to expose the whole of the heart and the great
vessels.

The region of dulness over the great vessels extends upwards from

the level of the third cartilages, sometimes as high as across the middle

of the manubrium, or within an inch of the top of the sternum, but

more usually to a little above the junction of the manubrium with the

VOL. iv. z

330 A SYSTEM OF MEDICINE.

long bone of the sternum, or about two inches below the upper eiid
of the bone. This space of dulness over the aorta and pulmonary
artery extends across the whole width of the sternum and reaches
some distance to the left of it, in the first and second spaces.

The area of the region of dulness over the heart itself and the
lower portion of the distended pericardium, may extend across the
chest from an inch or more to the right of the lower portion of
the sternum to an inch beyond the left nipple ; and from above down-
wards from tlie second cartilage to the lower edge of the sixth carti-
lage. The extreme measurement from side to side of the whole region
of pericardial dulness may vary from four and a half to six inches,
and somewhat diagonally from above downwards, from five and
a half to seven inches.

The lower portion of the region of dulness, from side to side, for
the extent of about two inches from above downwards, is situated
below the lower boundary of the heart ; and is entirely occupied by the
effused fluid, which here, as I have before shown, displaces the heart
upwards, and the diaphragm, stomach, and liver downwards to an ex-
tent corresponding to the amount of the effusion.

The width of the region of pericardial dulness in front of the great
arteries is usually about two inches, and this region usually ascends
above the upper boundary of the heart to an extent varying from one
inch to an inch and a half.

This upper region of pericardial dulness, over the great arteries,
which is two inches wide, is much narrower than the great region of
dulness over the heart itself, which at its upper portion is above
four inches wide, the greater width of the cardiac portion of the
region of dulness being gained chiefly to the left. This sudden
widening of the area of pericardial dulness from distension of the sac
gives that area a peaked form above, and an indented outline along
its left upper border, that distinguish it from the equally high and
extensive area of cardiac dulness due to adherent pericardium and
valvular disease, when the heart is enlarged in all directions and
especially upwards and to the left, and when the upper left border of
the region of cardiac dulness presents a very gradual inclination
downwards and to the left without a break. (Compare figure 42
with figure 43, p. 340.) This pear-shaped outline of the region of
dulness over the pericardium is quite characteristic, and indicates
with certainty the presence of extensive eflftision into the sac.

Among the forty-four cases, the upper boundary of the region of
dulness when the effusion had reached its acme was over the first space
or second cartilage in ten cases, over the second space in twenty-two,
and over the third cartilage in twelve. In those cases that suffered a
relapse, the first acme was as a rule higher, and the second, and still
more the third acme were lower than the single acme in cases that
had no relapse.

If the position of the upper boundary of the pericardial dulness over
the cartilages and their spaces is known, the whole area of the region

PERICARDITIS. 331

of dulness over the pericardium jnay be inferred with considerable
accuracy ; since the whole outline of that area shrinks when its upper
boundary is lowered, and widens when it is raised. In this respect with
certain definite reservations, the upper border of the region of pericardial
dulness over the cartilages and spaces to the left of the upper half
of the sternum, serves to measure the whole area of dulness and to
define its complete outline ; just as the ebb and flow of the tide, or the
rise and fall of a flood indicated on a measuring post, will tell anyone
accurately acquainted with the coast, or the contour lines of the
country, the exact area over which the land is covered by water.

If the upper boundary of pericardial dulness reach to the second
space, the contour line defining the dulness extends — to within an
inch of the top of the sternum ; an inch beyond the right edge of the
lower half of that bone ; and more than an inch below its lower end,
where it may descend as far as the tip of the ensiform cartilage ; to
the lower edge of the left sixth cartilage ; and about an inch beyond
the left nipple. (See figures 42, p. 340 ; 45, p. 356.) If the upper margin
of dulness be limited by the third space, the boundary line extends —
across the sternum on a level with the third costal cartilages ; to the
right edge of that bone ; and to fully half an inch below its lower
end ; to the upper edge of the sixth cartilage ; and to the left nipple.
(See figures 38, p. 335 ; 44, p. 356.) The lungs, the diaphragm, the fiver,
and stomach are all correspondingly displaced, to a greater degree all
round when the upper limit of dulness is over the second cartilage ;
and to a lesser degree all round when that limit is over the third
space. The intermediate position of the upper edge of dulness over
the other cartilages and spaces gives an intermediate outline of the
whole area.

The restrictions to this rule are due to age and sex, to previous affec-
tions of other organs, to valvular disease of the heart of old standing, to
coinciding affections of the lungs, especially the left lung, to the duration
of the attack of pericarditis and the occurrence of relapses, to accom-
panying endocarditis, to the progress of the disease, and to its termi-
nations, whether in complete restoration to health, the valves being
intact, in valvular disease, or in pericardial adhesions. These restric-
tions are numerous in appearance, but practically they seldom interfere
with the rule just stated of the correspondence of the whole area of
dulness with the boundary of a particular part of it.

The rule that the region of pericardial dulness in rheumatic
pericarditis enlarges over corresponding areas in different cases, holds
good in young persons of both sexes, and in women. In men,
however, the bony frame-work of the chest is larger, the lungs are
more ample and cover the heart to a greater extent, and the diaphragm
is lower than in boys, youths, or women. The result is, that in men
both the upper and lower boundaries of the region of pericardial
dulness are lower than in the classes just spoken of. Thus the upper
boundary of dulness during the acme was over the third cartilage in
8 out of 14 cases of rheumatic pericarditis in men ; while in the whole

2 2

332 A SYSTEM OF MEDICINE.

of those of the female sex so affected, except one, that boundary was
above the third cartilage. In nearly one-third, or 3 in 11 of the
male youths with rheumatic pericarditis, the upper boundary of the
region of dulness during the acme was over the third cartilage. This
is due to the fact that in the male sex, the lungs at a comparatively
early period are more largely developed than in the female sex.

When rheumatic pericarditis attacks a heart enlarged from
previous valvular disease, the pericardial sac, being more ample, is
capable of containing a larger amount of fluid, and the region of
pericardial dulness is of greater relative width than when the affec-
tion attacks the virgin heart.

If the lower lobe of the left lung shrinks, owing to the combined
effect of the compression of that lobe and of the left bronchus by the
swollen sac, and of pleurisy with or without pulmonary apoplexy, a
condition of things by no means unusual, the whole area of pericardial
dulness tends towards the left, and its left border comes into direct
contact with the ribs at the side.

CJianges in the Form of the Outline of Pericardial Dulness caused
by Variations in the Progress and Termination of the Affection. — If
the attack lasts long, the pericardial sac, as I have already stated,
becomes softened, it yields sideways, and becomes widened to the
left and right, while it is not proportionally lengthened above and
below (see figure 35, p. 307). This is especially to be noted when
relapses take place, and when the effusion, after lessening in quantity,
again increases. (See figure 48, p. 378.)

If the affection passes quickly through its stages, and the recovery
is perfect, the heart being restored to health, the changes of the in-
crease, the acme, and the decline of the pericardial effusion and of the
area of pericardial dulness pass through the course I have described.
(See figures 36, 37, p. 311 ; 38, 39, p. 335.)

If, however, the heart becomes^enlarged owing to the establishment
of valvular disease, the lessening and disappearance of the effusion
are delayed, and the area of dulness is somewhat widened and lowered,
especially towards the left

If along with valvular disease, adhesions of the heart are established,
the whole organ is enlarged, upwards, downwards, and sideways. The
outline of the area of dulness loses its characteristic pear-shaped
form, and its peaked outline over the great vessels gives place to a
gradual widening of that area from above downwards, that corre-
sponds with the enlarged outline of the heart itself. (Compare figure
42 with figure 43, p. 340.)

Prominence over the Eegion of tiie Pericardium.

Increased dulness on percussion over the region of the pericardium
is the only reliable sign of the increase of fluid in the sac. Increased
prominence of the costal cartilages over the heart, with widening of

PERICARDITIS. 333

the spaces between them, form, however, a secondary sign of some
interest and value.

In my paper before alluded to, I state that the distension of the
pericardial sac by fluid, besides displacing the surrounding organs,
pushes forward the sternum, elevates the costal cartilages from the
second to the seventh, widens the spaces between the cartilages and
ribs from the second to the sixth or seventh, pushes outwards the
sixth left rib, and causes some degree of prominence over the left
side.

This condition was observed with care in one or more of the cases
of pericarditis examined by me in the Nottingham Hospital I find
that prominence over the region of the pericardium was noticed by
me in 19 of 63 cases of rheumatic pericarditis under my care in St.
Mary's Hospital More than three-fourths of those patients (15 in 19)
were males, while only 4 were females. The cardiac prominence is
obscured in women by the mamma ; that sign having been observed in
only one-seventh of the female cases of rheumatic pericarditis (4 in
27), while it was noticed in nearly one-half of the male cases (15
in 36).

The increased prominence over the region of the heart was usually
noticed when the effusion into the pericardium was at its height, and
it lessened when the effusion declined. In the greater number of the
cases (12 in 19), the prominence over the region of the heart is de-
scribed in general terms, but in seven its area was specified. In one of
these it extended from the second cartilage to the sixth ; in two, from
the third to the sixth ; in three, from the third to the fifth ; and in the
remaining one, from the fourth cartilage to the sixth.

In these cases the cartilages yielded to the distension of the sac, and
were displaced by it forwards and upwards ; with the good effect of
somewhat relieving the pressure exerted by the swollen sac on those
important structures, the bifurcation of the trachea, the left bronchus,
the oesophagus, and the aorta, that are situated between the back of
the pericardium and the bodies of the dorsal vertebrae. The promin-
ence over the cardiac region caused by the forward pressure of the
enlarged pericardium, points out that a serious counter-pressure
backwards is exerted at the same time on the three vital tubes that I
have just named, which convey air to the lungs, and especially the
left lung, food to the stomach, and blood to the lower half of the
frame. Indeed, the true value of this sign is that its presence reveals
to us at the surface, the existence of deep and serious pressure on
important internal parts, a pressure that is augmented when the super-
ficial prominence increases, and that is relieved when that prominence
lessens.

It is to be remarked that at the same time that the sternum and
cartilages over the region of the distended pericardium are rendered
prominent with the effect of somewhat lessening the pressure, of the
swoUen sac upon the bifurcation of the trachea, the left bronchus,
the oesophagus and the aorta — the dorsal portion of the spinal

334 A SYSTEM OJf MEDICINE.

column deepens itself and curves backwards so as to afford increased
space for the swollen sac, and those important tubes that are com-
pressed by it At the same time the patient sits up, and even
leans forward, so as to allow of the gravitation downwards and for-
wards of the fluid in the pericardium. By this attitude, and the
deepened spinal curvature, indeed, the pressure of the distended sac
upon those vital parts is materially lessened, breathing and swallow-
ing are rendered less difficult, and blood is supplied through the de-
scending aorta with greater freedom to the body and lower limbs.

The Position of the Impulse of the Heart in Cases of

Pericarditis.

When the amount of fluid in the pericardium has increased so as to
enlarge the area of dulness on percussion over the region of the
heart, the seat of the impulse is raised and extended outwards.

I gave figures of three cases of pericarditis with great increase of
fluid in the sac, in my paper on the position of the internal organs,
in which the impulse was present in the third and fourth spaces,
instead of occupying its usual position in the fourth and fifth spaces.
In that paper, attention was I believe called for the first time to the
elevation of the impulse in cases of pericarditis with effusion into
the sac.

In thirty-seven of the forty-four cases of rheumatic pericarditis,
daily details of which are given in columns in the accompanying
tables, the exact position of the impulse during successive visits is
stated, in five others the impulse is described, but its situation is not
specified, and in the remaining two the impulse was almost or quite
imperceptible (see pp. 313 — 327).

In examining these cases I shall study the position of the impulse
from two points of view, (1) the elevation of its lower boundary ;
(2) its diffusion into the higher intercostal spaces during the period of
the increase of fluid in the pericardium.

(1) The Elevation of the Lower Boundary of the Impulse. — In fourteen
cases, the extent of dulness on percussion over the region of the
pericardium increased, and the effusion attained to its acme after the
first observation ; and in twelve of these the impulse occupied a higher
position at the time of the acme than at that of the first observation,
while in two its position was unchanged.

In twenty-two of the patients the amount of fluid in the peri-
cardium was at its greatest height or acme at the time of the first
observation; and as the effusion lessened, in eighteen of these the
lower boundary of the impulse fell, in three it was stationary, and in
one it became higher in position.

We thus see that in thirty of these thirty-seven cases of rheumatic
pericarditis, the lower boundary of the impulse was raised in position
when the amount of effusion in the pericardium was at its acme.

PERICARDITIS.

Via. 89.

For previous views ol this case, see figures SB, 87, page 811.

Figure 38, from a youth aged 17, affected with rheumatic pericarditis.

Prriod of the decline of the pericardial effusion.

Sixth ilay after the acme of pericardial effusion, eighth day after admission.

Tie pericardial effusion haa diminished to a great extent, and the sac, no longer dis-
tended, has contracted, bo that it has lost its pear-shaped form, and resumed more nearly
that of the heart itself, a little modified and enlarged by undue fulness above. The lower
liorder of the heart is much lower than during the acme, being situated behind the fifth
cartilage, and the lower boundary of the pericardium is much higher ; it no longer
protrudes into the epigastric space, but has shrunk upwards, being situated behind the
upper third of tho eusiform cartilage, and behind or nliove the upper edge of the sixth
left cartilage. The right ventricle and the apex of the left ventricle are exposed ; bnt
the upper part of the conus arteriosus and of the front of the left ventricle, the pul-
monary artery, and the ascending aorta, are covered with lung.

..... .1 of pericardial iMncss (see the Mack space) corresponds siith the lessened

amount of the pericardial effusion, and instead of being pear-shaped, or longer than it
is broad, as it was during the acme, it has now more nearly the contour of the natural
region of cardiac dulness, and is hroadcr than it is long. It still, however, presents a
peaked form at its upper border behind the sternum, where that border is on a level
with the third cartilage, and where it is still much higher than its upper border to the
left of the sternum, which is situated at the third left space. Its lower border is situated
behind tho upper third of the ensifomi cartilage ; and its right and left borders are
respectively behind the right margin of the sternum, and within the left nipple.

The impulse is felt in the first, second, third, and fourth left spaces, being feeble in
the fourth space. (See the curved and circular lines in those spaces.)

- doftl.
. s natural position, which is however still rather high.
Eighth day after the acme of pericardial effusion, tenth day after admission.
There is no pericardial effusion, and the chest has resumed its natural shape.
The region of cardiac dulness (see the black Space) has regained its natural form, and
o longer preternatural ly higher behind the sternum thin to tbe left of it. Its upper

336 A SYSTEM OF MEDICINE.

cartilage ; its right margin is a little to the left of the middle line of the sternum, and
its left border is folly half an inch within the mammary line.

In one-fifth of the cases (7 in 37) the lower boundary of the im-
pulse was pushed up as high as the third space, and in three-fifths of
them it was present in the fourth space (21 in 37). In two patients,
one with disease of the aortic and mitral valves, the other with that
of tiie mitral valve alone, of some standing, the impulse was seated
in the sixth space, in three cases it occupied the fifth space, and in
three it was felt over the third cartilage.

The existence of previous valvular disease, owing to the increased
size of the heart in such cases, exercised a marked influence on the
position of the lower boundary of the impulse, and as a rule lessened
or prevented its ascent during the acme of the effusion. Thus, of live
patients of this class, all of whom had affection of the mitral valve,
and one of them of the aortic valve also, in two the lower boundary
of the impulse occupied the sixth space, in two the fifth space, and in
one it was seated in the fourth space.

If we deduct from the thirty-seven cases these five with valvular
disease, which are exceptional both in their nature and as regards
the influence of the effusion on the seat of the impulse, we find that
in only one of the remaining thirty-two patients was the lower
boundary of the impulse as low as the fifth space during the acme of
the effusion.

These cases of previous valvular disease are exceptional in another
point of view. In three of these five patients the position of the
lower boundary of the impulse was not higher during the acme of the
effusion than at other times. If we deduct these five cases from
the thirty-seven under review, we find that in only three of the re-
maining thirty-two cases was the position of the lower boundary of
the impulse unchanged during the acme of the effusion, while in
twenty-nine of them it was definitely higher than in health.

Extent to which the Lower Boundary of the Impulse tvas Raised,
when the, Effusion into the Pericardium was at its Height or Acme. —
In the twelve patients in whom the acme of the effusion was
reached after the first observation of increased dulness on percussion,
and in whom the lower boundary of the impulse was then elevated,
the impulse at its lower boundary ascended two spaces in two instances
(compare figure 44 with figure 45, p. 356), a space and a half in one,
one space in six, and less than a space in three cases ; and it descended
after the acme two spaces in five instances, one space in five, less
than a space in one, and in the remaining case its descent was not
observed.

In the eighteen cases in whicli the effusion had attained to its acme
at the time of the first observation, the lower boundary of the impulse
subsequently descended two spaces in three patients, one space in
thirteen, one rib's breadth in one, and half a space in one case.

If we combine these thirty cases in one group, we find that the
lower boundary of the impulse was higher during the acme of the

PERICARDITIS. 337

effusion than in the natural state by two spaces in eight cases, by
one space in nineteen, and by less than a space in three cases.

Time occupied during the Ascent and the Descent of (lie Lower Bound-
ary of the- Impulse in connection respectively with the Increase, the Acme,
and the Decline of the Fluid in the Pericardium. — In the twelve cases in
which the impulse at its lower boundary ascended to its highest point
after the first observation, and during the period of the increase of the
pericardial effusion, the time occupied by its ascent was from one to
two days in nine cases, and from four to six days in three cases.

The lower boundary of the impulse fell from its highest position
to its natural one in from one to two days in ten cases, in from three
to nine days in eighteen, and in sixteen days in two out of a total
of thirty cases. The ascent of the lower boundary of the impulse was
therefore more rapid than its descent.

Relation between the Extent of the Effusion in the Pericardium, and
the Height of the Lower Boundary of the Impulse. — The clinical facts
just given show that the lower boundary of the impulse was raised
by the increase of the fluid in the pericardium ; and we find, there-
fore, as a rule, a relation between the extent of the effusion and
the height of the impulse in these cases of pericarditis. But this
rule is reversed in a small group of exceptional cases, amounting to
seven, in which the upper limit of the effusion was as high as the first
space or the second cartilage ; while the lower boundary of the impulse
was present in the sixth space in one, in the fifth space in two, in the
fourth space in three, and in the third space in only one of these cases.
Three of these patients in whom the impulse was low had valvular
disease of old standing, a condition that, as I have already shown,
prevents or lessens the ascent of the impulse.

(2) The Diffusion of the Impulse over the Higher Intercostal Spaces
during the Acme, and Decline of the Fluid in the Pericardium. — In
three-fifths of the cases (22 in 37) the impulse, at the time of the
acme of the effusion, extended upwards above its lower boundary to
the extent of one or more of the higher intercostal spaces. In more
than one-half of these cases the impulse was felt beating as high as
the second space (12 in 22), while in less than one-half of them its
upper limit was the third space (10 in 22). The extent to which the
impulse was felt in the higher spaces was naturally regulated by the
position of its lower boundary. Thus, the impulse was bounded below
by the fourth space in ten cases, and in eight of these it extended up
to the third space or cartilage, and to the second space in only two ;
while in eight other patients the impulse, which was bounded below
by the third space or cartilage, spread upwards to the second space.
According, therefore, to the degree to which the impulse was raised by
the increased amount of fluid in the pericardium, it was felt beating
in the second and third spaces, or the third and fourth spaces, instead
of, as in health, the fourth and fifth spaces.

In these cases there were two agencies at work : one, the increase
of fluid in the pericardium, which elevated the heart and its impulse

A SYSTEM OF MBDICINB.

Fro. 40.

Fio. 41.

Figure 40 from a housemaid aged 17, affected with rheumatic pericarditis.

Period of the first acme of pencartltal effusion , fifth day after admission.

The explanation or pericardial effusion and dulneas f<iven with figure 36, page 311,
applies also to this figure.

The pericardial effusion extends lean to the left and more to the right than in figure
37, page. 311 (acme of pericardial effusion), and is of about equal extent in the two
figures from above downward*. The heart, which is enlarged, is elerntcd hy the fluid, but
to a less degree than in figure 4], its lower boundary lieiug firol-ably situated behind the
lower border of tho fifth cartilage, and just above the lower end of the sternum.

The whole front of the heart is exposed, including the right auricle and ventricle,
the apex and front of the left ventricle, the ascending aorta within the pericardium, and
the pulmonary artery.

The region of pericardial dulneas (see the black space) extend* from a little nhove the
lower end of the manubrium and the second left space, down to the tip of the enniforni
cartilage, and the middle of the sixth cartilage ; and from n little over an inch to the
right of the lower hnlr of the sternum, to a little beyond the left mammary line. The
area of dulness includes (1, 1,) Die region of the great arteries; (2, 2,) that of the
heart; and (3, 3,) that of the volume of the effused fluid below the heart, and projecting
downwards into the epigastric apace.

The impuUc isles* elevated than in figure 37 (acme], heing situated in iho second, third,
and fourth spaces. (See the curved and circular lines in those spaces.)

two-thirds ; and ia also audible with pressure from the third to the fifth left cartilages
(right ventricle) ; and over, but not feyond the apex of the left ventricle.
A loud mitral murmur —> is audible extensively to the left of the heart.

Figure 41 from the same patient as figure 40.

Period of the decrease of the ptricartiial rffvtion after the first acme.

Eighth day after admission, tliird after the acme— for the sounds. Eleventh day after
admission, sixth after the acme — for the pericardial effusion and dulness, and impulse.

The pericardial effvsimi hns lessened considerably, but is still present in considerable
quantity. The right ventricle and the apex and front of the left ventricle arc completely
exposed ; and the left border of the right anricle, and the lower portions of the ascending
aorta and pulmonary artery, are also brought into view. The heart, (2, 2,) which U

PERICARDITIS. 339

enlarged, has dropped down into its natural place, and even extends beyond that place,
at its lower and left boundaries. The amount of effusion between the under surface
of the heart and the floor of the pericardium (8,8,) is very small.

The region of pericardial dulness (seo the black space) has lessened considerably in
area ; it extends from between the second spaces, behind the sternum, down to the lower
third of the ensiform cartilage ; from the third left space to the upper border of the sixth
cartilage ; and from the right edge of the sternum to a point an inch beyond the left
mammary line. There is reason to believe that adhesions have formed at the apex, so
that the latter boundary is not pericardial but cardiac The region of dulness over the
great arteries (1,1,) is still very marked but has materially lessened ; that over the
heart (2, 2,) being still extensive ; and that over the depending portion of the pericardial
effusion between the under surface of the heart and the floor of the pericardium (3, 8,)
being very narrow, indeed a mere strip.

The impulse of the apex is felt in the sixth space, considerably to the left of the nipple.
The position of the impulse elsewhere is not mentioned in the report, but 1 have riven
it in the figure as being present in the fourth and fifth spaces, because three days later,
at the time of the second acme, it was felt in those spaces, as well as in the second
and third spaces. (See the circles and curved lines in those spaces.)

The friction sound (see the zigzag lines, systolic thick, diastolic thin) on the seventh
day had increased considerably below and to the right, and lessened above and to the
left It was audible over the sternum from below, but not above, the level of the
second spaces, and thence down to the tip of the ensiform cartilage ; to the right of the
lower half of the sternum ; and over the left cartilages, from the third to the seventh,
where it extended about two inches below the heart ; but it was inaudible over the
region of the apex, "where there were probable adhesions.

For the later views of this case, see figures 42, 43, p. 340.

both at their lower and upper boundaries into the contracted space at
the higher part of the chest, and caused the heart to beat against
the left upper spaces ; the other, the enlargement from distension of
the right ventricle and especially of the pulmonary artery, owing
to the difficulty with which the blood passes through the lungs
from the combined effect of the pressure upon the auricles by the
fluid in the swollen sac, and the existence of endocarditis with
mitral regurgitation. The enlarged right ventricle and pulmonary
artery displace the lungs, and pulsate, the former against the third, the
latter usually against the second space ; and in that space the double
beat of the artery is then felt, the first being feeble, the second
sudden and like a shock, coinciding with a feeble first and intensified
second sound heard over the same situation. When the heart is much
raised, it is evident that the conus arteriosus must sometimes occupy
the second space, the pulmonary artery being elevated into the first space.

After the acme, when the amount of the fluid in the pericardium
lessened, the position of the impulse, as we have just seen, as a rule
descended at its lower boundary, but it generally retained its place
at its upper boundary. Sometimes, indeed, the impulse extended
upwards as well as downwards during the period of the lessening
of the effusion.

The clinical facts that I have just related as to the extension
of the impulse into the upper region during the successive periods of
the increase, the acme, and the decrease of the effusion into the peri-
cardium ; while its lower boundary steadily rose during the increase,
and fell during the decrease of the fluid, are to be traced I consider
to a succession of causes. I have just considered the two agencies
that are at work to extend the impulse into its higher region during

A SYSTEM OF MEDICINE

Fig. 42.

Fio, 43.

For previous views of this patient see figures 40, 41, page 388.

Figure 42, from a housemaid aged 17.

Period of the Mcoad acme of pericardial effusion owing to a relapse of pericarditis.

From the fourteenth to the eighteenth day after admission, from the tenth to the
fourteenth day after the first acme (figure 40), and from the third to the seventh day
after the period of decrease of the effusion illustrated in figure 41 . The period of the
acme lasted four days.

The explanations or pericardial effusion, prominence and dntness, given with figure 30,
at page 811, apply also to this figure.

The pericardial effusion has increased again to a very great extent The heart is con-
siderably enlarged, and is probably adherent at the apex ; its lower boundary is therefore
much lower than during the first acme, figure 40, and apparently reaches down to the sixth
cartilage, and the middle of the ensiform cartilage. The effusion has increased very
much, especially upwards, downwards, and to the right ; but owing probably to adhesions
at the apex, it has been stationary or has lessened in area at the left side — compared
with its amount and area during the period of decrease of the effusion after the first
acme shown in figure 41. The effusion extends much higher and more to the right
than during the first acme {figure 40), but it ia of the same extent at its lower and left
boundaries in this ss in the first acme. The area of the effusion was much wider in
relation to its length, and especially towards the loft, in the single acme shown in figure
37, owing to the enlargement of the sac froni long-continued distension, than it is in this
instance, in which the expansion of the sac to the left has been apparently stopped by the
probable adhesion of the apex and front of the left ventricle.

The whole front of the heart and groat arteries is exposed, including the right
auricle and ventricle, the apex and front of the left ventricle, and the ascending aorta and
pulmonary artery.

The region of pericardial dultieu (see the black space), corresponding to the pericardia]
effusion, extends very high, or to within an inch of the epistcrnal notch ; far to the
right, or nearly two inch™ to the right of the a termini ; low down, or below the tip of
the ensiform cartilage ; and owiug probably to adhesions at the apex, proportionally less
far to the left, or fully half an inch to the left of the mammary line. The region of
dnlneaa over the arteries is unusually high and narrow. Its width on the first day of the
acme waa little more than one inch ; but it had increased to about two inches on tint
fourth day, when its upper border was not quite so high as on the first day of the acme

PERICARDITIS. 341

and circles in those spaces). The lower boundary of the impulse has therefore been
elevated from the sixth space to the fifth since the period of the decrease of the effusion
following the first acme, shown in figure 41 : it is, nowever, lower in this second acme
than it was in the first acme, when it occupied the fourth space. *

The friction sound (see the zigzag lines, the systolic lines being thick, the diastolic thin)
ia scarcely audible anywhere without pressure, but with pressure it is heard, double, over
the whole region of the pericardial dulness except over the apex and front of the left
ventricle, where there are probably adhesions, and where a loud mitral murmur —>
]> re vail 8. The rubbing sounds are louder over the two lower thirds of the sternum and
to each side of it, than higher up.

Figure 43, from the same patient as figures 40, 41, 42.

Period of complete adhesion of the pericardium to the heart.

For pericardial dulness — fifty-two days after admission, thirty-nine to forty- three days
after the second acme.

For the impulse — eighty-eight days after admission, when the dulness, tested by post-
mortem examination, was about the same as on the fifty-third day after admission.

The region of pericardial dulness (see the black space) is very extensive, measuring
about seven inches from left to right, with a slight downward inclination, and nearly
five inches from above downwards. Its upper boundary was behind the lower border of
the manubrium ; its lower boundary, behind the lower end of the ensiform cartilage, the
sixth left space and the seventh left rib ; its right boundary was situated midway
between the right nipple and the edge of the sternum ; and its left boundary extended
to the sixth and seventh ribs at the outer side of the chest.

The impulse on the fifty- third day was present in the fourth, fifth and sixth spaces
from two inches within, to two inches without, the nipple line, and was quite absent
from the sternum and the spaces between the cartilages ; since that time the patient has
been getting gradually worse ; and the impulse has been becoming gradually stronger and
more extensive, and is now, on the eighty-ninth day, felt over the whole sternum,
the epigastrium, and the cartilages to each side, and on the left side down to the
seventh left rib, where it beats against the outer side of the chest (see the curved lines
occupying all that region). The impulse heaves up rather slowly during the systole,
and immediately after it, falls suddenly backward. The impulse in the first and second
spaces, over the pulmonary artery, is double, protruding slightly during the systole, and
going back with a flapping rapid movement during the diastole, conveying the impression
of a sharp impulse or shock, synchronously with the second sound. Ninety-first day.
The impulse is still felt over the sternum, but feebler than two days ago, similar in
character, but not felt

the periods of the increase and acme of the effusion ; the increase
namely of the pericardial fluid elevating the heart into the contracted
space of the chest above ; and the enlargement of the right ventricle
and pulmonary artery from obstruction to the flow of blood
through the lungs. During the decline of the fluid the first of
these influences is reversed, for the heart descends into its
natural place, where it beats with comparative freedom; but the
second influence, the enlargement of the right ventricle and pul-
monary artery from obstruction through the lungs, often remains in
full force to retain the impulse in its higher position ; and this
influence is frequently added to by other causes that have a like
effect. These additional influences include the thickening and mat-
ting of the inflamed pericardium ; the possible adhesion from pleurisy
of the left lung to the pericardium at its upper border ; and the defi-
cient or absent expansion of this portion of the lung from adhesion and
other causes, such as pulmonary apoplexy, and the imperfect general
use of the left lung. These views derive additional confirmation from
the fact that in all the cases save one in which the impulse extended

342 A SYSTEM OF MEDICINE.

over the higher spaces during both the acme and the decline of the
effusion, there was endocarditis with mitral incompetence, and in
several of them, aortic incompetence also.

Position of the Impulse after the Decline of the Pericardial Effusion
during the Later Stages of Rheumatic Pericarditis; and after its
Cessation. — When the effusion disappears and the heart resumes its
natural position, and when the lungs again cover the great vessels
and the upper part of the organ in front, the impulse as a rule
descends into its natural position, and is again felt in the
fourth and fifth spaces.

In those patients in whom the heart becomes again healthy after
the attack, the size, position and customary beat of the organ
are restored : but in those in whom valvular disease is established,
the nature and extent of the disease are made apparent by the force,
extent, and position of the impulse. When the resulting mitral
disease is severe, the impulse of both the right and left ventricles is
extended, and is felt beating from the lower half of the sternum to
the left nipple. When, however, the mitral affection is slight, and
such as scarcely or not at all to interfere with the function of the
organ, then the impulse resumes its natural boundary and strength ;
and thus the impulse becomes a true measure of the extent of the
valvular disease. When both the aortic and mitral valves are affected,
the apex-beat and the impulse generally of the left ventricle become
more markedly developed, the action of the right ventricle being still
unduly strong. In those comparatively rare cases in which the aortic
valve is alone affected, the right ventricle is untouched ; but the size
and force of the left ventricle are increased in exact proportion to
the increased labour thrown upon that cavity by the degree of the
crippling of the valve. The apex-beat and general shock of the
left ventricle become extended outwards beyond the left nipple, and
downwards into the sixth space, when the valvular affection is great ;
but they are held almost within the natural limits when it is slight.
When the heart becomes adherent and there is disease of one or more
of its valves, the impulse of the organ becomes extended in every direc-
tion— to the right, over and beyond the sternum ; to the left beyond
the line of the nipple; downwards, over the ensiform cartilage, and even
below it in the epigastrium ; and especially upwards, to the second
space and to the adjoining portion of the sternum. In some cases the
whole impulse bears at first forwards during the systole, and then
drags the walls of the chest in a characteristic manner backwards ;
while in other cases, in which there is complete fibrous attachment of
the adherent pericardium to the sternum, that bone and the adjoining
costal cartilages are steadily drawn inwards during the sys tole, and
spring forwards with a shock during the diastole. An essential dif-
ference is also established between the influence of respiration on
the area of the impulse of the adherent and the non-adherent heart.
When the heart is not adherent, a deep inspiration, by drawing down

PERICARDITIS. 343

the heart and covering it with the expanded lungs, causes a complete
transfer of the impulse from the fourth and fifth spaces to the epigas-
trium and the sixth and seventh cartilages ; but when the heart is
adherent, the outspread dragging impulse almost retains its position
during a deep inspiration, neither materially lessening its area over
its upper borders, nor materially increasing it below. There is, in
short, no transfer, such as occurs when there are no adhesions, of
the impulse during a deep breath from the intercostal spaces to the
en8iform cartilage and epigastrium and the adjoining left costal
cartilages. Thus in a patient who has recovered from rheumatic
endo-pericarditis we are enabled to judge by the position and force
of the impulse, whether the valves, if affected, are seriously or only
slightly affected ; and, by the extent to which the play of the impulse is
influenced by respiration, whether the valvular affection is combined
or not with extensive and binding adhesions of the heart.

Vibration or Thrill felt by the Hand over the Region of

Pericardial Friction.

A sense of vibration or thrill was felt over the seat of the friction
sound at the region of its greatest intensity in fully one-fifth of the
patients with rheumatic pericarditis (13 in 63).

In seven of the cases, or more than one-half of them, the thrill was
felt over the whole region of the impulse, extending in two instances
over the second and third left spaces, in one, over the spaces from the
second to the fifth, in three, over those from the third to the fifth, and
in one, from the fourth to the sixth spaces.

In two other instances the thrill was confined to the second space,
apparently over the pulmonary artery, in three to the region of the
apex, and in the remaining case it was present both over the second
space and the apex. In all these patients the friction sound was
harsh and grating, vibrating, or creaking in character.

In those cases in which the vibration was felt over the whole
region of the impulse, the thrill was present at the time of the acme
of the effusion, or in one instance two days after it (see pp. 313-315) ;
and the same may be said, with one exception, of those in which the
vibration was felt in the second space.

The duration of the thrill was short. It was observed for only
one day in seven cases, for two days in three, for three days in two
cases, and for four consecutive days in the remaining one. In two
cases (51, see p. 315; 40, see p. 313), the thrill, after being absent
from its previous seat over the body of the heart for several days,
returned over a limited space when the surfaces were comparatively
dry, the effusion having disappeared.

The character of the friction thrill or vibration is peculiar, and
differs from the thrill duo to altered blood-currents, chiefly in the
following points. The blood-thrill presents a succession of equal
vibrations, often like those made by a vibrating musical cord ; is

344 A SYSTEM OF MEDICINE.

diffused ; has a focus of greatest intensity, from which it lessens and
fades away all round ; gives the impression to the hand of being
deeply seated as well as superficial ; begins, when diastolic after the
impulse ends, and often continues, when systolic, for a short period
after the cessation of the beat of the ventricle ; retains its character,
position, focus of intensity, and general outspread, unchanged or with
only slight modifications from day to day ; and finally, has a long
previous history pointing to an affection of the heart, and probably
dating from an attack of acute rheumatism. The friction thrill or
vibration, on the other hand, is shallow, giving a sensation as if it
were made just under the hand by the rubbing together of two rough
surfaces; has often a grating, rasping or irregularly vibrating cha-
racter; presents no focus of intensity, but is spread, with varying
force, over the region of the impulse; begins and ends rather
abruptly, being limited to the period of the impulse and not passing
beyond or preceding it; does not end with an abrupt shock; is
short-lived and transient, and, if felt on one or two following days,
it always changes in extent, and perhaps in position, and alters in cha-
racter ; and finally has a short previous history of local pain, extended
dulness on percussion, increased prominence over the region of the
pericardium, and elevated impulse. Sometimes, however, the blood-
thrill and the friction-thrill are so much alike that they cannot be dis-
tinguished by the hand. The character of the thrill is, however, at
once cleared up by the ear ; the friction-thrill being accompanied by a
friction sound which is in all cases increased by pressure, and is
most vibrating, grating, or creaking and harsh at the very seat of the
vibration ; while the blood-thrill is accompanied by the murmur, usually
musical, that distinguishes the valvular affection.

The thrill of presystolic murmur is distinguished by the position
of the thrill over and to the left of the interventricular septum,
the peculiar large vibrating character of the murmur ; the abrupt
shock with which the thrill and murmur terminate ; the persistency
of the thrill, murmur, and shock from day to day ; and the long
previous history.

The character of the friction sound presented in the various cases
a close approximation to the character of the thrill or vibration.

The sensation conveyed to the hand when applied over the seat of
thrill in the thirteen cases under examination was not always of the
same character. Thus, under these circumstances the hand felt a sense
of grating or rasping in two, of vibration in four, and of thrill in seven
of the cases.

On listening over the region of the thrill or vibration in these cases
a loud harsh friction sound was heard in seven patients, in five of
whom the sound was described as being " to and fro ; w in five others of
them there was a noise resembling the creaking of leather ; in three
the sound was grating, in one rasping, in two vibrating, in one grazing,
and in one ".churning." In several of these cases the friction sound
presented, as we have already seen, different phases at different

PERICARDITIS. 345

periods of their progress. In all of them the friction sound became
less harsh and extensive^when the vibration or thrill over the region
of the pericardium ceased to be perceptible.

It is to be remarked that when the thrill was perceptible in these
cases, especially if it extended over the ventricles, and was not limited
to the region of the apex or that of the pulmonary artery, the area of
the friction sound was increased as well as the intensity. In one of
the cases the rubbing sound was audible over the whole front of the
chest, and in several of the patients it spread downwards to the ensiform
cartilage and to the left and right seventh and eighth costal cartilage.

The character of the friction sound, associated with the presence
of a thrill over the heart and great vessels, whether creaking or grating,
vibrating or rustling, or to and fro, will be considered in the next
section.

■

Auscultation.

Position and Character of the Sounds heard over the Heart and
Pericardium during the Early Stages of Pericarditis, — In more than
one-half of my cases of rheumatic pericarditis (33 in 63), I observed
the character of the sounds of the heart at or soon after the com-
mencement of the attack, and before the effusion into the pericar-
dium had arrived at its height. I was frequently surprised by the
rapidity with which the affection attained to its acme. In twenty-
three of these patients friction sound was heard for the first time
before the fluid in the pericardium had reached its greatest amount ;
and in fifteen of these the rubbing sound was detected only one day,
and in four two days before the time of the acme.

Modification of the Sounds of the Heart at the Commencement of
Pericarditis, before the Occurrence of Friction Murmur or Friction
Sound. — There were five cases in which the sounds of the heart
were modified before the occurrence of a friction sound, or the period
of the acme. In one of them the heart sounds were muffled two
days before the occurrence of the friction sound and the acme ; in three
of them those sounds were ringing in character from three to four days
before the acme ; and in one of these the systolic sound was rough and
unduly prolonged four days before that period. All the cases of this
group but one presented on pressure either a single or double murmur
or a rubbing sound subsequently to this modification of the heart
sounds, and before the occurrence of the acme.

Position andCharacter of the Friction Murmur, influenced by Pressure,
heard at the Beginning of Pericarditis: — A murmur, which was excited
or rendered more intense by pressure, was heard over the region of the
heart before the period of the acme of effusion into the pericardium
in eight cases.

Pain was felt directly over the seat of the pericardial inflam-

VOL. TV. A A

346 A SYSTEM OF MEDICINE.

mation in seven of the cases, being excited by pressure on the
surface of the chest in three of them. In .five of the cases the pain
was present at the same time as the appearance of a murmur on
pressure, and in two the pain preceded the murmur by a day or two.

In four cases the friction murmur was single and systolic. In four
cases a double murmur, excited or intensified by pressure, preceded
the friction sound and the acme of pericardial effusion. In the
last case of this group (49, see p. 327), a youth aged 17, a fatal case,
the friction murmur prevailed more or less through the whole of
the illness until the heart became adherent.

The double friction murmur, heard during the early period of peri-
carditis, is thus distinguished from the double murmur caused by
aortic incompetence, combined as it usually is with mitral regurgi-
tation. It is accompanied, and often preceded, by pain over the heart,
usually increased by pressure ; it comes into play suddenly ; its area
is b'mited to the middle, or lower half of the sternum, and the adjoin-
ing left, and, on rare occasions, right cartilages ; it is accompanied by
the natural heart sounds, but is not rhythmical with them, the heart
sounds and the murmur being heard as it were side by side ; it does
not begin with a double accent or shock, the double accent or shock
of the natural heart sounds, but is of equal intensity throughout ; it is
invariably rendered more intense by pressure, which often converts
it into a true to-and-fro frottement, and which always obscures or
silences the natural heart sounds. It is not accompanied by marked
visible pulsation of the great arteries in the neck, or by the sudden
pulse at the wrist of aortic regurgitation, audible when the arm is
raised ; it is accompanied by extended dulness on percussion over the
region of the pericardium ; and as a rule it speedily gives place to a
friction soimd, with which, however, it may co-exist, being audible
beyond the circumference of the friction sound especially below, and
on cither side.

In all these respects the double friction murmur contrasts notably
with the double aortic murmur ; which is not usually accompanied by
pain over the heart ; does not come into play suddenly ; is not
limited in its area to the middle or lower half of the sternum and the
adjoining cartilages — but extends also to the upper portion of the
sternum and to its right; is rhythmical with the natural heart
sounds ; commences with a double accent or shock ; is not rendered
to a material degree more intense by pressure, which never converts
it into a friction sound, and which never abolishes the double accent
with which the double murmur begins ; is accompanied by marked
visible pulsation of the carotid and radial arteries, the pulse of the
latter becoming audible as a shock when the arm is raised; is not accom-
panied by extension of dulness over the region of the pericardium ;
and does not give place suddenly to friction sound, but is persistent.

The single systolic friction murmur is not so easily distinguished
from the tricuspid murmur as from other systolic blood murmurs,
but their differences are sufficiently marked. The systolic friction

PERICARDITIS. 347

murmur is accompanied or preceded by pain over the heart, usually
increased by pressure ; comes into existence suddenly ; is limited
usually to the base of the right ventricle, being heard over the
middle or lower sternum, or over the fourth left space ; is accom-
panied by the natural first sound, but is not rhythmical with it,
the heart sound and the murmur being distinctly heard side by
side ; does not begin with an accent or shock, the accent or shock
of the natural first sound, but begins and ends with a single note
of equal intensity throughout; extends rarely beyond the period of
the systole into that of the diastole; is usually produced, and
invariably rendered more intense by pressure, so that it obscures
or masks the natural first sounds ; is accompanied by extended
dulness on percussion over the region of the pericardium; and
speedily gives place to a double friction murmur or a friction sound.

The several systolic blood murmurs may be thus distinguished from
the single or systolic friction murmur.

The tricuspid murmur is more likely to be taken for a friction
murmur than any other systolic murmur, for it is situated over the
front of the right ventricle — over and to the left of the lower half of
the sternum — and, like the friction murmur, it is a shallow sound,
and it may appear and vanish quickly. It differs, however, in these
respects ; it is rarely accompanied by pain and tenderness over the
heart; is never accompanied by the natural first sound over the
right ventricle, for that sound is converted into the murmur
always commences with an accent, the accent or shock of the first
sound of the right ventricle ; may be intensified, but is not changed
in character by pressure, which, however, brings the ear more close
to the murmur ; is not accompanied by extended dulness on per-
cussion over the pericardium ; and does not give place to a double
friction murmur or a friction sound.

The systolic mitral murmur is readily distinguished from the
friction murmur by the intensity with which it is heard to the left
of and below the apex ; and its great relative feebleness, or silence
over the right ventricle — to the left of the lower portion of the
sternum; and by its persistence. When the mitral murmur is audible
in the situation just spoken of it is feeble, and is accompanied by the
natural sounds of the right ventricle. The heart sounds and the
murmur are rhythmical and go well together ; and pressure, though
it makes the mitral murmur somewhat more clear, does not mask or
obliterate the healthy* sounds of the right side of the heart.

The direct aortic, and pulmonic systolic murmurs are distinguished
at once from the systolic friction murmur by their situation above
the level of the third cartilage ; the pulmonic murmur, which is often
scratching in character, and is therefore apt to be mistaken, when first
heard, for a friction sound, being limited to the second left space ; and
the direct aortic murmur being heard over the upper sternum, and to
the right of it, and in the neck over the carotid.

The essential features of difference between the friction murmurs

A A 2

348 A SYSTEM OF MEDICINE.

and the blood murmurs are these : — The friction murmurs do not
begin with an accent, but usually maintain the same tone and pitch
throughout ; while the blood murmurs begin with an accent or shock :
the friction murmurs are intensified and altered by pressure, becoming
sometimes rubbing in character ; while the valve murmurs are only
intensified by pressure : the friction murmur and the natural heart
sounds are heard at the same time, but they do not play together or
in unison, being audible as it were side by side, each having its
own rhythm ; and on pressure the friction murmur becomes so loud
and even rubbing in character as to mask and extinguish the heart
sounds ; while the blood murmurs are iu perfect accord with the heart
sounds : the friction murmurs come suddenly, with pain and increased
pericardial dulness, and are transient ; the blood murmurs come
gradually, without pain or increased dulness, and are permanent.

Friction Sound in Pericarditis before the Occurrence of the Acme
of the Effusion into the Pericardium. — Friction sound was heard during
the early stage of Pericarditis, in every gradation from a sound scarcely
to be distinguished from a murmur up to a grating, vibrating, or
creaking noise.

In a few of the cases, the early friction sound was not audible
until pressure was made over the heart. In. nearly all the cases,
the friction sound was double from the first, but in two, and, perhaps
three patients the sound was single and systolic when first heard.
In a small group of four patients, a smooth or feeble double friction
sound, intensified by pressure, came into play from one to fpur days
before the occurrence of the acme of the affection, when the friction
sound became louder and more harsh.

In the ^t great division, of cases of pericarditis with friction
sound before the acme, the double friction sound, as a rule, was
loud and harsh, was intensified by pressure, and set in suddenly;
and the effusion into the pericardium speedily attained to its acme
after the first observation of the friction. This set of cases divides
itself into three groups ; in the first group (1), the friction sound
became inaudible during the acme ; in the second (2), the friction
sound became less loud and harsh during the acme ; and in the third
group (3), the friction sound remained during the acme with little
or no change.

(1) In two cases, the friction sound, harsh at the onset, disap-
peared during the acme. It is difficult to explain the disappearance
of the friction sound at the time of the acme of the effusion in
these two remarkable cases on physical grounds, but the following
circumstances show that it was mainly due to lowering of the power
of the heart. It is natural to expect that when the fluid increases,
it should interpose itself between a portion of the right ventricle
and the anterior wall of the chest, and so limit the area of the
friction sound, and lessen its intensity. This will not, however,
account for the disappearance of the rubbing sound at the period of

PERICARDITIS. 349

the acme, since the impulse was then still perceptible, though higher
in position and less forcible.

(2) The second group of this division, in which a loud double
friction sound appeared suddenly before the acme of the effusion, and
became less lsud during the acme, consists of five patients.

The case of this group (33, see p. 319) that I shall relate, is
illustrated by the accompanying figures (44, 45, p. 350) ; during its
later stages, by figures 46, 47, 48, pp. 377, 378. A housemaid, aged
20, came in on the fifth day of her illness, the heart sounds being
natural. On the third day there was increased dulness on percussion
over the region of the heart ; and a to-and-fro friction sound over the
whole of the region of cardiac dulness, to which it was exactly
limited. the impulse was present, as before, in the fifth space,
but was higher in position. The dulness and the friction sound
extended from the sternum almost to the nipple, and froth the third
left cartilage to the sixth, but did not pass beyond the sternum to
the right, so that the rubbing sound was limited to the right ventricle.
It was stronger over the sternum than the cartilages, and became
everywhere much harsher on pressure. On the fourth, the double
friction sound was heard over the greater part of the sternum, and
was audible over the manubrium during expiration only. The friction
sound had somewhat the thafactet of a bellows murmur Over the
fourth space. It was not quite rhythmical with the sounds of the
heart, which were also audible. It was harsher and louder during
the systole than the diastole, and was rendered more intense by
pressure. On the fifth day, the effusion into the pericardium was at its
acme — reaching up to the second space and the manubrium. The
impulse was raised from the fifth to the third space. The area of
the friction sound was more extensive upwards, but more limited
below. It was heard over the whole sternum, being louder over the
manubrium on expiration, over the lower portion of that bone on
inspiration, and was most harsh and strong over the middle third of
the sternum. The rubbing sound was heard from the second to the
fourth cartilage, but not apparently below it, and was harsh in the
third space. A bellows murmur was audible over the fourth cartilage
on the light application of the stethoscope ; but when pressure was
made, a creaking noise was heard there during the systole, and
a rubbing sound during the diastole.

I believe that this group and this case represent the natural
progress of the friction sound from the commencement of pericarditis
to its acme when the effusion is at its height. During the first
blush of inflammation, the surfaces of the heart and the sac are
crowded with vessels, but are as yet scarcely coated with lymph.
A single or double friction murmur, induced or intensified by pressure,
may then be the only sound excited by the rubbing of the heart
against the pericardium. Speedily their surfaces become coated with
a finely honey-combed rugose covering ; and the amount of fluid in
the sac increases so as to enlarge the area of dulness over the

A SYSTEM OF MEDICINE.

c pericarditis (S3, see p.

he Hounds of the heart

'lit tin? space lietwccn
li elevates the heart to
ards and to each aide ;
: pericardium, and the

Figure U, from a housemaid aged 20. affected with rheums'
310).

Early period of the inrreast of the pericardii! effusion.

Firat day of the friction sound ; third day after admission,
were natural when she was admitted.

The pericardial effusion probably already occupies to some i
the under surface of the heart and the floor of the pericardium,
a alight degree, and, to a moderate extent, displaces the lungs 1
and the centre of the diaphragm, whore it forma the base of

subjacent portions of the liver and stomach downward*. Owing 10 me uispiaccuiem 01
the lungs] upwards and to enoh side fiuui befure 1 1 1 1.- licxd. the whole of the right ventricle
except tlio upper portion of the conns arteriosus, the inner or lilt border of the right
auricle, and the ajiex and a portion of the front of the left ventricle are exposed.

Probable region of pericardial dulness on j* inissiM (we the black spare). The out-
lines of the region of pericardial tHilnes-*, v.hic)i is increased in extent, are not described
on this occaiion, hut the extent of the friction sound and the position of the impulse are
given ; and I have assigned to the region of dulness an outline corresponding to the
region of friction sound and the position of the impulse. Tho region of pericardial dul-
ness hss not yet acquired the pyramidal or pear-shaped fomi tliat it presents during t)ie
acme of the pericardial effusion, hut still retains the general form of the healthy region
of cardiac dulness, hut its outline is considerably enlarged in all directions, and is higher
behind the sternum than over tiie cnrtilnpcs. It extends across from Die right edge of
the sternum to the left nipple : its i;| hit liourdnrv probably crosses the sternum on a
level with the upper edges .if the third costal cartilages, and occupies the thud space ;
and its lower boundary is prolubly situated a little above the middle of the ensiforni
cartilage, and the upper edge ol (lie sixth cartilage.

Third day. The impulse of the heart is felt at the fifth space below the nipple. (See

the circle in that ai

""■J

:, being slightly perceptible bch.ra- tlic nipple.

loud but aoft to-and-fro friction sound is heard over the sternum from below the ir ....
briam to its lower end, and up ,0 hut not beyond ; ^s rkdit border ; and over the fourth
and fifth cartilages and intermediate spaces, where i extends almost, hut not quite to
the nipple, where it is feebler than it is over the sternum. Tin- friction sound is rendered
much bawher by preasnre. Fonrth day. Tlic friction sound is nearly the satno in
extent, character uid area as it was yesterday, but it is now audible over the manubrium

PERICARDITIS. 351

daring expiration ; it is lower and louder below during inspiration than expiration ; and
it is louder generally during the systole than the diastole.

Figure 45 from the same patient as figure 46, affected with rheumatic pericarditis.

Period of tht first acme of pericardial effusion. Third day of the friction sound and
of the increase of pericardial dulness, fifth day after admission.

The explanations of pericardial effusion and dulness given with figure 36, page 311,
apply also to this figure.

The pericardial effusion completely distends the sac, which is pyramidal or pear-
shaped, as in figures 34, p. 305 ; 36, 37, p. 311 ; 40, p. 338 ; 42, p. 340. The extent of
the effusion, and of the displacement upwards and to each side of the lungs, and down-
wards of the diaphragm, liver and stomach may be inferred from the description given
below of the extent of the region of pericardial dulness on percussion. The whole front
of the heart is exposed, including the right auricle and ventricle, the apex and front of
the left ventricle, the pulmonary artery, and the ascending aorta within the pericardium,
owing to the extensive displacement of the lungs from before those parts.

TIic region of pericardial dulntss (see the black space) on percussion is pyramidal or
j>ear-shaped, like the distended pericardium. The upper and narrower region of dulness
over the great vessels (1, 1) is situated behind and below the lower half of the manubrium
and extends a little way into the adjoining first and second spaces ; the larger portion of
pericardial dulness, which includes the heart itself and the volume of fluid effused into
the space between its under surface and the floor of the pericardium (2, 2 ; 3, 3), extends
from the second space down to the lower bonier of the sixth cartilage, and almost to the
end of the ensiform cartilage, and from an inch to the right of the sternum to about
half an inch to the left of the ninple. The lower boundary of the heart (2, 2) is probably
situated behind the lower bonier of the fifth cartilage ; and the heart (2, 2) ox tends
from this boundary up to the third cartilages : and the volume of effused fluid between
the under surface of the heart and the floor of the epicardium extends from the lower
boundary of the heart down into the epigastric space, almost to the end of the ensiform
cartilage, and the lower edge of the sixth left cartilage.

TJic impulse has been elevated from the fifth to the third space, and extends outwards
to the nipple line. (See the concentric curves in that space.)

Tlie. friction sound (see the zigzag lines — systolic thick, diastolic thin) is double, and
extends from the nipple to the lower end of the sternum. It is most harsh about the
middle of the sternum, and is louder at the upper end of that bone during expiration,
and at its lower end during inspiration ; and is more intense during the systole than the
diastole. The frottcment is also audible over the left second, third, and fourth carti-
lages ; and is soft without pressure, but with pressure it is creaking over the fourth
cartilage.

A mitral murmur — > is audible at the apex.

For the later views of this case see figures 46, 47, 48, pp. 377, 378.

pericardium, and to expose the whole of the right ventricle and the
apex, but neither the right auricle nor the great vessels. The heart
is slightly raised and the apex beat ascends from the lower to the
higher part of the fifth space. A double friction sound is audible
over the whole region of pericardial dulness, to which it is exactly
limited, louder and more continuous during the systole than the
diastole, and rendered more intense by pressure, which brings into
full play both sounds, exciting a to-and-fro rustle or frou-frou.

When the effusion has increased to its utmost limits, the heart is
elevated, its impulse being raised from the fifth to the fourth or third
space ; the increased effusion displaces the lungs and so exposes the
whole surface of the heart and great vessels ; and depresses the central
tendon of the diaphragm downwards towards the abdomen, fluid being
alone present below the fourth space. The whole region of actual
friction is shifted upwards, and with it the whole region of the
friction sound ; which is no longer audible below the fourth or fifth
cartilage, but spreads outwards over the right auricle and the left

362 A SYSTEM OF MEDICINE.

ventricle, as well as the right ventricle ; and upwards over the great
vessels and to the top of the sternum. The friction sound silenced
below is intensified and extended above ; so that there is a transfer
upwards of the friction sound ; while the dulness on percussion in-
creases in all directions, upwards as well as downwards.

Four cases differed from the rest in this, that while the friction
sound spread upwards at the time of the acme, it also either
increased downwards, or, retaining its hold below, increased exten-
sively to the left side.

The comparative relative Area and Intensity of the Friction Sound just
bej 'ore1 , and during the Acme of the Effusion into the Pericardium. — In
twenty-nine cases the comparative area and intensity of the friction
sound were observed both before, and at the time when, the effusion
into the pericardium was at its height.

Area. — When the effusion into the pericardium increases, the
heart is raised, and the lungs are displaced upwards, and to the left
and right by the, increased fulness of the sac and the greater elevation
of the heart itself; for the organ is then pushed upwards from a wider
into a narrower space. It is natural to expect that, under these
circumstances, the area of the friction sound should steadily increase
upwards and to each side with the increase of the area of pericardial
dulness. This was found to be so in the great majority of instances.
Thus the area of friction sound was greater at the time of the acme
than before it in twenty out of the twenty-nine cases ; while it was
less under the same circumstances in only two of them. In six
patients, the area of the friction sound was equal before and during
the acme ; and in one case the friction sound was absent before, but
present at the time of the height of the disease.

These clinical facts show that when the curtain of lung in front of the
heart and great vessels is displaced by the distended pericardium and
the elevated heart., the friction sound spreads upwards, and to the
right and left ; so as to be audible over the whole front of the right
ventricle, the great vessels, the right auricle, and the apex.

The lower boundary of the friction sound, while it retains its
place, at the time of the height of the effusion, becomes softened in
character. The focus of intensity of the rubbing sound is shifted
upwards, with the upward shifting of the heart and its impulse ; and
the intensity of the sound is toned and graduated downwards, from
the seat of its focus to that of its inferior limit.

Intensity. — In nearly three-fifths (1G in 29) of the cases, the friction
sound was more intense ; and in fully one-third of them (10 in 29), it
was less intense, when the effusion into the pericardium was at its
height, than just before that time. The tendency, then, is for the
friction sound to increase both in intensity and area, during the acme.
The exceptions to this rule are, however, much more frequent as regards

1 At the time of the last observntion, made before the effusion ha«l reached its height.

PERICARDITIS. 353

intensity than area ; for the area lessened at the time of the acme,
in only two instances, while the intensity did so at that time, in ten
instances out of twentv-nine.

The area of the friction sound, then, is, as a rule, larger, and its inten-
sity greater at the time of the acme of the pericardial effusion, than
at that of the last previous observation, made from one to two days
before the acme. The exceptions to this rule are rare as regards the
area, but rather frequent as regards the intensity of the friction
sound, which is greater in one-third of the cases on the day before,
than at the time of the acme. The change, both in area and intensity,
is often notably rapid and great ; the character of the friction sound
being sometimes altogether altered, and its area remarkably enlarged
in the course of one or two days.

The Clmractcr and Area of (lie Friction Sound at the Time of
the Acme of the Effusion, into the Pericardium. — The friction
sound, audible over the region of the heart and arteries and the
pericardium during the acme of the pericardial effusion, presented
great variety of character, intensity, and area in the forty- four cases
under examination. I. In nine of those cases the friction sound
was accompanied during the acme by a thrill over the region of the
heart and great vessels ; and II. in thirty-five of them the presence of
a thrill was not observed. I. Of the nine cases with a thrill, (1) in
five a sound resembling the creaking of new leather; (2) in one a
grating sound ; and (3) in three a harsh friction sound was respectively
audible over the region of the pericardium. II. Of the thirty-five
cases in which a thrill was not observed, (1) in seven a creaking sound
was heard ; (2) in two the sound was grating in character; (3) in fifteen
a definite friction sound, intensified by pressure, which in two instances
excited a creaking noise, usually harsh, but sometimes not so, was
audible ; (4) in five the friction sound was soft in character, but was
rendered harsh or more intense by pressure, except in one instance, in
which pressure was not employed ; (5) in four a friction sound,
previously absent, came into play when pressure was made over the
region of the heart ; (6) in one friction sound, present during one, was
absent during two of the three days during which the acme lasted ;
and finally (7), in the remaining case a double friction murmur,
intensified by pressure was audible over the region of the pericardium
during the acme. The cases in the tables at pages 313-327 are
classified according to this arrangement.

I. — Cases vnth Thrill and (V\ a Creaking, (2) Grating, or (3) Harsh
F)iction Sound over the Heart (see pp. 313-316). — In nine of the forty-
three cases under review, a systolic thrill was felt over the heart, and
(1) in five of those cases a creaking; (2) in one of them a grating;
and (3) in three of them a harsh friction sound was audible at the
seat of thrill at the time of the height or acme of the disease.
In six of these cases the thrill was present over the right ventricle,
and, in some of those, but not in all, it was probably situated over the
left ventricle also ; in another of them it was present over the apex

354 A SYSTEM OF MEDICINE.

and the second space, but not over the right ventricle; in one of
the two remaining cases it was felt over the apex ; and in the other
one over the second space alone.

(1.) Creaking Friction Sound (see pp. 313, 314). — In three of the cases
with a thrill over the right ventricle, and in one of those with a thrill
over the apex alone, a creaking sound was audible over the seat of thrill.

One of these patients (4, see p. 313), a man aged 27, came in with ex-
tensive pericardial dulness ; a thrill over the right ventricle extending
from the fourth left cartilage to the sixth; a loud systolic creaking fric-
tion sound consisting of five vibrations, the diastolic sound being much
smoother than the systolic, over the seat of the thrill ; and a double
frottement extending widely over the front of the chest from the second
cartilage down to the ninth on both sides, and audible at the epigastric
space. The pericardial dulnessonthat day extended upwardstothe third
space, and on the following day to the third cartilage, when it reached
its greatest height. The region of thrill had increased upwards, and
extended from the third cartilage to the sixth. A creaking sound
was audible apparently over the whole seat of the thrill, but over the
fifth cartilage there was a vibrating, grating, systolic friction sound of
a churning character, which was creaking towards the end of the
systole, the diastolic sound being short and smooth.

(2.) Grating Friction Sound (see p. 315). — A grating friction sound
without a creak was present on the presumed day of the acme in one
case (51, see p. 315).

(3.) Harsh Friction Sound (see pp. 315, 316). — A harsh friction sound
was present with a thrill in three cases. One of these cases (16, see p.
315) a girl, aged 17, came in with an extensive impulse, a double thrill,
and a loud, double scraping sound over, but not below, the heart.
On the second day, there was loss dulness, and no note of thrill, and
the friction sound was less harsh and extensive : but, on the third
day, there was less effusion, the impulse was lower and more diffused,
and the friction sound was much more intense and extensive.

"We may, I think, say, on reviewing these cases, that at the time of
the acme of the disease, when a thrill is present over the right ven-
tricle, a creaking noise is audible over the seat of the thrill ; and that
from this noise, as from a focus, a to-and-fro sound radiates in all
directions over the front of the chest, reaching far beyond the limits
of the region of actual friction, becoming more feeble towards its
outlying margins, and spreading almost up to the clavicles, out to
or beyond the nipples, and down to the eighth or ninth cartilages ;
and that when the effusion lessens and the thrill disappears, the creak
vanishes, and the friction sound softens, and limits its area to the
region of actual friction, being bounded below by the sixth cartilage.
The reason for the great extension during the acme of the fric-
tion sound upwards, outwards, and downwards beyond the region of
actual friction in these cases is obvious. The heart, surrounded by the
distended pericardial sac, is displaced upwards into the higher and
narrower portion of the cone of the chest. It works in a confined

PERICARDITIS. 365

space, and rubs with its roughened surface against the roughened sur-
face of the pericardium ; and, the lungs being pushed aside, it presses
against the sternum and cartilages, and excites vibrations and a creak-
ing or grating friction sound over the walls of the chest in front of the
heart. The play of tlio two roughened surfaces of the pericardium upon
each other induces vibrations, sensible to the haud, that excite con-
sonant vibrations in the superimposed sternum and cartilages; and
these parts, acting as a sounding-board, transmit the sound to a distance
over the front of the cage of the chest in all directions, and espe-
cially downwards. When the thrill is limited during the acme to the
second space, over the pulmonary artery, or to the apex of the heart,
or is felt both over the apex and the second space, the creaking or
grating noise is limited to the seat of the thrill ; and the friction sound
does not extend beyond the region of actual friction, excepting
perhaps to a small extent over the circuit of the apex. When in
such a case the effusion lessens, the heart descends, and the thrill dis-
appears, the friction sound may spread downwards, so as to reach the
eighth cartilage.

II. Cases in which a Tlirill was not observed over the Region of the
Heart or Great Vessels (see pp. 316-327).

(1.) Cases in which a Sound like tlte Creaking of New Leather was
audible at the time of (lie Acme of the Effusion, no Thrill being present
(see pp. 316-318). — In seven of the forty-four cases under examination,
a creaking noise, usually systolic, was heard without a thrill at
the seat of the impulse of the heart at the time of the acme.

In all of these cases, and in several of those in which a thrill over
the heart was accompanied by a creaking or grating noise, as soon as
the fluid in the pericardium lessened and the heart descended, the
creaking noise was replaced by a comparatively smooth friction-sound.
This occurred on the day after the acme of the effusion in four of
the seven cases. This sudden disappearance of the creaking noise
with the diminution of the fluid and the descent of the heart, appears
to me to show that the presence or absence of the creaking noise
depended more on the position of the heart and on the degree and
kind of pressure exerted by it during its contraction ; than on the
character of the roughened coat of lymph covering the heart and
lining the pericardial sac, since that lining cannot have changed ma-
terially in one day when the disease was at its height. At the time of
the acme of the effusion into the pericardium, the heart is elevated so
as to occupy the upper and narrower part of the cone of the chest ;
and beats with force in its contracted space against the cartilages and
sternum which confine its movements. When the heart pulsates
thus against the walls of the chest, the movements of the former are
resisted by the pressure of the latter. The accumulated force of the
heart overcomes the resistance of the walls of the chest, and the
accumulated resistance of those walls then overcomes the force of the
heart ; these two opposite forces by turns arrest and overcome each
other and give rise to a series of tine jerks or vibrations that may

356 A SYSTEM OF MEDICINE.

give birth to a thrill, and a vibrating creaking noise. In one case, this
creaking noise consisted of five distinct vibrations ; and such a succes-
sion of vibrations forms, indeed, the essential nature of the thrill and
its attendant creaking sound.

The creaking sound, and the main varieties of friction sound,
may be imitated by rubbing the forefinger on the thumb with varyiug
degrees of force when the back of the thumb rests upon the ear.
"When the finger and thumb rub gently or with moderate force upon
each other, to and fro, the rubbing sound is smooth or harsh in pro-
portion to the gentleness or force employed. When, however, the
pressure exerted by the finger on the thumb is great, the resistance
to their onward movement on each other causes them to stop in a
succession of jerks, which produce a creaking noise.

When the fltiid decreases, the heart descends into the ampler space
of the chest; the organ moves with freedom; and, as it no longer
presses with a resisted force against the walls of the chest, the thnlJ,
vibrations, and creak give place to a moderated friction sound ; which
may be so harsh as to sound like the rubbing of sand-paper ; or so soft
as to resemble a murmur.

(2.) Vibrating, Grating Friction Sound (see pp. 318, 319). — The grat-
ing,vibrating friction sound ranks next to the creaking noise in intensity.
It is, in fact, a sister-sound to the creaking noise, with which it is
closely allied. Thus, it may be audible when there is a thrill, when
it may be heard alone, or associated with a creak; or it may by
pressure be converted into a creak; or it may precede or follow,
displace or be displaced, by that sound ; or it may, like it, be pro-
duced by pressure. The grating sound, like the creaking sound,
is the combined effect of pressure and friction, but the pressure is
usually less, while the rubbing surfaces are, 1 believe, more invari-
ably rough, when the sound is grating than when it is creaking. A
grating sound was audible during the acme of effusion in two or three
cases in which there was a thrill, and in two in which there was no
thrill ; and it was excited by pressure in two. It was, therefore,
observed in one-seventh of the cases (6 or 7 in 44).

We have already seen that the creaking sound is usually single, but
it is the reverse with the grating sound, which is usually double.
The grating friction sound is a jarring, grating, vibrating noise, rough
and to-and-fro in character, made in a succession of jerks, each jerk
being separately audible, and varying slightly, and the whole series
not combining to form one note like the creaking sound, but, as I have
just said, a jarring, grating, vibrating noise. I made out, as I have
already stated, that in one case the creak was composed of five vibra-
tions, or at the rate of twenty-two vibrations in a second; but, as I
took no special note of it, I do not know what number of vibratioDS
were made in a second by the grating noise. I believe, as I have
already hinted., that the grating noise is always associated with the
rubbing of the two harsh and roughened surfaces of the heart and peri-
cardium upon each other, but I have no direct prouf of this at present.

PERICARDITIS. 367

(3.) Harsh To-and-Fro Friction Sound, intensified by Pressure, at the
Time of the Acme of the Pepicardial Effusion (see pp. 319-324). —
Resume, including the whole of the preceding cases, whether with or
without a thrill. — We have just seen that a creaking noise, usually
systolic, was present over the heart at the time of the acme of the
disease in one-fourth of the cases in which the dulness was observed
at or about the period when the effusion was at its height (12 in
44) ; while in four other cases it was then excited by pressure, and
in two it was heard just before the acme of the effusion. Creaking,
therefore, was present as a primary sound in twelve cases; as a
secondary sound, or from pressure, in four cases ; and in two others it
was audible just before the acme. We have also seen that a grating
friction sound, usually double, was present over the heart when the
effusion was at or about its height, as a primary sound in three cases
in which there was no creaking, and in one or more in which there
was creaking; and as a secondary sound in two in which it was
excited by pressure ; while in four others it was present just before
or after the period of the acme of the disease.

Tf we combine the two sounds, we find that during the acme the
creaking and grating sounds were primary in fifteen cases, and
secondary, or excited by pressure, in six ; while they were associated
with each other in one or more. Besides these fifteen cases, in which
creaking or grating sounds were primary, there were nineteen cases in
which there was a definite friction sound, which was usually harsh; in all
of these it was double, or to-and-fro in character, being audible both
during the systole and the diastole of the ventricle, and in all but
two it was intensified by pressure. Three-fourths, therefore, of the
patients (34 in 44) in whom the pericardial dulness was observed
when at or near its height presented either a systolic creaking noise,
or a double grating, or a definite to-and-fro friction sound, usually
harsh in character.

Besides the nineteen cases in which there was a double frottement,
usually harsh, at the time of the acme ; there were seven cases in which
that sound was associated with a creaking noise ; and in one it accom-
panied a grating noise. In these cases the creaking or grating noise
was limited to that part of the right ventricle, or the apex, that was
pressing with the greatest force upon the costal cartilages or sternum,
while the double frottement pervaded and often overstepped the
rest of the heart and the great vessels.

If we group together the eight cases with harsh double frottement,
in seven of which the frottement was associated with a creaking sound
and in one with a grating noise, and the nineteen cases not so
associated, we find that in one-half of those twenty-seven cases the
character of the sound is definitely specified (13 in 27) ; while in
twelve it is described as a harsh double friction sound ; and in two
as a to-and-fro sound.

Of the thirteen cases in which the character of the double sound
was specified, in four it was described as being like that made by

35ft A SYSTEM OF MEDICINE.

rubbing with sand-paper ; in seven as being either rasping, or musical
planing, scraping, scratching, grazing or rustling, the latter sound
being a genuine frou-frou ; while in the remaining two the sound
resembled that made by sharpening a scythe.

In the whole of the twenty-seven cases except two, pressure with
the stethoscope intensified the double frotlcment ; it sometimes altered
or modified the character of the sound ; and in five instances it trans-
formed the double frottcmcnt into a creaking sound When the
creaking sound was thus brought into birth by pressure, or secondary,
it was usually double ; but when the creak was always present, or
primary, it was, as I have already shown, usually and essentially
single or systolic.

In all these cases the double frottement was essentially a to-and-fro
sound. The character and volume of the sound, and the relative
intensity of the to-and-fro, or the systolic and diastolic friction sounds,
varied over the different parts of the heart. As a leading principle,
the greater the pressure exerted by the heart, or auy portion of it,
during its action upon the cartilages or sternum against which it beat,
the more intense was the friction sound.

The friction sound in the remaining cases of this group was limited
to a comparatively small area.

In two of the nineteen cases, in both of which there was a thrill over
the right ventricle, the rubbing noise as I have already stated, extended
over the front of the chest, far beyond the region of actual friction.
These two cases, however, stand apart, for in the remaining seven-
teen the area of the friction sound was limited to the region of actual
friction ; with, however, this slight exception, that in six of the patients
the to-and-fro sound spread upwards to the top of the sternum, and in
one of them it was diffused outwards as far as the left arm-pit. The
upper limit of the distended pericardial sac and of actual friction is
rarely higher than the transverse centre of the manubrium, which is
about an inch below the top of the sternum ; therefore in the six patients
just spoken of, the friction sound extended itself upwards for from an
inch to fully two inches above the actual seat of friction over the
great vessels, which, at their higher portion, are partly covered by lung.

The explanation of this extension of the friction sound upwards
beyond the immediate seat of friction is the same as that of the
. diffusion of the friction sound over the front of the chest far beyond
the region of the distended pericardium and of actual friction, when
a thrill and a corresponding creaking noise are present over the heart.
The to-and-fro movements of the heart upon the pericardial sac, both
being covered with lymph, excite a to-and-fro sound which is audible
over the region of those movements. The vibrations that produce the
sound are communicated to the sternum, which is played upon by the
rubbing surfaces ; and the sternum, which acts as a sounding-board,
propagates the sound to its own upper end, which is at some distance
from the seat of the parent vibrations. The extension of the friction
sound beyond the region of actual friction depends on the loudness

PERICARDITIS. 359

and intensity of the rubbing noise, and the force with which the heart,
when it is rubbing to and fro, presses against the sternum and carti-
lages. Of the six cases in which the to-and-fro sound mounted to the
top of the sternum, in three there was a creaking sound over the heart,
with a thrill also in two of those ; in two others a creaking sound
was excited by pressure ; and in the remaining one a loud, harsh,
double friction sound was present over the region of the pericardium.
Although a creaking friction sound was audible over the apex in four
instances, in only one of them did the to-and-fro sound spread to the
left beyond the apex, but in that one the rubbing sound extended
outwards into the left arm-pit. In that case there was dulness over
the left lower lobe, and bronchial breathing between the left axilla
and the spine. It is, therefore, evident that the heart and pericardium
were displaced towards the left side owing to the condensation of the
left lung, and that this circumstance facilitated the extension of the
friction sound to the left axilla.

With these few exceptions, the region of friction sound coincided
in these cases with the actual region of friction at the time when
the effusion into the pericardium was at its height.

(4.) Cases in which a Soft Friction Sound, audible over the Heart at the
Time of the Acme of the Effusion into the Pericardium, was converted by
Pressure into a Harsh Rubbing Noise (see pp. 324, 325). — Four cases
with a soft friction sound, in which pressure rendered the sound harsh,
come under this heading, and in one of these the friction sound
elicited by pressure resembled the noise made by sharpening a scythe.
In a fifth case, with a similar friction sound, the pressure test was
not employed.

In these four cases a comparatively soft double friction sound was
intensified and altered by pressure, becoming converted in one
instance into a sound like that made by sharpening a scythe, and
in one into a rasping, grating noise. Here pressure expelled any
interposed fluid ; brought the opposite roughened surfaces of the peri-
cardium more closely into contact ; and aroused counter-pressure on
the part of the heart against the cartilages and sternum during its
to-and-fro rubbing movements. These effects spoke out not only in
a louder and more diffused, but also in an altogether altered sound ; so
that the soft sounds, sometimes so murmur-like as to be almost
doubtful in quality, became instantly transformed into a loud double
and broken noise, like that made by sharpening a scythe, or into a
rasping, grating, almost creaking sound.

(5.) Cases in which a Double Friction Sound, not otherwise
audible, came into play when Pressure was made over the Heart during
the time of the Acme of Pericardial Effusion (see pp. 326, 327). — In four
cases during the acme, on listening without making pressure, the
healthy sounds of the heart were alone audible ; but on making
pressure those sounds were either replaced or accompanied by a
double rubbing noise.

In three of these cases, at the time the effusion into the peri-

380 A SYSTEM OF MEDICINE.

cardium was at its height, when the stethoscope was applied lightly
over the heart, the natural heart sounds were alone heard, friction
sounds being everywhere inaudible. When, however, pressure was
made with the stethoscope, a double friction sound was immediately
brought into play, which could be suspended or renewed at will by
withdrawing or replacing the pressure. In one case the fric-
tion sound thus generated was limited to the region of the right
ventricle, and in another to the base of that ventricle ; but in a third
case it was diffused over the whole space occupied by the heart and
great vessels. The impulse was feeble in one of these patients, and was
felt over the right ventricle in another. It is difficult to say why
friction sound was absent without pressure over the seat of the impulse ;
but it is self-evident that if we pvess the cartilages or sternum inwards
upon the walls of the heart moving to and fro, those walls will work
with increased counter pressure against the resisting walls of the
chest ; and may thus elicit a friction sound when previously absent, or
intensify a friction sound already existing, owing to the increased
friction of the two roughened surfaces. In two of the cases a to-
and-fro sound was audible without pressure over the apex, and in
one of them over the lower border of the right ventricle also ; but it
was brought into play by pressure over the whole region of the heart
and great vessels.

The subsequent history of these cases illustrates with great clear-
ness the cause of the absence of friction sound without pressure, and
its presence with pressure during the acme of the disease. In three of
them (15, 8, 19), as soon as the effusion into the pericardium lessened,
the heart descended, and its impulse became stronger and lower; the
fluid interposed between the front of the heart at its lower border and
the pericardial sac disappeared ; and the friction sound came into
spontaneous play where it was before absent without pressure. That
sound, indeed, gradually augmented in loudness and intensity, and
increased in area upwards, sideways, and especially downwards.

(6) Case in which Friction Sound teas Absent for Two of the Three Days
during which the Acme of Pericardial Effusion lasted (35, see p. 327). —
This patient (35), a woman aged 21, came in with great pain and a double
friction sound all over the region of the heart. The pain was relieved
by leeches. Next morning the effusion was at its height, but the friction
sound had vanished and could not be brought back even by pressure.
That evening there was a return of pain, and a renewal of the friction
sound which lasted until next day, but again vanished on the fourth
day, when the effusion was still at its acme. She was in great distress
from pain over the heart, but the impulse was faint in the third and
fouith spaces. Next day there was less effusion, a lowered impulse,
and no distress, and friction sound was rendered audible by moderate
pressure over the right ventricle. Why was the friction sound absent
in this case of pericarditis ? When we consider that the impulse
was perceptible, it must be allowed that the answer is difficult. The
loss of blood on the second day and the great distress on the fourth

PERICARDITIS. 361

day may in some measure, however, account for the exit of the fric-
tion sound.

(7) Case in which a Friction Murmur was audible over the Heart at
the Time of the Acme of the Disease (see p. 327). — This case (49) of a
youth set. 17, presented a long history, and proved fatal on the forty-
eighth day. On examination after death, the heart was found to be
universally adherent by means of recent lymph. Throughout the whole
period, with rare and doubtful exceptions, the inflammation of the
pericardium was made evident, not by the ordinary friction sound, but
by a true friction murmur.

The Area of the Friction Sound during the Acme of the Effusion. —
The area of the friction sound when the effusion into the pericar-
dium is at its height may, on the one hand, be so extensive as to
cover the whole front of the chest, extending from the clavicles down
to the ninth right and left costal cartilages; or, on the other, be so limited
as to be confined to the middle or lower portion of the sternum. This
great diffusion, or narrow limitation of the friction sound at the
period of the acme of disease, is, however, comparatively rare; and, as
a rule, the area of the friction sound corresponds either with the area
of actual friction, or with that of dulness on percussion over the
pericardium.

The friction sound was audible over a great extent in all those
cases, amounting to nine, in which a thrill was felt over the heart or
great vessels, and especially in those in which it was perceptible over
the front of the right ventricle.

In all the cases with thrill the friction sound was audible over the
right auricle and ventricle, the outlying portion and apex of the left
ventricle, and the great vessels ; in all but one of them, also, it extended
to the top of the sternum, beyond the region of the distended peri-
cardium over the great vessels. In these cases, as I have already
explained, the friction sound was most intense over the region of the
thrill, and it radiated thence over a wide area, becoming gradually less
, intense from its focus to its extreme limits, being conducted by the
sternum and cartilages acting as a sounding-board.

In six of the twelve cases in which a creaking sound was heard
over the heart, the area of the friction sound extended down to the
seventh, eighth, or ninth costal cartilages ; but in five of these the
creak accompanied a thrilL In the remaining six cases the frottement
extended to the sixth cartilage, or occupied an unspecified space, to the
right and left of the sternum. It is evident, therefore, that the great
diffusion of the sound in these cases was due more to the thrill, than
to the creaking sound that was audible at the seat of the parent thrilL

I need not here specify the exact limits of the friction sound in the
remaining cases.

These clinical facts show that, when the effusion into the peri-
cardium is at its height, if we put out of view those cases in which a
thrill is felt over the right ventricle, the friction sound is, with a
slight exception, practically limited to the region of pericardial dulness,

VOL. IV. B B

368 A SYSTEM OF MEDICINE.

or rather of the heart and great arteries. This exception applies to
the presence of the friction sound over the upper end of the sternum,
which is fully an inch higher than the uppermost limit of that region.
This was observed in nineteen cases, and in ten of these no thrill
was noticed over the region of the heart or great vessels. In all
these cases the friction sound was conducted to the top of the manu-
brium, from the actual seat of friction by the sternum itself, acting
as a sounding-board.

When the lower boundary of the friction sound reaches to the lower
end of the sternum and the sixth cartilage, that limit is still within
the lower boundary of the region of pericardial dulness, which is situ-
ated, when the pericardium is completely distended, behind the
ensiform cartilage and along the lower margin of the sixth cartilage.
As I have already shown, however, the lower boundary of the heart,
and consequently of the region of actual friction, is, in the great
majority of cases, above the lower end of the sternum and the sixth
cartilage ; for the fluid in the pericardium presses the heart upwards,
and interposes itself between the lower border of the heart and the
walls of the chest in front of that border. The position of the impulse
is a good practical test of the position of the actual seat of friction.
In three of the seven cases in which the friction sound was audible as
low as from the seventh to the ninth cartilages, the impulse was felt
in the fifth space, and in one of them, a case of established valvular
disease with enlarged heart, in the sixth space. But with one single
exception, in which the beat of the heart was felt in the fifth space,
in all the rest of the cases the impulse was not present below the
fourth space, and in nine instances its lowest position was in the third
space. In the nature of things, the seat of the actual friction behind
the sternum, except at its upper portion, corresponded, as a rule,
pretty closely with its seat at the intercostal spaces.

In all the cases save one the friction sound was audible down to
the lower end of the sternum at the time of the height of the effusion,
and in twelve of them it was heard over the sixth cartilage. In all
these cases, therefore, it is evident that the friction sound was audible
below the actual seat of friction. The sternum is an excellent
sounding-board, and the conduction of the friction sound to the
lower end of that bone, by its own resonant vibrations, at once ex-
plains the presence of the sound at its lower end. The presence of
the frottement over the sixth cartilage, an inch below the actual seat
of friction, appears to me to call for a different explanation. The
observed facts are indeed different in these two cases. The sound
heard at the lower end of the sternum is, like that at its upper
end, usually of the same harsh to-and-fro quality, and of about the
same intensity as that audible over the two rubbing surfaces at the
middle of the bone. But this, as a rule, is not so with regard to
the friction sound audible over the sixth cartilage, for that is softer,
smoother, and less loud than the sound over the seat of the impulse,
from one to two spaces higher up. The presence of the soft mus-

PERICARDITIS. 363

cular space cute off the direct connection between the fifth carti-
lage and the sixth. The sixth cartilage is, however, directly attached
to the sternum, and that bone, acting as a sounding-board, doubtless
conveys some of its own resonant vibrations to the cartilage. But it
is to be noted that the sound over the fifth space, though softer and
feebler than that over the fourth space, is harsher and louder than that
over the sixth cartilage. It is self-evident that the sound over the
space can scarcely be conducted from the sternum ; and I think, there-
fore, that we must look to the fluid within the pericardium, and to the
inner surface and structure of the roughened and thickened peri-
cardium itself, as the principal media by which the sound is conducted
in these cases to the sixth cartilage.

If we except those cases in which a thrill is felt over the right
ventricle or at the apex, we find that when the sac is filled with
fluid the friction sound stops quite suddenly along the left and
right margins of the region of dulness over the pericardium. This
sudden arrest of the rubbing sound at its outer border is less
marked along the right than the left margin. This is, I consider,
explained, firstly, by the softer, smoother, and more equal character
of the to-and-fro sound over the right auricle than over the right
and left ventricles ; and, secondly, by the presence of fluid between
the compressed right auricle and the walls of the chest in front
of it, along its outer border. If, on the other hand, we look at the
left border of the distended pericardium, we find that there tjie solid
ventricles by their own pressure and action against the ribs and spaces,
displace the fluid and completely occupy the ground. Here we pass
suddenly from the loud double frottement made by the two rubbing solid
surfaces of the ventricle and the rib lined with roughened pericardium,
to the silent, soft, non-conducting surface of the lung.

We may, I think, conclude, with the qualifications just stated, that
when the effusion is at its height, as well as when it is increasing in
quantity, the friction sound is limited to the region of pericardial
dulness ; and, though with less rigour, to the region of actual friction ;
and that the law originally stated by Dr. Stokes, that the area of the
friction sound is usually limited to the region of the heart, is correct in
the great majority of cases, during the period of the acme of the effusion.

Before concluding what I have to state with regard to the area of
the friction sound, I would here estimate, as nearly as I can, the
extent to which the sound was heard over the various chambers of
the heart and the great vessels during the acme of the pericardial
effusion in the forty-four cases now under examination.

In one-half of the cases (21 in 44) the friction sound was audible
over the whole front of the heart, including the right auricle and
ventricle, the apex and a portion of the left ventricle, and the great
vessels. In seven or eight other cases it was heard over the right
auricle and ventricle, in four or five of which it was also present
over the apex, and in one over the great vessels. In fifteen other
cases the frottement was audible over the right ventricle, in nine of

b d 2

364 A SYSTEM OF MEDICINE.

which it was also heard over the apex, and in four or five over the
great vessels. In six of these cases the friction sound was limited to
the right ventricle. If, upon this estimate, we take- each portion of
the heart separately, we find that the friction sound was present
daring the acme over the right ventricle in the whole of the forty-
four cases under notice ; over the apex of the left ventricle in thirty-
four or perhaps thirty-five of those cases ; over the right auricle in
twenty-eight or twenty-nine of them ; and over the great vessels in
twenty-six or twenty-seven of them.

Ir^tensity and Character of the Fiction Sound over the different parts
of (he Heart and Great Vessels during the acme of the Effusion. —
When inquiring into the relative intensity and character of the fric-
tion sound over the different cavities of the heart, except the right
ventricle, and the great vessels at the time of the acme of the effusion,
I shall take into account the forty-four cases now under examination ;
but as regards the right ventricle I shall limit myself to the twelve
cases with primary creaking sound, the two with grating friction
sound, and the nineteen cases in which there was a harsh friction
sound intensified by pressure, which form a total of thirty-three cases.
Although the left ventricle forms the pivot of the heart's action,
and does its work with three-fold more power than the right ventricle,
I shall first examine the friction sound as it presented itself over the
right ventricle, because it forms the front of the heart ; covers the
left ventricle except at its left border and apex ; and is the main seat
of actual friction.

Right Ventricle. — As the right ventricle forms the front of the heart,
it is always in contact to a greater or less degree with the anterior
walls of the chest. Owing fo the distension of the pericardium during
the acme, and the elevation of the heart into the contracted space at the
upper part of the chest, the heart and great vessels are stripped of
the lung that covered them, and press directly forward upon the
middle and upper part of the sternum and the higher costal carti-
lages and intercostal spaces, from the second to the fifth.

The to-and-fro movements of the right ventricle, by rubbing against
the opposed surface of the sac, give birth to the to-and-fro friction sound
audible in front of the ventricle. Those movements play from right to
left during the contraction of the ventricle, and from left to right during
its dilatation (see Figs. 16, 17, p. 66). The sweep of the walls is very
extensive behind the sternum, at the junction of the auricle to the
ventricle ; thence it gradually lessens ; and comes to a stand-still near
the septum. The friction movements are therefore greater, and the
friction sounds are louder, at the sternal than the costal halves of the
cartilages. As the position of the ventricle is raised from the fourth
and fifth spaces to the third and fourth spaces, the frottejnent is usually
louder over the sternal portions of those spaces, and the adjoining
portion of the sternum, than elsewhere.

As the movements made during the emptying of the ventricles are
active, and those made during the filling of the ventricle are passive,

PERICARDITIS. 365

the increased pressure made by it upon the cartilage and sternum
during the systole often intensifies the frottement, and, as I have
already shown, may even transform it into a reaking noise. Thus,
of the thirty- three cases under examination, in six there was a systolic
creak over the right ventricle ; in thirteen the systolic friction sound
was louder than the diastolic; in two the systolic and diastolic
sounds were equal; and in twelve it is not stated whether there
was any difference between the two sounds.

From these clinical facts it is evident that the active friction sound
made during the contraction of the ventricle is, as a rule, louder than
the passive friction sound made during its dilatation. In a small
minority of cases, however, the two sounds are equal, and a true to-and-
fro sound is produced, the diastolic portion of which speaks with the
same intensity, length, and continuousness as the systolic portion.
In these cases I believe that the impulse is feeble, and that the
systolic friction sound, like the diastolic, is, so to speak, passive, and is
not intensified by the greater pressure from within of the anterior
wall of the ventricle upon the walls of the chest.

The conus arteriosus of the right ventricle calls for special notice.
It is situated behind the third space and the two adjoining cartilages,
and as it enjoys extensive play during the systole, when its move-
ments are twofold, from above downwards, and from left to right, the
friction sound is often notably harsh, loud, and to-and-fro in that
situation. Sometimes it is there creaking or grating, when it may be
accompanied by a thrilL It sometimes resembles the sound made by
rubbing together two opposite surfaces of emery paper, of stuff or
of silk ; or it is rasping, or scratching, or rustling when it may present
a true frou-frou; or it may, though less frequently, be soft in
character. A friction murmur is, however, rarely or never present in
this situation. Pressure readily intensifies and alters the friction
sound over the conus arteriosus, and sometimes converts it into a
creaking sound. As the conus arteriosus is covered in health by a
thin layer of lung, it is not usually the early seat of friction
sound ; but as the lung, when once displaced from before it, does not
readily replace itself, the rubbing sound is often heard in this
position up to a late period in the history of the case. The friction
sound is notably double or to-and-fro over the conus arteriosus, and
this may be accounted for by the ready completeness with which the
right ventricle spontaneously fills itself during the ventricular
diastole.

The Apex and Outlying Portion of the Left Ventricle. — The apex
and outlying portion of the left ventricle are in health covered by the
lung. The extent to which the lung thus affords a protection for the
apex depends upon the vigour of the individual, the size of the chest,
and the amplitude of the lungs. The portion of left lung immediately
covering the apex is a thin tongue, the lowermost protruding angle of
its upper lobe, which laps round the apex of the organ, and inter-
poses itself between that part and the ribs.. During the diastole,.

366 A SYSTEM OF MEDICINE.

'when the ventricle is inactive, the covering of lung is complete ; but
when the ventricle contracts, owing to the combined muscular rigidity
of the organ, and the outward pressure of the blood that is compressed
by the contracting cavity, it pushes aside the tongue of lung in front
of it, so that the apex sweeps against the ribs and their interspaces.
It is thus in young persons and those who are not robust ; but in
strong adults, inured to exercise, the average size of the lung is in-
creased, and the apex is so embedded in the lung, that its proper beat
cannot be felt, except perhaps at the end of a forcible expiration, or
when they lie on the left side. In one instance (12, see p. 317) and
in one only an dbscuie friction sound was heard over and limited to
the «pex before it was audible elsewhere. This was on the day of
admission, but on the following day it had left the apex, and trans-
ferred itself to the whole right ventricle and right auricle. I can
offer no explanation of this exceptional sign.

As a rule, the friction sound was, as I have said, limited at first
to the right ventricle; but as the disease advanced, the increased
fluid in the pericardium displaced the left lung and laid bare the
apex, so that the friction sound spread itself from the right ventricle
to the left.

When the effusion was at its height the heart was raised, and
the apex-beat was felt in the fourth, or even the third space, at
or just above and beyond the nipple. Friction sound was probably
audible over the apex during the acme in thirty-four of the forty-
four cases now under notice ; it was absent from that point in nine ;
and its presence there was doubtful in one case.

The movement of the apex is, in its nature, the reverse of that of
the right ventricle at its junction with the right auricle ; for while,
during the systole, that part moves from right to left, the apex moves
from left to right, and from below upwards. As the active sweep of the
apex takes place during the contraction of the ventricles, it is natural
to expect that the friction sound at the apex should be mainly systolic,
and the examination of my cases shows that this is so. Of the thirty-
four cases in which a friction sound was audible over the apex, in
six it was heard during the systole only; in ten the frottemmb was
double, but was more intense and prolonged during the systole than
the diastole; and in none was it stated that the two sounds were of
equal intensity during the two periods. In six cases there was a
creaking friction sound, usually systolic, at the apex.

When the lower lobe of the left lung shrinks under the double
effect of pulmonary apoplexy within the lung, and pleurisy on its
exterior, on the one hand ; and of compression of that portion of the
lung and of the left bronchus, by the great distension of the pericar-
dium, on the other, the apex becomes completely exposed, and extends
far to the left. In one such case (25, see p. 317), a youth, aged 17, a
systolic creaking sound was audible over and beyond the apex, and
the friction sound extended far to the left, ceasing suddenly in the axilla.
Bight AuricU* — The right auricle is in health completely screened

PERICARDITIS. 367

from the anterior wall of the chest by the middle lobe erf th& right
lung, which separates it from the middle of the sternum and the costal
cartilages to the right of the lower half of that bone. Friction
sound is therefore never audible over the right auricle until the
portion of lung that is interposed between it and the right cartilages
is pushed aside by the advancing tide of effusion, so as to lay bare
the auricle. When the effusion into the pericardium was at its
height, a friction sound was audible over the right auricle in three-
fifths of the cases (28 or 29 in 44).

The expansion of the right auricle is quite passive, and its contrac-
tion is made with so little exercise of force, that its movement to the
right during its period of filling, and its movement to the left during
its period of emptying, are made so quietly, that it exerts no pressure
on the cartilages during its to-and-fro movements. It is natural to
expect that the to-and-fro frottement, the frou-frou produced by
the passive double friction of the right auricle, should be made up
of two equal sounds, and as a rule those two sounds were equal over
that cavity.

In twelve of the twenty-nine cases in which friction sound was
audible over the right auricle, the systolic and diastolic sounds were
equal ; in eleven the frottement was double, but the relative intensity
of the two sounds was not described ; and in one a systolic sound,
almost creaking in character, was audible over the right auricle.
In this last exceptional case a similar almost creaking noise was
heard over the base of the right ventricle at the lower portion of
the sternum, and that was evidently the source of the rubbing
sound over the auricle.

The two sounds made respectively over the right auricle during
the two alternate movements of its dilatation, with contraction of the
ventricle, and its contraction with dilatation of the ventricle ; are not
only equal in character, intensity, and continuousness ; but they are
also more soft and smooth in tone than they are over the ventricle ;
this contrast being most remarkable in some of those cases that
present a thrill and a creaking sound over the right ventricle, and
the diffusion of a harsh double friction sound over the whole front
of the chest extending downwards even to the eighth or ninth
right and left cartilages.

The question here arises whether under these circumstances the
soft double friction sound audible over the cartilages to the right of
the lower sternum is due to the immediate friction of the subjacent
right auricle ; or to that of the right ventricle, transmitted through the
fluid and softened in its transmission ? I think that we must infer
that the latter is the usual source of this sound, when we consider
that the yielding right auricle is compressed by the fluid in the peri-
cardium at the time of the acme. Why under these circumstances,
the two sounds are usually equal, I cannot say.

The Ascending Aorta and Pulmonary Artery. — In health the two
great arteries lie behind the upper half of the sternum and the

368 A SYSTEM OF MEDICINE.

spaces to the left of it, above the level of the third cartilages. They
not only have the bony protection thus afforded t hem, but they are
additionally sheltered by a thin covering of lung that is interposed
between them and the bony shield in front, and is made up of the
inner adjoining margins of both lungs. The aorta is guarded by the
strongest portion of the sternum, and the pulmonary artery lies
behind the second space and cartilage, and the adjoining margin of the
sternum. In the early stages, therefore, of pericarditis, friction sound
is never audible over the great vessels. When the fluid increases, the
distended pericardium and the elevated heart and great vessels push
the double curtain of lungs to each side, so as to bring the great
arteries into contact with the sternum and the first and second spaces
and cartilages. The heart and great vessels then, as I have already
said, occupy the narrower space in the upper portion of the cone of the
chest, and there is now no longer room both for them and for the portion
of lung superficial to them in health, which is therefore displaced.

In considering the character of the friction sound over the two
great arteries, we must distinguish the aorta from the pulmonary
artery. The roots of those arteries, including under that term their
apertures, valves, and sinuses, descend and ascend fully half an
inch during the successive periods of the systole and diastole of the
ventricles ; the movement of the systole being more active than that
of the diastole.

The root of the pulmonary artery is situated at the front of the
heart, and when the lung is displaced from before it, the artery lies
immediately behind the second, and sometimes also the first, left in-
tercostal space, the second costal cartilage, and the adjoining border of
the sternum. The movement of the pulmonary artery, like that of
the conus arteriosus from which it springs, is downwards and from
left to right during the systole, and the reverse during the diastole.
The friction sound over the pulmonary artery, is not, therefore, so far
as I know to be distinguished from that over the conus arteriosus. The
to-and-fro sound caused by those two adjoining and connected
parts 'must resemble and blend with each other; but while that of
the pulmonary artery is situated over and above the second space and
the adjoining border of the sternum ; that of the conus arteriosus
extends downwards from that point to the fourth cartilage, but widen-
ing to the right, so as to occupy the whole breadth of the centre of
the sternum.

A peculiar systolic scratching noise, that somewhat resembles a
friction sound, is sometimes audible over the pulmonary artery during
the course of acute rheumatism, and is generally associated with
endocarditis. This sound is evidently caused by the vibration of the
blood advancing during the systole along the artery when not in a
state of tension ; and is to be distinguished from a friction sound by
its limited area, the sound being confined to the second space, and
not accompanied by friction sound elsewhere over the heart ; its re-
striction to the period of the systole and its consequent total want of

PERICARDITIS. 360

a to-and-fro character ; its freedom from change when pressure is made
over it ; its unaltering character on successive days ; and the absence
of pain over the heart or other symptoms or signs of pericarditis.

The root of the aorta instead of being exposed in front, like that of
the pulmonary artery, is buried deeply in the centre of the heart,
being covered by that artery, the conns arteriosus, and the left border
of the right auricle. The root of the aorta cannot therefore cause a
friction sound. The ascending aorta, where it comes into view above
the right auricle and behind the lower half of the manubrium, is in
health deep in situation, being covered by the adjoining margins of
the opposite lungs. When, however, the heart and great vessels are
lifted upwards by the advancing invasion of the fluid in the pericar-
dium, the lungs are displaced from before the ascending aorta, which
may possibly be pressed against the back of the manubrium. Even
then, however, it can only excite a partial friction sound, for its move-
ments, which are downwards and upwards, are very slight.

Friction sound was audible at the manubrium over the ascending
aorta and the adjoining portion of the pulmonary artery at the
time of the acme of the effusion into the pericardium, and especially
during expiration, in twenty-six or perhaps twenty-seven of the forty-
four cases under review ; but this friction sound was evidently not
generated by the double movement of those vessels, but was conducted
upwards by the sternum, acting as a sounding-board, from the harsh
double friction sound over the right ventricle. This was shown by
that sound reaching with full intensity to the top of the sternum,
which is a little above the transverse aorta, in twenty-six or perhaps
twenty-seven of the forty-four cases ; and by the close correspondence
between the' character of the double frottement over and above the
great vessels at the upper half of the sternum, and that over the
right ventricle, at the lower half of the sternum.

At the time of the acme of the effusion into the pericardium
the whole heart is raised, and the lungs are separated from each
other in front, so that the pulmonary artery, the conus arteriosus
and the rest of the right ventricle, the apex and outlying portion of
the left ventricle, and the right auricle are uncovered, and brought
into immediate contact with the walls of the chest in front of them.

The whole front of the right ventricle bears upon the sternum and
left cartilages with varying force. Sometimes it produces a thrill during
its contraction, which may extend over its surface from the third to
the sixth cartilages, and is often accompanied by a systolic creaking
sound. At other times, sometimes with, but generally without a
thrill, a double grating sound or a harsh friction sound of various
tones, the systolic sound being usually louder than the diastolic,
springs up over the whole right ventricle. In rare instances the two
sounds are equal. More rarely a soft friction sound, rendered harsh
by pressure, or a to-and-fro sound, excited by pressure but absent
without it, is present over the right ventricle.

370 A SYSTEM OF MEDICINE.

A friction sound is heard over ihe apex during the acme in about
three-fourths of the cases. The apex may, like the right ventricle,
present a thrill and a creaking sound during the systole; or a loud,
prolonged systolic friction sound, and a short, feeble diastolic one. In
no instance are the systolic and diastolic friction sounds equal over
the apex.

During the acme the right auricle in two-thirds of the cases
presents over its surface, to the right of the lower half of the
sternum, a double, smooth, to-and-fro murmur or friction sound,
equally loud during its dilatation and contraction. This double
smooth frottement over the right auricle is probably transmitted,
softened in its transit, through the fluid, from the noisy and active
right ventricle.

The friction sound, if any, that may be made during the acme by
the ascending aorta and the adjoining portion of the pulmonary artery
behind the manubrium, is almost always masked by the friction sound
of the right ventricle, which is conducted by the sternum acting as a
sounding-board, the sound being thus conducted in more than half of
the cades to the upper end of the bone.

The double frotUment proper tp the pulmonary artery when
covered with lymph is undoubtedly audible during the acme over the
second space, where it must resemble and blend with the double
frottement proper to the conus arteriosus.

In every instance pressure intensifies the two friction sounds ; and
it sometimes transforms an ordinary frottement into a creaking or
grating sound ; or a soft friction sound into a harsh rubbing noise ; or
it excites a friction sound when one was previously absent.

Second Acme. — Benewed Increase of Effusion into tlie Pericardium
owing to Relapse. — In eleven cases the effusion into the pericardium,
after it had reached its height and commenced to decline, again
increased in quantity, and attained to a second acme. Another case
that had a relapse and a second acme, that was admitted during the
period of the first acme, has not been included in the inquiry that is
about to follow. In five of those eleven patients under consideration
the fluid, after declining for a second time, again increased so as to
present a third acme of pericardial effusion, and in one of the five
there was a fourth wave of increase.

I shall examine in these casSs with relapse and renewed acme, the
comparative height of the pericardial effusion; the extent of the
heart's impulse ; the area and intensity of the friction sound ; the
severity of the general illness ; and the intensity of the accompanying
endocarditis, and its permanent effect on the functions of the valves
of the heart during the period of the later acme.

Extent of tlie Effusion into the Pericardium. — In five of the cases
the effusion into the pericardium was equal in extent during the first
and the second acme ; while in five it was greater, and in one it was
less, during the first than the second acme. In six of the cases, from

PERICARDITIS. 371

two to five days, and in five of them from six to eight days, elapsed
between the end of the first period and the beginning of the second
period of the height of the effusion.

Position of the Impulse. — In six of the cases, and probably in a
seventh, the impulse at its inferior boundary occupied a lower
position by from one to two intercostal spaces during the second
acme of the effusion than the first (compare Figs. 48, p. 378 ; and
42, p. 340 respectively with Figs. 45, p. 350 ; and 40, p. 338) ; in two
cases the impulse occupied the same position during the two periods ;
in one instance it was imperceptible throughout ; and in one it was
very feeble.

We thus find that in the great majority of the cases the impulse of
the heart was lower during the second acme of effusion, or the period of
relapse, than during the first acme. The reason is, I think, evident When
the fluid in the pericardium begins to increase during the early period
of pericarditis, the heart, which is then yielding in structure and usually
of the natural size, is steadily floated upwards by the increasing tide of
effusion into the pericardium, which may indeed compress the auricle,
and lessen the size of the heart. The heart, under the double influence
of the inflammation on its exterior, and the resulting thick coating of
lymph, on the one hand ; and the inflammation on its interior, and
the resulting crippling of valves, enlargement of cavities, and thickening
of walls, on the other, becomes increased in size. The whole organ is,
in fact, enlarged, and it is often unyielding in its position owing to
its tough new covering, and perhaps to partial adhesions that may
have already connected the double surfaces of the thickened peri-
cardium and the heart, especially along and near the septum ; and
although the renewed increase of fluid elevates the heart to a certain
extent, this second elevation of the impulse is not usually so great as
the first elevation.

Thrill. — A thrill was felt over the heart for the first time during
the second acme in three of the cases. In two of them the thrill was
present over the apex, and this was the natural effect of the lowered
position, greater prominence, and increased force of that portion of the
heart during the second acme than the first. In the other case the
thrill was present over the second left space, but in this patient the
second acme was the true one, for the effusion was considerably higher
during the second than the first acme. A thrill is, in fact, more
frequently present over the second space during the first acme than
the second, and over the apex during the second acme than the first,
for the reasons that I have just stated.

Area and Intensity of the Friction Sound during tlie Second Acme
of Increased Effusion, into the Pericardium. — During the second acme
of the pericardial effusion a creaking friction sound was audible over
the heart in four cases, and a grating noise in one; a to-and-fro
sound in five patients, and a double Motion murmur increased by
pressure in one.

In five of the cases the area of the friction sound was greater, and

372 A SYSTEM OF MEDICINE.

in four it was less during the second than the first acme of the effusion
into the pericardium, and in two it was of equal extent during both
periods. In five of them the friction sound was audible over a
lower position during the second acme than the first, and in none
of them was the friction sound lower during the first acme than the
second.

In like manner, the friction sound was more intense in six cases,
and less intense in four, during the second acme than the first ;
and in one it was of equal intensity during both periods. In four
of the patients both the area and the intensity of the frottemtnt
were greater, and in three they were both less, during the second
than the first acme.

The following agencies, on the one hand, tend to increase the area
and intensity of the friction sound during the second acme as com-
pared with the first : — The greater size of the heart ; the increased
thickness and force of its walls ; the lowered position of the organ
and its impulse ; and the greater roughness and toughness of the
lymph covering the heart and lining the pericardium.

The following, on the other hand, tend to lessen the area and
intensity of the friction sound during the second acme as compared
with the first: — The greater extent to which the lungs sometimes
cover the heart; the restraint placed on the movements of the
heart, and especially of the right auricle, by the thickness and
toughness of its envelope of lymph; and the adhesions that have
often already taken place between the pericardium and the heart ; and
especially along the septum, between the ventricles, and at the apex.
Vital influences blend with and counteract these physical influences
in producing the result.

My analysis of the cases does not enable me to assign to each of
those causes its proper share in the production of these effects.

In the one fatal case the heart was universally adherent, and in
that patient the friction sound was less in extent and intensity during
the second acme than the first, owing, I consider, to adhesions that
had already begun to form between the heart and the pericardium.

The friction sound, as we have seen, was lower in extent during
the second acme than the first in one-half of the cases (5 in 11), owing
to the lower position of the heart and its impulse during that period.

In five of the cases the friction sound maintained the same character
during the second acme as during the first, but in six others it was
altered. Thus, one that had a friction sound on pressure, one that
had a smooth friction sound harsher on pressure, and one that had a
harsh friction sound 'creaking on pressure during the first acme, pre-
sented, all of them, a creaking friction sound during the second acme ;
while one with a to-and-fro sound during the first, gave a grating
noise during the second acme.

From what I have just said, it is evident that the influences
tending to increase the area and intensity of the friction sound
during the second acme were in greater force than the influences

PERICARDITIS. 373

tending to lessen them ; and that the friction sound was usually more
intense and more extensive, especially downwards, during the second
acme than the first.

Comparative Area and Intensity of the Friction Sound just "before,
during, and soon after the Second Acme of Effusion into the Pericar-
dium.— The friction sound is, as a rule, louder and more extensive
during the second acme of pericardial effusion than either just before
or soon after that period. At this stage, therefore, the frottement
increases with the advance, and decreases with the decline of
the fluid.

Degree of the General Illness during the Second Period of Increased
Pericardial Effusion. — In five of the cases the illness was extreme, in
three it was severe, and in three it was slight or probably so during
the second acme.

Of the five cases in which the illness was extreme, the face was
anxious in four; there were choreal movements and rigidity, chiefly
of the left arm, in one ; breathing was laborious in one and quick
in four, the respirations ranging from 32 to 48 ; pain was present
over the heart in one, and in another pain was felt, apparently in the
side, on a deep breath ; swallowing was difficult in two ; one had
diphtheria ; and one raised phlegm tinted with blood.

The patients who were thus affected with relapse of the inflamma-
tion of the pericardium suffered more frequently with symptoms of
great severity during the first than the second period of the increase
of the effusion into the sac. Thus during the first acme in seven
patients the illness was extreme, including the five in which it was
so during the second acme, and in three it was severe. In one case
the symptoms were not described.

Of the seven cases in which the illness was extreme during the
first acme, perspiration was very profuse in three; the face was
anxious, pallid, livid, or of a leaden hue, in four ; there were slight
choreal movements in one ; breathing was quick in five, the respira-
tions ranging from 40 to 48 ; pain was present over the heart in four*
of those seven patients and in two others in whom the symptoms
were less severe ; and swallowing was difficult or painful in three.

We thus see that pain attacked the region of the heart in six cases
during the first acme, and in only one case during the second acme.
The breathing also was more urgently affected during the first acme,
when they numbered from 40 to 48 in the minute ; than during the
second acme, when they ranged from 32 to 48.

On the other hand, depression and anxiety were more marked
during the second acme than the first.

The general illness was much more often extremely severe during
the first acme in those cases that suffered from a relapse, than during
the single acme in those that had no relapse. Thus of those patients
in whom there was a renewal of the acme, the illness was extreme
during the first acme of the effusion in two-thirds (7 in 10 or 11),
and severe in one-third (3 in 10 or 11) ; while of those who had no

374 A SYSTEM OF MEDICINE.

renewal of attack, the illness was extreme in only one-third of the
cases (10 in 30 or 32), severe in one-half (14 in 30 or 32), and not
severe iD one-fifth (6 in 30 or 32). In one case of the series with a
relapse, and in two cases of the series without a relapse, the symptoms
were not recorded.

Intensity of the Endocarditis accompanying the Pericarditis dwring
the, Second Acme of the Effusion; and Permanent Effect of the Endocarditis
on the Valves. — All the cases that had a relapse of pericarditis were
affected with endocarditis in an intense degree. One of the patients
had old-standing disease of the mitral and aortic valves ; and in seven
of them valvular disease was established when they left the hospital,
the mitral valve being affected in all of them, and the aortic valve
also in three. In three cases the mitral valve, which was incom-
petent during the attack, owing to inflammation of the valve, com-
pletely regained its function.

The proportion of cases in which the valves were permanently
crippled among those who were affected with relapse of the pericarditis
was much greater than among those who were not so affected. Thus
the valvular incompetence became permanent in two-thirds of the
patients with relapse of the affection (7 in 10), three of them being
affected with both aortic and mitral disease ; and in only about one-
fourth or one-third of those who had no relapse (11 in 52 and 7
others who left with lessening murmur.)

These clinical facts tend to make it probable that when there is a
relapse of the inflammation of the exterior of the heart, there is a
relapse also of the inflammation of the interior of the heart and
its valves ; and that the inflammation when thus prolonged tends to
cripple the valves for life.

Second Relapse of Pericarditis with a Third Acme of Pericardial
Effusion — In five of the eleven cases with relapse and a renewed
increase of effusion into the pericardium, after the fluid began to
•decline, there was a second relapse, and the fluid increased in quantity
for a third time. In one of those cases there was indeed a third
relapse followed by a fourth acme of pericardial effusion.

In one of the cases the effusion into the pericardium was equal in
amount during the first acme, the second, and the third, the wave of
increase rising on each occasion to the same height. In two of them
the fluid was equal in quantity during the first acme and the third,
but was less during the intermediate period of renewed increase ;
and in the two remaining cases the wave of increased effusion
lessened on each repetition, the effusion being less during the third
acme than the second, and less during the second acme than the first.

In those five cases from three to five days elapsed between the second
acme and the third.

The impulse, at its inferior boundary, was lower during the third
acme than the first in three of the cases ; and it was lower in one case
and higher in another during the third acme than the second ; while

PERICARDITIS. 375

its position was unchanged during those two periods in a third. In
one of the cases the impulse Was imperceptible throughout, and in
another it became so at the period of the third acme.

The presence of a thrill was not observed in any of the cases
during the third acme.

The friction sound is in a declining state during the third acme.
The frottement was of a definite rubbing to-and-fro character, inten-
sified by pressure, in only one of the four cases during the final acme.
In one of those patients the friction sound was double and smooth
in character; in another it was single and systolic ; in a third it was
almost [like a bellows murmur ; and in the remaining case it was
absent with light pressure, but firm pressure brought a to-and-fro
sound into existence.

Four of the five patients belonging to this group were affected
with great general illness during the final acme ; their breathing was
distressed and rapid, numbering respectively from 36 to 60 in the
minute ; while two of them had pain in the chest, and the remaining
two pain in the region of the heart.

The Area and Intensity of the Friction Sound during the Decline of
the Pericardial Effusion. — In forty-three cases the comparative area
and intensity of the friction sound were observed both when the
effusion into the pericardium was at its height, and during the period
of its decline.

(1) The friction sound spread downwards to a greater extent during
the decline than the acme of the effusion into the pericardium,
in three-fifths of the cases (26 in 43.) (2) In less than one-fourth
of the cases (10 in 43) the reverse took place, the friction sound
being more extensive, and especially downwards, during the acme
of the effusion than when the fluid diminished. (3) The area of the
friction sound extended downwards to an equal extent during the
acme and the decline of the effusion in a still smaller proportion
of the cases (7 in 43).

(1) Cases in which the Friction Sound spread downwards to a greater
extent during the Decline than the Height of the Effusion into the Peri-
cardium.— I shall consider (1) the time of occurrence ; and (2) the
duration of the downward extension of the friction sound in these
cases ; (3) the area; and (4) the character of the sound ; and the posi-
tion of the heart and its impulse and thrill ; and (5) the degree of the
general illness during the period in question.

1. Time of the Occurrence of the Downward Extension of the Friction
Sound. — The friction sound spread rapidly downwards soon after the
fluid in the pericardium began to decline in all but a very small pro-
portion of these cases. Thus the rubbing sound had already extended
downwards to its lowest position in four-fifths of the patients (21 in
26) during the first three days after the acme. During the three fol-
lowing days the descent of the rubbing sound appeared in four more
ef the cases ; but in the last of these this condition came into play quite

376 A SYSTEM OF MEDICINE.

suddenly on the twelfth, and still more on the fourteenth day after the
fluid began to lessen.

2. Duration of the Extreme Downward Extension of the Friction Sound.
— The downward extension of the friction sound lasted in these cases
for a very short period. In two-thirds of them (17 in 26) it was ob-
served during only one day, and in but two cases, or rather one, did it
last over three days. This extension downwards of the friction sound
during the decline of the fluid was therefore short and transitory.

3. Area of the Downward Extension of the Friction Sound. — When
the fluid in the pericardium, after having reached its height, lessens
in quantity, the heart descends, its impulse is lowered by from one to
two intercostal spaces, and the friction sound extends downwards.
The area of the rubbing noise is, as a rule, by no means limited to the
area occupied by the heart itself; but spreads downwards to an extent
varying from one to four inches below the lower boundary of the
heart. The friction sound does not, in these cases, diffuse itself downwards
over the whole breadth of the region below the heart ; for it is usually
silent over the front of the abdomen in the epigastric space ; while it
is present along the right and left seventh and even eighth costal
cartilages that bound that space to the right and left ; and over the
ensiform cartilage that dips downwards from the lower end of the
sternum at the centre of that space.

The rubbing noise is usually heard with equal intensity over the
right and the left seventh and eighth cartilages. Sometimes indeed
the sound was louder and more extensive over the right seventh and
eighth cartilages than the left ; and it appeared as if in those cases the
cartilages that rested on the liver conducted the sound better than the
cartilages that covered the stomach. The contrast between the harsh
rubbing noise heard in some cases over those cartilages, and the com-
plete silence present over the intervening epigastric space was very
remarkable.

The friction sound, besides travelling downwards, extended also up-
wards in one half of these cases (14 in 26) when the fluid in the peri-
cardium lessened, and the heart and its impulse descended. In one
third of the patients (8 in 26) the area of the friction sound was equally
high over the front of the chest during the period of the acme of the
effusion into the pericardium, and that of its decline.

In four instances the whole area of the friction sound shifted bodily
downwards when the pericardial effusion lessened, and the heart and
its impulse descended ; so that the upper and lower borders of that
area were then simultaneously lowered. In these four cases while
the lower boundary of the region of friction sound descended from
the sixth to the seventh cartilages ; its upper boundary descended v\
two of them from the second left cartilage to the third, and in the
other two from the third cartilage to the fifth.

In two-thirds of those cases (16 in 26) in which the friction sound
extended much downwards after the acme, it was also audible up to
the top of the sternum. In three of those cases the friction sound so

PEBICARDITI8.

Fig. 46.

Fio. 47.

For previous views of this case, see Figs. 44, 45, page S50.

Fitf. 46, from it housemaid aged 20, affected with Theumatic pericarditis (33, tee p. 319).

Period of the decline of the pericardial elusion after the first nemo.

Fifth day after the acme of pericardial effusion, seventh day after the first observation
of the friction sound and increased pericardial dulness, and ninth day after admission.

The pericardial effusion has lessened much since the period of the acme, its upper
boundary (1, 1) having descended from the middle of the manubrium to the middle "

amount of fluid between the under surface of 4he heart and the floor of the pericardia
(3, 3}, though still considerable, has tptidelitl; Jessened by at least one half. The right
ventricle, the inner or left half of the right auricle, and the apex and front of the left
ventricle are exposed ; but the great arterue are covered with lung.

The region of pericardial duimu (see the black apace) probably extends from the
' Mean Ae third cartilages, and from the fourth left cartilage,

middle

a between t

and from a little to the right of the hwer half of the sternum tt . .

lower boundary of the heart is behind -the upper edge of the sixth rib, and the top of the
ensiform cartilage.

The impulte has descended from the third space during the acme, to the fourth and
fifth spaces. (See the circular and curved lines in those spaces.)

A double friction snuiwi (nee the zigzag lines — ayatolie linaa thick, diaatolio thin), which
is more harsh on making pressure, is heard over the whole length of the sternum ;
which is most intense at the middle of the bone, and is louder at its lower end during
inspiration, and over the manubrium during expiration ; a creaking sound is andible
during systole over the third, fourth, and fifth loft spaces ; and a friction Bound is heard
to the right of the lower portion of the st "*"

this figure.)

t spaces i and a fr
(The nipple is t

-s Figs. 44, 45 (page 350), 46, and 48.
■ial effitlioa ; second view, tak~ **
slight and transient second acme, when the fluid was again declining.

Bemarkable extension of the friction sound over the greater part of the front of the
chest, and especially downwards.

Tenth day after the first acme of pericardial effusion ; twelfth day after the first obser-
vation of the friction sound and of pericardial dulness ; fourteenth day after admission ;
and four days before the occurrence of a second acme.

VOL. Tf. C C

iTO

A SYSTEM OF MEDICINE.

The pericardial effusion has diminished. There is therefore less fluid between the
under surface of the heart and the floor of the pericardium (3, 3) ; the roughened front of
the heart is more dry, and is closer to the corresponding roughened surface of the peri-
cardial &sc ; the heart (2, 2), which is somewhat enlarged, is lower in position ; and the
upper boundary of pericardial effusion (1, 1) is lower, and its inferior boundary is some-
what higher than when Fig. 46 was taken five days previously. The whole right
ventricle, the left border of the right auricle, and the apex and front of the left ventricle are
exposed ; while the great arteries and part of the conns arteriosus are covered with lung.

The region of pericardial dulnea (see the black apace), which is bounded above by the
fourth cartilage, and below by the sixth cartilage, is probably rather leas extensive above,
below, and to the right, than in Fig. 46, taken on the ninth da; after admission.

The impulse is lower, stronger, and more extensive than in Fig. 46, and is present
from the third to the fifth spaces, and up to or beyond the mammary line (see the
circular and curved lines in those spaces) ; and gives therefore direct evidence that the
heart is lower in position, and that the effusion has lessened.

The friction tounet (see the zigzag lines — systolic lines thick, diastolic thin) has gained
a very great extension, being audible over a great part of the front of the chest, from
the first costal cartilage to the seventh left and the eighth right cartilages ; and from the
top of the sternum to the bottom of the ensiform cartilage. This extension of the friction
sound is especially marked downwards, where it extends for about four inches below the
heart, and is lower on the right than on the left side, reaching over the right eighth
cartilage in front of the liver, and the seventh left cartilage in front of the sternum.
Thia is the reverse above, when the rubbing sound extends four inches to the left, and
only about two inches to the right of the sternum.

The friction sound is harsher than it was yesterday ; over the midatarnum it is louder
during the systole than the diastole ; and it is intensified by pressure ; over the manu-
brium, the to-and-fro sounds are equal ; over the ensiform cartilage, friction sound ia
present during inspiration ; it is creaking during systole over the second and first
spaces ; aud it becomes louder below the niainina during inspiration.

For previous views of this case, see Figs. 44, 15, page 850, and 46, 47 on the preceding

Fig. 48, from a housemaid affected with rheumatic pericarditis (33, seep. 31B).
Third acme of pericardial effasian (the second acme was very slight and transitory).
Thirteenth day after the Erst seme ; eighteenth day after admission.

PERICARDITIS. 379

The pericardial effusion is greatly increased, but its extent and limits are not definitely
described. If we compare this third acme with the first acme (Fig. 46, page 377), we
find that the distended pericardium, though it contains less fluid, is wider in relation to
its length ; that the heart is larger ; and that the lower boundary of the heart is lower,
in this the later and renewed, than in that the earlier and original acme. In the first
acme the heart was not vet enlarged, or, being compressed by the fluid in the distended
sac, was possibly lessened in size ; and the walls of the pericardium were still unyielding,
so that the swollen sac took the form that it would naturally take if artificially distended
with fluid (see Figs. 33, 34, page 305). In this, the third acme, the heart has become
enlarged both by pericarditis and by mitral endocarditis ; the lower boundary of the
heart, although elevated by the accumulated fluid, is lower than in the first acme ;
and the walls of the pericardium have become thicker, softer, and more yielding than in
health, so that the distended sac yields to the right and left, where it meets with no
resistance, to a greater extent than it does upwards and downwards, where it meets with
much resistance ; and is therefore wider in relation to its length than it was during the
first acme, when its form was more purely pear-shaped. The whole front of the heart
and great vessels is exposed, including the right auricle and ventricle, the- apex and
front of the left ventricle, the pulmonary artery, and the ascending aorta within the
pericardium. The fluid has evidently interposed itself to a greater extent between the
surface of the lower portion of the front of the heart and the walls of the chest during
this, the third acme, than during the first acme.

The region of pericardial dulness (see the black 8}»ace), the limits of which are not
described, corresponds in general form and outline to the pericardial effusion, and evi-
dently extends more to the right and left, and less upwards and downwards than it did
during the first acme.

The impulse has again been elevated at its lower boundary, and this time from the
fifth space, as in Fig. 47, page 377, to the fourth space, where it is feeble ; and it is
felt over the third space during expiration. (See the concentric circles in those spaces.)
The lower boundary of the impulse is therefore lower by one space than it was during the
first acme, when it occupied the third space (see Fig. 45, page 350).

The friction sound (see the zigzag lines— systolic lines thick, diastolic thin) is softened,
and is limited in area, being heard over the middle region of the sternum, where it is
double, and although frictional in character is almost like a bellows murmur ; and is
audible over the second and third spaces during the systole.

Later progress of this case. — On the following day, the nineteenth after admission,
the friction sound was almost creaking, or like the sound made by rubbing with sand-
paper, over the second and third left spaces. On the twenty-first day, or the fourth after
the third acme, the extent of dulness over the pericardial region had lessened ; and a
double friction murmur, which was not rhythmical with the sounds of the heart, was
audible over the base of the right ventricle, and became harsh on pressure. The friction
murmur was still heard on the following day, but after this it was scarcely audible.

covered the front of the chest as to be audible up to the clavicles,
while in one of them it reached the first cartilage. In the whole
of these cases the friction sound extended from two to nearly four
inches above the actual seat of friction. The region of pericardial
dulness was limited above in all but three of the patients by the
third intercostal space or the fourth cartilage ; and the space between
this limit and the top of the sternum nearly measures the extent to
which the frottement extended above the seat of the friction

When the fluid in the sac declines, the roughened heart rubs against
the roughened pericardium, and in doing so bears directly upon the
lower half of the sternum with which it is almost in contact ; owing to
the removal of the anterior layer of the fluid, and the despent of the
heart aud its impulse. The sonorous vibrations excited by the move-
ments of the heart are directly conveyed to the sternum, and that
bone and the costal cartilages attached to it act as a sounding-board
and transmit the rubbing noise in all directions.

c c 2

380 A SYSTEM OF MEDICINE.

In three of the cases the sound was audible over the whole front of
the chest. Usually, however, it extended only slightly to the right,
and over a greater extent to the left of the loweT half of that bone.
As a rule, therefore, the rubbing noise extended in a straight line
from the top to the bottom of the sternum, and there it divided into
two diverging lines, one along the right, the other along the left seventh
cartilage, where they form the boundaries of the intervening epigastric
space. The area of friction sound thus extending along the sternum
and the right and left seventh cartilages closely resembles in shape
the inverted letter J^. Since however the friction sound also extends
downwards over the ensiform cartilage, its area is somewhat like a
trident with a short central prong.

In one-fifth of the cases (5 in 26) the area of the friction sound
dwindled during a short period after the time of the acme, and then
suddenly expanded, and especially downwards, at a later date during
the decline of the effusion.

In one case the friction sound alternately lessened and increased in
area and intensity during the ten days that intervened between the
termination of the acme, and the time at which the frottement had a
remarkable downward development

4. Character and Intensity of the Friction Soxind ; and Position of
the Heart and of its Impulse and Thrill. — At the time that the fric-
tion sound spread downwards when the effusion lessened, the sound
was intense, loud, and of a marked character in all but three or four
of the twenty-six cases that belong to the group under consideration.

In nine of those cases the friction sound was creaking (6), or
grating (3) ; in thirteen it was harsh and loud ; and in four its
intensity was not specified.

The friction sound in the twenty-six cases under review, as a rule,
gained in intensity as it gained in area ; and lost in intensity as it lost
in area. Thus in all but six of the cases, the rubbing noise became
more harsh when it increased in extent ; and in all but two of them it
became softer when it lessened in extent.

When the effusion lessened, the impulse, while it descended at its
lower boundary, was still felt beating in the higher spaces into which
it had been forced during the acme in fully one-fourth of the cases
(5 in 19) : while, curiously, the impulse ascended to a higher space
than it had occupied during the acme in six other patients.

A thrill was felt over the heart in five of these twenty-six cases
during the acme of the effusion. In four of these the thrill disappeared
when the effusion lessened, and in one it remained, though with
lessened intensity. In three other patients a fresh thrill came into
play during the decline of the fluid ; in two of them over the apex, and
in the other case at the second space.

In these twenty-six cases, when the effusion into the pericardium
lessened, the heart, relieved from the pressure of the fluid, descended
into its natural space, and even below and beyond it. The heart thus
relieved, beat with increased force ; its right cavities were enlarged,

PERICARDITIS* 381

owing to the increased supply of blood from the system, and the con-
tinued resistance offered to the flow of blood through the compressed
lung and the incompetent mitral calves ; and, as the general result,
its anterior walls played with greater power and noise upon the
sternum and cartilages, and the friction sound was heard over a
largely increased area.

5. Degree of the General Illness. — At the time that the area of the
friction sound was most extensive, especially downwards, when the
fluid in the pericardium lessened, twenty of these twenty-six cases
were less ill or in better health, three of them were probably better,
and three were worse in health than they were during the acme.

In a large proportion of the cases under review, when the fluid in
the pericardium lessened, the heart descended and gained freedom of
movement and power, and the general health improved; and as a
natural result the friction sound increased in extent, and especially
downwards. The comparatively dry roughened surface of the heart
rasped to and fro upon the roughened surface of the pericardium.
These influences combined to cause the increased harshness and ex-
tension of the friction sound; which, starting from its focus of greatest
intensity over the right ventricle, radiated in all directions over and
beyond the region of the heart and the great vessels, outwards to the
right and left, upwards to the summit of the sternum, and especially
downwards over the ensiform cartilage and the diverging right and
left seventh and eighth cartilages.

(2) Cases in which tJte Friction Sound was audible downwards to a
greater extent during than after the Acme of the Effusion. — In ten
cases the friction sound was audible to a greater extent downwards
when the effusion was at its height than during its decline.

Two series of influences are at work in these cases, acting at different
times, to enlarge the area of friction sound during the acme, and to
lessen it during the decline of the effusion.

1. When, during the acme, the friction sound is creaking or grating,
being sometimes associated with a thrill, over the right ventricle, and
when it radiates thence in all directions, softened in character, beyond
the region of actual friction, the heart, raised by the increased effusion
into the narrower space at the upper part of the cone of the ohest,
beats with increased force directly against the sternum, the higher
cartilages, and their spaces, and so excites an intense and widely
diffused friction sound.

When the fluid lessens the heart descends and is again partially
covered with lung ; and as it beats over a smaller extent, and with less
pressure against the sternum and cartilages, the friction sound lessens
in intensity and area.

2. When the friction sound is of moderate intensity and extent
during the acme, it sometimes lessens during the decline of the
effusion. Tn these cases the impulse at its inferior boundary is not
notably lowered, while it disappears from the upper spaces. In some
of these cases the action of the heart is throughout feeble ; and probably

•t

382 A SYSTEM OF MEDICINE.

in others of them slight adhesions take place at the apex and septum
which restrain and lessen the descent of the heart/the rubbing move-
ments of the right ventricle, and the area and intensity of the friction
sound over the higher intercostal, spaces.

(3) Cases in which the Friction Sound extended Downwards to an
equal extent during and after the Acme of the Effusion. — In seven
cases the friction sound was of equal extent during the two periods,
when the fluid in the pericardium was at its height and was declining.

Character and Intensity of the Friction Sound during the Decline of
the Effusion, and the Relation of the Intensity to the Area of the
Friction Sound.— I shall examine these conditions during three
periods in the order of time of the decline of the effusion, (1) the
beginning of the decline of the effusion; (2) the gradual and the
interrupted progress of the decline of the effusion ; and, (3) the final
dying away of the friction sound ; and (4) shall then inquire into cases
in which the ordinary friction sound gave place to a friction murmur
towards the end of the attack.

1. Character and Intensity of the Friction Sound at the Beginning of
the Decline of the Effusion. — When the amount of fluid in the pericar-
dium began to lessen, if the friction sound increased or diminished
in intensity, it usually increased or diminished also in area.

As a rule, the friction sound increased in intensity and area in those
cases in which the frottement extended further downwards after than
duringjthe acme; while it lessened in intensity and area in those in which
the friction sound spread more downwards during the acme than after it.

When the friction sound spread downwards during the decline of
the effusion, the sound gained in area in nearly every case (25 cases
in 26), and in intensity in two-thirds of the cases (18 in 26).
We thus see that while an increase in the intensity of the frotte-
ment almost invariably leads to an extension of its area — for I find
only one exception to this rule — and while a diminution of its intensity
likewise generally causes a diminution of its area; yet, in certain
cases, the friction sound gains in extent, though it lessens (4 cases in
43) or remains unchanged (3 cases in 43) in intensity. This is
explained by the lowering of the heart, and the consequent descent of
its impulse during the decline of the effusion in all the cases — the
surface of the roughened organ being thus brought into more exten-
sive contact with the sternum at its lower half, and with the corre-
sponding costal cartilages : while in the small number of cases in
which, although the friction sound gains in area, it is lessened or not
increased in intensity, the heart, released from its confinement in the
contracted space of the chest above, where it rubbed with force and
noise against the sternum and cartilages in front of it, finds itself
moving with ease in its proper place in the lower and wider part of
the chest, and so presses with less force and less noise than before on
the sternum and cartilages in front of it. The causes of the increased
intensity as well as area during the decline of the effusion, which, as

PERICARDITIS. 383

we have just seen, occur in the great majority of the cases under
examination, have been already considered at page 381.

2. The Gradual and Interrupted Progress of the Decline of the Effusion.
— In thirty- one of the forty -three cases now being examined, the
effusion in the pericardium steadily and gradually declined, and, as we
have already seen, in twelve of them, owing to relapse, the effusion
after beginning to decline, again increased in quantity generally once,
sometimes twice, and on one occasion even a third time.

The progress of the friction sound during the decline of the effu-
sion was rarely uniform. It was in several of the cases silenced
and suspended for a time (6 in 43); it more frequently, however, when
in full play, became feebler during a short period, and then again
louder (13 in 43). In a larger number of the cases the frottement,
after attaining to its greatest intensity, more or less steadily lessened
in loudness and extent until it finally disappeared (23 in 43).

In one case the friction sound suddenly and permanently disap-
peared after an attack of syncope. In this patient, a girl, the friction
sound vanished when the action of the heart became enfeebled ; and
she died in a second attack of syncope a few hours after the first
attack.

Cases in which the Friction Sound vanished and reappeared during
the Decline of the Effusion. — In six of the forty-three cases under
review and in one other patient the friction sound disappeared and
reappeared during the decline of the effusion. In five of these cases
the frottement was absent for from two to three days, and in one of
them for about seven days.

In three of the patients the friction sound, as in the case just
referred to, vanished for- a time after the application of leeches for the
relief of pain.

If we view these cases as a whole, and take into the survey the
case of the female servant who died from a second attack of syncope,
the first attack having permanently quenched a loud and pervading
friction sound, we shall, I think, see that when the force of the heart's
action and the volume of the blood in circulation are lessened — either
by immediate syncope, by loss of blood from leeching, by diarrhoea,
sickness, or other exhausting influences, by pain in or over the organ,
by extreme distress in breathing, or more often by a combination of
several of these lowering agencies — then the nibbing sound, when in
full play, may gradually or suddenly vanish, and may suddenly
rekindle into full volume after a longer or shorter period of silence.

Cases in which the Friction Sound lessened and then increased in Area
and Intensity during the Decline of the Effusion. — In thirteen of the
forty-three cases under examination, and in three other cases, the
friction sound, when in full play, lessened in extent and intensity, and
after a longer or shorter interval again resumed more or less nearly
its full sway.

In one of these sixteen cases the diminution of the frottement was
associated with sudden faintness ; in two with loss of blood from

384 A SYSTEM OF MEDICINE.

leeching ; in eight with increase of the general illness — in seven of
which as the health improved the friction sound resumed its extent
and intensity — in two with an amelioration of the symptoms ; in two
with irregularity and intermission of the pulse and the action of the
heart ; and in two the state of the health is not described.

In eight cases the diminution of the friction sound corresponded
with an increase of the general illness, which showed itself generally
by an anxious expression, accelerated and difficult breathing, and pain
over the heart ; sometimes with cough and rusty phlegm ; and some-
times with abundant perspiration. With the renewed increase of the
rubbing sotmd there was in all these cases, save perhaps one, a
marked improvement in the health ; manifested usually by a compa-
ratively cheerful expression, more easy respiration, lessening or absent
pain over the heart, and assuaging of cough with diminution of
phlegm.

(1) Duration and (2) Progress of the Friction Sound during the
Decline of the Effusion. — (1.) Duration. — The friction sound lasted for
a very variable period during the decline of the disease.

In the group of thirty-one cases that had no relapse and no return
of the effusion into the pericardium, the friction sound lasted from
three to niueteen days, its average duration being ten days.

In the group of twelve cases that Suffered from relapse with
return of the effusion into the pericardium, the friction sound lasted
from eleven to twenty-two days, its average duration being fifteen
days.

(2) Progress. — Cases in which the Maximum Development of the Friction
Sound took place during the Decline of the Effusion. — Period between
the Maximum Development and the Cessation of the Friction Sound.
— In thirteen of the nineteen cases under examination the area
of the friction sound steadily lessened from the day of its maxi-
mum extension to that of its final disappearance. It contracted
gradually from right to left and from left to right, from above down-
wards and from below upwards, towards the centre or focus of actual
friction. It thus died away from beyond and over the great vessels,
the right auricle, and the apex, and from the region that it had pre-
viously occupied below the lower boundary of the heart. Towards
and over the region of actual friction it step by step concentrated
itself, and after lingering over the right ventricle with softening tones
for a shorter or longer period, it quietly died away. Tn about one-half
of the cases (6 in 13) this subdued sound outlived the period
of its greatest intensity and extent for from one to two days ; in the
remainder, for from three to seven days ; and in only one did it
exist for nine days.

The front of the right ventricle was, as I have just said, the last
home of the friction sound, as it had been indeed the seat of its
birthplace. As the position of that ventricle varied in different
patients accordingly as the heart was larger or smaller in size, higher
or lower in situation, the final seat of the softened friction sound

PERICARDITIS. 385

varied in different cases, from the left third and fourth cartilages to
the fifth or sixth ; and from the middle third of the sternum to the
ensiform cartilage.

There was a general but by no means invariable correspondence
between the area of the friction sound on its last observation, and
the position of the impulse.

In only three of the nineteen cases now under review did the im-
pulse occupy the same position when the friction sound was heard
for the last time, as when it was most extensive. In four cases it
had descended at its lower boundary from the fourth space to the fifth ;
and in four cases it had disappeared from the upper space at the time of
the last observation of the frictioQ sound, when compared with the time
at which it was predominant. There was therefore in these patients a
tendency for the heart and its impulse to take up a lower position, and
to be covered to a greater extent with lung as the friction sound was
about to disappear, and the case advanced towards its termination. On
the other hand, in two other cases the impulse gained ground above, and
appeared in the second space for the first time when the frottemerU
was heard for the last time.

The descent of the impulse both above and below when the case
advances to recovery and the friction sound is dying out, appears to me
to be the natural bias in these cases when the heart is not adherent,
and descends irto its natural situation; when the right ventricle
and pulmonary aitcry are not greatly enlarged ; and when the upper
lobe of the left lung expands in front so as to cover the pulmonary
artery and the upi cr portion of the right ventricle.

When, however, the heart becomes more or less adherent ; when
the pulmonary artery and right ventricle become enlarged owing to
mitral regurgitation; when mitral incompetence is combined with
adherent pericardium ; when the walls of the pericardium are thick-
ened ; or when the left lung does not expand in front of the upper
border of the heart so as to cover the pulmonary artery and the
conus arteriosus ; and notably when two or more of these conditions
combine their influence, then the impulse tends to remain in or attain
to the higher intercostal spaces, and especially the second space.

In one remarkable case belonging to the group of nineteen now
under review, the friction sound was lost on the fifth day after the
acme, and reappeared on the twelfth day with greater intensity and
over a larger area than at any previous time. In three other cases
the friction sound, after gradually diminishing in intensity and area,
became suddenly reinforced ; and in two others a similar diminution
and increase of the frottement took place but to a comparatively
slight degree.

3. The final dying away of the Friction Sound. — The friction sound
offered greater variety in different cases just before the time of its
extinction than at any other period of its existence.

(1) In a very small number of the cases (4 in 43) the friction sound,
when in full play, suddenly disappeared ; (2) in two-fifths of them (16 in

386 A SYSTEM OF MEDICINE.

43) the froltcrnent, after being more or less loud up to a certain date,
Tapidly declined, and vanished in one or two days ; (3) in a fifth of them
(8 in 43) the decline of the friction sound was gradual ; (4) and in
two-fifths of them (16 in 43) the ordinary rubbing sound gave place
towards the end of the case to a friction murmur sometimes double,
and increased by pressure (8), sometimes double and excited by pres-
sure (5), sometimes single and systolic and intensified by pressure (2),
and in one case a single friction murmur was excited by pressure.

4. Cases in which the ordinary Fiction Sound gave place to a Friction
Murmur towards the end of the attack. — In fifteen patients, and possibly
in a sixteenth, a friction murmur was audible in lieu of the ordinary
friction sound towards the end of the attack of pericarditis.

We have already seen that in a certain number of cases, at the be-
ginning of the attack, the ordinary friction sound was preceded by a
friction murmur : and that in one remarkable case a friction murmur
prevailed throughout the whole course of the disease to the exclusion
of the usual rubbing sound. I would here refer to what has already
been said as to the friction murmur as it was observed during the
beginning of the attack, at pages 345-348.

In one case a systolic friction murmur audible on making pressure,
and in another case a systolic friction murmur increased by pressure,
was respectively the final sign of pericarditis.

In six cases a double friction murmur was audible on pressure
towards the close of the affection. One of the cases of this group (47,
see p. 318), a servant girl aged 20, presented on the seventh day, when
the effusion was at its height, an extension of the frottement, when
there was a double grating friction sound. On the eleventh, when
the effusion was declining, there was a feeble murmur-like friction
sound over the right auricle, to the right of the lower sternum ; and
later in the day the heart sounds were natural over the lower
sternum, but pressure brought out a double friction murmur not
quite rhythmical with the sounds of the heart. A systolic friction
sound was audible over the left fifth cartilage. On the fourteenth
day a faint double murmur was still excited by pressure over the lower
sternum. This was the last day of undoubted pericardial friction
sound, but on the eighteenth day a double grating friction sound
burst out on pressure at the end of a deep breath, that was probably
pleuritic.

In several of these cases a friction murmur either prevailed over
the right ventricle during the early stages, or was limited to certain
favourite spots, such as the right auricle, when the friction sound was
at its height Later, the friction murmur gradually again developed
itself as the harsher friction sounds became softened, and at length
spread itself over the heart. Soon, however, this disappeared as a
constant sound, but for one or two final days of the disease it could
be again awakened by making pressure over the right ventricle. Several
of these cases ended with a double friction murmur that was intensified
by pressure.

PERICARDITIS. 387

In addition to these cases in which the friction murmur prevailed
exclusively towards the termination of the disease, there were others
in which, while the friction sound was harsh, and even creaking or
grating over the focus of its greatest intensity, it was yet so toned down
towards the lewer margins of the area of rubbing sound, especially at
and below the ensiform cartilage, that a double friction murmur was
audible there, when a loud double grating noise was heard over the
right ventricle. In some of the cases also, when a creaking, or grating,
or rasping sound prevailed with a thrill over the right ventricle, a
double friction murmur was audible over the right auricle. Here the
stormy noises prevailed over the forcible ventricles, and the soft mur-
muring sounds over the passive auricle.

The occurrence of a creaking, grating, or harsh friction sound
depends on the force with which the heart contracts and presses
against the cartilages and sternum, and on the roughness of the lymph-
covered rubbing surfaces ; the creaking sound being mainly excited
by pressure, the grating noise by the roughness of the two surfaces
when the one rubs actively upon the other. The friction murmur, on
the other hand, is due to the gentle or restrained movements of the
heart, and the comparative smoothness of the rubbing surfaces all
over the heart, that occur towards the end of the attack. It may
also be present in its softest and most murmur-like tones over the
comparatively smooth and feeble right auricle, and below the heart
over the epigastrium, when the attack is at its height, and is speak-
ing with the greatest harshness and noise over the more vigorous
parts of the OTgan ; and when the harsh friction sound is evidently
softened and rendered murmur-like during its transmission through
the fluid intervening between the seat of active friction, and the
comparatively distant surface of the chest over the right auricle or
the epigastrium.

I have already given the distinctions between the friction murmur
and the valvular murmur when inquiring into the occurrence of the
former during the first blush of the affection. The rules that apply
to the distinction of the friction murmur during the early period of the
attack apply also to its distinction during the later period These
rules have been already given at pages 346-348, but the following is a
rSsumS of the more important distinctions between the friction murmur
and the valvular murmur : —

The friction murmur is not rhythmical with the natural heart-
sounds, but the two sounds are heard side by side ; the valve murmur
is rhythmical with the natural heart-sounds, and the two sounds are
in perfect unison. The friction murmur does not begin with an accent
or shock, but is of equal tone throughout ; the valvular murmur begins
with an accent or shock, the accent or shock of the corresponding first
or second sound which serves as the starting-point for the murmur.
The friction murmur is greatly intensified, and is often altered in tone
on pressure ; the valvular murmur is brought nearer to the ear by
pressure, but is not altered in tone.

388 A SYSTEM OF MEDICINE.

There are certain differences between the early and the late friction
murmur, although their characters in the main correspond.

In situation the early and late friction murmurs for the most part
correspond, being generally seated over the base or body of the right
ventricle. The early friction murmur was situated to the left of the
sternum in six cases (6 in 8), in four of which it was also heard over
the sternum ; and it was present over the sternum alone in two cases
(2 in 8). The late friction murmur was audible over the sternum
alone in four cases ; over that bone and to the left of it in five ; to the
left of the sternum alone in four; and to the right of the sternum in three
cases, including one case in which it was also audible to the left of the
sternum. From these figures it would appear that the early friction
murmur is always situated over the right ventricle ; but that while
the late friction murmur is present over the right ventricle in seven-
eighths of the cases, it is audible over the right auricle in one-fifth of
the cases.

The late friction murmur is smoother and more equal in tone ; more
prolonged ; less rustling and more murmur-like; more alike in tone and
intensity during the systole and the diastole ; varies less from day to
day ; and lasts much longer than the early friction murmur. Pressure
intensifies both of them and often modifies their tone, but I think that
the early friction murmur is more frequently converted by pressure
into a true rubbing sound than the late friction murmur.

The complication of a co-existing aortic murmur with the friction
murmur is more frequent during the late than the early period of the
affection.

The Character and Tests of Pericardial Friction* Sound.

I shall, before concluding the subject of pericardial friction sound,
briefly consider the characteristic nature and tests of that sound, in-
cluding its character and rhythm ; its position and extent ; the influence
exercised over it by respiration ; its variation from day to day in cha-
racter, intensity, rhythm, position and extent ; and finally, the effect
upon it of external pressure over the region of the pericardium during
pericarditis, or the pressure test of friction sound.

Character of the Pericardial Friction Sound. — The friction sound
when in full play, and of its usual to-and-fro character, speaks for itself.
I have already illustrated, in the preceding pages, the clinical history
of the forms and variations, the growth, ripening, and decline of the
friction sound. When the friction sound is smooth and soft, almost
resembling a murmur, or when a friction murmur is present, the sound
no longer declares itself, from its very nature, to be of a rubbing quality,
and requires for its distinction that other points shall be considered
besides the tone, nature, and to-and-fro quality of the sound. The
clinical history and distinguishing characters of the friction murmur
during the early advance and the late decline of the attack of peri-
carditis have been given respectively at pages 345 and 387.

PERICARDITIS. 389

The Rhythm of the Friction Sound. — In a large proportion of my
cases it was noticed that when the friction sound was not of its com-
pletely developed to-and-fro and rubbing character, that is, during both
the advance and the decline of the pericarditis, the healthy sounds of
the heart were heard along with the double or single friction sound.
The natural sounds of the heart and the friction sounds were never
welded or incorporated together, but were each of them heard separately,
and, so to speak, side by side. They did not seem to begin or end
together ; and although they were both sounding at the same time, they
yet appeared to be completely separate and apart. They were not,
therefore, rhythmical with each other. That the natural heart sounds
are in play within the period of the to-and-fro friction sound is evi-
dent, for when that sound becomes sufficiently loud and continuous,
whether by the natural advance of the disease, or by pressure made
from without, the sounds of the heart are overwhelmed, being masked
by the predominant rubbing noises.

When the to-and-fro friction sound is loud, harsh, and in full play,
the systolic and diastolic sounds being equal in duration— though
rarely in loudness, the systolic sound being the louder — each sound
seems almost to fill up its respective space, leaving two very short
intervals of silence between the two sounds. These two friction sounds
never begin with an accent or shock, but they commence, continue,
and end as a rule with the same tone throughout. In these respects
they differ from the natural heart sounds. The first sound always ends
in a shock, followed by a short but definite space between itself and
the second sound ; and the second sound consists in a short shock,
followed by a prolonged space between itself and the first sound. The
mitral murmur always begins with a shock or accent, the shock of the
first sound, and the munnur fills up the space more or less completely
between that shock and the second sound. The diastolic aortic mur-
mur also commences with a shock or accent, the shock of the second
sound, and it usually fills up the space but not always completely,
between that shock and the first sound. The absence of a commenc-
ing shock or accent from the friction sound or friction murmur and
the presence of a commencing shock or accent with the valve
murmurs distinguish those two classes of sounds from each other.

The first contraction of the ventricles precedes by an appreciable
period the flow of blood from them into the great arteries ; and after that
flow has ceased, the exterior of the heart is still in motion. The play
of the surface of the heart against that of the pericardium therefore pre-
cedes, accompanies, and follows the natural first sound of the heart, and
precedes and accompanies the coinciding valvular murmur if present.
The closure of the aortic valve precedes the second sound by the tenth
of a revolution of the heart's action. The diastolic frottement therefore
both precedes and follows the second sound ; and accompanies a diastolic
murmur, if present, throughout its whole period. The friction sound
being made by the moving exterior of the heart, is in relation to the
healthy heart sounds and the valvular murmur, which spring from the

390 A SYSTEM OF MEDICINE.

interior of the heart, as if it were made, so to speak, by an instrument
playing outside the room, while they are made as if by an instrument
playing inside the room. The friction sound is therefore a surface
noise, working apart from, and often over-riding the healthy heart
sounds and the valvular murmurs. The healthy heart sounds and the
valvular murmurs are, on the other hand, internal noises made simul-
taneously and by the same parts, and playing together inseparably and
in unison.

When listening to the two sounds, the frictional and the natural
heart sounds, playing together but not in concert or unison, I have
found it very difficult to say whether the systolic friction sound com-
menced before the first sound of the heart or not For the reasons
just given, however, and that a considerable space of time intervenes
between the beginning of the systole and its final shock, amounting
to about two-fifths of the healthy revolution of the heart's action, it
is evident that the commencement of the systolic friction sound must
precede the final shock of the first sound. In one case I heard a short
brush at the beginning of the systole, and this no doubt represents the
natural beginning of the prolonged systolic friction sound. As a rule
the systolic friction sound is of equal tone throughout, whether it is
creaking, grating, rubbing, or rustling ; but in one instance that sound
became suddenly less loud about the middle of its course, and re-
mained so to the end of the systole, the second half of the sound being
weaker than its first half.

In one instance a systolic brush, excited by pressure, occupied the
latter two-thirds of the systole ; in another a systolic whiff, excited by
pressure, extended into the diastolic period ; and in a third, a double
brush was excited by pressure, the systolic being the longer, and each
brush occupied a part of the systole and a part of the diastole. I state
these signs as I heard them, but cannot account for them.

The diastolic friction sound presents much greater variety in cha-
racter and rhythm than the systolic friction sound. While the sys-
tolic sound is usually continuous through the whole of its proper period,
the diastolic friction sound is often of short duration ; when it is, I
believe, usually present about the beginning of the diastole, and when it
accompanies but is separate from the natural second sound : in one
instance, however, the natural second sound was followed by a diastolic
graze. Sometimes there was a double graze or rub during the diastole ;
when the entire friction sound resembled the noise made by sharpen-
ing a scythe, having one forward or systolic, and two backward or
diastolic strokes. When the friction sound was to-and-fro, the second
sound appeared generally to be equal in duration, but not in loudness,
to t".. first. When a creaking sound was present it was mostly limited
to the systole : this was not so, however, with the grating noise, which
was usually a double sound.

The diastolic sound was usually equal in intensity and length to the
systolic over the right auricle, both sounds being in all but one instance
soft in character. This double soft to-and-fro sound over the right

PERICARDITIS. 391

auricle was evidently transmitted, softened during its transit, from the
loud speaking right ventricle, through the fluid, to the cartilages in
front of the right auricle*

The diastolic friction sound was often absent, and, relatively to the
systolic friction sound, was always short and feeble over the apex. In
more than one instance, in adults, the diastolic friction sound at the
apex appeared to have in it a peculiar twist.

Respiration exercised in many of my cases a definite and speaking
influence upon the area, and in a few of them upon the intensity of
the friction sound. The friction sound became more loud or harsh in
three cases during expiration, and in four during inspiration ; and in
one the frottement disappeared at the end of a deep breath.

The area of the friction sound increased below during inspiration in
a large number of cases, or thirty-one, while in a much smaller number
of instances, or eight, it increased above during expiration.

The Friction Sound varied in character, intensity, rhythm, and posi-
tion from day to day. The clinical history contained in the previous
pages of the friction sounds during pericarditis is pervaded throughout
with instances of the great daily variability of the friction sound in all
its relations. This changing condition of the friction sound during
the successive phases of the disease is one of the important characteristic
features of that sound. This feature has been already abundantly
illustrated.

Position and Extent of the Pericardial Friction Sound. — Dr. Stokes1
in 1834 stated that the friction sounds in pericarditis are audible
generally only over the region of the heart. I stated independently,
in 1843, that I had never heard the friction sounds beyond the region
of the heart.2 We have seen in the previous pages that during the
advance of the effusion, and usually during its acme, the friction sound
is limited to the region of the heart, but that in certain cases with a
thrill, the friction sounds spread during the acme from the seat of the
thrill as from a focus, in all directions, over the front of the chest, and
especially downwards.

Dining the period of the decline of the effusion, the friction sound, as
we have seen, also often extends beyond the region of the heart, over
the front of the chest, and especially downwards to the seventh and
eighth, and even the ninth cartilages (see pp. 376, 380). The various
changes in the area of the friction sound are given in the previous
pages, and to those I refer for the more extended study of this subject.

The position, limitation, and extension of the pericardial friction
sound supply characteristic differences between pericardial friction
sounds and endocardial murmurs.

*&.

The Effect of Pressure with the Stethoscope over the region of the
Pericardium during Pericarditis on the Friction Sound ;orihe Pressure
Test of Pericarditis. — I called attention in 1843, in my paper on the

1 Dublin Journal, iv. 60.

1 Situation of the Internal Organs. Prov. Med. Trans., xii. 62.

392 A SYSTEM OF MEDICINE.

situation of the internal organs,1 to the effect of pressure made with the
stethoscope over the region of the pericardium in rheumatic pericarditis,
in intensifying or even bringing into play a pericardial friction sound.
Since then Dr. Walshe — who, in the British and Foreign Medical
Review, very kindly reviewed my paper just referred to, soon after its
publication, and Dr. Stokes, independently observed this sign. This
effect of pressure is thus spoken of by Friedrich. " Sehr brauchbar
is das von Sibson, Walshe, und Stokes, angegebene Zeichen, das
namlich Eeibungs gerausche bei Druck mit dem stethoskop st&rker
werden, was allerdings Endocardial Gerausche nicht thun." 2

The pressure test shows itself in two ways, (I.), when pressure over
the region of the heart elicits a friction sound that was previously
absent ; and the other, (II.), when pressure made over the seat of a fric-
tion sound intensifies, changes, or modifies that sound.

I. Influence of Pressure over the region of the Heart in exciting a
Friction Sound not previously audible (see Table I. at p. 328). — Pres-
sure made with the stethoscope over the region of the heart elicited a
friction sound not otherwise audible in twenty-nine of the forty-four
cases that are included in the tables of cases of pericarditis given at
pages 313 — 327, and in the special Table at page 328, in all of which
cases the acme of the pericardial effusion was observed. As might
be expected, it was usually (1) during the period of the commencement
of the attack or (2) that of its decline that this sign was observed ;
and a friction sound otherwise latent was also thus brought into play
by pressure (3) at the time of the acme of the effusion in four patients
whose cases have already been touched upon at page 359, and in one
case during a second acme of the effusion.

1. Friction Sound excited by Pressure during the onset and early period
of the attach of Pericarditis. — In eight cases, as has just been stated,
the attack of pericarditis first declared itself by a friction sound induced
by pressure over the region of the heart. As a rule this sound, so
awakened, was smooth in character. In three instances it appeared as
a single or double friction murmur, in one as a whiff, and in one as a
soft to-and-fro sound. In the other three cases, however, the rubbing
sound was more marked, being harsh and systolic in one, of a winnow-
ing character in another, and creaking, in the third of those cases.
In three of these eight cases, pressure was required to bring out the
friction sound over the right ventricle during the advance of the
effusion. The friction sound was excited by pressure made, in six cases
over the sternum, in one over the fourth cartilage, and in one over
the heart. As a rule the spontaneous friction sound partook some-
what of the character of the friction sound previously generated by
pressure. Thus it was creaking in the case in which it was originally
creaking ; harsh in one of those (23) in which it was harsh ; to-and-fro
in that in which it was to-and-fro (56), rather smooth in the patient
(28) with a systolic friction murmur ; and a double friction murmur

1 Prov. Med. Trans., xii. 540.

9 Friedrich, Die Krankheiten des Herzens, page 229.

PERICARDITIS. 393

prevailed through the long history of the fatal case (49), in which a
double friction murmur was originally aroused by pressure.

The acme of the pericardial effusion usually occurred in these cases
very soon after the first appearance of the excited friction sound, or
from the first to the third day, in six of the eight cases.

2. The four cases in which a friction sound, otherwise absent, was
elicited by pressure during the acme of the disease have been already
considered under their proper heading at page 359.

3. Friction sound excited by Pressure during the decline of the effusion
into the pericardium ; and during tlie dying away of the attach — In the
great majority of the cases in which pressure was required to elicit the
friction sound during the period of the decline of the pericardial effusion,
this sign was a prelude to the dying away of the friction sound. Thus
in nineteen of the twenty-four cases that belong to this class the frotte-
ment never again appeared as an independent sound ; and the attack
of pericarditis was coming to an end. In three of the cases the
friction sound, after being for a time only audible when excited by
pressure, reappeared for from five to ten days as an independent
to-and-fro sound. There was a complete suspension of the friction
sound in connection with extreme general illness in two of these
cases (45), and the return of the spontaneous friction sound was in both
of them associated with improvement of health, and was preceded by
the appearance of a pressure friction sound.

The friction sound became inaudible except on pressure in nearly
one-half of the cases under examination during the first four days
after the acme of pericardial effusion (11 in 24); and in more than
one-half of them this sign came into play from five to twenty-one days
after the occurrence of the acme (13 in 24).

The character of the spontaneous friction sound last observed before
the pressure friction sound was called forth was, with few exceptions,
decidedly of a subdued tone.

The lower two-thirds of the sternum was the favourite seat of the
pressure friction sound which was heard in eleven of the cases over
that bone, including two in which it was heard over the ensiform
cartilage. In seven of the cases the rubbing sound was excited by
pressure over the cartilages from the third to the fifth, in one other
instance over the second space, and in one over the fourth space.
Besides these cases the pressure friction sound was heard over the
heart in one case, the right ventricle in three, and the apex in three.

II. Influence of Pressure over the Region of the Heart in intensifying
a Friction Sound already present (see Table II. page 328). — Pressure
exercised a marked influence on the friction sound in all but one of
the forty-four cases under inquiry, and in that single exception there
is no mention of the employment of pressure over the region of the
heart during the attack of pericarditis. Pressure, therefore, as a
means of diagnosis, and of illustrating the clinical conditions of the
friction sound in pericarditis, is essentially interwoven into every part
of what has gone before in relation to friction sound in that affection ;

VOL. IV. D D

394 A SYSTEM OF MEDICINE

and one part has been devoted to the study of cases in which a soft
friction sound audible over the heart at the time of the acme of the
effusion into the pericardium, was converted by pressure into a harsh
rubbing noise (see page 359). It is not, therefore, needful to give
here again in a detached form what has already appeared distributed
naturally through the preceding pages.

In four instances or observations, an endocardial murmur was masked
on pressure by the occurrence of a friction murmur or friction sound.
A. friction murmur was modified by pressure in fifteen instances : a
systolic murmur being intensified (in 3), rendered double (in 1), or
transformed into a double friction sound (in 1), by the employment
of pressure ; and by the same means a double friction murmur was
intensified in five and converted into a double friction sound in four
instances. In a few instances (3) a friction sound resembling a
murmur acquired its complete frictional character by pressure ; and
in a greater number a systolic friction sound was thus intensified
(in 4), or rendered double (in 5). An ordinary friction sound usually
double, sometimes soft or grazing (in 18), sometimes of the usual
to-and-fro character (in 38), sometimes harsh (in 18), was intensified,
or altered in tone, or rendered more harsh in seventy-four instances
or observations. As a rule a succession of observations was made
upon each case, and the same patient often reappears a^ain and
.again under the varying phases of the friction sound, and of the
influence of pressure upon that sound.

I have not, as a rule, illustrated in this summary the various trans-
formations that the friction sound may undergo under the touch of
pressure ; but those two remarkable noises, the grating and the
creaking friction noises, have been separately analysed, and all the
instances in which either of those sounds replaced another character
of friction sound, or was strengthened by pressure, are given in the
summary at page 328, and in this place.

INFLUENCE OF PRESSURE IX INTENSIFYING A PERICARDIAL FRICTION

SOUND.— Continued from p. 323.

Friction Sound rendered Creaking by Pressure.

Friction sound Systolic friction sound rendered almost creaking by pressure, 31 , acme, 3rd space,
rendered almost J ^ double fri<-'tion sound (bellows murmur) almost creaking on pressure, 30,
creaking bv \ *cn*e.

nrMunra Double friction sound rendered almost creaking by pressure, 6, acme, 3rd space,

pressure. j 40, acme, 39, after acme, 123, acme ?

Systolic friction murmur rendered creaking by pressure (diastolic rub), 33, acme,

4th cart 33, 3 days later.
Musical friction sound, changed to creak on pressure, 30, acme, 3rd space, (30,

2 days later, systolic creak produced by pressure).
Friction sound like sandpaper rubbing, creaking on pressure, 30, after acme, J2,

acme T double friction sound.
Orating sound changed to creaking by pressure, 45, after acme.
Harsh double brush, replaced by double creak on pressure, SO, before acme.
Friction sound rendered creaking by pressure, 33, after 2nd acme, 33, ditto, 44,

second acme.

{To and fro sound partly creaking, increased by pressure, 40. after acme.
Creaking systolic friction sound, increased by pressure, 34, acme, 43, acme, 42,
after acme.
Systolic creaking friction sound, double creak on pressure, 7, acme, 4th space,
122, acme ?

Friction sound

rendered creaking

by pressure.

PERICARDITIS. 395

A friction sound of indefinite quality was rendered grating by pres-
sure in six instances, and in two a grating friction sound was inten-
sified or rendered more harsh by pressure. A creaking friction sound
was in an especial manner the offspring of pressure when applied over
the seat of an ordinary friction sound, since in six instances a friction
sound, double in all but one, was rendered almost creaking by pressure,
and in twelve instances, various kinds of friction noise, grating, harsh,
smooth, and murmuring, were transformed by pressure into a creaking
sound; while in two others, pressure converted a systolic creaking
sound into a double creaking sound. These eighteen instances
occurred in fourteen different cases. Iu each of two of these patients
a creaking sound was excited by pressure four different times in the
course of the clinical history of the case ; showing a strong tendency
to the repeated recurrence of this sign when it has been once excited.
In six cases a creaking friction sound was rendered more intense by
pressure, and only one of these cases appears also among those just
spoken of in which an ordinary friction sound was converted by
pressure into a creaking sound.

Although I have only noticed in the summary those two mote strik-
ing noises, the grating and the creaking, as being excited by pressure,
yet there are many other friction sounds of a definitely individual
character that are thus brought into existence. These sounds differ
in no essential respect from those that are spontaneously excited from
within by the simple rubbing of the heart against the pericardium,
when their opposing surfaces are covered with roughened lymph. Pres-
sure over the heart affected with pericarditis excited — either originally
or by transformation, among my various cases — a single and a double
friction murmur; a whiff; a single, and more often a double brush ;
rustling, grazing, scraping, scratching, and sawing friction sounds ; a
double sound like that made by rubbing with sand-paper ; and a peculiar
double sound, broken during the diastole, that brings to my ear a noise
like that made by sharpening a scythe. A to-and-fro sound was not
unfrequently excited by pressure. I again and again noticed that
under the influence of pressure the two friction sounds, and especially
the diastolic one, became more continuous.

Owing to the increased intensity and continuousness of the friction
sound caused by pressure over the heart in pericarditis, the natural
sounds of the heart which were previously audible side by side with
the friction sound, but were not strictly rhythmical with it, were
frequently silenced under the influence of pressure.

dd2

390

A SYSTEM OF MEDICINE.

The Movements of Inspiration in Pericarditis.

In the Cases included in the following Table the movements of
respiration were observed with the aid of the chest measurer.

TABLE SHOWING THE MOVEMENTS OF RESPIRATION IN

PERICARDITIS.

L— CA8E3 IN WHICH THE RE3PIRATORY MOVEMENT8 OF BOTH THE CHEST AND

THE ABDOMEN WERE OBSERVED.

* Explanation. — These figures indicate the movements of respiration in hundredths of an inch.

For explanation of Symbols, see page 226.

15 (See p. 326). Female, set 16. Z$.

1st day.
Friction
whiff on
pressure,
pain left
side.

Rib. Rt.
2nd 15*
6th 6
9th 9

abdom. 6
abd. below)
ens. cartiL J

lft
%.*
2.
7.
9.

-10.

7th day

Better,

pericardial {

effusion

less.

(Rib. Rt lft
2nd 16 12.
6th 6 6.

9th 9 7.

abdom.- 10 S.
abd below \ Q
ens. cartiL J" 8-

4th day.

Acme of

pericardial

effusion.

19th day.

No
friction
sound,
better.

Rib. Rt
2nd 26#
6th 6
9th 14
abdom. 6
abd. t*low
ens. cartiL

15. •
6.
6.
6.

Rib. Rt. Lft
2nd 9 7.
6th 8 2.

abd. below \ .
ens. cartiL J
abdomen at
navel

Vth day.
Acme of
pericardial /
effusion,
less pain

heart,
reap. 52.

15th day.

Friction
sound
more

limited;
feels

better.

rRib. Rt.
2nd 6
6th 2

6th 3

0th 7

abdm. 6
nbd. below \
ens. cartiL)

lft.
4.
2.
S.
6.
0.

-8.

10th day.
Reap. 48.

Rib.
2nd
0th
9th

22nd day.
Weak.

Rt.

15
4

abd. below \
ens. cartiL j
abd. at navel

Lft.
15.

18tb day.
Lying on
right side,
friction
sound on
pressure.

Rib. Rt. lft
2nd 8 4.
6th 1 1.

7th 7 3.

9th 7 4.

abdm. 4 4.
bel. ens. car. —6.
abd. at navel 7.

rR\b. Rt. lft.

2nd 14 12.

6th 7 4.

9th 10 7.

abdm. 3 6.

abd. below I Q

ens. cartiL f
I abd. at navel 4.

(below ens. i .
cartiL ) °*
ditto, deep «,
breath, J *•

83rd day.— Below ensifonn
cartilage, deep breath, 50.

1st day.
Pn. IfL side,
ill a week
No friction

sound.

(L
J 2:

Rib.
nd
6th
9tb
abd.

Rt-.

20
6
4
6

14t,
15-20.

8th day.

Acme,

resp. 54, ]

pain side. I

Rib.

6th

9th

abd.

ens.

Rt,

9
below i
caitiL )

I4t
8.

-1.

6th day.
Pain in
epiga-
strium.

Rib.

2nd

6th

9th

abdm.

abd. below

ens. cartiL

}

12.*
3.
6.
8.

-8.

26th day.

abd. below ensi-
form cartiL 10.
bd. at navel 16.

36 (See p. 316). Female, aet. 20. j£

12thday.

Feels

better.

Resp. 50.

21st day.
Better, as-
pect good,

resp. SO,
no friction

sound.

Rib. Rt Lft
2nd 18 12.
6th 5 8.
abdm. 8 2.
abd. below)
ens. cartiL J
abd. at navel 0.

Rib. Rt. lft
2nd 12-2010-15
6th 6 f

9th 10 „
abdm. 8 10.
abd. below \ .
ens. cartiL ) *'
do. deep breath 20
abd. at navel 6.

87th day. — Below ensiform
cartilage, deep breath, 90.

6 (See p. 324). Female, aet, 15. «=£>

12th day.
Better, but

reap. 55,

no friction

sound.

Rt.

18
6
9
1

lft
16.

2.
-8.

4 (See p. 313.) Male, aet 27. ^

2nd day.

Acme,

very ill,

resp. 86,

Rib.

2nd

6th

lth

abd.

7-9

Lft.
7-10.

5.
12.

3rd day.
Better.

Rib.
2nd
6th
9th

abd. below i
lens. cartiL i

Rt.
6
6
»»

IJt.
i.
3.
9.

12.

7th day.

abd. b. ens. c. — 2.

Rib. Rt lft
2nd 6 7.
6th 4 2.
9th 4 7.

abd. at navrt 2".

PERICARDITIS.

397

6th day,
Acme,

pain over
heart

■•/

18 (See p. 323). Female, set. 18. ^

Rib.

2nd

6th

9th

abd.

ens.

Rt.

SO
7

10
below
cartil.

20.
6.

14th day.— Slight friction Round.

8th day.
Pain in
chest,
friction
sound.

Rib.

2nd

6th

9th

abdm.

Rt.
30
6
15
- 8

7th day.
8 days af-
ter acme,
very ex-
tensive
friction
sound.

6th day.

Acme,
lessening
pais over

heart

8th day

before

acme pain

in heart

10
9
9

abd. below)
ens. cartil. |
abd. at navel

Lfl.
20.

►»
t.

-2,
-4.
0.

11th day.
Acme.

/RQ>.
2nd
6th
9th

abd.

Rt.
30

6
10

abd. below \
ens. cartil. /
abd. at navel

0.
8.
7.
3.

-4.

19 (See p. 326.) Male, set. 23.

Rib.

Rt.

lift-

2nd

20.

6th

ft.

9th

10th day.
Improv-
ing, It 88
friction
sound;
lea
pleurisy.

Rt. Lit.
25 20.

Rib.
2nd
6th 9

9th 13
abdm. 12
abd. below \
, ens. cartil. J

10.

13th day.

Better.

very slight

friction

sound.

26 (See p. 324). Male, set. 25. <Zt

m. L/l
20 20.

10.
10.
10.

10th day.

Reap. 22,

better,

friction

sound.

Rib.

2nd

6th
10th
abdm.

Rt
8

16
9

20.

abd. below )
ens. cartil. f
abd. at navel

20.
40.

13th day.

Jbetter, sits

\ip in bed,

friction

sound on

pressure.

Rib.

Rt.

X/fc

2nd

12.

6th

9th

12.

abdm.

10.

ab. b.

ens.

c. 2.

abd. at nav

el fty

Rib.

Ifl.

2nd

16.

6th

10.

abdm.

36.

abd. below

} 30.

ens. cartiL

abd. at navel 40.

49 (See p. 327). Male, sot. 17.

Rib.

Rt.

7th

abdm.

Acm*y } ~~ *Ddomen below ensiform cartilage, -7.

II.- CASES IN WHICH THB RESPIRATORY MOVEMENTS OF THE CENTRE OF THE

ABDOMEN WERE ORSERVED.

16 (8ee p. 827X Male, set 17. ;~^ <21st day, no friction sound ...

A.— Case* observed— (\) below the Ensiform Cartilage, and (2) at the Navel.

I (12th day, second acme ... Below ens. cartiL, -3, at navel, 4.

l86th day ...

!4th day, acme, pain epigast
5th day, after acme
6th day, ,,

16 (8ee p. 816). Fern., set 17. ^ 2nd day, acme ?

r * 1 1st day, acme ...

40 (8ee p. 313). Male, set 17. 3 < 7th day, after acme

"^ (15th day, friction sound

B.— Cases observed below Ensiform Cartilage.

61 (See p. 815). Male, set 22. ^
86 (8ee p. 327.) Fern., set 21. ^

( 4th day, acme ]

1 7th day, decline of fid.

1 9th day, second acme

\ 29th day, well. Deep breath

66 (8ee p. 324.) Male, set. 16.

!5th day, after acme
11th day, improving
32nd day, clothes on. Deep breath
-^— ^( 1st day before acme

it A l3lxl <Jay' aelne

™ ▼ 1 11th day. well

•0

»t

•12.

10.

•t

»»

10.

12.

mei

it below

ens.

carta.

.-*.

»»

6.
9.

t»

>»

,,110-170.

-2,

i»

»»

5<V

»»

16.

»t

»i

0.
1.

»t

-7.

* •

.»

17.

88 (Bee p. 325). Fern., set 22 "£ J1?"1 day' second acme ...

"■> 122nd day, 3rd acme

18 (See p. 316). Fern., set 19. r£ J?H\,dfty' ***** acme *"

10 (See p. 521). Fern,, set. 24. ^t IHS ^ay' acme

^ i zotn uay ... ... ...

44a (See p. 823). Male, set 14. £> 6th day, after first acme

18 (See p. 814). Fern., «t 26. o-> 4th day, acme, or after

68 See p. 318). Male, set. 26. £j£ 5th day before friction sound ... Movement below ens. cartil. 5.

64 (See p. 820). Male, set 35. Z$. 8th day, no friction sound ~ „ „ " 20.

»i »» tt ••

Mvt bel. ens. cartil. or lower, 4.

308 A SYSTEM OF MEDICINE.

The movement* of respiration were affected in pericarditis in three
different relations ; (1) those of the ribs ; (2) those of the abdomen on
each side, just below the eighth cartilage ; and (3) those of the centre
of the abdomen.

(1.) The respiratory play of the upper ribs was more than doubled
in extent in three-fourths of the cases observed (5 in 7), so that
respiration was as a rule high. This was due to the arrest or restraint
of the action of the diaphragm caused by the extensive inflammation
of the central tendon of the diaphragm, where it forms the floor of the
pericardium.

In one (4) of the two exceptional cases, the movements of the
second ribs were not at all or only slightly augmented throughout
the whole period of the illness ; but iij the other case, in which the
respiration was greatly accelerated, the action of those ribs, which
was slight during the acme of the affection, was much increased during
the -decline of the effusion.

The respiratory Movement of the ribs on the left side of the chest
was less than that of those on its light side, as might naturally be
expected, in more than one-half of the cases (5 in 8) ; but in the
remaining three patients the action of the two sides was nearly equal
both during the acme and the decline of the pericarditis. The dif-
ference in the movement of the two sides of the chest was not, as a
rule, limited to the ribs adjoining the pericardium, but extended along
their whole range, from the second to the ninth. The study of the
Table will show, however, that there were some exceptions to the rule
that the play of the ribs was restrained throughout on the left side ;
since in two of the three cases in which the two sides of the chest
moved with equal freedom, the ninth left rib was greatly restrained
in its movements.

(2.) The lateral movements of the abdomen below the eighth carti-
lages were greatly restrained in three-fourths of the cases (6 in 8) ; and
the respiratory play of the left side of the abdomen was muck less than
that of its right side in the same proportion of cases (6 in 8).

(3.) The inspiratory movement of the abdomen below the ensiform
cartilage was either reversed (in 12), arrested (in 1), or restrained (in 6)
in every case of pericarditis in whioh thajb sign was observed. This is
at once accounted for by the inflammation, in that disease, of the central
tendon of the diaphragm where it forms the floor of the pericardium,
. which leads to the virtual paralysis of the central portion of the dia-
phragm. This fact, that the anterior wall of the epigastric space,
instead of advancing, recedes during inspiration, gives us a physical
sign of great value in the diagnosis of pericarditis, and of the advance
and decline of that disease. Thus in the first case in the Table (15),
a girl, aged 16, the anterior wall of the abdomen below the ensiform
cartilage fell backwards during inspiration for the tenth of an inch
during the three early days, when the disease was at its acme ;
then, as the tide turned and the effusion diminished, the abdomen
receded less and less up to the seventh day, when it did so for

PERICARDITIS. 39»

only the fiftieth of an inch ; after this itregained its natural forward
movement, and on the twenty-sixth day the abdomen at the epigastric
space advanced as much (the tenth of an inch) as it had receded on
the day of admission. In the other case (56), the front of the abdomen
advanced the sixth of an inch on the day of admission, when the peri-
carditis had scarcely pronounced itself; the sixteenth of an inch on the
third day, when it had reached its acme ; and the fifth of an inch on the
eleventh day, when it had declined and disappeared. In my paper on
the movements of respiration I showed that in health the abdomen at
the navel advanced during inspiration a quarter of an inch or a little
more, but I did not ascertain the respiratory movement at the epiga-
stric space. A short time ago I observed, with Mr. Eossiter, the
respiratory movements of the abdomen in eleven patients in St.
Thomas's Hospital, several of whom were convalescent, and one had
pericarditis ; when we found that the inspiratory advance at the epi
gastric space varied from the sixth to the fifth of an inch. The latter
was also the extent of the advance in two healthy men. I consider
that this forward movement fairly represents the healthy respiratory
play of the part in question ; that in pericarditis, as a rule, the whole
of this advance is lost ; and that in addition the play is reversed to the
extent of from the fiftieth to the tenth of an inch. It is worth noting,
in conclusion, that in the case of pericarditis observed by Mr. Eossiter
and myself in St. Thomas's Hospital, a boy, aged 12, in whom the
disease was at its height, the wall of the abdomen receded during
inspiration at the epigastric space from the sixteenth to the twentieth
of an inch, and at the navel from the thirty-fifth to the fiftieth of
an inch.

CASES OF BBIQrTPS

DISEASE EXAMINED AFTER DEATH
With Especial Ebfbh«ncb to thr Ooodb-

CONDITION 0*

— — —

I
|

]

a
I

I
I

loot* BrtRht'i, Dl*.
eue following '
Bearlst Fotbt . 1

Unrl of uiturtl li™ . . .
Ditto wilk partial Pcritardltit

Hurt Urge or vert lira . .
Sin of heiirt nat deecrtbed

iivn I ...

"a
l

!•

19ft

Ditto vU* partial J
Aeat) Bright'! Dh- J
Mk witt antral P

FtltT Kidney . .,'

Henrtof nntirmldw. . . .

Henri lerge or veryinrge. hyptid.
Ditto witE antral Ptriardilit.
BluofbenrtnatdeKhbed. .

It lit .-. n'ilJi jvrfnil Ptricardittl .

lbT

ij'3°

MtV/o

ID
«■*•/

i'i

a
I

l t

6«°/o IS*/.
"tj T

"a ~i

"a i

i„.»„^f^i

U'J

STVo

Sft

»/■

**>/.

□mrralu Kidney.
Kidney leuened'

Hmrtur™iiii.l.i».^r.(|i).

_»■!»,'<,

=
_

i'a

[

DiUdifUA partial PirioirdtdJ .

■< 9

]

■

-""

*0
23-4=/„

Ditto \oil\ Qneral PtrkardUU

Onnulir Kidney. ' '' "ll'"r \ •"', ' v l"?? °V
Kiilney nf iwtn- 1 | EgW«|T-» VT^V
ger thin mtunL J, ., ,, ,', . L r| , ar^-ribea .

117

24 : 8

Tl-WoiTWe

ur°/0

•».'•

Ti"

B4%

101 | S3

63 S% »*/

»t*>„

o»>

1
I

h
si

1
i

\
I

\
j

--6

i3s

■

siil

;;:

--; =

:::

-::-

11
"i
"a

B
1
"i

]

ta%
it

•*•

SS"S%

4
9

'3
"a

1
"j

i
■

":i

ir
i

1
is-s%

»'*"Ai

":)

i'i

70%

"j
»
.1

~^r

11%

WT<V«

*>/.

(1 r,, .

t
S

"j
It

13
S

.-.

11
1

!■■.

M
Bl'6%

4»
1

1
"»

Ii
41'/.

-"'■■

M-W/o

117%

«■ <•

4 7%

«*•/.

CASES OF BRIGHTS DISEASE EXAMINED AFTER DEATH AT

Cu«0f ICttMluil]

Bwt of Mturti da . . .

II- :il t 1.1V ulUTT Lire
IIMi in'Il gtncni! I'crvimlitl

Embc.lf.mof Ki'dnir. Hwrf very Urge ■
Own. oft I H^rtfMjUrgo

Ditto vith partial Pericardial .

'I lll'ATt uniall

■ llwirt "f ii'i'n

I'oUl CUM of.

li:n iff! ,../:;«! (',■,(■■,.,■',.'.■.

lientl nUxilup ....
i)U(o villi p«un'! /', ,,,.(,■■;,';.(
/)ir.'„ ;■ iflk ,u,rtMiJ PtrkoitiilU
Heart 1mk« or verr f -j n , ■■ ■ . l.vi-1.
/.liii.i i<-ifi -wa.-ivn' y. c .1.1,1

Gifto I'.'il* ,-p,-fi',n' P.i,'.-.i,.f.'rj.

CrJcnlna In Kidney, ]

>f heurt not deecribod .

neplultla frc
rrtaSctnro, &r. "

Ditto. Total ......

-■WntlttjKMraJ JVrdnrdiiil.

T"T*t, Hnmiai or Cud . .

ii TIeart nraa.ll
' Hewt of natural sUe . . .
Dilfo ril* fl««ial Pericardii!!
Hart rallior large ....

t\ i

■ Cakolni In kidney, pelyli, or

ST. MARY'S HOSPITAL DURING THE YEARS 1851-69— (continued.)

403'

» Stricture, or affection of prostate or bladder 01) J PF«mia (l) ; calculus in ureter (1).

404 FREQUENCY OF PERICARDITIS, PLEURISY, PERITONITIS, AND
PNEUMONIA IN CASES OF HEIGHT'S DISEASE OF THE KIDNEYS.

Caie» ommm •" Ebolaso as

8KrIL.HO.

Dr. Drfght (i7*»V tlatpilal lUporti, I.

[ml., (r:-,,, ! 11-. ,-■■: :-'ii, \ ,

Dr. Gripilit »i'»l It.rl.-B UVuy'. ffw.j.ifcill
Bqw-U, MtOIld MliM. I.) . . . , , ,1
Dr. Ongniy (i'rffiu ««d. Jo*ni„ »olM

xxxvl., xixvu.) i

Ur. I'liiislisHi ((>., >,'..<r.iii!iirl)rfc*eraliwi<
-■/ KiVn.>«] J

IV J< itl IJ l/ll' ■■■■ ! ■■' A'!.'". II') ■ - ■

nr.*i:vH(i;..,/. ;/,-(, to;.. ncw«r,vul.)

" " wlmi.('MDrT,pi>)

ik-u-.i, r"-i .^.>i,.!iu.iri,->) . . .

IV Mi|].-r(A,|-.l'.!f.». in Sffl'llIJ'fKr) . .
■ir T'.l.-ii.'f.J c.'.if .'■ r„.,v..l WIU i

_'r. UmI-i I- MX...' ■•■! I HtwtllliKOK).

IV. ui M KL'uni-i (K.i.jll'i ita<.««) .

Ur Cir.-. mM.I [T»bl« i-ontribuW tol

lathor (51. MaT^j J7»p. IMK-lforfMil
end, isal-flB) '

Dr Clwnbn* IDtannlam Partofootrum) .

ClUS OBSERVED in OK1MI.

Mllmstan (tf. BrfffJUcit Nimntrniitl

l««>i) J

Fr. ri.ti- {['. Brifhticht .v«fnilTiirii**B*ii>
BMiilwrgrrtnnrtalv'J ^«AJb) . . .

ri-ii -I

M-^.i.T J nvWj .(rf*;-/, III.) . . .
TUugel

T[i'Lr>(rr.:;.'.'.- I":',-'. ■'.-.i.1, r.i.-l n /'. l-.Mh.

SoHnttetn i'frrenl-miiHUitoii, p. 105)
Ditto (dIHo p. 103)

.1. ■ ■■ nil I .

BUlu (WjiminHW.)

C.SEJ 01HERTID IK tlUia

MJiirin s..i..n i;^ fj.'Mmfnurt*) . .

IIK.n'.! Ii"-li. I.",,.,) . .

I1.-..,ii.iv| ,-,.. (i.,„.,, ,',-., C,,,:,.. A. in!

Ditto (d(l!o Chlldn

mux (EbtfcIuji. iki. St. W«d.) . ,

lonheid (On Distant of India) .

ISSSj-

■leesl

Hi the •ddltlaii of Dr. Clumbenl **4 et

FREQUENCY OF PERICARDITIS, PLEURISY, PERITONITIS, AND 405
PNEUMONIA IN THE VARIOUS FORMS OF BRIGHTS DISEASE.

Pericar-
ditis.

Pleurisy.

Perito-
nitis.

Pneu-
monia.

•sE.

ACUTE BRIGHT* DISEASE FROM SCARLET FEVER.

Casks below 16 Years or Age. I J

"Dr. Dickinson (OnAlbuminv ria, from Tables \\ 91 '
kindly communicated to the Author) . .1

Dr. Greenfield (from ditto) '4' 1 0 0

The Author {St. M ary's Hosp. Post Mort Rtc.y 40 2 2

Total

Case* abote 15 Tears or Age.

Dr. Greenfield (loc. cit.)

The Author (St. Mary's Hospital) . .

linl4

7o/o
0
0

1 in 5
20-7o/o

6 or 7

0
0

Total 5' 0 > 1

ACUTE BRIGHTS DISEASE, NOT FROM

Cases below Id Tears or Aoe.

Dr. Dickinson (loc. cit.) 3 0 0

Dr. Greenfield {inc. eit.) 1 0 1

The Author [St. Mary's Hospital) .... 1 0 0

4
lin7
13 8"/o

Total

Cakes above 16 Years or Aoe.

Dr. Dickinson (loc. cit.)

Dr. Greenfield (loc. cit.)

The Author {St. Mary's Hospital)

Total

Cases ih which the Age was not
specified.
Bamberger, "first stage," [loc cit.) . .

Total with Acute Bright's Disease, not from)
Scarlet Fever. All ages J

4
8

liu7

I430/0

ltn65

15-40/c

1 in 78
13o/o

SCARLET

0
0
0

in 14

7o/0

1 in 65

15 -40/0

1 in 6*5

1540/0

6 or 7
1 in 5
2lo/o

"I 2~~
FEVER

1
0
0

•••

1
1
0

linlS

77o/o

1 in 13

7-7o/0

2
1 in 7
14-jo/o

4
1 in 6 5
15'4o/0

1 in 4-8
20*5o/o

•••

1
1

•••
•••

•••
•••
•••

Transitional Cases, passing from Acute Bright's Disease to the Fatty or Large White Kidney.

Dr. Dickinson (loc cit.)

CASES WITH

Dr. Dickinson (loc. cit.)

Bamberger, "second stage," (loc. cit.). .

Dr. Wilks (toe ciL\ "large white." 23
"coarse,- 5: ••fatty," 17, some with
lardaceous Kidney

The Author (51. Mary's Hosp. P. M. Records)

FATTY

•I

0
23

Total with Fatty Kidney

136

0
1

I ° I

LARGE WHITE

j lin
I 16<

in 62

60/0

lin 27

370/0

lin 4

25 80/0

1 in 4 5

22o/0

0 I

KIDNEY.

1
1

lin 31

3-2o/o

lin 15

6-6<Vo

*••

• ••

•■•

•••

—

•••

lin 4

25o/o

• ••

•••

lin 6

17o/0

Dr. Wilks (toe. cit.)

Dr. Dickinson (On Albuminuria) .
Dr. Grainger 8tewart (loc. cit.) . .
Bamberger, "third stage." (toe cit.)
Author (St. Mary's Hospital) . . .

GRANULAR KIDNEY, CONTRACTED.

Total with Contracted Granular Kidney

I28

lin 10

IO0/0

326

1 in 6

16 80/0

4
30
1 in 4-3
28 4o/o

~~ 47~~
1 in 4*8

2lo/o

2
3
0
0
6
1 in 21 J
470/0

1 in 20-5

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1

lin 10

IO0/0

1 in 9

11%

• ••

•••

• ••

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• ••

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• •■

• ••

LARDACEOUS (AMYLOID) DISEASE OF KIDNEY.

Dr. Dickinson (toe. cit., " depurative ") . .
Dr. Grainger Stewart (toe. cit.)

Author (St. Mary's Hospital, Lardaceous)
Disease actual and probable) j

Total with Lardaceous Disease of Kidney .

48
50

120

2
lin 11

*Vo

1 in 13 3

7-5o/o

6
3
3

1 in 7

14'JO/o

1 in 10-8
»-2o/o

4
lin 5 2
19-4o/o

1 in 10-8

9-2o/o

3
1 in 7
14-So/o

lin 85

117%

406 A SYSTEM OF MEDICINE.

Pericarditis in Bright's Disease of the Kidneys.

Dr. Bright, in the first volume of Guy's itospital Reports, gives 100
cases of albuminuria, seven of which, according to the tables, and eight
according to his description, had pericarditis. Subsequently Dr.
'Gregory and Sir James Christison, in Edinburgh; Martin Solon,
Becquerel and Bayer in France; and Malmsten in Germany, gave
each of them a series or summary of cases of Bright's disease, in all
of which cases, except those communicated by Malmsten, pericarditis
was either infrequent or absent.

Dr. Taylor called attention, in 1845, to the large proportion in which

• cases of pericarditis are affected with Bright's disease, and to the fre-
quency with which pericarditis occurs in cases of Bright's disease. He
found that out of thirty-one patients with pericarditis, nine, if not

• eleven, had Bright's disease ; and that of fifty post-mortem inspec-
tions of cases with Bright's disease, five, or one in ten, had pericarditis.

Several years later, or in 1851, Frerichs published his important work
on Bright's disease, which contains a valuable table showing various
conditions that existed in 292 cases collected by him from various
sources, and including 21 observed by himself. He states that in 13

v of those collected cases there was pericarditis ; that is in only 4 J per
cent, or 1 in 22 of the cases. This return, which has been, and still is,
much quoted, gives a lower proportion of attacks of pericarditis in
Bright's disease than in the cases given or enumerated by Dr. Bright

' (7 or 8 per cent, or 1 in 14 or 12), Dr. Taylor (10 per cent, or 1 in
10), M. Rayer (5*4 per cent, or 1 in 18), and Dr. Gregory (5 per cent,
or 1 in 20) ; and a higher proportion than in the cases observed by
Becquerel (4*6 per cent. or 1 in 62). Frerichs appears to have overlooked

: some of the cases of pericarditis in his analysis. To test his figures,

I examined as nearly as I could the same cases or tables given by the

observers quoted by him, and I find that in a total of 326 cases, 17 or

19 had pericarditis, or about 5*5 per cent, or 1 in 18.1

During the nineteen years, ending in 1869, 285 cases of Bright's

• disease were examined after death in St. Mary's Hospital, and of these
25 or 1 in 11*3 or 88 per cent, were affected with pericarditis ; which
was present therefore somewhat more frequently in those cases than
in 1,691 collected cases of Bright's disease, 136 of which, or 1 in 12*3

• or 8* 17 per cent, had pericarditis.

Besides the twenty-five cases of pericarditis noted in the records of St
Mary's Hospital, there were fifteen of partial or doubtful pericarditis ;

• but these cases ought not, I think, to be taken into the general account.

If we separate the various forms of Bright's disease occurring in
. St. Mary's Hospital from each other we shall see the proportion in

• which each form was affected with pericarditis.

1 Frerichs. Dr. Bright, 100 cases ; Sir James Christison, 14 ; Dr. Gregory, 87 ; Martin

• Solon, 8 ; Rayer, 48 ; Becquerel, 45 ; Bright and Barlow, 10 ; Malmsten, 9 ; Frerichs, 21 ;

* Total, 292. Author. The same authorities respectively ; 100, 14, 39, 10, 55, 45, 9,
-83,21 ; Total, 826.

Cases of pericarditis in the above, Frerichs, 13 ; Author, 17 or 19.

PERICARDITIS. 407

SUMMARY.

Acute Bright's disease, from scarlet fever, total number, 6 ; affected
with pericarditis, 0 ; with partial pericarditis, 1.

Acute Bright's disease, not from scarlet fever, total number 15 ;
affected with pericarditis, 2, or 1 in 7*5, or 13 3 per cent. ; with
partial pericarditis, 0.

Fatty or large white Kidney, total number, 62 ; affected with peri-
carditis, 1, or 1 in 62, or 1*6 per cent. ; with partial pericar-
ditis, 5.

Contracted Granular Kidney, total number, 128; affected with
pericarditis, 13, or 1 in 10 or 10 per cent.; with partial pericar-
ditis, 7.

Granular Kidney of natural or large size, total number, 34 ; affected
with pericarditis, 3, or 1 in 11*3, or 88 per cent.

Granular Kidney, grand total number, 162 ; affected with pericar-
ditis, 16, or 1 in 10, or 10 per cent. ; with partial pericarditis, 7.

Lardaceous disease of Kidney, actual and probable, total number,
22 ; affected with pericarditis, 2, or 1 in 11, or 9 per cent.

Nature of Kidney disease doubtful, 11 ; affected with pericarditis,
4, or 1 in 2*7, or 36 per cent. ; partial pericarditis, 2.

Total number of cases of Bright's disease, 285 ; affected with peri-
carditis, 25, or 1 in 11 '3 or 88 per cent.; with partial pericar-
ditis, 15.1

Calculus in kidney, pelvis, or ureter, or dilated pelvis (hydro-
nephrosis), total number, 12 ; affected with pericarditis, 0.

Suppurative Nephritis from stricture, &c, total number, 13 ; affected
with pericarditis, 1, or 1 in 13, or 7*7 per cent.

That I might enlarge the area of observation, I have brought to-

f ether from various sources, including the returns from St. Mary's
lospital, in the accompanying Table, the number of attacks of peri-
carditis in 1,681 cases of Bright's disease; and the number of attacks
of pleurisy, peritonitis, and pneumonia, in 1,228 cases (see p. 404).

I have also given in another and more extended table (see p. 400),
the number of cases witli pericarditis, pleurisy, and peritonitis, pneu-
monia, pulmonary apoplexy, and purulent deposit or abscess of the
lung; and certain conditions of the heart and aorta in the various forms of
Bright's disease among the 285 cases examined at St. Mary's Hospital ;
distinguishing also those cases in which the heart was small, of natural
size, rather large, and large or very large, giving separately those various
conditions as they appeared in the cases affected with pericarditis.

Among the cases of Bright's disease collected from various sources,
8'1 per cent, or 1 in 12*3 were attacked with pericarditis.

These cases are arranged in three sections devoted respectively to
England, Germany, and France ; and the occurrence of pericarditis

1 For details of the cases of partial pericarditis see pages 411, 413.

408 A SYSTEM OF MEDICINE.

in Bright's disease is here shown to be most frequent in Germany (1 in
9*5, or 104 per cent.), and least frequent in France (1 in 33, or 3 pei
cent), while it is of medium or average frequency in England (1 in
11- 9, or 8*4 per cent).

Comparative frequency of Pericarditis in the various Forms of Bright }s
disease. — I have added to the table of 1,682 cases collected from many
sources, a series of secondary tables (see p. 405;, showing the relative
frequency of pericarditis, pleurisy, peritonitis, and pneumonia in the
various forms of Bright's disease, in a certain number of the cases ;
and I shall here inquire into the frequency of pericarditis in the
different forms of that disease.

Pericarditis is not frequent in caseS of acute Bright's disease from
scarlet fever in the young, since it only occurred in 1 in 14, or 7 per
cent, of the patients under 16 years of age. The tendency to pericarditis
in children in such cases is slight, as was pointed out to me by Dr.
Dickinson, who kindly supplied me with the valuable tables of his
cases of that class, amounting to 21. Pericarditis is on the other hand
frequent in acute Bright's disease in the adult, since it was present in
1 in 6£ or 15*4 per cent, of those cases. The value of these returns
has been greatly added to by the cases of acute Bright's disease kindly
communicated to me by Dr. Greenfield.

During the transitional period, when acute Bright's disease slowly
gives place to the fatty or large white kidney, pericarditis is probably
frequent,sinceitoccurred inoneof Dr. Dickinson's four transitional cases.

When, however, acute Bright's disease instead of recovering passes
into the second or chronic stage, in the form of large white kidney,
the tendency to general pericarditis disappears, since it only occurred
in 1 in 27 or 37 per cent, of the collected cases, and one in 62, or
1*6 per cent, of the St. Mary's Hospital cases, and the kidney in that
single case was in the third or contracted stage of fatty disease. Five,
however, of the St. Mary's Hospital cases with fatty kidney had partial
pericarditis, showing that this affection, although still inherent, does
not tend to develop itself in that form of the disease.

The two great and opposite forms of Bright's disease, the fatty
kidney, or the chronic stage of acute Bright's disease, and the contracted
granular kidney, show a marked difference in the proportion with which
they were respectively affected with pericarditis ; which attacked those
with contracted granular kidney from six to four times as often (1 in
10 * and 1 in 6 2) as those with fatty kidney (1 in 62 J and 1 in 26'6 *).

Cases of lardaceous disease of the kidney have pericarditis with a
moderate or average frequency (1 in 11, or 9 per cent.,2 and 1 in 13*3,
or 7*5 per cent.2).

Inquiry into the influence respectively of the fatty kidney, and the
contracted granular kidney, in the production of pericarditis. — When
inquiring into the influence of these two forms of Bright's disease
in the production of pericarditis it may be well to consider two points

1 Id 285 cases examined after death in St Mary's Hospital.
9 In the collected cases.

PERICARDITIS. 409

which appear to be associated with the production of pericarditis,
though for different reasons ; (1) the proportion in which cases with
fatty and contracted granular kidney were affected respectively with
pleurisy, peritonitis, and pneumonia : and (2) the relative proportion in
which the heart was enlarged and its left ventricle was hypertrophied in
those two forms of disease ; and the immediate relation, if any, that the
enlarged heart may have had to the production of pericarditis.

1. Pleurisy attacked 60 of the 285 cases with Bright's disease
occurring in St. Mary's Hospital ( 1 in 4*8 or 21 per cent.1 and 1 in
6 or 16*4 per cent.2) It will thus be seen that in these cases of
Blight's disease pleurisy was twice as frequent as pericarditis (1 in
11*3 1 and one in 123 2). We have here a marked difference between
the pericarditis of acute rheumatism and the pericarditis of Bright's
disease, since while in the former disease, or acute rheumatism, the
inflammation of the pericardium is much more common than that of
the pleura ; the pleurisy when present, being usually either due (1)
to the spreading of the inflammation of the pericardium to the pleura,
or (2) to pulmonary apoplexy which is the consecutive effect of
the double inflammation of the heart, inside and out ; in the latter
affection, or Bright's disease, the pleurisy is an independent affection,
and is, as we have just seen, twice as frequent as pericarditis in the
cases under inquiry.

The same in principle may be said of peritonitis, which is practi-
cally unknown in acute rheumatism ; while it occurs nearly as often as
pericarditis in Bright's disease ; the numbers being 93, or 1 in 13,2 and
19, or 1 in 15 * of peritonitis against 100 or 1 in 1232 and 25 or 1 in
11*3 * of pericarditis.

Two-fifths of the cases of pericarditis were also affected with pleurisy
(10 in 25) and three-fifths were free from that affection (15 in 25);
while only 2 in 25 of those cases had peritonitis.

The relative frequency of pleurisy and peritonitis on the one hand,
and pericarditis on the other, varied much in the different forms of
Bright's disease.

In acute Bright's disease from scarlet fever in the young, pleurisy
occurs three times (1 in 5) and peritonitis twice (1 in 7) as often as
pericarditis (1 in 14) ; but it is otherwise in acute Bright's disease in
the adult, not from scarlet fever, since in such cases pericarditis is as
frequent as pleurisy (each 1 in 6*5), while it is twice as frequent as
peritonitis (1 in 115).

Pleurisy attacks many more cases (1 in 41 and 1 in 4*5 2) with fatty
kidney than pericarditis (1 in 62 * and 1 in 27 *) ; while in those
with contracted granular kidney, pericarditis (1 in 10 l and 1 in
6*) occurs, judging by the collected cases, nearly as often as pleurisy
(1 in 4*3 * and 1 in 48 2). Although pleurisy is rather more frequent,
pericarditis, as we have seen, is much less so in cases with fatty than
in those with contracted granular kidney ; and it is therefore evident

1 In 285 cases examined after death in St Mary's Hospital.
' In the collected cases,

VOL. IV. K s

410 A SYSTEM OF MEDICINE.

that the causes producing the two inflammations have but little in
common, and that the one rarely excites the other. Peritonitis occur-
red twice as often (1 in 31 l and 1 in 152) as pericarditis in cases with
fatty kidney, while pericarditis attacked three times as many as
peritonitis (1 in 21) in those with contracted granular kidney.

Pleurisy and peritonitis (each 1 in 10*8 2) were both of them more
frequent than pericarditis (1 in 13*3 *) in cases of lardaceous disease
of the kidney.

Pneumonia, which when it occurs by itself is an occasional cause of
pericarditis, while it is less common (1 in 6*4 l and 1 in 76 2) than
pleurisy (1 in 4*8 l and 1 in 6 2) is more common than pericarditis in
cases of Bright's disease. Those two secondary affections, pneumonia
and pleurisy, were of exactly equal frequency in cases of acute Bright's
disease, whether from scarlet fever or not ; so that what has been said
with regard to the latter of those affections applies to the former.

Pneumonia was common (1 in 4 * and 1 in 6^ and pericarditis
was rare (1 in 62 * and 1 in 27 2) in cases with fatty kidney. It was
almost the reverse in those with contracted granular kidney, in which
pneumonia (1 in 101 and 1 in 92) scarcely equalled pericarditis in num-
ber (1 in 10 l and 1 in 6 2). The proportion of pneumonia was, there-
fore, about twice as great in cases with fatty, as in those with contracted
granular kidney, while pericarditis, rare in the former, was frequent in
the latter form of the disease, making it evident that there was little
in common between the production of pneumonia and that of pericar-
ditis in these cases. Pneumonia was present in only one-third of the
cases of Bright's disease that were affected with pericarditis (8 in 25).

2. Enlargement of the heart, usually with hypertrophy of the left
ventricle, was present in one-half of the cases of Bright's disease under
review (129 in 259) in which the size of the heart was described.
The heart was large in more than half of the cases of pericarditis
in which the size of the heart was defined (10 in 19 3); or 10 in 129
of the total number of cases of Bright's disease with enlargement of
the heart. Pericarditis occurred in six cases in which the heart
was of natural size (or 6 in 61). It would thus appear that 1 in 10*1
of the latter in which the heart was natural in size, and 1 in 12*9 of
the former, with hypertrophy of the heart, had pericarditis. This
would seem to say that hypertrophy of the heart had no apparent
influence in the production of pericarditis in these cases. If, however,
we add the cases in which the heart was small (23), none of which
had general pericarditis, to those in which it was natural in size (61),
we find that 6 in 84 or 1 in 14 of those combined cases had that affection.
If to these we join the cases in which the heart was rather large (45) 3
of which had pericarditis, the result is that 9 in 129 or 1 in 14*3 were
thus attacked. From this analysis, it would appear that enlargement
of the heart exercised a definite but not a predominant influence
over the production of pericarditis in cases of Bright's disease.

1 In 285 cases examined after death in St. Mary's Hospital. * In the collected cases.
3 The size of the heart was doubtful in six cases with Pericarditis.

PERICARDITIS. 411

Although hypertrophy of the heart is absent in almost one-half of
the cases of Bright's disease with pericarditis, we know that in every
form and case of that disease, whether acute or chronic, fatty or gra-
nular, the action of the left ventricle is unduly strong ; for it has to
send the poisoned blood through vessels of great tension that oppose
resistance to the onflow of the blood. The result is that in every
case of Bright's disease, the left ventricle, whether hypertrophied or
not, is beating with undue force ; and thus tends, by the pressure
of its walls with undue force against the pericardium, to induce
pericarditis. The heart is prevented from becoming enlarged in many
cases of Bright's disease by the exhausting loss of albumen, the gene-
ral waste, and the lowering character of the disease. This especially
applies to cases of fatty, lardaceous, and suppurative kidney. The left
ventricle, notwithstanding the great waste of tissue that goes on in
those cases, is actually hypertrophied in a certain proportion of them ;
and it is so in the greater number of those with acute Bright's disease,
in spite of the waste of tissue entailed by the great loss of albumen
and blood in such cases. We have already seen that in acute rheu-
matism, over action of the heart tends to induce pericarditis. It is,
therefore, consistent with analogy, reason, and the clinical facts, that
in Bright's disease over-action of the heart should increase the ten-
dency to pericarditis, that tendency being already resident in the
disease. May it not be that on the one hand, the lessened force of the
heart, induced by the weeping of albumen, dropsy, and other secondary
wasting diseases in cases with fatty disease of the kidneys, explains
to some extent the rarity of general pericarditis (1 in 62 l and 1 in
27 2), and the comparative frequency of partial and undeveloped peri-
carditis (1 in 12*4), in that disease ? and that on the other hand, tlio
increased size and action of the heart in cases with granular kidney,
which usually lose little albumen, are not dropsical, and are free from
exhausting secondary disease, tend to increase the frequency of
general pericarditis in that affection (1 in 10 * and 1 in 6 *) ?

Although the cases of partial pericarditis, which amounted to fif-
teen, cannot be classed rightly with those of general pericarditis ; for
the partial variety appears to have a tendency to remain partial, and
those cases are not usually included among those with pericarditis, yet
those cases ought to be studied. One of ' the fifteen cases of partial
pericarditis had acute Bright's disease from scarlet fever (1 in 6 or
16*6 per cent.) ; five of them had fatty kidney (5 in 62, or 1 in 12*4,
or 8 per cent.) ; seven of them had contracted granular kidney (7 in
129, or 1 in 18*3 or 5*5 per cent.) ; and in two the state of the kidney
was not specified.

The proportion in which partial and general pericarditis respectively
attacked the different forms of Bright's disease somewhat correspond.

In four of the cases of partial pericarditis the heart was very large,
(1 in 32*2), and in three it was rather large (1 in 15); while in five of

1 The cases of Bright's disease examined after death in St. Mary's Hospital.
J * The collected cases.

EE 2

412 A SYSTEM OF MEDICINE.

them the heart was of natural size or small, (1 in 16*8) and in three
the size of the heart was not described.

It thus seems that great enlargement of the heart does not favour
the persistence of partial pericarditis, but rather tends to develop
it into general pericarditis.

Amount of Fluid in the Pericardial Sac in Pericarditis from Bright9 s
Disease. — The amount of fluid in the pericardial sac varied consider-
ably in the twenty-five cases of pericarditis from Bright's disease, the
smallest quantity being two drams, and the largest about a pint, in
which case the contents of the sac were purulent.

In one-fifth of the cases (5) the contents of the pericardium are not
described ; and in one-fifth of them (5) there were recent adhesions.
The sac contained only a small quantity of serum, or not more than
one ounce in one-third (5) of the remaining cases (15) ; a moderate
amount, or a few ounces, in another third of them (6) ; and much
fluid, eight ounces in one instance, a pint in another, in the remaining
third (4) of those cases. It is evident that the presence of adhesions,
or of a small, a moderate, or an abundant amount of fluid in the
pericardium, depends on the stage of the pericarditis at the time of
death ; and that in the several cases the fluid had either been re-
moved, or was lessening, increasing, or at its height, when the final
observation was made. It may, 1 think, be admitted that in the
pericarditis of Bright's disease there is less effusion in the pericardium
than in rheumatic pericarditis ; but from the evidence here given it
would appear that there is no very material difference in the amount
of fluid in the sac at the time of death in the two classes of cases.

Character of the Exudation on the Surfaces of the Heart and Pericar-
dial Sac in Pericarditis from Bright }s Disease. — In a small proportion
of cases the lymph covering the heart and lining the pericardium in
case of pericarditis from Bright's disease presents the same pale and
rough surface, firm to the finger, with " cat's-tongue "-like projections,
so usual in pericarditis from acute rheumatism. It was thus in
two of the twenty-five cases that were examined after death at St.
Mary's Hospital. In two other cases also, both of acute Bright's
disease, a rather firm layer of fibrin easily peeled off from the heart,
leaving a finely-injected red surface underneath.

In the majority of cases of pericarditis from Bright's disease the
exudation differs from that usual in rheumatic pericarditis. Universal
adhesions of the heart, rare in the latter, are common in the former
affection ; the heart having been completely adherent in three instances,
extensively so in one, and doubtfully so in another of those cases.
There was pus in the sac in two cases. The lymph — was soft, granular,
imperfectly organized, or in patches in six, in two of which the
presence of pericarditis was perhaps doubtful ; or was bloody or very
red on the surface, or mixed with blood in three of the twenty-five
cases of pericarditis from Bright's disease. These conditions, which
affected nearly two- thirds of those cases, are rare or unknown in
rheumatic pericarditis. The remaining cases were less definite in

PERICARDITIS. 413

character, the heartin four of them having been covered byrecent lymph,
while in two the pericardium was affected with " recent pericarditis."

Appearances in Partial Pericarditis, — The cases of partial or doubt-
ful pericarditis varied much in their features. In four of them flakes
of lymph floated in the serum contained in the pericardial sac, the
surfaces of the heart not being named. Pericarditis was limited,
slight, or in traces or patches in seven other cases, and in two more it
was highly vascular or congested. One case presented rough lymph
easily detached, leaving an apparently healthy surface ; and in the last
instance there was a red fluid containing flakes of lymph in the sac, and
lymph on the heart, the surface of which was healthy. These two
cases, and the four in which flakes of lymph floated in the serum,
were probably free from actual pericarditis.

Physical Signs of Pericarditis Occurring in BrigMs Disease. — Dr.
Taylor gives careful reports of nine cases of Bright's disease with pericar-
ditis, in three of which there was a friction sound, while in six of them
there was no definite sign of the affection. In three of these six cases
there were complete recent adhesions, rendering friction sound im-
possible. In one of the three cases in which pericarditis was not
discovered during life, a layer of soft lymph coated the heart, but
there was no lymph on any part of the loose pericardium, and this
appears to account for the want of friction sound. In one of the
three cases that presented a friction sound, a double creaking noise
was heard between the apex of the heart and the sternum ; and the
heart and sac were covered with soft, slightly rough lymph.

In two of the three cases without friction sound, excluding the
three with complete adhesions, and in two of the three with friction
sound, there was no adequate explanation, after death, of the absence of
that sound in the two former cases, in which the opposed surfaces
of the heart and sac were rough and scabrous ; nor of its presence
in the two latter case? in one of which there were extensive adhesions
of the heart ; while in the other the surface of the heart was simply
red from fine injection, and there were but a few spots of lymph on
the anterior coronary artery.

I possess notes of the symptoms during life, and the appearance
after death of nine fatal cases of Bright' s disease with pericarditis.
I cannot find the notes of a tenth case with regard to which 1 find
two lines of an abstract of symptoms. In seven of the cases immediate
signs of pericarditis were observed, and in three of them the signs of
pericarditis were not observed.

Cases in which the Signs of Pericarditis were not Observed. — In one
patient, a man, aged 61, with granular kidneys, the heart, which was
very fat, was covered and the sac was lined with recent lymph. On thB
third day after his admission, on which day he died, the heart's action
to the left of the ensiform cartilage was loud ; and loud mucous rattles
were audible all over his chest. In the second case, a man, aged 47,
the opposite surfaces of the pericardium, and the heart, at its base, and
along the great vessels were rough with a deposit of fibrin. This

414 A SYSTEM OF MEDICINE.

patient was in the hospital fifty-two days, hut there is only one
note of the state of his heart, which was on the fifth day after his
admission, when its sounds were rather loud.

I cannot find the notes of the remaining case with Blight's disease
and pericarditis ; but the following is the brief abstract preceding the
notes of the examination after death. " At first, doubling of the first
sound, afterwards systolic murmur after epistaxis," so that friction
sound was evidently not observed in this case.

Cases in which the Signs of Pericarditis were Observed. — (1) A creak*
ing noise with a thrill was present in three of the seven cases of peri-
carditis with friction sound; (2) a creaking sound without a thrill
in two of them, and (3) in ihe remaining two there was a "friction
sound."

(1.) Cases with Thrill and a Creaking Friction Sound over the
Seat of the Impulse, and Frottement extending far beyond and especially
below the Region of tlu Pericardium. — There were three cases of this
class. One of them a woman, aged 32, who was in the hospital for a
week, presented after death some fluid in the pericardium, and a rough
deposit of recent lymph of a bright red colour, which covered the heart
and lined the sac. On the day after her admission a systolic murmur
was audible over the cardiac region. Two days later, when she com-
plained of pain going across the chest, the upper border of cardiac dul-
ness was situated at the third space ; and a rasping, creaking friction
sound, chiefly systolic, was heard all over the front of the chest,
and down to the eighth and ninth costal cartilages, its maximum
intensity being at the centre of the sternum, and during the middle of
the systole. Next day a strong thrill extended over the heart from
the right of the sternum to the nipple, and as high as the third cartilage ;
and the creaking sound was triple, being exactly like that made by
the rise and fall and rise in the saddle. On the following day, the fifth,
the thrill was less intense, and there was a triple creak at the apex, the
friction sound being still audible over the lower cartilage ; and two
days later she died.

The second patient, a woman, aged 27, with contracted granular
kidney, and pericarditis, had several patches of recent lymph on the
surfaces of the heart and the free pericardium, and presented a double '
thrill, a double creak, and an extensive friction sound, which were all
absolutely suspended for one day, under the influence of flooding.

The third case, a man, aged 33, had mitral-aortic incompetence,
and highly albuminous urine. The heart and pericardium were greatly
increased in size, and the right ventricle was covered with- a white
fibrinous structure, rough to the finger, like a cat's tongue. On admis-
sion he had pain over the heart ; and for two days, mitral and double
aortic murmurs were audible. He became worse, and on the fourth
day the diastolic murmur disappeared. On the ninth day he was
drowsy, a strong thrill was felt with each impulse from the third
cartilage to the fifth ; a loud grating double friction sound was present
over the seat of the thrill, the rubbing noise radiating thence up to

PERICARDITIS. 415

the top of the sternum, down to the eighth cartilages, and to the left
and right ; a leather creak was audible at the apex ; and a sound of a
friction character was heard behind, over the dorsal spine. On the
next day, when he died, the vibration had increased, and extended
from the third to the seventh cartilages ; it lessened in extent above,
on inspiration, below, on expiration ; and was accompanied by a loud
creak during systole, and a fainter creak during diastole, the sound
spreading from the seat of the vibration over the front of the chest,
and the upper third of the belly.

(2.) Cases with a Creaking Friction Sound, no Thrill being Observed,
over the Seat of the Impulse, and a Frottement extending beyond, and
especially below the Region of Pericardial Dulness. — One of the two
cases of this class was a young married woman, with granular disease
of the kidney. A firm coating partly in ridges and partly like a
cat's tongue covered the heart and lined the sac. On her admission
a creaking systolic friction sound was audible at the apex, in the
fifth space. Four days later, when the pericardial dulness was at its
acme, reaching up to the third cartilage, her respirations being fifty,
the friction sound was no longer creaking but presented itself as an
occasional brush ; but three days after this, or on the eighth day,
there was a loud leather creak over the whole region of the peri-
cardium. After this the friction sound almost disappeared; but on the
twelfth and preceding days it had again burst into full play as an ex-
tensive leather creaking noise, covering the whole pericardium, and
extending down to the seventh cartilage ; and eight days later she died.

In the second case, a man, aged 30, with small, probably granular,
kidneys, recent, bloody, honey-combed lymph lined the pericardium
and covered the heart On the day of his admission the two sounds
of the heart were indistinct. Next day the impulse was extensive,
and a loud double creaking sound, more intense during systole, occu-
pied the whole region of the heart, extending downwards to the
seventh and eighth cartilages, and into the epigastrium. During the
next few days the frottement was much smoother and more restricted
in area. On the eighth day he was weak and in distress ; the friction
sound was audible over the whole pericardium, and beyond it, from the
top of the sternum to the lower cartilage; and he could scarcely swallow
or speak : and in the evening he died.

(3.) Cases with " Friction Sound!' — One of the two cases of this
class, a man aged 38, with granular kidney of full size, had recent
lymph over the whole surface of the heart, and in some places the heart
and pericardium were adherent by cord-like prolongations of lymph.
On the fifty-seventh day there were doubling of the second sound, and
a murmur over the third cartilage. On the seventy-fifth day, which
was eight days before his death, " double friction sound over the peri-
cardium," was noted for the first time. Three days later the pericardial
friction sounds, which were scarcely audible without making pressure,
were mingled with pleuritic friction sounds ; but after this he was too
ill for examination*

416 A SYSTEM OF MEDICINE.

The other patient.an old woman, with contracted granular kidney and
pericarditis, the whole surfaces of the heart and sac being covered
by recent soft granular lymph, complained, on the twenty-first day
after her admission, of great pain at the region of the heart Next day
there was pericardial dulness, and friction sound was present between
the sternum and the left nipple ; and three days later she died.

Several of these seven cases of Bright's disease and pericarditis pre-
sented certain broad features in common. In three of them a thrill
or tactile vibration could be felt over the region of the heart's impulse,
extending from the third to the fifth, the sixth, and in one instance
the seventh cartilages. In one of those cases the thrill extended from
the right border of the sternum across the chest to the nipple. In
these three cases, and in two others in which a thrill was not observed,
a loud sound like the creaking of new leather, usually double, but more
intense and prolonged with the systole, was audible over the whole
seat of the thrill, or when that was absent, over the region of the
heart's impulse. The friction sound was, however, in none of the
five instances restricted to the area of the thrill or impulse, or
even of the distended pericardium; but extended upwards to the
top of the sternum, downwards to the right and left along
the seventh and eighth costal cartilages, and over and even below
the ensiform cartilage. In these cases the wide-spread friction
sound became softer in tone, and especially downwards, as it widened
away from the focus of its greatest intensity. In two of these five
cases with creaking and extended friction sound, the deposit of
fibrin or lymph on the surface of the heart was firm and like a cat's
tongue, in one of them it was rough, in one it was bloody and
honey-combed, and in the fifth, patches of recent lymph were
present on the heart.

In three of these cases there was a period of complete or partial
suspension of the creaking and extensive friction sound ; which after
spreading with great intensity and over a large area, became silent or
feeble and contracted in area for a time, and then suddenlv burst
forth again with full intensity, and over a wide space. It was evident
that under these circumstances, some influences were at work exciting
the heart at the time of the creaking and wide-spread friction sound,
and depressing the heart when that sound ceased or became feeble.
In one instance, the suspension of the thrill and creak was traced to
the influence of flooding.

In the two other patients the surface of the heart is described as being
covered with recent, and in one of them with soft, lymph. In neither
of them is it noted that the coating of lymph was rough. In
both of these cases it is simply stated that a " friction sound " was
present over the region of the heart.

In all of these patients pressure intensified the friction sound.

Cases with a Friction Sound that were not Fatal, or not Examined
after Death. — Besides these seven fatal cases of Bright's disease with
pericarditis in which friction sound was observed, during life, I find

PERICARDITIS. 417

three other cases in which the signs of pericarditis were observed when
the patients were in the wards.

One of these cases, probably fatal, admitted during the recess,
very imperfectly recorded, presented a pericardial friction sound, which
was chiefly present at and below the left nipple.

Another patient, a carpenter, aged 35, had Bright's disease and aortic
regurgitation of some standing. On the eighty-second day he had
great pain in the heart, and four days later a rough double noise
resembling a friction sound was audible over the cardiac region. Four
days after this there was dulness over the pericardium from the third
space downwards, and pain over the heart, relieved by leeches ; and
next day a to-and-fro friction sound was audible over the heart, which
continued for six days ; after which, when he was in distress from
aching over the heart, and sickness, the rubbing noise vanished, being
replaced by the lost diastolic murmur of aortic regurgitation. This
case left the hospital in improved health.

The last case of Bright's disease with friction sound, was one of
great interest, a cab-driver, aged 45. His urine was loaded with albu-
men, and contained coarse granular and fatty casts. There was, on
the fourth day, an extensive impulse, and a remarkable doubling of
the first sound heard all over the region of the impulse, which was
heard along with, but apart from, a peculiar pericardial friction sound
chiefly systolic, which was audible for two inches below the nipple.
This sound which wa3 rasping at first, became creaking two days
later, and five days after that, was only audible when pressure
was made over the same spot, the sound being like that caused by
rubbing together two pieces of emery paper. Next day there was
great extension of the friction sound, which required no pressure
for its production, over the whole region of the pericardium ; and four
days later, the seventeenth after admission, the friction sound was
soft, double, and murmur-like, chiefly heard on pressure, and was ac-
companied by the natural heart sounds, with which it was not rhyth-
mical. I could not make out which sound had the start of the
other. For a few days a systolic friction murmur was audible on
passing beyond the nipple line, and a double rustle was heard on pres-
sure down to the twenty-eighth day. The extensive doubling of the
first sound held its ground throughout, and on the forty- fourth and
fifty-third days a little frottement was again present, produced by
pressure. On the sixty-fifth day he felt lighter over the heart, and a
tremor or thrill was perceived, extending over the cardiac region from
the right to the left nipple. A loud double new-leather creak extended
over the whole of this region, but the rubbing noise spread far and
wide, being heard from axilla to axilla, and down the ensiform and
seventh and eighth cartilages. The thrill and creak retained their
intensity and area for five days, but on the 6 th day the thrill was feeble,
and the creak was replaced by a to-and-fro sound extending from the
third to the sixth cartilage. Doubling of the first sound was mixed
up with the friction sound, but pressure intensified the latter and

418 A SYSTEM OF MEDICINE.

extinguished the former. On the seventy-third day there was no
thrill, and a systolic friction sound, double on pressure, was present
between the fourth and sixth cartilages. Two days later the rubbing
sound was no longer audible without pressure, and was quite lost on the
seventy-ninth day. In this remarkable case the friction sound waa
present over a limited region near the apex, from the fourth to the
twenty-eighth day ; came into play slightly on the forty-fourth and
fifth-third days ; and on the sixty-fifth day burst out, with a thrill, with
great intensity over the region of the impulse, and radiated thence as
from a focus, all over the front of the chest, and down to the eighth
costal cartilages, being audible with a lessening area and diminishing
intensity to the seventy-fifth day. This long and intermittent duration
of pericardial friction sound appears to me to be peculiar to the peri-
carditis of Bright's disease, and is certainly never found in rheumatic
pericarditis.

These ten cases — which I have given with some detail, as, with
the exception of Dr. Taylor's cases and two related, in this respect
briefly, by Traube, I have found no cases of pericarditis from Bright's
disease in which the signs are related — presented features that
are common in them, but are comparatively rare in rheumatic peri-
carditis. A thrill was present, as we have just seen, in four of these
cases or almost one-half (4 in 10) ; and a sound like the creaking of
new leather was heard in six of those cases, or more than one-half
(6 in 10), over the seat of the thrill or impulse ; and that radiated
thence as a softening sound over the front of the chest, beyond the
region of the pericardium, and downwards over the ensiform cartilage
and the seventh and eighth costal cartilages. These signs were much
less frequent in rheumatic pericarditis, since a thrill was present in
only one-fifth of those cases, or 13 in 63, and was distributed over the
region of the impulse in only seven, was limited to the second space
in two, to the apex in three patients, and to both those regions in one ;
and a creaking friction sound was present at or near the time of the
acme of the pericardial effusion in about one-fourth of those cases,
or about 18 in 63. The long duration of the friction sound, and its
frequent suspension, observed in several of those cases of pericarditis
from Bright's disease, likewise distinguish them from those with
rheumatic pericarditis.

Calculus in Kidney, Pelvis, or Ureter; or Dilated Pelvis: — and
Suppurative Nephritis from Stricture, &c. — I have added, in the
Table of Pericarditis in Bright's disease, two sections of cases that,
without ranking under that affection, float upon its borders; and
substantially belong to the same disease in this respect, that the blood
is poisoned, owing to the retention within it of the debris of the
broken-up tissues of the body, owing to the imperfect action of the dis-
eased kidney. In the first series, the secreting structure of the kidney is
often atrophied by the backward compression of the organ, owing to
the distension of the pelvis from the presence of calculus in the ureter,
pelvis, or kidney. None of these cases, amounting to twelve, had

PERICARDITIS. 419

pericarditis. In the second series of cases, numbering thirteen, there
was suppurative disease of the pelvis or kidney, owing mainly to
stricture, or disease of the prostate, or bladder (in 11 cases); in one
case, to calculus in the ureter, and in another to pyaemia. One of these
cases had pericarditis.

I refer to the table for the general condition of these two sets of
cases.

Pericarditis, neither Rheumatic nor from Bright's Disease.

Rheumatic pericarditis, so common in the wards, is rare in the post-
mortem room ; and pericarditis, as we have seen, occurs in as many as
eight or nine per cent, of all fatal cases of Bright's disease. Although
uncomplicated pericarditis is a very rare affection, yet its association
with other diseases when fatal, and generally as an effect of those
diseases, is by no means rare. There is no single malady that is
associated with pericarditis nearly so often as the two just mentioned ;
yet if we combine all the other fatal cases with that affection, except
those with Bright's disease and acute rheumatism, we shall find that
pericarditis is found on examination after death nearly twice as often
in those combined affections as in Bright's disease, and three or four
times as often as in fatal cases of acute rheumatism.

The records of the examinations made after death at St. Marv's
Hospital during the nineteen years ending 1869-70 contain forty
cases of pericarditis that were neither rheumatic nor from Bright's
disease. The accompanying summary shows that thirty-nine of these
cases of pericarditis were associated with some other disease, general
or local, and that in only one case was the affection uncomplicated.

Besides these forty cases of pericarditis, there were sixteen with
partial or slight pericarditis.
{ In addition to these cases I have analysed in one view (1) Dr.

Chambers' complete and valuable table of the causes of pericarditis
in 136 cases observed after death in St. George's Hospital during ten
, years ; (2) thirty-seven cases with pericarditis published in the Patho-

logical Transactions ; and (3) seventy-nine cases collected from various
sources.1 .

A. Three cases of pericarditis and three of slight pericarditis had
pyaemia, one had scarlet fever, and in one the affection was associated
with tubercular disease of the suprarenal capsule; B. twelve cases of peri-
carditis were associated with affections of the heart or aorta; C. fifteen
with affections of the lungs or pleura ; D. one with ulcer, and one with
cancer of the oesophagus ; E. five with affections of the abdomen ; R
\ and besides these cases of secondary or associated pericarditis, there was,

i Corvisart (6) ; Bertin (5); Andral (9) ; Bouilland(16) ; Dr. Stokes (18 including 4
from Testa) ; Dr. Law (2) ; Sir Thomas Watson (8) ; Tringel (18) ; Dr. Graves (5) ; Dr.
Mayne (8) ; Dr. Green (1) ; Dr. Beattie (2) ; and Dr. Thwaites (1) ; Total, 70 case*

II. ASSOCIATED WITH BRIGHTS DISEASE

UMa

"— BS2»-«" "■— ej»**«

*
"T

adb!jL

.s:,.

«n1!:i"

]

A Pericardii!!, tit., amoclated will, t,.m i , r
conititutlor.il dlniM :-
S«oudirTlndam.p7*mia,r>hlFMt eryslp.
With acarlct fever and initial ,„ii,,(ii,i:i.i.
With dteeaae or the eopra-t. mil <Ui.si:li* .
With cancer, notlncldng. I ID cancer ot heart

S— Psrlcardltia, Ac. Aeaociated wllh affectiona
of the Burt :-

Tiibercnlar porieardltia (bul h bad iilit.riii.ia)

Anenrlam of the aaceuding aorta. . , .

Cancer or beart (total rnu or cancer M) .

Heart enlarged without v : . Incom-
peteuue or any otber diHaae
(t. valvee heallhy In elm ....
b. with aomothteaenlngof mitral valve.

n*
1

13G

1
Id

U
a

i
ii

180
111

~S37

7i
i

12
t)

"*"

«
w

ii
i

~13~

■

15S~

7o4

...

•

~2
5

..!

:::

S
9

4
*
1

Aortic regurgitation— a. ascending aorta,

a. aorta atharoiaatoni, valve dliwawd .
e. aorta dilated, valve in™™ --tent,

Mitral-aortic valve-diaeaae

Trlouapld valve-dlaeaaa

Total with valvular dlaease .

C— Perleanlltla, 4c. aaenclatetl with Affectloni
or the Lung! and Pleura :—

Pleurtiy, not with empyema or pneumonia.
Empyema, not Including P ■■ I ■ ■. . . .

Phthlals. not Including pneumothorax, j .
empyema, S ; tubercular pericarditis, *J .

C— Tout,

D— rertcarditia, *c. associated with ulcer, I,

t— Pericardltli two with Altec, of llio AM". : -
Abeceaa or liver. Sa ; [ol rti
Diaphreg. hernia, 1 : lunir.
Parltonitia, Including tl tnbeuin Ijij Ti..i 1 f . nit i -,
not including s phtbiaia. Total caaei .

E— Toi-ar.

F - Peri card! tia appar not aaeo. vrith other affec

Pericardial adhesion ; heart heal t :.v. naL In ilie

1
4

1*5

-§

651

285! 26

4 ; pblhliia, 10 ; peritouitla. 4

nut albuminuria nr general dropaj- : —
asaee of aorta, fi : mitral aortic lalvc-

SuPPLUSMTABT Tabli, thowing the Six* of the Heart in the eaeei enumerated in the
preceding Table, (1) in their total number ; (2) in Wiom wt'A PtrieardHU, complete

and partial; and (3) vrith Pericardial Adheeioni.

—

--.^-^fu-.-*.^

■ ','?:.; "ii; :;„';,■"■

*._*

£i",;ld"X"l

i
j

1
1

;

Scirtet ftier. . . .
Addlton'i dii«us . .
C»ncer (not inolndint
loitllbwncerof luit

4
4

i'i

u
u

:
.

1
1

1
"l

1
1

■"

1
I

'6
J

1
3

A-To»l . .

13G

4 ft

a-m*nia of man [<»(

Wound of nwtt . .

I uU-r ■■:!!. i: MliiMrdltii

II sunn |>1 i r»t*l enlnrgc-

inenlof h*»rt. nM
with tdlM. perl. .

Mitral rcsiirgil ■.n.'ii
Vllral oh.Uu.iUon. .

Mitni-«nrtic mlvo'dii
Tricuspid valve digram
Fatty dsetneritloD i>

11
n
ii
il

■

t
1

,0,0

■•■
I

:
l
1

■
7

IWttl (i.fi.-r 1. ir 0/ *,.;.

a*d ptrUnrdto'h. .

Total mill, valr*i,t<- •!••-

ISO

118

104
71

14 |l

21
15

„ | ~

„

...

C-fliun.no/ Itiaj.arn

Pnenmo-thoni . . .
PhUiSiii ...

Bronehitli ....
Einphyituu ....

tf
U

1»

.'■

i'i

;;

6 LI

H
It
N

1
1

12
*

C-Totai. . .

237

105

Jl|ft

D— Vtan,' Canm of
(EtajJuiffia.

-7

■

E— Dunurj nf Abtloim.
Pentonllli. loclu. 6 o
tub*reulr.pMitonltla
notinclu .l«(iilitlilsl!i
Atvtu ol Urtr. ^ ; o
dUptir. 1 ; dlaphr

mcttdwlth ■tonuirli, 1

71
8

■

i
T

■*■■

1
1

T
l

1
U

104
28

E-TOTAL . .

Uncoinpllc pericard,
Uucom(iliisat«l perl
cardial adlioaiiina .

1
1

OB.NC T..T.L [ 661

138

12 4

10B

Diioiirt Uniur. j MS

til

a sysikm or MSDicnrm.

a PEWCABDmS IN ITS ASSOCIATION WITH OTHEB I
Cat* collected from all Sources.

«_

ill

SI.-::.'- li-.;

i_
I'

1
1

5
5

t-Witll j:.-rii Til "1 1,.'l:-.r;:i1-„.„i,,l In-;.'..-.- ; .

„-B

KrynllWM (In eluded with Py__tn._, St «-_..)■■_ Hoqilul) .

Tnbcri'iilne .li-.-.i.---. ^ 11. [,l i.ivil .-iiTiaulp . ......

Tubercle

(1-W ill. Altec-lon* of tlii? Hurt md Aorta. •—

2«~,:2-

Is"

■

"5"

1
1
*

"To-

Blow i!V.r rli, li™rt(l), |Y;, ;::■;• ,.f [!,. .[. riium fl) . . !
Crniccr of iii-nri ] ., -i- i . ..:■' m-n .:r i,, i^lil.ourluHnl ....

•;•

Kilrl-.ji.l ,|[, .;,:■.,■ ,.,f Wl.Us.il' 111'.! 1

~la~

EnlntKCiim-iit "1 lit in t, v. i ill ■■in ,i.-i-. a: .1 . iiii.i_ntloua . .

OJUODH iimlfannntlvii

ft- Willi Alleetioiiii ot Uii? LAW nn.l Pleuri :—

Plll.-111IL...liLl UIIIUUHJ- WJtl, |,UM|I„1)

i
i

Indefinite nl._i.riua o! till' rlK-.il ° \

li— Willi wo. mi] (1); ■lough.;.); nicer {!); «ni ..nt-or (1) or

15
I

l
1

_.'— IrVflh Arr.ellon. .if lln- ..Wi.iii.ii. iui'ludin,! Hi.' hj.ii.lirnj.-i ii :—
DJaulffiigUMtii- Il.tlii.i (1) . tillN.jilr l-.jiiii._-i Ti-.L null ,l..]ii!i.li

Absceaa of liter (S); oue i-ommuuicile'd wltli pcrldr- |

r.rico.dltla, li..!. jn.odnli.il with olhet mab.-lie.iis ....

Gn.s-n Total . .
* Mot iii.iln.llni. tbw tr-.n Britli-'. di.ci.e.

lse

40*

IB'

U !

78 i

PERICARDITIS. 423

as I have just said, one in which the affection appeared to be primary,
or uncomplicated.

A. General Diseases. — One of the three cases of pyaemia was a school-
boy whdse leg was doubled up under him five days before^his admission.
He came in with hurried breathing, blue lips, and tenderness over the
chest and abdomen ; on placing the hand over the heart a sense of
friction was felt, and a loud pericardial friction sound was heard all
over the cardiac region. He had delirium, and died during the night
The surfaces of the heart and sac were covered with recent lymph in
ridges, and connected by threads ; and the muscular substance of the
heart was firm, and contained numerous minute purulent dots scattered
through the fibres of the left ventricle. Dr. Trotter observed this
patient

This case is typical of a frequent method in which pysenria induces
pericarditis. In such cases the inflammation does not at once attack
the surface of the heart, but spreads to it from the points of suppura-
tive inflammation minutely scattered through the muscular walls of the
organ, just as pleurisy is caused by the masses of suppurative inflamma-
tion spread through the lungs. Dr. Moxon l has seen several cases of
pyaemic abscesses of the heart, mostly in youths with suppurative
periostitis, or acute necrosis of the long bones, in which pericarditis
was often caused by the bursting of small abscesses into the pericar-
dium. This is not however the invariable mode in which pericarditis
is caused by pyaemic abscesses of the heart, since in my case, just given,
and in Mr. Stanley's,2 there was evidently no rupture of the minute
collections of pus in the walls of the heart. Dr. Moxon finds that in
cases with pyaemic inflammation of the lung near its surface the pleura
becomes involved, and thus every diseased portion of tissue is covered
with a layer of lymph ; and that when general pleurisy takes place,
the abscess has generally burst into the pleura, and so caused the
serous inflammation (p. 328). This well represents the parallel condi-
tions in cases of pericarditis caused by pyaemic abscesses in the heart.

Another case may be named, a man, who had rigors on the day after
being operated upon for perineal fistula, and was seized on the follow-
ing day with violent pain in the region of the heart, the sounds of
which were natural. Next day there was a distinct pericardial fric-
tion sound, which was feeble in the evening, and was not again dis-
tinctly audible. He died on the twelfth day after the operation, and
the pericardium was found to be adherent to the heart by a thick
layer of recent lymph. In this case, unlike that related above, the
pyaemic inflammation evidently struck directly at the pericardium,
since violent pain seized the heart the day after the operation, and
next day there was a pericardial friction sound. These two cases
show the rapidity with which the processes of inflammation pass
through their stages in pyaemia.

Pyaemia, including with it erysipelas, was a much more frequent

1 Lectures on Pathological Anatomy, by Dr. Wilks and Dr. Moxon, p. 122.
* MedAco-Chirurgical Transactions, vii. 323.

424 A SYSTEM OF MEDICINE.

cause of pericarditis in Dr. Chambers' cases observed in St. George's
Hospital (22 or 23 in 81 or 1 in 3*8 of the cases of pericarditis that
had neither acute rheumatism nor Bright's disease) than in those
recorded in St. Mary's Hospital (3 in 46 or 1 in 13 6 ; or including
partial pericarditis 6 in 56 or 1 in 9*5).

Fever, in which the serous inflammations are rare, was only asso-
ciated with pericarditis in six instances among those from every source.
This does not include one of small-pox, properly pysemic, nor one of
scarlet fever.

Those constitutional diseases, tubercle, cancer, and syphilis, were very
rarely complicated with pericarditis, or in only one each among the
whole of the combined cases, not including however tubercular
pericarditis or cancer of the heart, in which the action of the disease
was strictly local.

One single instance of chorea, which is so closely connected with acute
rheumatism, had pericarditis. This occurred among the collected cases.

The case of pericarditis associated with disease of the suprarenal
capsules is figured at page 307. This man could not lie down, his
chest was universally dull on percussion in front and at the left side, and
the sounds and impulse of his heart were absent. Upon these grounds
Sir James Alderson, under whose care he was, correctly inferred that
he had pericarditis.

B. Affections of the Heart and Aorta. — In one case, a man,pericarditis
was caused by a wound of the heart. The right ventricle was pene-
trated by a wound about half an inch long, and the surface of the heart,
and that of the pericardial sac were covered with recent lymph, stained
red in many places. He survived the injury nearly five days. The
left ventricle was penetrated by a wound half an inch long. In
another patient who survived nearly two days, fibrinous coagula were
found on either side of the wound, but there was no definite note of
pericarditis. Pericarditis was caused by an injury inflicted over the
region of the heart in two of the collected cases.

Local affections of the pericardium itself, and of the immediately
adjoining structures, whether bearing upon it from within, and
occupying the walls of the heart or ascending aorta ; or from without,
and seated in the neighbouring tissues, all tend to produce pericarditis.
Tubercular pericarditis occurred in two instances ; and as tubercular
disease of the pericardium is rare, it is evident that this affection has
a strong tendency to inflame the surface of the heart.

Among the affections of the structure of the heart that excited
pericarditis by bearing outwards upon the pericardial surface of the
heart, there were four cases with cancer of the heart ; two with fibroid
disease of the heart, in which the disease extended to the surface of
the organ ; and two of abscess of the heart, in one at least of which,
described by Dr. Graves, there was no pyaemia, and in which instance
the abscess contained two ounces of pus, and did not therefore cause
pericarditis by bursting into the sac. These cases are derived from
all sources.

PERICARDITIS. 425

Aneurism of the heart was the cause of pericarditis in another
patient, a well-formed woman, aged 53. The pericardium was dis-
tended with about eight ounces of fluid, and was adherent in front to
the right ventricle., and behind to the left ventricle by quite recent
attachments. The mitral valve was thickened and incompetent. An
aneurism was discovered, on examination, in front of the left ventricle
about the size of a small orange. The walls of the left ventricle were
thickened, but in the position of the sac there was not a trace left of
muscular tissue, and the wall was only formed by the parietal layer.

In all these cases, whether of cancer, fibroid disease, abscess, or
aneurism of the heart with pericarditis, the inflammation of the
surface of the heart is excited in the same manner. The new mass,
projecting into the pericardium, and bearing upon it during the active
contraction of the organ with a rude and unaccustomed force, excites
inflammation in the opposite surfaces of the heart and the pericardial
sac, and so establishes pericarditis.

Aneurism of the ascending aorta excited pericarditis in eight of the
cases derived from all sources ; and three of the twenty-six cases of
that affection observed in St. Mary's Hospital, presented evidence
of previous pericarditis in the form of pericardial adhesion. In these
cases the pericarditis is excited by the constantly enlarging aneurism
bearing upon the pericardium, in the same manner that it is excited
by cancer, abscess, fibroid disease, and aneurism of the heart

Cases with valvular disease of the heart, including all its varieties,
without Bright's disease, were attacked with pericarditis in definite,
but by no means frequent numbers, since that affection appeared in
only 6 of the 117 fatal cases in which the valves of the heart were
incompetent (1 in 20). These proportions are increased if we strike
out the thirty cases of the class under examination in which there
were complete adhesions of the heart, and in which pericarditis was
therefore forbidden. Thus corrected, the attacks of pericarditis number
6 in 87 (or 1 in 14'5). It will be interesting to ascertain whether
valvular incompetence with Bright's disease was more frequently
visited with pericarditis, than when it existed free from that affection.
In 78 cases of Bright's disease with imperfection of the valves, 5 had
pericarditis (1 in 15*6), or, deducting nine in which the heart was
completely adherent, the numbers stand 5 in 69 or 1 in 14. From
these comparative results it would seem that Bright's disease scarcely
increases the tendency to pericarditis in valvular disease of the heart,
for the proportion is almost identical in the two sets of cases. Partial
pericarditis was present in 4 of the 117 cases with valvular insuf-
ficiency that were free from Bright's disease ; and in three of the 78
cases of that class in which the kidneys were affected.

The six cases of pericarditis have been just distributed over the
whole series of cases with valvular disease, the varieties of the
affection being merged under one common title. If, however, we dis-
tinguish the different affections of the valves from each other, we find
a remarkable difference in the proportion in which they were respec-

VOL. IV. F F

426 A SYSTEM OF MEDICINE.

tively attacked with pericarditis. The cases of mitral incompetence
included all but one of those attacks of pericarditis, or 5 in 32 ; or,
deducting 12 with complete adhesions of the heart, 5 in 20 or 1
in 4 of those cases were thus affected. The remaining instance of
pericarditis appeared in one of the thirty-one cases of mitral-aortic
insufficiency, or, deducting fourteen with complete pericardial
adhesions, 1 in 17 of those cases. Not one of 32 cases with aortic
valve-disease, or of 20 cases with mitral obstruction, had pericarditis.

Pericarditis in cases of valvular disease had a strong but not exclu-
sive preference for mitral incompetence among the collected cases,
including those in the Pathological Transactions, for among eleven
cases in which the affection of the valve was specified, eight had
mitral insufficiency, while two had mitral-aortic, and one had aortic
valve-disease. May not the comparative frequency of pericarditis in
mitral valve-disease be due to the resistance to the flow of blood
through the lungs, and the consequent distension of the right ventricle
with blood ; the powerful action of that ventricle, which presses so
strongly upon the walls of the chest in front; and the fulness of
the coronary veins — which occur in the final stage of that affection ?

The cases of pericarditis in Bright's disease, with valvular insuffi-
ciency, were equally distributed over the whole series ; two with mitral
incompetence, one with mitral contraction, one with aortic, and one
with mitral aortic valve-disease being thus affected.

Pericarditis attacked one case in which there was hypertrophy of
the heart without valvular disease, or any other complication except
pericardial adhesion. There were altogether eleven cases of hyper-
trophy of the heart thus circumstanced, and as in six of them the
heart was adherent, rendering pericarditis impossible, that affection
attacked one in five cases of this class.

It will be well to inquire as to the proportion in which pericarditis
attacked cases with and without hypertrophy of the heart. The
heart was enlarged in 130 out of 655 cases of all the kinds
enumerated in the supplementary table at page 421, that were free
from Bright's disease, and among these 130 cases, 12, or 1 in 11, had
pericarditis. The heart was diseased in 86 of those cases in wliich
the organ was enlarged, excluding eleven without other complications
except adhesion ; and including those cases with adherent pericar-
dium, the heart was not diseased in 45 instances. Of the cases just
referred to, 26 of the 86, and 9 of the 45, had pericardial adhesions,
and could not therefore have pericarditis. After deducting the oases
with adhesions, 7 in 60 (or 1 in 8*6), with disease of the heartland
•5 of the 36 (or 1 in 7), without other affection than hypertrophy of
that organ, had pericarditis. Without going into detail it may be
briefly stated that of the rest of the cases, after deducting those with
adherent pericardium, 6 in 104 (or 1 in 17) of those in which the heart
was Tather large, 4 in 267 (or 1 in 66) of those in which that organ
was natural in size, and 1 of the 26, in which it was small, :had
pericarditis.

PERICARDITIS. 427

These returns make it evident that enlargement, or hypertrophy
of the heart exercises a powerful influence on the production of
pericarditis. Besides the cases enumerated, there were 107 (or 1 in
6) in which the size of the heart was not described, and of these sixteen
(or 1 in 6*7) had pericardial adhesions, and* nineteen (or 1 in 4,
excluding those with adhesions) had pericarditis. It thus appears
that the size of the heart was not described in nearly one-half of the
cases with pericarditis, owing evidently to the mind of the reporter
being preoccupied by the morbid anatomy of the inflamed organ. One
of the cases in which the size of the heart is not noted had mitral
incompetence, and may therefore be ranked with those in which the
organ was enlarged ; and ten of them had pneumonia (in 6), pleurisy
(in 3), or empyema (in 1). In these ten cases the labour of the right
ventricle must have been increased and prolonged, with the effect of
enlarging the right side of the heart. This would tell more on
the cases with pi euro-pneumonia than in those with simple pleurisy
or empyema, but in such cases, with much effusion into one side of
the chest, the obstacle to the stream of blood through the lungs is
often great. This was well evidenced in a case, already alluded to at
page 140, of extensive effusion into the right side of the chest which I
saw through the kindness of Dr. Wane. Mr. James Lane drew off a
large quantity of fluid from the affected side. Before its removal there
was a mitral murmur and doubling of the second sound. The doubling
disappeared when the fluid was being extracted, and after a time the
murmur vanished. In these cases, therefore, the prime effect of the
spreading of inflammation from the pleura to the pericardium was
heightened by the added secondary influence of the increased size
and labour of the right ventricle.

C. Eight patients with pneumonia (8 in 46), three with pleurisy
(3 in 26), and two with empyema (2 in 17) had pericarditis. In
all these cases (13 in 89), whether the primary affection, was pneu-
monia or pleurisy, it was the pleurisy affecting the outer surface of the
pericardium, and spreading thence to its inner surface, that immediately
kindled the pericarditis.

Three of the eight cases with pneumonia and pericarditis were
under my care, but in none of them did I detect a friction sound.

Two of the three cases with pleurisy and pericarditis were my
patients, and in both of them friction sound was heard. One of these
was a little girl, who had been attacked a fortnight before with pain
in the left side and over the heaTt, and was brought to the hospital in
the mother's arms, in distress, pale, and breathing hurriedly. There
was extensive pleurisy of the left side, and next day there was dulness
on percussion, and a double, rather smooth friction sound over the whole
pericardium. Chorea soon appeared, and on the seventh day, when
there was a mitral murmur, the effusion had reached its acme. Two
•days later, when the friction sound was limited to the lower sternum,
she died. The other case was a man who had been ill six months
with pleurisy of the left side. On the eleventh day after admission

F F 2

428 A SYSTEM OF MEDICINE.

double pericardial friction sound came into play, and continued to the
nineteenth day. After two days it vanished from over the heart, and
was only audible at the apex ; it was thus ten days later, and on the
following day he died. The heart was almost universally adherent by
yellow lympn.

Although in these thirteen cases the pleurisy excited inflammation
of the exterior of the pericardial sac, which travelled through its fibrous
structure to its interior, and then attacked the surface of the heart ;
yet in many of the seventy-six other cases with pleuro-pneumonia or
pleurisy the exterior of the pericardium was inflamed, and yet the sac
proved to be a barrier to the inflammation, which did not extend
inwards so as to excite pericarditis. We have seen that in rheumatic
pericarditis the inflammation habitually travels through the fibrous
walls of the sac, and attacks its exterior, or pleural surface, exciting
pleurisy; so that pericarditis tends to pass from within outwards
much more than pleurisy of the pericardium does so from without
inwards.

A case of pleurisy with pericarditis, under my care, that recovered
presented a peculiar pericardial friction sound on pressure, to the left of
the lower sternum, that lasted about three weeks.

I have just alluded to the important secondary influence which the-
increased size and force of the right ventricle exercises in reinforcing
the primary influence of the extension of the inflammation from the
pleura to the pericardium in cases of pneumonia and pleurisy.

Pericarditis attacked two cases of phthisis out of a toted number
affected with that disease amounting to 12. This does not include
the two cases of tubercular pericarditis with phthisis already spoken of.
Dr. Stokes gives an important case communicated to him by Dr.
McDowell in which pneumo-pericarditis was caused by a fistulous
communication between the pericardium and a small cavity at the-
summit of the right lung ; the apices of both lungs were healthy, but the
bases of both lungs were solidified from a deposit of miliary tubercle and
from pneumonia.1

D. Two cases were attacked with pericarditis owing to disease of
the oesophagus where it passes behind the pericardium. In one of
these patients, who was under the care of Dr. Chambers, the oesophagus
was ulcerated from the bifurcation of the trachea to half an inch above
the diaphragm. The ulcer gave way into the pericardium, which was
filled with fluid from the stomach, and the interior of the sac was
lined, and the heart was covered with recent fibrin.

The other patient, with cancer of the oesophagus behind the peri-
cardium, a woman, aged 47, a cook, under my care, complained of
slight difficulty in swallowing, referred to the fauces. A to-and-fro
friction sound, louder with the diastole than the systole, was audible
over the cardiac region, being most intense over the sixth cartilage,
and heard from thence to the ninth cartilage. Pleural friction was
also present. This patient died on the fifth day after admission,

* Dr. Stoke9, On Diseases of the Heart and AorPr, p. 25.

PERICARDITIS. 429

E. There was a small and remarkable group of cases, in which
pericarditis was caused by affections involving the diaphragm. One
of them had diaphragmatic hernia; two others had abscess of the
liver involving the diaphragm ; and another had a tumour connected
with the pericardium, and communicating with the stomach.

In the case of diaphragmatic hernia which was under the care
of Sir James Alderson, the stomach, omentum, spleen, and transverse
colon were forced through an opening into the left side of the chest,
which contained six pints of liquid, parfly digested blood, partly food.
The heart was displaced to the right of the sternum, and there was
pericarditis.

In one of two other cases an abscess, with thickened walls, con-
taining several ounces of greenish pus, was situated between the pericar-
dium and the liver, involving the diaphragm, and communicating with
a small abscess in the liver. The pericardium contained many ounces
of puriform fluid, and its lining membrane and the surface of the heart
were " hypenemic," the latter being very red and velvety. In the
other case, the diaphragm was pushed up by the liver in a conical pro-
jection, which was formed by an abscess occupying the interior portion
of the left lobe of the liver, and the contiguous part of its right lobe.
The pericardium contained two or three ounces of turbid fluid, and
the surface of the heart was roughened by a recent deposit of lymph.
Dr. Graves gives an important case in which pneumo-pericarditis
was caused by a hepatic abscess which communicated with the peri-
cardium and the stomach.

In the fourth case the pericardium was full of thick yellow fluid
and there were some nodules on the aorta; a dense white tumour
which was interposed between the pericardium and the diaphragm was
softened in the middle, and formed a cavity which communicated with
the stomach and spleen, and resembled an ulcer.

One case of peritonitis out of a total of 64 had general, and another
had partial pericarditis.

F. There remains one fatal case of pericarditis in which there was
no evidence that the affection was secondary to, or associated with,
any other disease.

In this patient, a woman, aged 44, the pericardium was nearly the
eighth of an inch thick, and its sac contained a large quantity of sero-
purulent fluid. The surfaces of the heart and the sac were covered
with recent layers of plastic deposit, which was arranged at the base
in a honeycomb shape, and was lengthened out at the apex into
bands. The heart was small, hard, and contracted ; the lungs were
congested behind ; and there was a quarter of a pint of brown fluid
in each lateral cavity of the chest.

Two cases of pericarditis, under my care in St. Mary's Hospital,
presented no other definite affection. One of these, a schoolboy, aged
12, was attacked, eighteen days before his admission, with pain in
both sides of the chest, worse in the left. On admission the impulse
of the heart was in the fifth space, there was fulness over the pericar-

430 A SYSTEM OF MEDICINE.

dium, dulness from the second cartilage to the sixth, and a loud to-and-
fro sound, which was intensified by pressure, over the same region and
up to the top of the sternum. Next day the dulness had lessened, but
the friction sound was strong and grating, and extended beyond the
region of dulness. For several days it was more feeble and limited ;
on the fourteenth, and two days later, it was again louder, but on
the nineteenth day it had vanished. The other patient, a pregnant
woman, took cold six weeks before admission. The heart's action
was tumultuous, and on the third day the impulse extended from
the sternum to two inches and a half beyond the left nipple, a to-and-
fro sound appeared over and below the region of the heart, and a
mitral murmur at the apex. Next day an impulse of a grating
character, almost a thrill, extended over the region of the friction
sound. These signs continued with variations, b\jt lessening, and on
the fourteenth day the impulse had shrunk inwards for two inches
and a half, being bounded by the nipple line. Three days later a
systolic murmur was converted by pressure into a friction sound, which
disappeared on the eighteenth day.

The Treatment of Pekicabditis.

Pericarditis, as we have just seen, is so rarely met with except as a
combination of, or associated with, some other disease, that in the
treatment of such cases we have to consider mainly the primary
affection, and along with this the local management of the secondary
inflammation of the pericardium. I shall of course here practically
limit myself to this latter and local point. It will be important,
however, to touch upon the measures, in the treatment of the main
disease, that may tend to prevent the occurrence of pericarditis.
I shall briefly consider (1) the preventive treatment of acute rheu-
matism, in relation to the possible occurrence of pericarditis and (2)
the local treatment that the presence of pericarditis may render
desirable in those diseases which are more or less frequently compli-
cated with that affection.

(1) The chief objects to be kept in view in the treatment of acute
rheumatism are (1) the mitigation of the endocarditis that is the usual
and natural effect of that disease, and (2) the prevention of pericar-
ditis, which, though the frequent, is not the customary complication
of that disease. Fortunately the measures that tend to palliate the
inflammation of the interior of the heart, tend also to prevent the
inflammation of the exterior of that organ. The Address in Medicine,
given at the meeting of the British Medicine Association in Newcastle-
on-Tyne, was devoted to the treatment of acute rheumatism by rest and
the relief of local pain, with a view to prevent pericarditis and lessen
the severity and permanent ill effects of endocarditis. The publisher
of this work will supply the reader, if he desire it, with a copy of that
Address. The absolute rest of every limb and joint ; and the soothing

PERICABDITIS. 431

application of the belladonna and chloroform liniment, sprinkled on
cotton wool, to the affected joints, supported by flannel, applied over
the seat of pain with uniform and comfortable pressure, are the most
important measures in the treatment of acute rheumatism for the
prevention of pericarditis. The rest and support of the affected
joints should be strictly maintained for several days after the
disappearance of the local inflammation ; for the too early use of an
affected joint or limb, after the relief of pain and swelling, often leads
to a relapse, first attacking the joints of the over-used limb, extending
to other joints, and often producing endocarditis and pericarditis.
I have given, at pages 210, 211, brief notes of six cases in which a
relapse of the joint affection, usually thus occasioned, induced endo-
carditis and pericarditis.

2. The employment of a few leeches, and the application of
cotton wool or a poultice, sprinkled with the belladonna and
chloroform liniment, over the region of the heart during the early
and painful period of an attack of pericarditis, are the means
that I have for a long time employed in the treatment of that
affection.

I have before me the collected notes of 36 cases of pericarditis, in
which several leeches were applied over the region of the heart. In
29 of these cases there was pain over the region of the inflamed
pericardium, and in 7 of them there was no note of the presence of
pain. In 24 of the cases suffering from pain, marked relief, sometimes
complete, followed upon the application of the leeches ; and this relief
in a fair proportion of the cases so speedily followed the local bleeding
that the relief must be attributed to the leeching. Brief notes of
cases in which the application of leeches relieved the pain over the
region of the inflamed pericardium will be found in the preceding
pages (211, 219, 231, 238). The local bleeding, besides assuaging the
local pain, lessened the oppression in the chest and the difficulty of
respiration in many cases.

In one instance leeches were applied over the seat of pain five
times ; although on each occasion relief seemed to follow, yet the pain
soon again increased.

In five cases leeches gave little or no relief. Although in these
cases pain was not materially lessened by the local bleeding, yet in
every instance but one, its action on the patient's state seemed to be
favourable. In that patient (17), whose case has been already referred
to at pages 219, 232, 235, and 237, there was pain over the heart,
the action of which was very tumultuous at the time of admission.
Leeches were applied with great relief, but unfortunately the bleeding
from one of them could not be stopped, and she lost much blood.
After this the action of the heart was irregular and intermittent, and
she was evidently weakened by the haemorrhage. She finally died
after a long and severe illness, which was closed by an attack of
small-pox.

The employment of leeches produced a definite but very variable

432 A SYSTEM OF MEDICINE.

effect on the friction sound, and tended to lessen the force and extent
of the impulse. Sometimes the friction sound was lessened in
intensity (in 8), but as often it became more intense (in 8) after the
local bleeding. In one patient (35, pp. 327, 360) its effect was to
suspend the rubbing sound, which had been previously extensive and
rough, for one day ; but in the evening pain returned, and with it the
frottement over the region of the heart. Another patient (16) on
admission had excessive pain across the heart, where there was a
double thrill, and a double harsh scraping friction sound ; four leeches
were applied ; and next morning there was scarcely any pain, no
friction sound, and no note of thnll. The friction sound returned on
pressure that afternoon, and was again present on the following day.
In one instance — I speak from memory — I examined a patient with
pericarditis immediately after the withdrawal of leeches, and found that
the friction sound that had been previously audible was entirely
abolished. This disappearance of the friction sound in such a case
is evidently not due to any change in the character of the lymph on
the surfaces of the heart and sac, although their vascularity may be
lessened, but to the diminished force of the action of the organ. In
direct confirmation of this, we have already seen that in several cases
friction sound was abolished, suspended, or softened, by the weakening
of the action of the heart (see pages 235, 360).

The effect of leeching the region of the heart on the amount of
effusion in the pericardium in cases of pericarditis was not very
marked. The leeches were applied at the time of the acme of the
effusion in ten cases, and in all of them but two the amount of
effusion had lessened on the following day, and in the remaining two
on the third day after the local bleeding, which lessened local pain in
eight of these cases. To balance these instances, in eight others the
effusion increased after the application of the leeches, and attained its
acme in a day or two ; at the same time, however, the pain over the
region of the heart was relieved in six of those cases, but was not
so in two of them.

Blisters applied over the heart are frequently employed in the
treatment of pericarditis. I resorted to them occasionally up to the
year 1856. I cannot, however, find any instance in which they
appeared to be of service, and they were certainly, in some cases, a
source of discomfort. It is evident that a blister over the region of
the heart adds a second and outward inflammation to the primary
and inward inflammation, and it therefore, unless there is a counter-
balancing gain, increases the eviL Blisters were the definite cause of
mischief in a case that I shall have occasion to quote when I speak
of the removal of the fluid from the distended pericardium. In that
instance they were applied seven times in succession over the pre-
cordial region. A blister cannot alter the lymph covering the heart
and lining the sac ; and cannot directly lessen the amount of fluid in
the pericardium, which as we have again and again seen, tends of itself
to diminish rapidly when it has reached its acme. It appears to me

PERICARDITIS. 433

that a blister over the distended pericardium would rather increase
than lessen the morbid supply of blood to those inflamed parts to
which it is so contiguous. Blisters, besides inflicting local injury,
taint the blood by increasing its fibrin, and are apt to lead to a
secondary and low kind of inflammation in distant parts, and perhaps
even to degrade the character of the pericardial inflammation itself,
and to prolong its existence.

It may be said that exciting pain at the surface of the chest in these
cases lessens the severity of the internal pain. This is true, but this
effect may be induced innocuously, by the application of chloroform
over the seat of suffering, combined with belladonna liniment, sprinkled
on cotton wool, and covered with oiled silk.

Paracentesis of the Pericardium. — We have seen again and again
that when the fluid in the pericardium has reached its acme, it very
soon begins to diminish.. It is therefore evident that puncture of
the pericardium is very seldom called for. In some rare instances,
however, the quantity of serum in the sac is so great as to interfere
seriously with the action of the heart, breathing, swallowing, and
speech ; owing to the compression of the auricles and venae cavae, the
trachea and left bronchus, the oesophagus and the descending aorta ;
and the inflammation of the recurrent nerve. Generally the fluid of
itself lessens so quickly that these threatening symptoms pass by
without real danger to life. In some rare instances, however, life is in
danger owing to the distension of the pericardium, and then paracentesis
of the pericardium may become urgently called for.

Riolan,1 in 1649, proposed that in dropsy of the pericardium, the
sac might be opened by trephining the sternum an inch from the
ensiform cartilage. Senac,2 and Laennec,3 at long intervals, both gave
the same advice, the point selected by Laennec being immediately
above the ensiform cartilage. Desault4 attempted to open the
pericardium between the sixth and seventh ribs, and Larrey,6 between
the fifth and sixth ribs ; but they both evidently failed to enter the
pericardium. Romero6 opened the pericardial sac in three cases of
" hydro-pericardium," twice with success, through an incision made
in the fifth space, near the junction of the cartilages to the ribs,
this wound being made, partly to explore, partly to open the pericardium
or the pleura. The first circumstantial account of tapping the pericar-
dium was in a patient of Skoda's, with pericarditis from cancer of the
heart, operated upon by Schuh in 1840,4 who first inserted a trocar by
a perpendicular puncture through the third space close to the sternum
over the great arteries, and failing to get fluid, penetrated the sac through
the fourth space and obtained a certain amount of reddish serum. This
patient lived for nearly six months, and died with extensive cancer of

I Encheiridium Anatomicum ct pathologicum, p. 213.
f Senac, de la Structure du Cceur, ii. 369.

3 Laennec, Traiti de V Auscultation Mediate.

4 Trousseau et Las^gue, Arch. Gen. de Med. Nov. 1854.

5 Bid. des Sc. Midicalcs, v. xL, p. 370. These cases are given imperfectly.

434 A SYSTEM OF MEDICINE.

the chest.1 In 1841 Heger performed paracentesis of the pericardium
in another patient of Skoda's, with pericarditis. He entered the
pericardium through the fifth space, two inches from the left border
of the sternum. Altogether 1500 grammes (about 48 ounces) of a
brownish serum, finely flocculent, escaped, and nineteen days later,
the fluid having reaccumulated, he again punctured the pericardium at
the same place, and 500 grammes (about 16 ounces) of a reddish
troubled fluid escaped in the course of four hours. This patient died
51 days after the second operation. The pericardium was in great part
adherent, and there were nine and five pints respectively in the two
sides of the chest, and a tubercular cavity of the left lung. These two
patients died from the primary diseases, cancer, and tubercle ; but both
operations were successful.

Behier thought that he punctured the pericardium through the sixth
left space in a case related by him in 1854 ; the patient died twenty-six
days afterwards, but there was no pericarditis, and no mark of punc-
ture in the walls of the sac. Jobert,2 in 1854, after cutting the skin
punctured the pericardium with a trochar, in a case of pericarditis,
a patient of M. Trousseau's, through the fifth left space, 1*2 inch from
the edge of the sternum. The cannula was agitated by the beating of
the heart — the fluid came at first in drops and then very slowly, and
altogether 400 grammes (about 13 ounces) of liquid flowed in the
course of an hour-and-a-half. The patient left the hospital eleven
weeks after the operation, suffering from phthisis. Trousseau,3 in 1856,
operated on another case, and opened the chest with a bistoury below
the nipple through the nearest intercostal space, and penetrated into
the pericardium, from which flowed nearly 100 grammes (about three
ounces) of a red serosity ; and twice as much yellow serum came from
the pleura. The patient died five days after the operation. The last
of the French operators that I shall name was M. Aran,4 who in 1855,
after cutting through the skin, penetrated the pericardium with a
trochar through the fifth space, about an inch from the extreme limit
of pericardial dulness, and withdrew about 350 grammes (fully 11
ounces) of reddish transparent fluid, and then injected a solution of
iodine.1 Twelve days later he tapped a second time and withdrew
1,350 grammes (about forty ounces) *of albuminous liquid. This
patient recovered from the operation, but three months later presented
signs of phthisis.

I have now to speak of two important cases of pericarditis with
symptoms threatening life, in which Dr. Clifford Allbutt resolved with
his colleagues on the performance of paracentesis of the pericardium.

1 Trousseau and Lasegue publish this case at length in the Archives, but in his
Clinique Mklicale Trousseau states that Sehuh penetrated in his first puncture a mass of
cancer, altogether of a thickness of six inches, which had invaded the sternum. It was
not, however, until more than a month after the operation that this tumour showed
itself. Arch. G. de Med., 1854, p. 520.

9 Trousseau et Lasagne, Arch. O. de Med., 1854.

3 Trousseau, Clinical Medicine. New. Syd. Soc.y iii. 865.

4 Bulletin de V Academic Royalc de Attdicine, xxi. 142.

PEEICABDITI3. 435

One of these cases was operated upon by Mr. Wheelhouse, who vividly
describes the condition of the patient and the steps of the operation.
He found the patient sitting up in bed, his head resting on his
hands, his elbows on his knees, struggling for breath. I quote the
following from his description, and refer to his paper for the full
details of the operation ; and the precautions adopted during its per-
formance : — " I chose for my purpose a small trochar. This I placed
on the upper margin of the fifth rib, half an inch to the left of the
sternum ; and inclining it upwards and inwards, thrust it steadily
forwards through the intercostal space towards what I believed to be
the centre of the ventricle. I pushed it onwards until I could distinctly
feel the movements of the heart with the instrument; and then,
sheathing the point, I advanced the cannula well up to the heart, until
I could feel and see, and demonstrate to those around, the impulse of
the heart as communicated to the instrument. The trochar was then
withdrawn, and the fluid allowed to escape. This it did at first in a
steady stream, which soon subsided into a saltatory flow coincident
with the heart's contractions. The fluid consisted of a pale pink
coagulable serum, and, upon the whole, about three ounces escaped.
During the operation the patient gradually obtained relief; and after
the cannula was withdrawn, the bed-rest was removed, and he was
able to lie down."1 This patient completely recovered, and was in
perfect health the other day when Mr. Wheelhouse, in reply to my
inquiries, kindly informed me as to the state of the patient. In the
second of Dr. Clifford Allbutt's patients Mr. Teale drew off, as Mr.
Wheelhouse had done, through a fine cannula five ounces of fluid
which gave the patient great relief. The reaccumulation of the fluid
called for a second operation, which was performed with considerable
relief. Finally, however, this patient, a girl, died of bronchitis.2

The operation has been performed within the last three years on
three occasions, and I owe the references to these cases to the kind-
ness of Mr. Holmes. M. Villeneuve, in 1873, operated by means of the
aspirator, on a child with arching and fluctuation over the precordial
region. He punctured the tumour at its most prominent part, and
removed two syringe-fulls of serum. On withdrawing the cannula a
jet of liquid spirted out of the wound, which remained open owing to
the internal wall of the cavity having been very much thinned by the
repeated application of blisters, seven of them having been placed one
after another, without any improvement, on the same place. A peri-
cardial fistula, yielding pus, was established and did not heal up until
the sixth month after the operation.8 In the other case, a man in
whom paracentesis of the chest and abdomen had already been per-
formed, Dr. Valtosta, in 1874, opened the pericardium by making an
incision over the fifth space, commencing about half an inch from the
sternum. The layers of muscles were then carefully divided and an

1 Sec British Medical Journal, Oct. 10, 1868, p. 885.

2 See Dr. Clifford Allbutt's important paper, Lancet, 1860, i. 807.
8 London Medical Record, iii. p. 532.

436 A SYSTEM OF MEDICINE.

elastic dilatation was felt. A puncture was made in this, the point
of a small trochar was introduced, and about ten ounces of fluid was
removed with immediate relief. This patient died four weeks after
the performance of the operation.1 M. Chairon contributed a third
case in 1875, in which more than 1000 grammes (about 33 ounces) of
liquid were removed from the pericardium. The result is not given.
With reference to the method of operation, he says the spot to be
preferred is the fifth intercostal space, at an intermediate point between
the nipple and the sternum, rather nearer to the former, always being
guided by the apex of the heart. The aspiratory method should, he
considers, be preferred.2

Proposed Operation for Paracentesis of the Pericardium. — This
operation cannot well be called for unless the amount of effusion into
the pericardium be so great as to compress the venae cava* and the
auricles, the oesophagus, trachea, and left bronchus, and the descending
aorta, so as to interfere with the action of the heart, swallowing,
breathing, and the supply of blood to the abdomen and lower limbs.
Under these circumstances the pericardial sac is greatly distended
downwards towards the abdomen, and the heart itself is elevated. The
result is that the mass of the fluid occupies a large space below the
heart, measuring between one and two inches from above downwards,
between the lower surface of the ventricles and the floor of the peri-
cardium, where it is formed by the central tendon of the diaphragm ;
which is depressed downwards almost or quite to the level of the
upper border of the sixth space, in the manner represented in the
figures at pages 311, 338, 340, and 378, and also, in principle, in
Pirogoffs important work.

When it is considered that in these serious cases the lower border
of the heart is above, while the mass of the fluid is below the level of
the lower edge of the fifth cartilage, I advise that the fine trochar,
such as that used by M. Aran, Mr. Wheelhouse, Mr. Teale, and M.
Chairon, should be inserted into the distended pericardium at a point
just above the upper edge of the sixth cartilage at the lowest part of
its curve, more than an inch within the mammary line ; and that the
instrument should penetrate gently inwards with a direction slightly
downwards, so that it may advance into the collection of fluid below
the level of the heart ; and that the liquid should be slowly and gently
extracted by the use of a syringe or the aspirator. By this proceeding
the collected fluid will be alone penetrated and the heart will be quite
untouched. Extensive incisions, and the injection of irritating fluids
should be of course avoided.

In every case in which the heart has been previously healthy, and
is of the natural size, its lower border is elevated above the level of
the fifth space when the effusion into the pericardium is at its height,
so that in such cases the procedure I have advised, which has the
sanction of Aran's and Chairon's operations, can be performed with
ease and safety.

1 London Medical Record, iii. p. 275, 532. * JbiJ, p. 694.

PERICARDITIS. 437

When, however, the heart is enlarged owing to the existence of
valvular disease of some standing, the heart is sometimes, as in the
cases spoken of at page 336, to be felt beating in the fifth or even
the sixth space at the time of the acme of the effusion, when the
urgent distress and danger of the patient may demand paracentesis
of the pericardium. Under such circumstances, which can be readily
discovered by ascertaining the position of the impulse — which should
always be some distance above the point of penetration, for a thin
layer of fluid interposes itself between the surface of the heart above
its lower border, and the front of the chest — another point than that
just indicated in the fifth space must be chosen for the operation. This
point should then be selected at the space bet\vreen the left edge of the
ensiform cartilage and the right border of the seventh cartilage in the
epigastric region ; or, if needful, owing to its margin being covered by
the seventh costal cartilage, the ensiform cartilage, at its left border,
may itself be perforated, first with the point of a bistoury, and then
with the fine trochar. Trousseau states that Larrey advised that the
puncture of the pericardium should be made through this space ; but
in the operation which he performed with a view — erroneous in this
instance — to enter the pericardial sac, that great surgeon, as we
have seen, entered the cavity of the chest between the fifth and sixth
ribs. The lower border of the fully-distended pericardium is usually
a little above, and sometimes even below, the lower end of the
ensiform cartilage, as in figure 42, page 342 ; which is from a case,
exactly in point, with mitral regurgitation and enlargement of the
heart ; and the pericardium may therefore be safely punctured through
a point corresponding to the middle or the lower portion of that
cartilage. The presence or absence of the impulse of the right
ventricle in the epigastric space, and the position of the lower
border of the pericardial dulness in that space, must be previously
ascertained. Those two important points of diagnosis, which can be
readily made, will prove a safe guide to the surgeon as to the place
which he should select for the operation, which he will rightly fix
sufficiently below the seat of the impulse, so as to avoid the heart ;
and sufficiently above the lower border of pericardial dulness, so as
to prevent the cannula being tilted upwards when the floor of the
pericardium elevates itself as the sac is being emptied. When he
pushes the trochar onwards he must use all the precautions so clearly
described by Mr. Wheelhouse, so that if the point of the instrument
comes upon the front of the heart, he may withdraw the trochar at
the same time that he gently presses the cannula forwards and
downwards.

In the great majority of cases the fluid, after it has reached its acme,
soon begins to lessen, and continues to do so steadily from day to day.
Under these circumstances I do not advise the use either of aperients,
which tend to disturb and lower the patient, or of diuretics. If,
however, the quantity of the fluid is stationary, or lessens very slowly >
then diuretics mav sometimes be of use.

438 A SYSTEM OF MEDICINE.

ADHERENT PERICARDIUM.

BY FRANCIS SIBSON, M.D. F.R.S.

The discovery of adherent pericardium during life is in some cases
impossible, and in some, doubtful or difficult ; but in others, and these
are amongst the most important cases, its existence may be ascertained
during life on reasonable and well-ascertained grounds.

When the adhesions are partial, or when the heart, though com-
pletely adherent, is small, is not bound by external adhesions to the
anterior walls of the chest, and is covered to the natural extent by the
lungs, their expansion being free and unconstrained, then the varying
relation of the heart and lungs to the chest is quite natural, and the
diagnosis of the adhesions is impossible. If the adherent heart be
enlarged, and is not attached to the lower half of the sternum and the
cardiac cartilages by combined pericardial and pleural adhesions, so that
the active or automatic and the passive or respiratory movements of
the heart are scarcely or but little interfered with, the inspiratory
expansion of the lungs is freely permitted, and the diagnosis of the
adherent pericardium may be difficult, obscure, or even impossible.

When, however, the heart is, as usual, enlarged, being often affected
with valvular disease, the adhesions may be short, fibrous, and binding ;
and the front of the organ may be fixed to the two lower thirds of the
sternum and the adjoining cartilages by pleuro-pericardial adhesions,
so that the automatic and respiratory movements of the heart, and the
inspiratory expansion of the lungs are restrained : thus the discovery
of the adhesions during life may generally in such cases be made
by a careful study of the physical signs; its diagnosis being the
more certain and easy in proportion as the heart is more enlarged,
and more firmly fixed to the anterior walls of the chest

Anatomical Description of Adherent Pericardium.

Partial Adhesions. — Pericardial adhesions vary greatly in firmness
of tissue and length of fibre, and when they are partial they are
usually longer than when they arc general.

Four conditions seem to regulate the position, extent, and firmness
•of partial adhesions of the heart. (1.) The amount of movement of the
various parts of the heart and arteries ; for it is evident that the more

ADHERENT PERICARDIUM. 439

limited the movement of any part, the greater must be its tendency
to adhesion : the relation of the surrounding sac (2) to the heart ;
and (3) to the outer borders of the pericardium, which are close to the
heart, and are therefore more often adherent: (4) the gravitation of
the heart in the fluid, since the posterior or depending parts of the
heart, when the patient lies on the back, attach themselves readily to
the parts on which they rest.

Partial adhesions take place most frequently near the apex and
along the line of the ventricular septum ; at the outer border of the left
ventricle and the outer side of the right auricle, where the movements
of those cavities are most limited, and to which parts the outer borders
of the sac cling ; the posterior surfaces of the left auricle and of the
ventricles which rest upon the sac ; and the great arteries at their higher
parts, where the extent of their movement is least, and where they
are most contiguous to the pericardium. The visible commencement
of the ascending aorta is often free from adhesions, owing to the
hollow, containing liquid, formed in front of that part of the vessel,
between the appendix of the right auricle and the origin of the
pulmonary artery. In several instances a patch of the right ventricle,
to the right of the septum, and midway between the pulmonary artery
and the lower border of the ventricle, was adherent when the rest of the
ventricle was free ; and it is to be remarked that this patch is the part
of least movement, or stable equilibrium, of the walls of the right
ventricle (see fig. 16, page 66). A frequent seat of partial adhesions
is a point a little above and to the left of the apex of the heart.
These adhesions near the apex frequently become stretched and at-
tenuated, and at length give way. Several pendulous, filamentous,
fibrous bands often hang from this point, near the apex, on the surface
of hearts that are free from internal disease ; but which display white
fibrous patches on their surface ; the filaments and the patches being
evidently alike the result of a previous attack of pericarditis.

The parts of the surface of the heart and arteries that are usually
not adherent when other parts are so, are the front of the right ven-
tricle, especially in the neighbourhood of the right auricle and pul-
monary artery, and above its own lower border; the appendix and
ventricular border of the right auricle ; and the parts of the aorta and
pulmonary artery nearest to the heart, those being the parts that have
respectively the greatest extent of movement during the action of the
heart, as may be seen in the figures at page 66.

General Adliesions. — The adhesions are formed of fibrous threads of
variable and often of considerable length, and they usually allow of
a fair amount of movement of the heart. Long and loose adhesions
interfere but little with the free play of the heart ; but short, close, and
firm attachments embarrass the action of the organ. The length of
the fibres of adhesion varies over the different parts of the heart; their
length usually corresponding to the amount of movement, and the power
exercised by the respective parts during the action of the oigan. The
adhesions are generally longer at the apex than elsewhere : those oyer

440 A SYSTEM OF MEDICINE.

the left ventricle are longer than those over the right ventricle ; those
over the auricular portion of the right ventricle are longer than those
over its body and near the septum, and I believe that the same
applies to the left ventricle also. The adhesions over the right auricle
are much shorter than those over the right ventricle; and the auricular
appendix is contracted in size by the fibrous covering. The attach-
ments of the left auricle, the aorta, and the pulmonary artery are
generally closer than those of the right auricle.

When the adhesions are long and loose, and the heart is free from
valvular disease, and from any other influence tending to cause enlarge-
ment of the organ, the size of the heart is usually natural. It was
thus in two of the cases examined after death at St. Mary's Hospital,
in four cases that I observed at Nottingham, in many of those
referred to by Dr. Stokes, in ten briefly described by Dr. Gairdner, and
in 34 out of 90 cases collected by Dr. Kennedy.

When pericardial adhesions are associated with valvular disease,
the heart is always enlarged. It was so in 25 out of 2& cases, and in
the remaining instance, a case with mitral contraction, the heart
was rather large. I have compared a double series of cases of
valvular disease side by side, in one series with, and the other without
adherent pericardium, and, not going here into details, I may say that
the cases with adhesions were on an average five and a half ounces
heavier than those in which there were no adhesions, an increase that
was to a considerable extent accounted for, in many instances, by the
augmented thickness and weight of the pericardial sac. The increased
size of the heart would seem, therefore, in such cases, judging by this
analysis, to be traceable more to the affection of the valves, than
to the adherent pericardium. We find, however, that in two-thirds
of the cases without valvular disease in which the pericardium was
adherent, the heart was enlarged (12 in 19) ; and in one-fifth of them
it was rather large (5 in 19) ; while in only one-tenth of them the organ:
was of natural size (2 in 19). These proportions are borne out by Dr.
Kennedy's important analysis of collected cases of adherent pericar-
dium, who found that in fifty instances the heart was enlarged, in
thirty-four it was of natural size, while in five it was atrophied.
We may therefore conclude that in cases with the double affection of
valvular disease and adherent pericardium, the valvular disease is the
essential cause of the enlargement of the heart ; yet that the adhesions,
by giving an additional spur to the action of the organ, add to the
more important enlarging effect of the valvular disease of the organ.

It is the natural effect of pericarditis for the inflammation to spread
from the pericardial to the pleural surface of the fibrous sac. When,
therefore, the pericardium becomes adherent to the heart in those
cases, it becomes adherent also to the walls of the chest in front of the
pericardium. These pleural adhesions often occupy an extensive
space in front of the chest, and may extend from the second left
cartilage to the sixth ; from the manubrium to the upper half of the
ensiform cartilage ; and from the right border of the sternum to the

ADHERENT PERICARDIUM. 441

apex of the heart, to the left of the nipple line, as in the cases referred
to in former pages, and there described. Though these are extreme
instances, yet they are typical of many cases with pleuro-pericardiai
adhesions.

When the adhesions are short and powerful, and when, being pleuro-
pericardiai, they bind the walls of the heart extensively to the walls
of the chest in front of them, a great and constant strain is put upon
the ventricles ; for they cannot contract upon themselves to expel their
contents until they have dragged the sternum and cartilages powerfully
inwards. The ventricles thus expend their force in two directions, one
towards the interior to expel their contents, resisted in doing so by
valvular incompetence; the other from the exterior, to compel the
front of the chest, which is united to them like a solid buckler, to
share in their contraction. Under these influences the ventricles tend
to undergo a change in form, and to become flattened out, the one in
front of the other. Two cases observed by me in Nottingham were
thus influenced. The enlarged and thickened right ventricle, instead
of sweeping half round the left ventricle, usually cone-shaped, lay
directly in front of it ; and the septum between the ventricles, instead
of bulging forwards into the right cavity, became flattened.

When the adhesions, being extensive and pleuro-pericardiai, are not
short and close, but of moderate length, and do not, therefore, bind
the sternum and cartilages to the heart like a buckler, they do not
seriously embarrass the commencing action of the ventricles; but
during their contraction, the ventricles at length begin to draw upon
the walls of the chest ; and in the course of the systole they drag
those walls inwards.

When the adhesions are, as usual, longer and less solid, the ventricles
contract more after their wont, and retain more or less perfectly their
power. The right ventricle is usually enlarged as well as the left, but
not always, for the size of the ventricles is necessarily influenced by
the valvular affection. When that affection is mitral or mitral aortic,
the right ventricle shares the labour and the enlargement with the left
ventricle ; when the aortic valve is alone affected, the left ventricle is
often alone enlarged; and when there is mitral obstruction, the
enlargement may mainly affect the two auricles, that of the ventricles
being somewhat moderate.

The ventricles, when the pericardium is adherent, tend to enlarge
outwards in every direction, and especially upwards to the manubrium,
as well as downwards, into the epigastric space, to the right, and to the
left. The great arteries are lifted up on the top of the ventricles
into an unusually high position, and are crowded into the narrowed
space at the top of the chest, almost as high as the root of the neck.

When the adhesions are dense, strong, and contracted they sheathe
the wThole heart in a tight, tough envelope, wThich grasps the auricles
and ventricles, prevents their free expansion, and forcibly lessens
the organ.

VOL. iv. o G

442 A STSTBM OF MEDICINE.

Physical Sigss of Adherent Pericardium.

Clinical History. (A) From a succession of Observers. — Dr. Burns,
in 1809, gave cases to show that when the pericardium is adherent,
pulsation is felt in the epigastrium — a sign that had been previously
observed by Korner — caused, he says, by the repercussions of the heart
affecting the liver, which is the immediate seat of the pulsation.1 He
gives a case of adherent pericardium in which Dr. Rutherford found
a strong pulsation of the heart, accompanied by a jarring motion,
most remarkable at the contraction of the ventricles. Heim, according
to Kreysig,2 observed that a hollow appeared under the ribs during
each systole when the pericardium was adherent. Sander3 found, in
a case of adherent pericardium with great enlargement of the heart.

deepening of the space on the left side of the ensiform cartilage,
followed quickly by a shock, perceptible to the hand; fulness over the
cardiac cartilages ; and extensive impulse over the front of the chest.

Corvisart' noticed that in these cases respiration is high, and this
he connects with the trouble of the whole heart caused by the laborious
action of the diaphragm, to which it is attached by the adhesions.

Dr. Hope,s in 1839, observed that pericardial adhesions sometimes

' Burns, on the Diseases of the Heart, p, 62.
1 Kreysig, Die KranktuUm des Hcnen\ ii. 825.

* Bu/tluiiand Bibliothck d. p. Beilktude, Bd. 51, 120.

* Corvuort, Bur let Maladies du Caur, p. 35.

* Dr. Hi>pe, on tlso Disease* of the Beart, p. 1D4.

&#-_•' >z::

ADHERENT PERICARDIUM.

caused a prominence of the cardiac cartilages, sometimes an abrupt
jogging motion of the heart, corresponding with the systole and the
diastole, that with the diastole having the character of a receding
motion suddenly arrested. In the recital of four of his cases, to wliich
his general account does little justice, he states that they presented a
second or diastolic shock or back-stroke.

Dr. Williams,1 in 1840,rem:irked that when the pericardium adheres
both to the heart when enlarged, and to the walls of the chest, the
heart pulsates in close contact with those walls ; so that the pulsations
are felt very widely, extending upwards as well as downwards,
drawing in the intercostal spaces at each systole ; and that respiration

does not lessen the region of cardiac dulness on percussion, and of
impulse. Dr. Law, in a communication that I have not been able to
find, states that change of posture does not alter the position of the
impulse.

In my paper on the situation of the internal organs, I, in 1844,8
described four cases of adherent pericardium, and gave figures showing
the position of the internal organs after death, two of which figures
I reproduce here (see Figs. 49, 50). In one of these cases, a young
woman, the heart was small in size, and presented during hie no
physical sign of disease of the heart, but the pulse was very feeble ;
she had palpitation, dyspnoea, and anasarca ; and her lips were blue.

444 A SYSTEM OF MEDICINE.

The heart was very large in the three remaining cases, two of which
had mitral regurgitation, and the third had nam>wing of the mitral,
aortic, and tricuspid orifices. One of the two cases with mitral
disease has been already described, and is figured at page, 350. In
the other case of the same class, the impulse was very strong and
jogging ; shaking and heaving the whole chest. The apex protruded
strongly; the lower half of the sternum advanced firmly at the
beginning of the systole, and fell back gradually and firmly during its
continuance. The lower end of the ensiform cartilage receded during the
systole ; the impulse was irregular, 140 to 160 (see figure 49, page 442).

The remaining case with adherent pericardium presented physical
signs that differed materially from those observed in the two other
cases. The obstructed, mitral, and aortic apertures tested by the cone,
each measured half an inch, and the tricuspid orifice three-quarters of
an inch. The heart was very large, weighing thirty-two ounces ; and
all its cavities, and especially the ventricles, shared in the enlargement.
The following were the physical signs : — " Strong protruding impulse
at the apex between the sixth and seventh ribs. During the systole,
the sternum and the left and right costal cartilages over the right
ventricle became steadily depressed ; immediately after the systole
they advanced with a shock.?1 (Sec Fig. 50, p. 443.)

In the general description I thus defined the character of the
impulse in the two classes of cases just given : " The sternum, costal
cartilages, and xiphoid cartilage are heaved forward firmly and
steadily at the beginning of the systole ; and during its continuance
those parts fall back steadily and quickly, coinciding with the mode
of systolic contraction of the right ventricle. In some cases the
sternum and costal cartilages spring forward with a jerk during the
diastole."

M. Bouillaud,"2 in 1846, described a sign by which he had been able
to announce the existence of adherent pericardium in six or seven
cases. It consisted in evident retraction of the pericardial region ;
the movements of the heart not being free, but embarrassed or
curbed. He does not state during what period in the revolution of the
heart's action the depression of the pericardial region took place.

Skoda,8 in 1852, published an important paper on the diagnosis of
adherent pericardium, in which he gives a critical account of most
of the communications just analysed, and reports of three cases
observed by himself. In the first case, a youth, there was dulness on
percussion, equal in extent during inspiration and expiration, from the
second left space to the ensiform cartilage, and from the middle of the
sternum to the left nipple ; and fulness over the second space, which
advanced during the systole and sank in during the diastole ; the
third, fourth, and fifth spaces deepened with the systole and filled out
with the diastole ; the heart's impulse was feeble, and the apex-beat

1 Loc. cit. p. 562.

3 Traiti de Nosographie Mtdicalc, i.

3 Zcitschrift dcr Gescllschaft dcr Acrztc zu Wien, 152, i. 306.

ADHERENT PERICARDIUM. 445>

was imperceptible. The heart sounds were natural, but the second
sound was split over the pulmonary artery. The pericardium was
tied to the walls of the chest by filamentous bands, and was universally
adherent to the heart, which was natural in position ; the right
ventricle was enlarged, the right auricle wTas changed into a stiff -crumb-
ling tuberculous mass, and the conus arteriosus was widened, its
walls being only a line in thickness.

The second case, which passed through all its stages under Skoda's
eye, a youth, was admitted with pericarditis. The friction sound,
then loud and extensive, became feeble and limited to the apex on
the loth, and was lost on the 19th day. On the 37th day there
was a systolic deepening of the third, fourth, find fifth spaces, and the
apex-beat was imperceptible. A month later, when he left the
hospital, during each systole, besides the indrawing of the spaces,
there was indrawing of the lower half of the sternum, which sprang
forward after the systole with a perceptible shock. He was admitted
ten weeks later with pneumonia, when the heart-signs were unchanged,
and he died fully six months after his first admission. The right
ventricle was enlarged ; the valves were healthy ; the heart, which lay
in the middle of the chest, was firmly adherent to the pericardium,
which was, in turn, strongly glued to the walls of the chest by a
tuberculous exudation.

Skoda's third case was a man, with narrowing of the mitral orifice,
ascites, and oedema. The region of cardiac dulness remained unchanged
during inspiration and expiration. There was a considerable deepening
of the fifth space during the systole, after which the hollow quickly dis-
appeared, and a shock was perceived there at the beginning of the
diastole. After his death, five months later, the pericardium and pleura
were found to be universally adherent, and the right side of the heart
was considerably enlarged.

These cases, published by Skoda, form a valuable addition to the
clinical history of adherent pericardium, for the true points of
diagnosis have here been clearly observed, stated, and confirmed ; and
are given with force, and as the effects of the central cause,
the doubly adherent pericardium. They do not, however, present
any new points of diagnosis, for it will have been seen, in the
previous narrative, that he has been anticipated by one or more authors
in the observation of each diagnostic sign. Thus the systolic deepening
of the intercostal spaces had been observed by Heim and Dr.
Williams, the return shock over the previously retracted space by
Sander, and the great extent of the cardiac space upwards, and the
non-diminution of that space, by Dr. Williams and myself; while the
retraction during the systole of the lower half of the sternum, and its
advance with a shock immediately after the systole, was observed by
myself in the case already given.

Great diagnostic value is to be attached to the principal points
specially illustrated by Skoda's paper, namely : the systolic indrawing
of the lower sternum or intercostal spaces by the contraction of the

446 A SYSTEM OF MEDICINE.

adherent heart ; and the diastolic shock or back-stroke that immediately
follows, given by the return elasticity of the chest-walls.

Cejka,1 in 1855, published four cases of adherent pericardium, three
of which confirm, with more or less precision, the points illustrated
in Skoda's paper. In one of them, with contraction of the aortic
orifice, there was systolic indrawing of the third, fourth, and fifth
spaces, and so strong a blow was given by the return elasticity of the
chest walls that it was like the impulse of the heart. In another
instance, an old man with adherent pericardium, a chronic affection
of the lungs, dilatation of the aorta, and thickening of the mitral valve,
the fifth and sixth spaces were drawn inwards with each systole, and
became quickly even with each diastole. The impulse was not per-
ceptible, and there is no note of diastolic backstroke. In the third
patient, with aortic aneurism, the vaulting of the sixth left space,
caused by the systole, gave place towards the end of the case to a
slight drawing inwards of the corresponding region. Cejka's fourth
case of adherent pericardium, also with aneurism of the aorta,
presented no impulse and no apparent drawing inwards during the
systole.

Clinical History. (B) Cases observed in St. Mary's Hospital and at
Nottingham. — 1. Cases emmincd after Death. — The pericardium was
completely adherent in fifty-one, and partially so in nine of the cases
free from Bright's disease, recorded after death in St. Mary's Hospital
up to the year 1870. (See the table at p. 420.) Besides these,
seventeen of the cases with Bright's disease had universally, and three
of them had partially, adherent pericardium.

Eheumatic pericarditis had evidently been the cause of the adhe-
sions in more than one-half of the cases, since of those with complete
adhesions, 29 in 51 that were free from Bright's disease, and 9 in 17
with Bright's disease, had valvular disease of the heart; while the
valves were affected in 7 out of 8 of those with partial adhesions that
were free from Bright's disease, and the three cases of that class with
that affection.

General adhesion of the pericardium was rarely associated with
disease of the aortic valve (2 in 32), and with mitral obstruction
(1 in 21), in cases free from Bright's disease, while that affection was
very frequent in such cases with mitral and mitral-aortic valve disease
(13 in 33 of the former and 11 in 31 of the latter affection). Adherent
pericardium was present in one case with disease of the tricuspid
valve. Partial adhesions of the pericardium were noted in one case with
aortic regurgitation, in two with mitral obstruction, in none with mitral,
and in two with mitral-aortic regurgitation, without Bright's disease ;
since the aortic valve was affected in 1 in 4 of the cases, while only
two had mitral and two had mitral-aortic disease. Among the cases
of complete (17) and partial (3) adhesions with Bright's disease, 4 (in

i VUrUljdhrschrifl fUr die praktische Ecilkund, 1355, 128.

ADHERENT PERICARDIUM. 447

21) had aortic valve- disease, 5 (in 29) had mitral and 2 (in 20) had
mitral-aortic valvular disease, and 1 (in 9) had mitral contraction.

Aneurism of the ascending aorta was the evident cause of adherent
pericardium in three instances (3 in 25), and cancer of the heart in
one (1 in 10).

There was no other affection of the heart or aorta, excepting
enlargement of the organ itself, in more than one-third of the cases
with complete adhesions (19 in 52). The adhesions were not accom-
panied by any other affection in less than one-half of these cases (7 in
19), and they were complicated in more than one-half of them with
pyaemia (in 2), apoplexy (in 1), pneumonia (in 3), empyema (in 2),
phthisis (in 3), or peritonitis (in 1). All those affections, excepting
the last two, were acute ; and they could not, therefore, have given rise
to the adhesions. Phthisis, and especially empyema, which is so often
associated with phthisis, may, owing to the duration of those diseases,
have induced first pericarditis and then adhesions. Notwithstanding
this, the whole of those cases may be taken into account when consider-
ing the effect of pericardial adhesions on the size of the heart, for
none of them by themselves cause enlargement of that organ, excepting
pneumonia, and, less often, phthisis, both of which affections tend
to increase the right ventricle in size.

The heart was enlarged, its valves being thickened but competent
in one instance, in fully two-thirds of the cases with adherent
pericardium that were free from any other cardiac disease, and in
which the size of the heart is mentioned (11 in 16) ; it was rather
large in three of them ; and in only two instances was the heart of
its natural size. We may however, 1 think, estimate that in one-third
of these cases the adhesions did not cause an increase in the size
of the heart. These results do not differ materially from those
arrived at by Dr. Kennedy,1 who found that in 90 cases of adherent
pericardium in which valvular disease was not present, the heart was
of natural size — " healthy " — in 34, or fully one-third, hypertrophied in
51, or three-fifths — being dilated also in 26 — and atrophied in 5.

Tt is proved that pericardial adhesions do not necessarily cause
enlargement of the heart. I saw four cases in Nottingham in which
the heart was of natural size and one in which it was lessened ; Dr.
Gairdner 2 gives brief notes of ten cases in which the heart wras not
morbid, and by inference was not affected in size ; and Dr. Stokes 3
informs us that Professor Smith found that general adhesions of the
pericardium corresponded with atrophy or with hypertrophy of the
heart in nearly equal proportions.

We may, I think, safely conclude from what has gone before that
adherent pericardium may, and often does, exist without influencing
the size or healthy function of the heart ; that in a few rare instances
it may induce atrophy of that organ ; and that in nearly two-thirds of

1 Edinburgh Medical Journal, iii. 980.

2 Ibid, Feb. 1851.

8 Dr. Stokes, Diseases of the Heart, , I

448 A SYSTEM OF MEDICINE.

the cases it tends to cause an increase in the size of the heart, both
as regards the thickness of its walls and the capacity of its cavities.

We have just seen that the heart was enlarged in the majority of
the cases of adherent pericardium that were free from any other affec-
tion of the heart itself. When we take this into account it is natural
to expect that the heart should be more enlarged in cases with
valvular disease when they are affected with adherent pericardium
than when they are not so ; and the analysis of the cases of this class
that were recorded at St. Mary's Hospital by taking a simple average
of the weights of the hearts with valvular disease, with or without
pericardial adhesions, gives some support to this anticipation, as will
be seen by the examination of the following summary of the average
weight of the heart in those cases.

Average weight of the heart in cases of valvular disease with and
without adherent pericardium. The cases were not affected with
Bright's disease except where specified.

Mitral regurgitation, pericardium adherent (4) . average weight, 21 ounces.
Ditto, pericardium not adherent (14) . . . ,, ,, 16*6

Ditto, with BrigliCa disease, pericardium adherent (3) ,, ,, 25

Ditto, pericardium not adherent (19) ... „ „ 19*4

Mitral obstruction, pericardium adherent (1) . . ,, ,, 21

Ditto, pericardium not adherent (14) . . . „ ,, 14

Aortic regurgitation, pericardium adherent (2) . ,, ,, 26*7

Ditto, pericardium not adherent (23) ... ,, ,, 22

Mitral-aortic regurgitation, pericardium adherent (6) „ ,, 26*3

Ditto, pericardiuin not adherent (12) ... ,, ,, 22

Total of combined valvular diseases, without

Bright's disease, pericardium adherent (13) . . ,, ,, 23*3

Total of combined valvular diseases, without

Bright's disease, pericardium not adherent (63) ,, ,, 19 ,,

This method is far from doing scientific justice to the question
before us ; for cases of all ages, both sexes, and various degrees of
disease, are brought together under one common heading, although
in reality many of these cases differ materially from each other.
Notwithstanding this, a rough and ready answer is given to us that is
probably not far from the scientific truth. We find, then, that the
average weight of the heart in the thirteen cases of valvular disease,
with adherent pericardium, was 24 J ounces, wliile its weight in sixty-
three cases of a like kind, in which the pericardium was not adherent,
was 19 ounces, or 5£ ounces less than the first series. It is to be kept in
view that the pericardium was included with the heart in the first set
of cases, and what its average weight may be under the varying
circumstances I do not know. It may, however, I think, be concluded
that in the cases of valvular disease of the heart the existence of
adherent pericardium tended to increase the size and weight of the heart,
but not to a great extent.

The size of the heart, as we have seen, lias been usually described;

*»
it

»>

>»
tt

»»

ADHERENT PERICARDIUM. 44&

its weight being often given, in the cases with adherent pericardium
observed in St. Mary's Hospital. The relative size of the different cavi-
ties of the heart has, however, only been described in 11 of these cases.
*I have, therefore, with a view to discover the influence that the presence
of adherent pericardium may have on the size of the various cavities
of the heart and the thickness of their walls, brought together 18
additional cases from various sources — or 29 in the whole — in which
the general condition of the various cavities of the heart was described,
and which are given in the following summary : —

Cases with adherent pericardium in which the size of the different
cavities of the heart was described : —

1. — Cases in which both ventricles were enlarged (hypertrophy and dilatation) 16

Of these, 6 were free from valvular or other heart disease (1 had Blight's
disease) ; 10 had valvular disease (3 aortic, 2 mitral, 3 mitral-aortic,
regurgitation, 2 mitral contraction).

2. — Cases in which the right ventricle was enlarged, the left being not so

(in 1), or small (in 1), or not described (in 3) 5

Of these, 3 were free from valvular disease, 1 had mitral regurgitation,
and 1 aneurism of the aortic sinuses.

3. — Cases in which the left ventricle was enlarged, the right being small

(in 1), or not described (in 7) 8

Of these 8 had no valvular disease, 1 had aortic, and 8 mitral, regurgi^

tation, and 1 had aneurism of the apex of the left ventricle.

Total 29

There was valvular disease of the heart (15), or aneurism of the
heart (1) or aorta (1) in 17 of these cases, and as those affections
exercise a definite influence of their own on the size of the cavities of
the heart, they must be left out of view in considering the direct effect
of adherent pericardium on those cavities. The same must be said of
one instance with Bright's disease among the remaining 12 cases in which
there was no valvular or other affection of theheart or aorta. Hyper-
trophy and dilatation of both ventricles existed in 5 ; of the right
ventricle in 3 ; and of the left ventricle in the remaining 3, of these
11 cases. From this it would appear that adherent pericardium, when
it produces enlargement of the heart, tends to affect both ventricles to
an equal but varying degree.

2. Physical signs observed during life in cases with adherent
pericardium admitted into St. Mary's and the Nottingham Hospitals.
— I have observed nine cases with adherent pericardium in
St. Mary's Hospital, and have added one recorded there by Dr.
Markham ; and have examined seven such cases at Nottingham, four
of which I published in 1844, and have given briefly above. There
was no valvular disease of the heart in three of these seventeen
cases, while in the remaining fourteen, one or more of the valves was
affected, mitral regurgitation being present in nine of them, mitral-
aortic regurgitation in three, and mitral obstruction in two, of those
cases.

450 A SYSTEM OF MEDICINE.

In one of the three cases in which the valves were healthy, in which
case Bright's disease was present, the sounds of the heart were natural
but weak, and the presence of impulse was not noted. In another of
them, a man, with empyema and lardaceous disease of the kidney,
the heart being only slightly enlarged, the impulse was at one time
imperceptible, but afterwards, when it could scarcely be felt over
the ribs, it was perceived over the ensiform cartilage. In these two
cases, and in that of the same class already alluded to at page 439,
in which the heart was small, the presence of adherent pericardium
could not, I think, have been discovered during life.

The signs of the heart were not noticed in one of the cases in
which adherent pericardium was associated with mitral regurgitation,
an old man who presented various sonorous noises over the lungs.
In one of two cases, both men, with mitral disease, observed at
Nottingham, in which the heart was very greatly enlarged, the left
ventricle was greatly hypertrophied and dilated, the right being so
to a minor degree; and the impulse was feeble, the second sound,
distinct over the sternum, was scarcely audible at the apex, and the
lungs were (edematous. In the other case, with hypertrophy of both
ventricles, the impulse was inconsiderable, but was diffused over
the whole left mammary region.

The next case is an important one, reported by that careful and
accurate observer, Dr. Markham, for it shows that the apex-beat may
be strong, and far to the left, in some unusual cases of adherent
pericardium. In this patient, a girl, the impulse was heaving and
extensive, and was violent far to the left of the nipple line, and
beneath the sixth rib. The second sound was very loud over the pul-
monary artery, but was absent at the apex. M. Aran likewise describes
a case of adherent pericardium, in which the apex-beat was present
in the sixth space, three-and-a-half inches from the sternum, and the
systolic impulse was strong and progressive, and was not followed by
a diastole impulse. Skoda takes exception to my observation that the
apex protruded extensively to the left in two of my cases published
in 1844, given briefly above at pp. 439, 440. We shall see that the apex-
beat is usually feeble, and does not often extend far to the left in
cases of adherent pericardium ; but it was certainly otherwise in this
case of Dr. Markham, in that of M. Aran, and, I would say, also in my
two published cases. It appears to me that in this patient, and in
the other cases just given, there was no sign characteristic of
adherent pericardium.

The next instance was too ill for careful physical examination,
and presented a feature unusual in cases with pericardial adhesion?.
The healthy impulse was much more diffused than natural, bein.u
present in the epigastric space and four or five intercostal spaces,
and the lower ribs retracted during the diastole, which is a nuv
occurrence. The apex-beat, which was felt in the fifth and sixth
spaces, did not extend outwards so far as the nipple line. The twu
following instances present features that were sufficient to characterize

ADHERENT PERICARDIUM. 451

them during life as being affected with adherent pericardium. In
the first of these cases, the left ventricle was hypertrophied, the right
ventricle was small, and both the auricles were very large. The apex-
beat was seated in the sixth space, an inch to the left of the nipple
line, and 5^ inches from the sternum, and in spite of the great and
extensive hypertrophy of the left ventricle, was feeble. The second
sound, which was heard over the right ventricle, was faint at the apex.
There was, on the 54th day after admission, a diffused impulse chiefly
over the cardiac cartilages, extending down to the seventh costal
cartilage, and to the ensiform cartilage. The impulse advanced
quickly and fell back suddenly during the systole, and was followed
with a sharp sudden shock or jerk over the whole region of the
impulse. There was slight pulsation of the liver below the ensiform
cartilage. Breathing was rather high, the movement being chiefly at
the upper part of the chest, with retraction at its lower part. The
other case, equally remarkable, and the last of the series with mitral
incompetence, had points of close resemblance to the last, with points of
marked difference. In this case the front of the heart adhered strongly
to the inner surface of the sternum through the medium of the
pericardium. The walls of the right ventricle and auricle were much
hypertrophied, while the left ventricle was only somewhat thickened ;
thus reversing the conditions that were present in the former case.
There was some fulness over the region of the heart. The impulse
over the heart, and especially over the right ventricle, was very
extensive, spreading from the third to the seventh cartilage ; and from
the right cartilages, across the sternum and ensiform cartilage, to the
sixth left space, an inch-and-a-half beyond the nipple line. The impulse
was peculiar, and told remarkably on the sternum, first heaving that
bone forwards with sudden force, and then drawing it backwards with
great strength. " The heart " (or rather the front of the chest) " seemed
to be dragged backwards during each systole. The apex-beat was
feeble, low down, and far to the left, in the sixth space, an inch-and-
a-half beyond the nipple line. There was some pulsation of the liver
in the epigastric region. The second sound was loud and plunging
over the right ventricle, and feeble at the apex, where a mitral murmur
was loud and extensive. Afterwards the fulness over the heart, and
the extent and force of the impulse lessened, but the beat of the
heart retained its remarkable character, first advancing, and then
forcibly retracting, during the systole. Later still the apex-beat, which
was very weak, extended only a very little beyond the nipple line.
Notwithstanding this contraction of the region of the impulse, it
extended from right to left over a width of six inches. A deep
inspiration caused a marked lowering of the upper and lower borders
of the region of the impulse, in spite of its great extent. After a
few days he became drowsy, felt tight in the chest, and died three
weeks after his admission." It is to be remarked that while in the
previous case a diastolic shock or back-stroke followed the systolic
retraction, which was preceded by a systolic advance ; in this case

452 A SYSTEM OF MEDICINE.

there is no note of back-stroke, though I cannot vouch for its absence ;
but the sudden systolic heave followed by a forcible systolic retraction
of the sternum and cartilages, as if those parts were dragged backwards
by the heart clinging, as it were, to its buckler, pointed definitely to
adherent pericardium as the cause of the chain of signs.

The two cases of adherent pericardium with mitral-aortic incom-
petence present, like the last two cases, physical features that denote
the presence of the adhesions, though not perhaps with the same
emphasis as the two first related. In the first case, a youth, the heart
was of very great size, so as completely to cover the left lung. On
his admission, three months before his death, the impulse was gradual,
but ended abruptly with a shock ; and extended from the third cartilage
to the sixth, but scarcely beyond the nipple line ; there was also a
marked general pulsation over the whole liver, both in front and at
the right side. A month later the impulse had extended itself to the
left, being diffused, and shaking the whole of that side of the chest,
the apex-beat being an inch-and-a-half to the left of the nipple line.
Afterwards the impulse extended more to the right and was felt in
the epigastrium, but its characteristic features are not again described
The other instance was a boy, and in him the heart, which was con-
siderably enlarged, clung so close to the sternum and cartilages that
it was found best to remove the viscera en masse from behind. There
was fulness over the cardiac region, and the beat of the heart, which was
extensive, reaching down to an inch-and-a-half below the sternum, and
extending thence to the seventh cartilage, was of a peculiar character,
beginning with a diffused heaving impulse, which gave way to a
sudden and sharp retraction. He always said, after this examination,
that he felt better, though he really was not so, and eight days later
he died.

The two remaining cases with adherent pericardium had mitral
contraction. In one of them, a young woman, the heart was very
large ; the impulse extended from the second space to the seventh
costal cartilage and the ensiform cartilage, and, even when she lay ou
the left side, the apex beat was feeble. As in the last case, there was
strong pulsation over the whole liver, extending from the front to the
back. The remaining case with adherent pericardium and mitral
contraction was observed by me in Nottingham in 1835, and although
it presents no signs characteristic of the adhesions, is perhaps of
interest, as being, so far as I know, the earliest case in which the so-
called presystolic murmur was described. The size of the heart is not
given, but there was no hypertrophy of either ventricle. The mitral
opening was half an inch in diameter. A thrill, extending over a
large space, was communicated to the hand when applied over the
apex, which was terminated by a jerk. A peculiar purring sound was
heard at the apex, the vibrations being longer and louder as the time
progressed, the sound ending in a strong loud clear jerk, synchronous
with the pulsation. The sound occupied two-fourths of the time, no
other being audible at the apex.

ADHERENT PERICARDIUM. 45

JRi-mmi of the Physical Signs observed in Cases of Adherent Pericar-
dium.— The steady retraction of the lower half of the sternum during
the whole of the systole of the ventricles, and the sudden starting
forwards of the lower half of the sternum at the beginning of the
diastole with a return shock or blow, was observed in my own case,
published in 1844, and in one of Skoda's given in 1852.

The drawing inwards of the cardiac intercostal spaces during the
systole was first observed by Heim, and afterwards by Dr. Williams,
by Skoda in three cases, and by Cejka in three more.

This sign, which is sometimes present in other cases, renders the
existence of adherent pericardium probable, and especially if this sign is
still present when the patient draws a deep breath ; but if it is followed
by a diastolic shock the diagnosis of that affection is certain. The exist-
ence indeed of a diastolic back-stroke taken by itself pronounces that
the heart is adherent. This sign, which generally gives the impression
of a double impulse, was first noticed by Sander ; afterwards by Dr.
Hope in four cases of adherent pericardium ; in the two typical instances
just given and described respectively by myself and by Skoda, who
observed it in another instance ; by Cejka in one, and by myself in
two others given above.

A double movement of the systolic impulse, first forwards with a
heaving motion, then backwards with a forcible retraction, was observed
by myself in a case in the Nottingham Hospital, to the description of
which Skoda takes exception, and afterwards in three other cases in
St. Mary's Hospital. The outward pressure, equal in every direction,
of the blood contained in the ventricle during its contraction naturally
forces forwards the walls of the chest in front of it at the beginning
of the systole. During the continuance of the systole, the adherent
sternum resists the contraction of the heart, but in the struggle
the bone yields, and is drawn forcibly inwards by the active
ventricle.

The non-diminution of the region of pericardial dulness and of the
impulse was observed by Dr. Williams ; and the absence of change in
the position of these signs when the patient lay on the left side was
noticed by Dr. Law.

The non-diminution of the area of pericardial dulness and impulse
is undoubtedly a valuable sign of adherent pericardium ; in one of my
cases, however, the impulse below was unusually strong at the end
of expiration, and in another of them the upper and lower borders of
the impulse palpably descended during a deep inspiration. This is
indeed different from the diminution of the extent of dulness and
impulse, and, what is still more important, from the bodily transfer
during a deep breath of the seat of the dulness and impulse from the
cardiac cartilages and the fifth space near the nipple, to the epigastric
region, including the ensiform cartilage and the adjoining seventh costal
cartilage. One of my cases illustrates in its own manner the other
point just referred to — the non-shifting of the seat of the impulse when
the patient turns on the left side. In that case, when the patient lay

450 A SYSTEM OF MEDICINE.

•

The signs of the heart were not noticed in one of the cases in
which adherent pericardium was associated with mitral regurgitation,
an old man who presented various sonorous noises over the lungs.
In one of two cases, both men, with mitral disease, observed at
Nottingham, in which the heart was very greatly enlarged, the left
ventricle was greatly hypertrophied and dilated, the right being so
to a minor degree; and the impulse was feeble, the second sound,
distinct over the sternum, was scarcely audible at the apex, and the
lungs were ©edematous. In the other case, with hypertrophy of both
ventricles, the impulse was inconsiderable, but was diffused over
the whole left mammary region.

The next case is an important one, reported by that careful and
accurate observer, Dr. Markham, for it shows that the apex-beat may
be strong, and far to the left, in some unusual cases of adherent
pericardium. In this patient, a girl, the impulse was heaving and
extensive, and was violent far to the left of the nipple line, and
beneath the sixth rib. The second sound was very loud over the pul-
monary artery, but was absent at the apex. M. Aran likewise describes
a case of adherent pericardium, in which the apex -beat was present
in the sixth space, three-and-a-half inches from the sternum, and the
systolic impulse was strong and progressive, and was not followed by
a diastole impulse. Skoda takes exception to my observation that the
apex protruded extensively to the left in two of my cases published
in 1844, given briefly above at pp. 439, 440. We shall see that the apex-
beat is usually feeble, and does not often extend far to the left in
cases of adherent pericardium ; but it was certainly otherwise in this
case of Dr. Markham, in that of M. Aran, and, I would say, also in my
two published cases. It appears to me that in this patient, and in
the other cases just given, there was no sign characteristic of
adherent pericardium.

The next instance was too ill for careful physical examination,
and presented a feature unusual in cases with pericardial adhesions.
The healthy impulse was much more diffused than natural, being
present in the epigastric space and four or five intercostal spaces,
and the lower ribs retracted during the diastole, which is a rare
occurrence. The apex-beat, which was felt in the fifth and sixth
spaces, did not extend outwards so far as the nipple line. The two
following instances present features that were sufficient to characterize

ADHERENT PERICARDIUM. 451

them during life as being affected with adherent pericardium. In
the first of these cases, the left ventricle was hypertrophied, the right
ventricle was small, and both the auricles were very large. The apex-
beat was seated in the sixth space, an inch to the left of the nipple
line, and 5^ inches from the sternum, and in spite of the great and
extensive hypertrophy of the left ventricle, was feeble. The second
sound, which was heard over the right ventricle, was faint at the apex.
There was, on the 54th day after admission, a diflused impulse chiefly
over the cardiac cartilages, extending down to the seventh costal
cartilage, and to the ensiform cartilage. The impulse advanced
quickly and fell back suddenly during the systole, and was followed
with a sharp sudden shock or jerk over the whole region of the
impulse. There was slight pulsation, of the liver below the ensiform
cartilage. Breathing was rather high, the movement being chiefly at
the upper part of the chest, with retraction at its lower part. The
other case, equally remarkable, and the last of the series with mitral
incompetence, had points of close resemblance to the last, with points of
marked difference. In this case the front of the heart adhered strongly
to the inner surface of the sternum through the medium of the
pericardium. The walls of the right ventricle and auricle were much
hypertrophied, while the left ventricle was only somewhat thickened ;
thus reversing the conditions that were present in the former case.
There was some fulness over the region of the heart. The impulse
over the heart, and especially over the right ventricle, was very
extensive, spreading from the third to the seventh cartilage ; and from
the right cartilages, across the sternum and ensiform cartilage, to the
sixth left space, an inch-and-a-half beyond the nipple line. The impulse
was peculiar, and told remarkably on the sternum, first heaving that
bone forwards with sudden force, and then drawing it backwards with
great strength. " The heart " (or rather the front of the chest) " seemed
to be dragged backwards during each systole. The apex-beat was
feeble, low down, and far to the left, in the sixth space, an inch-and-
a-half beyond the nipple line. There was some pulsation of the liver
in the epigastric region. The second sound was loud and plunging
over the right ventricle, and feeble at the apex, where a mitral murmur
was loud and extensive. Afterwards the fulness over the heart, and
the extent and force of the impulse lessened, but the beat of the
heart retained its remarkable character, first advancing, and then
forcibly retracting, during the systole. Later still the apex-beat, which
was very weak, extended only a very little beyond the nipple line.
Notwithstanding this contraction of the region of the impulse, it
extended from right to left over a width of six inches. A deep
inspiration caused a marked lowering of the upper and lower borders
of the region of the impulse, in spite of its great extent. After a
few days he became drowsy, felt tight in the chest, and died three
weeks after his admission/' It is to be remarked that while in the
previous case a diastolic shock or back-stroke followed the systolic
retraction, which was preceded by a systolic advance ; in this case

452 A SYSTEM OF MEDICINE.

The two cases of adherent pericardium with mitral-aortic incom-
petence present, like the last two cases, physical features that denote
the presence of the adhesions, though not perhaps with the same
emphasis as the two first related. In the first case, a youth, the heart
was of very great size, so as completely to cover the left lung. On
his admission, three months before his death, the impulse was gradual,
but ended abruptly with a shock ; and extended from the third cartilage
to the sixth, but scarcely beyond the nipple line; there was also a
marked general pulsation over the whole liver, both in front and at
the right side. A month later the impulse had extended itself to the
left, being diffused, and shaking the whole of that side of the chest,
the apex-beat being an inch-and-a-half to the left of the nipple line.
Afterwards the impulse extended more to the right and was felt in
the epigastrium, but its characteristic features are not again described.
The other instance was a boy, and in him the heart, which was con-
siderably enlarged, clung so close to the sternum and cartilages that
it was found best to remove the viscera en masse from behind. There
was fulness over the cardiac region, and the beat of the heart, which was
extensive, reaching down to an inch-and-a-half below the sternum, and
extending thence to the seventh cartilage, was of a peculiar character,
beginning with a diffused heaving impulse, which gave way to a
sudden and sharp retraction. He always said, after this examination,
that he felt better, though he really was not so, and eight days later
he died.

The two remaining cases with adherent pericardium had mitral
contraction. In one of them, a young woman, the heart was very
large ; the impulse extended from the second space to the seventh
costal cartilage and the ensiform cartilage, and, even when she lay on
the left side, the apex beat was feeble. As in the last case, there was
strong pulsation over the whole liver, extending from the front to the
back. The remaining case with adherent pericardium and mitral
contraction was observed by me in Nottingham in 1835, and although
it presents no signs characteristic of the adhesions, is perhaps of
interest, as being, so far as I know, the earliest case in which the so-
called presystolic murmur was described. The size of the heart is not
given, but there was no hypertrophy of either ventricle. The mitral
opening was half an inch in diameter. A thrill, extending over a
large space, was communicated to the hand when applied over the
apex, which was terminated by a jerk. A peculiar purring sound was
heard at the apex, the vibrations being longer and louder as the time
progressed, the sound ending in a strong loud clear jerk, synchronous
with the pulsation. The sound occupied two-fourths of the time, no
other being audible at the apex.

ADHERENT PERICARDIUM. 46

JRe'sumi of the Physical Signs observed in Cases of Adherent Pericar-
dium,— The steady retraction of the lower half of the sternum during
the whole of the systole of the ventricles, and the sudden starting
forwards of the lower half of the sternum at the beginning of the
diastole with a return shock or blow, was observed in my own case,
published in 1844, and in one of Skoda's given in 1852.

The drawing inwards of the cardiac intercostal spaces during the
systole was first observed by Heim, and afterwards by Dr. Williams,
by Skoda in three cases, and by Cejka in three more.

158 A SYSTEM OF MEDICINE.

together by the backward portion only of the effect of the recoil of the
aorta walls, which expands itself in every direction -r and that force of
recoil ia itself but a portion of the original propulsive force of the left
ventricle, which presses with its full power upon the closed mitral valve.
The surfaces or lines of contact and closure of the mitral valve extend
along and just within the borders of its two flaps. This border of
contact is not a mere edge, but a surface or line of adaptation, made
up of the small bead-shaped cells, that dove-tail into each other along
the margins of the flaps ; those flaps being held in their place by
the simultaneous contraction of the papillary muscles, acting on
their tendinous cords; the result is that the margins of contact of
the mitral flaps press against each other when the valve is shut with
much greater tension, force, and concentration, than the margins of
contact of the aortic valve ; under the triple agency of a finer margin
of contact, greater pressure of blood, and the muscular force and
tendinous traction proper to the valve. The mitral valve, which is
situated in the muscular centre of the ventricle and in the focus of its
internal inflammation, is more immediately and frequently subjected
to endocarditis than the aortic valve, which has broader surfaces of
contact, less pressure of blood, and no muscular and tendinous
traction.

Endocarditis, as I have said, does not therefore attack the very
rim of the flaps of the mitral valve at the attachment of their out-
spreading tendinous cords, but the line or margin of contact just
within the edges of the valves. When the mitral valve is inflamed,
a frill of small bead-like granulations lines the whole proper border
of contact and closure of the valve; and tends to prevent their
perfect adaptation, and to cause regurgitation through the valvular
aperture when the ventricle contracts. These prominences consist of
a swelling and granular disintegration of the connective tissue, with
softening of the intercellular structure. Each of these prominences
is covered by a cap of fibrin deposited from the blood in the manner
well represented by Rindfleiach.1 Endocarditis affects the surfaces of
contact of the aortic valve in the same way that it affects those of
the mitral valve.

This is the usual manner in which endocarditis affects the mitral
and aortic valves, whether the parent affection, rendering those parts
prone to inflammation, be acute rheumatism, chorea, or pyaemia.
Sometimes, however, the inflammation deepens at its original seat on
the surfaces of contact of the mitral valve, and extends beyond
those surfaces, so as to affect a large portion of the flaps of the
valve on their ventricular surface. Under these circumstances, the
Inflamed, softened, and thickened structures may undergo granular
degeneration, and its ventricular layer may become broken ox ulcerated.
The auricular layer of the valve thus tends to yield before the pressure
<>f the blood, which forces its way through the breach in the ventricular

1 Loc. cit. p. 281, fig. 87.

ENDOCARDITIS. 459

layer, and to form pouches or aneurisms protruding into the left
auricle. The auricular layer may then be involved in the inflammation,
and become in turn subjected to granular disintegration and breaking
up of tissue, so that the flap of the valve may become perforated.
The fibrin of the blood deposits itself everywhere on the inflamed
surfaces, often in the form of vegetations, which may become
extensive ; and thus the fibrin often lines, closes, and conceals the
perforation.

We have already seen how many points in its favour, as regards
its tendency to endocarditis, the aortic valve presents over the
mitral; and it presents another in this respect — that while the
pressure of the blood bears directly upon the inflamed surface of
contact of the mitral valve during its closure at the time of the
systole, the pressure of the blood does not bear upon the inflamed
ventricular surface of contact of the aortic valve when it is closed
at the time of the ventricular diastole, but upon the uninflamed
upper or aortic surface of the valve. Although this condition,
favourable to the aortic valve, exists, I have seen preparations
in which a small aneurism, or aneurisms, of one or more of the flaps
of the aortic valve protruded downwards into the ventricle.

The advantages are not, however, entirely on the side of the
aortic valve when it is affected with endocarditis ; for a serious
counterbalancing disadvantage exists under such circumstances,
as I shall now mention. The sesamoid body, and the margin
or surface of contact of the valve on each side of the sesamoid
body, which are the seat of endocarditis when it affects the aortic
valve, receive the direct pressure of the column of blood in the
aorta; and those parts, which are softened by the inflammation,
tend therefore to be pushed downwards towards the ventricle
during the ventricular diastole; with the effect of sometimes pro-
ducing retroversion of the sesamoid body, and to a greater or less
extent of the softened flap, of which it is the centre. We here
see the great disadvantage in which the inflamed aortic valve is
placed from the want of tendinous cords and papillary muscles to
support its flaps when rendered soft and yielding by endocarditis.

Another special evil accruing to the aortic valve from a similar
class of cause, is the tendency of the sesamoid body, and the
adjoining portion of the flap affected with endocarditis, to lay hold
of deposits of fibrin from the regurgitating stream of blood, with
the effect of establishing a chain of fibrinous vegetations, which
form one upon another, and which hang pendant into the left
ventricle, being forced in that direction by the return current of
blood. When this chain of fibrinous concretions forms upon either
the right or the left posterior flap of the valve, it is driven down-
wards and backwards by the stream of regurgitation, so as to beat
against and rest upon the anterior flap of the mitral valve, with
the effect of causing ulcerative endocarditis of that flap. As the
blood regurgitating from the aorta into the ventricle beats upon

n h 2

460 A SYSTEM OF MEDICINE.

that flap, it parts with its fibrin which clings to the inflamed
surfaces of the mitral valve, and forms on these a second chain of
fibrinous concretions.

The flaps of the mitral valve are, as we have seen, the principal
seat of endocarditis, but inflammation may also attack the papillary
muscles, and especially where they are brought into contact with
each other towards the end of the systole, and cause fibroid
degeneration of those muscles. The tendinous cords may also
sometimes become inflamed, softened, and disintegrated, when the
grave result of rupture of the cord may ensue.

I have just given a series of notable instances of the occurrence
of endocarditis, locally excited by the contact with each other of
the two opposing surfaces of the valve ; of two adjoining papillary
muscles ; and of a pendant chain of fibrinous concretion beating
against the anterior flap of the mitral valve. These are not the
only parts of the interior of the heart that may be inflamed from
this cause, for wherever two Surfaces of the endocardium come
into contact with and rub against each other, endocarditis may be
excited in both of those surfaces. The influence of the labour of
the left ventricle and the mutual contact of its internal surface
in tending to produce endocarditis is illustrated in an original and
able manner by Dr. Moxon. I would refer to his work and to the
others already named for the study of the various effects of endo-
carditis.

Among the effects of endocarditis, I would here simply name the
formation of vegetations on the inflamed valves, already in part
illustrated ; the production of embolism by the washing away from
the vegetations of fibrin into the current of the blood ; the ulceration
of the surface of the endocardium; the establishment of valvular
disease from the thickening and enlargement of the valves ; the con-
traction, adhesion, or retroversion, and perforation of their flaps ; the
rupture of the tendinous cords ; the formation of aneurisms of the
valves ; the fibroid and atheromatous degeneration of the fibrous and
muscular structures of the ventricle ; the production of aneurisms of
the heart ; and other effects that will be found described in the
works to which I have referred.

II. -CLINICAL [HISTORY OF RHEUMATIC ENDOCARDITIS.

The accompanying analytical tables of 325 cases of acute rheu-
matism under my care in St. Mary's Hospital during the years
1851-66, show the proportion in which those cases were free from
endocarditis, and were threatened with or attacked by that affection ;
and the number that were attacked by pericarditis, distinguishing
those with established endocarditis ; also those in which endocarditis
was doubtful, and those in which it was absent.

The analyses contained in the tables sufficiently indicate the
reasons for arranging the cases in the manner adopted.

ENDOCARDITIS. 461

TABLE SHOWING THE CONDITION OF THE CASES OF ACUTE

RHEUMATISM, WITH ESPECIAL RELATION TO THE ABSENCE OB
PRESENCE OF ENDOCARDITIS.

/. — Cases of Acute Rlieumatism in xchich there icas no Endocarditis.

Affection of joints somewhat severe or moderate, no general illness, no palpitation, signs over heart

not named ............ 2

Joint affection slight, some general illness, heart not named . . . IS

Joint affection not, or scarcely severe, some or little general illness, heart sounds healthy . -. 10

Joint affection not, or somewhat severe, some or considerable general illness, heart not named . 5

Joint affection not severe, some or considerable general illness, heart sounds healthy . . 10

Joint affection severe, some general illness, heart not named . . . . 6

Joint affection somewhat severe, considerable general illness, heart sounds healthy, or loud and

ringing ... . . . . . . . 7

Joint affection severe, some general illness, heart sounds healthy ..... 11

No description of state of joints, or general illness, heart sounds feeble . . ... 1

Joint affection not, or rather severe, slight or no general illness, Klight prolongation of first sound . 7

Joint affection rather severe, slight or no general illnesH, doubtful occasional obscure murmur . 1

Previous valve-disease, mitral regurgitation «^> . . . 2

Death, delirium . , . . . . . . . 4

I.— -Totax ......... 70

II. — Cases of Acute Rheumatism in which Endocarditis was threatened.

Some general illness, pain over the cardiac region, heart not named ..... 1

Great general illness, pain left side, or region of heart, signs of heart not named 2

Great general illness, pain left side, heart sounds healthy ...... 3

Great general illness, pleurisy, heart sounds healthy . . . . 1

Great f r considerable general illness, pain left side, or region of heart, heart sounds healthy . 8

Great general illness, delirium, pain left side ... . . . . 1

Considerable general illness, first sound very loud ....... 3

Considerable general illness, doubling of first sound . . . . 1

Considerable general illness, first sound or heart sounds feeble or indistinct .... 3

General illness, pain over region of heart or left side, first sound indistinct or muffled . 2

Slight general illness, prolonged first sound ........ 13

Great general illness, prolonged first sound ........ 3

Great general illness, lung affection, prolonged first sound . . . . 4.

\ General illness, pain in region of heart or chest, prolonged first sound .... 10

1 Little general illness, faint or obscure murmur early or late in the attack . . . 5

Considerable general illness, obscure murmur after cessation of attack (endocarditis probable) . 1

Previous valve disease, considerable general illness .... .... 2

ll.-TOTAL 63

III. — Cases of Acute Rheumatism in which Endocarditis was probable.

Great general illness, pulmonary ai>op]exy in 1, prolonged first sound (situation Unknown), almost
a murmur in 1, a pulmonic murmur in 1 .

Great general illness, severe cough in 2, prolonged first sound at apex, almost a mitral murmur
in t, almost a tricuspid murmur in 1, a pulmonic murmur in 3

Great general illness, prolonged first sound at right ventricle, almost a tricuspid murmur, and a
pulmonic murmur ...........

Slight general illness, tricuspid murmur <— , ending in prolonged first sound in 1 . . .

Slight general illness, previous or established mitral regurgitation jw murmur did not vary

materially in 1, murmur became louder in 1 . ^^ ^ . .

Considerable general illness, previous or established mitral-aortic regurgitation "^ v » aortic

murmur absent at first in 1, mitral murmur became musical in 1 , . .

III.— Total .... ..... 13

432 A SYSTEM OF MEDICINE.

IV. — Cases of Acute Rheumatism in which Endocarditis was present without

Pericarditis.

Prolongation of first sound, almost a murmur, pain in heart 1, in chest 1, extreme general illness 2

Tricuspid murmur <— , murmur absent on recovery^— o . . . . .7

Tricuspid murmur <— , murmur lessening on recovery <- . 0

Tricuspid murmur <— Total . . 13

Mitral murmur — >, murmur disappearing on recorery o— > .25

Mitral murmur — >, murmur lessening on recovery •> . . 10

Mitral murmur — >, murmur established on recorery — > . . .14

Inflammation of mitral valve — >, died, murmur In 1, no note of murmur in 1

Mitral endocarditis — > Total, mitral murmur in 50, no note of murmur in 1 51

Aortic murmur y murmur disappearing on recovery^ . 5

Aortic murmur y aortic regurgitation established on recovery y . . . .5

Aortic murmur y Total ......... 10

Mitral-aortic murmur y— > murmurs disappearing on recovery o— >y ... 3

Mitral-aortic murmur, mitral murmur established, aortic murmur disappearing «->y . 2

Mitral-aortic murmur, mitral-aortic regurgitation established — >y .... 4

Mitral-aortic murmur,— >yToTAL ......... 0

Previous valvular-disease, mitral regurgitation «=>> .... . . 6

Previous valvular-disease, mitral and tricuspid regurgitation ir£> .... 3

Previous valvular-disease, mitral regurgitation, adherent pericardium aortic regurgitation*^ J, 1

Previous valvular-disease, aortic regt;rgitation v . . . . 3

Previous valvular-disease, mitral-aortic regurgitation (tricuspid murmur 2) 4^ >Jjf . 9

Previous valve- disease.— Total ..... .22

IV.— Total cases*of Endocarditis ..... *107

V. — Cases of Acute Rheumatism with Endo-Pericarditis.

( Tricuspid murmur <- 3 . j*[n"nTlr dif QJTJ?5 on ™c°very«-o • \\ 3
Heart iMurmur established on recovery <— . 2J

previously J Mitral murmur -» 36 . . ftftrW11 ?,C°V'' "o*?*1 °^ 17' \ nol
healthy, S , I aortlc 1 l> mitral-aortic-o^. | x _ J ™

Aortic murmur J, 1 . . . \Murmur lessening on recovery, mitral -»
^ Mitral-aortic murmur ->^6* \Mur. estb. on rec, mitral -» 11, mit.-aor. -» ^ y~ 16

Total eases of endocarditis in which the heart was previously healthy . 46

Cases of endocarditis, with prcv. valv. disease, mitral c^> 5, mitral-aortic ^ X 3 . .8

Total cases with endo-pericarditis ..... 54

IV., V.— Total with Endocarditis .... 161

VI.— Cases of Acute Rheumatism with Pericarditis; Endocarditis being

doubtful .3

VII. — Cases of Acute Rheumatism with Pericarditis in which there was no

Endocarditis G

V., VI., VII. Cases of acute rheumatism with Pericarditis.— Total . 6;t

Gbaxd Total of Cases of Acute Rheumatism . . . 325

* 108 cases of Endocarditis appear in the Tables at pages 187-188. I find that one of those cases has

been accidentally enumerated twice over, a woman, aged 23.
Correct errors of press in the Table at page 216 thus— (1) line 9, for 1 read 6 : (2) line 12, for mitral-
aortic read mitral-aortic 5 ; (3) lino 16, for total 10 read 19.

ENDOCARDITIS. 463

I have considered the cases of endocarditis according to the
character of the valvular affection of the heart due to the inflam-
mation of the interior of the ventricle, and have arranged these
cases into those (I.) with an uncomplicated tricuspid murmur ; (II.)
with mitral regurgitation; (III.) with aortic regurgitation, (1) not
accompanied by a mitral murmur, and (2) accompanied by a mitral
murmur ; (IV.) with prolongation of the first sound without a mur-
mur; (V.) with endocarditis supervening upon previous valvular
disease.

I. — Cases of Kheumatic Endocarditis wrrn an Uncomplicated

Tricuspid Murmur. Symbol <-

In a moderate proportion of the cases of rheumatic endocarditis
under my care in St. Mary's Hospital during the fifteen years ending
1866 — amounting to 13 out of a total number of 107, or one in eight
—there was a murmur over tlie right ventricle from regurgitation
through the tricuspid valve, without a mitral murmur. In nearly all
of these cases there was a greater or less amount of general illness,
and in one-third of them (4) there was pain in the region of the heart.
A tricuspid murmur was present also in 2 cases, in which endo-
carditis was probable, and in 2 that have been included, with a little
doubt, among the cases of pericarditis.

In the majority of these cases the murmur had disappeared when
recovery was established ; and in the remainder the murmur was then
diminishing in loudness, extent, and clearness.

This tricuspid murmur is usually present over the body of the
heart, or, in other terms, over the right ventricle ; and extends from the
lower half of the sternum to a line a little within the left nipple,
which line corresponds with the ventricular septum, and from the
third to the sixth cardiac cartilage. The presence of this murmur in
these cases over the right ventricle in the early stage of endocarditis,
and that, too, when no other murmur prevails, naturally suggests to
the mind at first sight that it is due to endocarditis affecting the right
ventricle and the tricuspid valve.

This inference is, however, forbidden by the following considerations.

(1) Endocarditis, and disease the result of endocarditis of the
tricuspid valve, are very rarely discovered on dissection in those who
have died from rheumatic inflammation of the interior of the heart,
or from valvular disease, the effect of such inflammation.

(2) The tricuspid murmur, when uncomplicated with disease of the
mitral valve, was not established in any of my cases, but had either
ceased altogether, or was steadily declining on the recovery of the
patient.

(3) The tricuspid murmur was frequently associated with a mitral
murmur, and less often with a mitral-aortic or an aortic murmur of
recent origin.

A tricuspid murmur was present over the right ventricle in one-

464 A SYSTEM OF MEDICINE.

half, or 27 in 50, of the cases with recent mitral murmur. In 7 of
those 27 cases the presence of a tricuspid murmur was somewhat
doubtful. In eight of those cases the mitral was preceded by the
tricuspid murmur, and in six of these the tricuspid murmur had ceased
to be audible when the mitral came into play. In thirteen other
cases both murmurs were present when they were first noticed, which
was at the time of admission, in fully one-half of those patients. The
mitral murmur appeared before the tricuspid in five cases. The tri-
cuspid murmur disappeared when the mitral murmur was still audible
in two-thirds of the cases (16 in 27) ; both murmurs ceased at the same .
time in seven instances ; and in four the tricuspid murmur outlived
the mitral. A tricuspid murmur was also present in one-third, (3 in
10), of the cases of endocarditis with mitral disease of old standing.

A tricuspid murmur was present in two or three of the eight
cases of mitral-aortic, and in about four of the ten cases of aortic,
regurgitation of recent origin; and in two of the five cases with
aortic, and none of the seven instances with mitral aortic valvular
disease of old standing affected with endocarditis.

(4) I have observed tricuspid regurgitation as a marked and
lasting feature in a case of button-hole contraction of the mitral
valve; in several instances in which the tissue of the lung was
permanently condensed, owing to repeated attacks of bronchitis ; in
patients affected with contracted granular kidney, in whom obstruc-
tion of the pulmonary circulation, with enlargement of the right
ventricle, had followed upon obstruction of the systemic circulation,
with its attendant tension, dilatation, and thickening of the systemic
arteries, and hypertrophy of the left ventricle.

These circumstances point irresistibly to the conclusion that the
tricuspid regurgitation is usually due to the so-called " safety-valve "
function of that valve, and not to endocarditis of the right side of
the heart. In all these cases resistance to the flow of blood through
the lungs has induced tension of the pulmonary artery, and distension
of the right ventricle and auricle, with, as a result, incomplete closure
of the tricuspid valve. The pent-up blood flows back through that
aperture, and upon the veins of the system; with the effect of distending
those veins, and of giving proportionate relief to the blood gathered up
in excess in the pulmonary vessels. At each contraction of the right
ventricle, indeed, instead of the whole of the blood flowing forwards
into the over-charged pulmonary artery, a portion of it flows back-
wards into the right auricle, and vense cavse.

Inflammation of the left side of the heart, even when there is no
regurgitation through the mitral orifice, impedes the flow of blood
from the lungs into that side of the heart ; and the accumulation of
the blood in the pulmonary vessels, thus caused, induces and is
relieved by the tricuspid regurgitation.

The tricuspid murmur was present on admission in two of the
thirteen cases of endocarditis in which that murmur existed without
mitral regurgitation. In nine of the remaining cases, the tricuspid

ENDOCARDITIS. 465

murmur was not observed until from two [to seven days after ad-
mission, and generally on the fourth or fifth day. In one case the
murmur did not appear until the 26th day after admission.

In nine of these instances the duration ftf the illness before their
admission is stated. In one of them the murmur appeared on the 7th
day ; in five, from the 10th to the 12th ; and in two, from the 14th to
the 16th day after the beginning of the attack of acute rheumatism ;
and we may therefore infer that the tricuspid murmur generally comes
into play about the 10th or 12th day of the primary attack.

In four instances the murmur was preceded by a prolonged first
sound over the right 'ventricle, and in one by a very loud, and in
another by a peculiar booming first sound.

In five of the cases there was direct evidence of endocarditis at
the time of admission, in the shape of pain in the heart, and a pro-
longed first sound ; although the murmur did not pronounce itself
fully until several days had elapsed. In two of them, indeed, the
murmur did not appear until there was a marked improvement in the
general symptoms.

The duration of the tricuspid murmur in these cases was very
variable. In two instances it was only observed once, and in eleven
it disappeared in from two to nineteen days ; in eight the murmur
when last noticed had become much more feeble, and in three of
these the first sound became prolonged at the apex, at the time that
the tricuspid murmur was diminishing. In three cases a pulmonic
murmur, which indicates lessened tension of the pulmonary artery,
appeared when the tricuspid murmur was lessening.

From these observations we are entitled, I consider, to infer: —

1. That the appearance of a tricuspid murmur over the body of the
heart, extending from the sternum to the nipple, and limited to that
region, which corresponds to the right ventricle, is usually the effect
and the evidence of endocarditis affecting the left side of the heart.

2. That when this murmur is neither coupled with nor replaced by
a mitral murmur, we may safely foretell that when the inflammation
leaves the heart, the valves will be perfect and the organ free from
disease.

A tricuspid murmur, as I have already remarked, is often the pre-
lude, and for a time the accompaniment, of mitral murmur in cases of
rheumatic endocarditis. The latter murmur, however, in two-thirds
of the cases (16 in 27) outlives the former, which is essentially a
transient murmur. I have already given the proportion in which
mitral regurgitation is accompanied, preceded, or followed by a
tricuspid murmur (see p. 463).

The duration of the tricuspid murmur in these cases, in which it
was associated with a mitral murmur, though variable, was usually
short. In ten instances it was only heard once, and that generally
on the day of admission, but in one half of these the existence of
the murmur was doubtful ; in six cases it was audible for from two
to seven days, and in seven from nine to sixteen days ; while in

452 A SYSTEM OF MEDICINE.

The two cases of adherent pericardium with mitral-aortic incom-
petence present, like the last two cases, physical features that denote
the presence of the adhesions, though not perhaps with the same
emphasis as the two first related. In the first case, a youth, the heart
was of very great size, so as completely to cover the left lung. On
his admission, three months before his death, the impulse was gradual,
but ended abruptly with a shock ; and extended from the third cartilage
to the sixth, but scarcely beyond the nipple line; there was also a
marked general pulsation over the whole liver, both in front and at
the right side. A month later the impulse had extended itself to the
left, being diffused, and shaking the whole of that side of the chest,
the apex-beat being an inch-and-a-half to the left of the nipple line.
Afterwards the impulse extended more to the right and was felt in
the epigastrium, but its characteristic features are not again described.
The other instance was a boy, and in him the heart, which was con-
siderably enlarged, clung so close to the sternum and cartilages that
it was found best to remove the viscera en masse from behind. There
was fulness over the cardiac region, and the beat of the heart, which was
extensive, reaching down to an inch-and-a-half below the sternum, and
extending thence to the seventh cartilage, was of a peculiar character,
beginning with a diffused heaving impulse, which gave way to a
sudden and sharp retraction. He always said, after this examination,
that he felt better, though he really was not so, and eight days later
he died.

The two remaining cases with adherent pericardium had mitral
contraction. In one of them, a young woman, the heart was very
large ; the impulse extended from the second space to the seventh
costal cartilage and the ensiform cartilage, and, even when she lay on
the left side, the apex beat was feeble. As in the last case, there was
strong pulsation over the whole liver, extending from the front to the
back. The remaining case with adherent pericardium and mitral
contraction was observed by me in Nottingham in 1835, and although
it presents no signs characteristic of the adhesions, is perhaps of
interest, as being, so far as I know, the earliest case in which the so-
called presystolic murmur was described. The size of the heart is not
given, but there was no hypertrophy of either ventricle. The mitral
opening was half an inch in diameter. A thrill, extending over a
large space, was communicated to the hand when applied over the
apex, which was terminated by a jerk. A peculiar purring sound was
heard at the apex, the vibrations being longer and louder as the time
progressed, the sound ending in a strong loud clear jerk, synchronous
with the pulsation. The sound occupied two-fourths of the time, no
other being audible at the apex.

ADHERENT PERICARDIUM. 45

Rdsum6 of the Physical Signs observed in Cases of Adherent Pericar-
dium.— The steady retraction of the lower half of the sternum daring
the whole of the systole of the ventricles, and the sudden starting
forwards of the lower half of the sternum at the beginning of the
diastole with a return shock or blow, was observed in my own case,
published in 1844, and in one of Skoda's given in 1852.

The drawing inwards of the cardiac intercostal spaces during the
systole was first observed by Heim, and afterwards by Dr. Williams,
by Skoda in three cases, and by Cejka in three more.

A double movement of the systolic impulse, first forwards with a
heaving motion, then backwards with a forcible retraction, was observed
by myself in a case in the Nottingham Hospital, to the description of
which Skoda takes exception, and afterwards in three other cases in
St. Mary's Hospital. The outward pressure/equal in every direction,
of the blood contained in the ventricle during its contraction naturally
forces forwards the walls of the chest in front of it at the beginning
of the systole. During the continuance of the systole, the adherent
sternum resists the contraction of the heart, but in the struggle
the bone yields, and is drawn forcibly inwards by the active
ventricle.

468 A SYSTEM OF MEDICINE.

murmuring, and becomes grazing, rubbing, grating, or creaking in
character.

When pericarditis supervenes upon a tricuspid murmur, the pressure
testis sometimes in* the early stage almost essential to the discovery of
the friction sound ; sometimes, however, the patient under these circum-
stances is so ill that you cannot make pressure. Local pain will then
usually guide the treatment, and time will clear up the obscurity.

In five of my cases, aortic regurgitation was accompanied by a tri-
cuspid murmur ; and in two of these by a mitral murmur also.

Cases of endocarditis with aortic regurgitation present obstruction
to the flow of blood through the lungs, and so may cause tension of
the pulmonary artery and tricuspid regurgitation; more, however,
owing to the inflammation of the interior of the left cavities and
the mitral valve itself, than to the aortic regurgitation, which is
rarely sufficient in volume to induce congestion in the lungs. This is
shown by the clinical fact that there were four instances with tricuspid
murmur in the sixteen cases of endocarditis in which there was
recent aortic regurgitation, in seven of which there was mitral regur-
gitation also ; while there was no instance of tricuspid murmur in the
fourteen cases of endocarditis in which there was aortic regurgitation
owing to the previous disease of the valve, in one-half of which cases
there was mitral regurgitation also.

A tricuspid murmur was present in three cases of endo-pericarditis;
and in two of those cases the murmur was persistent ; while in one
of them it disappeared, after the recovery from acute rheumatism.

I will give here the proportion in which a tricuspid murmur was
present in cases of acute rheumatism with endocarditis under my care
from October, 1866, to 1869, treated by means of rest.

There were altogether 31 cases of endocarditis in a total of 74 of
acute rheumatism, and in none of those thirty-one cases was one
tricuspid murmur present without a mitral or other murmur.

While the tricuspid murmur unaccompanied by another murmur was
absent in those cases ; although it was present in the proportion of one
in eight of such patients treated during the previous fifteen years ; the
proportion in which the conjoint tricuspid and mitral murmurs were
present was fully maintained in the cases treated by rest. Mitral
regurgitation was present without aortic regurgitation in twenty of
those cases, and of these, tricuspid murmur was present in nine, or,
if we add two doubtful cases, in eleven instances.

In none of these instances did the tricuspid murmur precede the
mitral ; in four the two murmurs appeared at the same time ; in fou*
the mitral preceded the tricuspid murmur by from one to three days,
and in one (45) by nine days.

In three of these cases the mitral murmur outlived the tricuspid ;
in two it was the reverse ; in three they were combined to the last,
and in the remaining case the mitral murmur probably lasted beyond
the tricuspid.

The relation of prolongation of the first sound over the right
ventricle to tricuspid murmur will be considered at pages 473, 492.

ENDOCARDITIS. 469-

II. — Cases of Rheumatic Endocarditis with a Mitral Murmur.

Symbol -»

The mitral and the tricuspid valves, while they correspond in
general structure and function, differ essentially in the construction
and arrangement of their flaps and in the whole setting of the valve.

The tricuspid valve, as I have already stated, is composed of three
great flaps and several intervening small ones, which meet somewhere
about the centre of the valve ; and the aponeurotic ring which forms
the base of those flaps is surrounded on all sides by muscular walls.
(See figs. 1, 2, pp. 40, 41 ; and fi^s. 13, 14, 15, pp. 55 — 57.)

In health, when the ventricle is not over-distended, the flaps of the
valve adapt themselves to each other perfectly, and close the tricuspid
aperture completely during the contraction of the ventricle.

When, however, the cavity is over distended, as it is under the
various circumstances which I have already described, the flaps of
the valve adapt themselves only partially to each other, especially, so
far as I have observed, at the meeting-point of the three great flaps,
and regurgitation ensues. The so-called " safety-valve " function of the
valve is thus brought into play, with the effect of relieving the tension
of the vessels of the lungs, and throwing the blood backwards
upon the veins of the system.

The result is that the tricuspid murmur is, with rare exceptions,
not a sign of inflammation of that valve, but of the over distension of
the right ventricle, caused by obstruction to the flow of blood through
the lungs.

The mitral valve is formed of one great semilunar or convex flap,
the base of which is incorporated with the powerful aponeurotic struc-
ture that is continuous with the two posterior sinuses of the aorta ; and
of a crescentic or horse-shoe flap, complex in structure, being formed
of three segments, set in the muscular walls at the base of the left
ventricle. The setting of the base of the valve is therefore two-
thirds muscular and one-third aponeurotic. There is no tendency in
the aperture to widen outwards at the base of the valve equally in all
directions, for the aponeurotic structure, when healthy, though elastic,
is practically unyielding. The single anterior semilunar flap, held
in check by its proper chords and fleshy columns, fills up the pos-
terior crescentic flap with perfect adaptation. The edges of the
opposed flaps press against each other with increasing force in propor-
tion to the increasing pressure of the blood on their under surfaces ;
and the over distension of the left cavity does not, owing to the
structure to which I have alluded, readily tend to widen the orifice
and open up the valve. The healthy mitral valve, therefore, when
the left ventricle is not greatly enlarged, possesses only under circum-
stances of extreme backward pressure or forward resistance a func-
tion like the " safety-valve " function of regurgitation with which the
tricuspid valve is endowed. Such a function of the mitral valve would
indeed be the opposite of a " safety " valve function, for it would

470 A SYSTEM OF MEDICINE.

immediately endanger the lungs by throwing the blood backwards
upon their vessels. (See figs. 1, 2, pages 40, 41 ; and figs. 7 — 12, pp.
50—52.

The result is that when the right ventricle is over distended, it
relieves itself backwards through the tricuspid aperture upon the
veins of the system ; and that when the left ventricle ife over-distended,
it, with rare exceptions, relieves itself directly forwards upon the
arteries of the system, and so the lungs are spared in both instances.

I derive the more important evidence of the correctness of this
view from the well-understood pathological history of aortic regurgi-
tation from widening of the orifice of the aorta, owing to atheroma of
its walls. In those cases the cavity of the left ventricle becomes
greatly, sometimes enormously, enlarged, and yet I know of compara-
tively few instances of this land in which the mitral valve was there-
fore incompetent.

Mitral regurgitation, without disease of the structure of the valves,
occurs most frequently among cases in which there is great arterial
tension owing to Bright's disease, and great consequent distension of
the left ventricle ; in which cases there is often also an atheromatous,
or thickened state of the mitral valve, with, as an effect, widening of
the fibrous portion of that aperture, and possible regurgitation.

Mitral murmur is, as a rule, neither a sign of over-distension of
the left ventricle, nor of a supply of blood to that cavity too small
in amount, or too thin in quality.

The existence then of a mitral murmur in a first attack of acute
rheumatism is a direct sign of inflammation affecting the left side of
the heart

Mitral regurgitation, not connected with previous disease of the
valve, and without aortic regurgitation, was present in 50 out of 107
cases of rheumatic endocarditis under my care in St. Mary's Hospital,
from 1851 to 1866, and in 20 of 31 such cases treated by rest from
1866 to 1869. In twenty-five of the earlier series of cases the
murmur had disappeared, and in ten others it was lessening at the
time of the patient's recovery, while in fourteen of them the murmur
seemed to be established ; and it was absent in one and present in the
other of two fatal cases of mitral endocarditis at the time of death.
In the cases of the later series the corresponding numbers were
thirteen, four, and three, the latter being the only cases in which the
murmur was established at the time of the patient's recovery.

In one-half of the cases of both sets the mitral murmur was heard
on the day of admission or the next day ; the numbers being 28t in 50
of the first set, and 9 in 20 of the second set. The murmur presented
itself within six days of admission in three-fourths of the remainder,
or seventeen of the earlier and nine of the later series, and from 8 to
17 days after admission in the remaining cases, amounting to one-
seventh of the whole.

Among the thirty-seven cases of endocarditis, combining the two
series, admitted with mitral murmur, one-third, or eleven, had been ill

ENDOCARDITIS. 471

from 2 to 7 days, nearly one-half, or fifteen, from 8 to 14 days, six
from 2 to 4 weeks, two for a longer time, and three for an unknown
period.

The mitral murmur became audible after admission in thirty-six
cases, and of these the murmur appeared in six during the first 7
days, in eleven from 8 to 14 days, and in eight from 15 to 28 days
after the beginning of the attack of acute rheumatism ; in six at a later
period ; and in three at a time unknown.

The mitral murmur may be present in full force on the third day
of the attack, or its appearance may be delayed until the fortieth day.
In a fair proportion of the cases, amounting to one-fourth, it is deve-
loped during the first week, and in the larger number, or two-thirds,
before the end of the second week.

Gcmral illness. — In nearly every case of endocarditis the patient
presents great or considerable general illness. Thus in sixty-two of
the seventy-one cases of mitral endocarditis the illness was great or
considerable, in two it was definite, and in five it was slight ; while in
two there is no description of the general state of the patient.

In most of the few exceptions to this rule of the presence of great
general illness in these cases, the murmur was established at the time
of their admission, and the severity of the attack was already mitigated
or passing away.

Those cases in which there was no endocarditis, present a very
different aspect, since in scarcely one-third of them was there consider-
able general illness.

As might be expected, constitutional illness was more severe and
frequent in those instances in which there was a threat of endocarditis,
though its existence was not actually demonstrated by valvular incom-
petence, since in nearly two-thirds of them the general illness was
either great or considerable.

The illness in cases of endocarditis is peculiar. It differs from and
is superadded to that due to simple rheumatic inflammation of the
joints, and is such as to call the attention of the physician to the state
of the heart.

The face may be flushed all over, the forehead, nose, lips and chin
being of as high a colour as the cheeks, a state that is usually associated
with profuse perspiration, drops of sweat standing in beads on the
surface — a condition, however, that may be present in cases with severe
affection of the joints without endocarditis. Thus when endocarditis
exists the face loses the brightness, glow, and smoothness, and the
variety of hue and tone of health, and becomes clouded, being dusky,
dull, or ashy in hue, or glazed, or unduly white, or even of a bluish
tint. The countenance, no longer expressive of interest in things and
persons around, or even of pain in the limbs, is marked by internal
trouble. The aspect of the patient is altered, often profoundly so,
being anxious, depressed, or indifferent. The eye loses ita lustre and
expression, and becomes heavy and dull.

Sleep is often absent, the nights being restless ; but this is perhaps

472 A SYSTEM OF MEDICINE.

more often due to the inflammation of the joints than to that of the
interior of the heart.

The nervous system is often gravely affected. Delirium at night, the
patient wandering, muttering, and complaining, is occasional, but rare ;
it occurred in two instances, in which the affection of the heart was
evidently the primary exciting cause of the mental trouble. In
another patient the head was confused on the third day.

Choreal movements, as we have seen, are in some instances a
definite effect of endocarditis, especially of the non-rheumatic kind,
traceable frequently to cerebral embolism; but choreal movements,
and indeed embolism, were of very rare occurrence in my cases of
rheumatic endocarditis uncomplicated with pericarditis. In one in-
stance the patient, previously anxious, and with sordes on his teeth,
was nervous and fidgetty ; and in another, starting appeared on the
6th day, having been preceded on the 4th day by pain in the heart.

Sickness is occasionally present It was so in four of my cases.
These cases, however, point not to the stomach as the cause of sickness,
but rather and usually to the state of the nervous system, and more
immediately to that of the brain itself; as in a case in which giddiness
and sickness appeared together, and in another in which sickness was
preceded by restlessness.

Failure in the power of the heart is an occasional occurrence in
cases of endocarditis. Thus, two of my patients were attacked with
fainting. One of these fainted on the day of admission, and again on
the thirteenth, and on the following day was sick, so that failure of the
heart may be a cause of sickness. In the other case pain in the heart
and fainting appeared on the seventeenth day after admission. We
may fairly attribute the fainting in these cases to the actual failure of
the heart itself, caused by the internal inflammation of that organ.

The pulse is often quick, feeble, and fluctuating. I believe that
it is dichrotous, but I have not employed the sphygmograph in
any case of endocarditis, being perhaps deterred by the state of the
wrist.

Perspiration is often especially profuse and of long continuance ;
sudamina being also present in some of the more severe cases.

The breathing is usually affected, being more or less quickened. In
rare instances pulmonary apoplexy or extravasation is the result of the
difficulty to the flow of blood through the lungs, which is the general
effect, varying in degree, of endocarditis.

The chain of symptoms here described points mainly to the
affection of two great functions. The nervous power is lowered ; and
the circulation of the blood through the fine vessels of the lungs and
the body is enfeebled.

Pain in the Region of tJis Heart. — Pain in the region of the heart,
sometimes severe and lasting, sometimes slight or transient, amounting
perhaps only to uneasiness, was present in about one-fourth of
the cases of tricuspid and of mitral murmur belonging to the earlier
series, and in one-half of the later series, treated by rest. If to

ENDOCARDITIS. 473

these we add other cases having mitral or tricuspid murmur in
which there was pain in the left side, or in the chest ; the proportion
thus affected reaches to nearly one-half in the first series, and to fully
one-half in the second.

The pain in the heart was sometimes, but not generally, severe. In
a few instances the pain was increased or excited by pressure. We
may fairly infer that in those cases pericarditis was imminent or was
actually present, though not, except in rare instances, with such
intensity as to cause even a transient friction sound.

Palpitation was very rarely complained of, but fainting, as I have
already stated, occurred in two instances.

Prolongation of the First Sound occurring during the Early Period of
Mitral Endocarditis. — In one-half of my patients affected with mitral
regurgitation, as wre have just seen, a murmur was established at
the time of admission. In one-half of the cases in which the
murmur was not thus established, prolongation of the first sound
preceded, and was merged into, the murmur. In all but one of those
cases the first sound was prolonged at the time of admission, and in
that case and two others a tricuspid murmur was then in full play.

The tricuspid murmur was likewise heralded by prolongation of
the first sound in one-half of the cases in which that murmur was not
already present at the time of admission.

In a number of the cases, the exact position of the prolongation of
the first sound was not defined ; but wherever it was so, the mitral
murmur was preceded by prolongation of the first sound at the apex ;
and the tricuspid murmur by prolongation of the first sound over the
front of the heart, or the right ventricle.

I think that no cardiac sign is more readily recognized than pro-
longation of the first sound, and yet there is none so difficult to define.
That this is so, however, is natural, for it is a transition sound. It
forms, as we have just seen, the transition from a clear healthy first
sound to a murmur ; and as we shall see, at a later period, in a large
proportion of the cases, it forms a transition between a mitral or
tricuspid murmur when dying out, and the restoration of the healthy
first sound. In one-half of the cases in which the prolongation
preceded the murmur, there was a double transition, the murmur
being both preceded and followed by prolongation of the first sound.
This prolongation is sometimes so like a murmur that it is difficult to
make the distinction, and this is especially the case just before the time
of transition, when the prolongation precedes the murmur; and just
after that time, when it follows the murmur.

Prolongation of the first sound is the absence of silence and the
presence of a wavering, grave, feeble sound during the interval between
the first and second sounds. It is not the prolongation of the shock
of the first sound which is itself significant, being sometimes a pre-
cursor of the more telling signs of endocarditis. The prolongation of
the first sound is not the same as the natural loud vibrating character
of that sound over the superficial cardiac region which ia slwv^V

vol. iv. ^ \

474 J SYSTEM OF MEDICINE.

always present in cases of anaemia, when the muscular force of the
ventricles is maintained, and even in excess, but when the blood is
scanty and thin, being deficient in red corpuscles.

Prolongation of the first sound is, I repeat, a feeble, indeterminate,
wavering sound, that fills up the space between the first and second
sounds, which space is silent in health. It presents every gradation,
from a sound so feeble that it is with difficulty discovered, to a sound
so murmurlike that it can scarcely be distinguished from the murmur
into which it so often ripens. Prolongation of the first sound was
noticed on the first day of observation in fourteen cases ; the prolonga-
tion developed into a murmur in two-thirds or nine of those cases
before the seventh day after admission ; and in the remaining third, or
five, between the seventh and fourteenth days. In two other instances
the prolongation, absent on the day of admission, appeared on the
•following day, and in the other after a lapse of four days.

It is evident that in all these cases the endocarditis was present before
the appearance of the murmur for a period of time at least as long as
the previous period of duration of the prolongation of the first sound.

There are other modifications of the first sound, besides its prolonga-
tion, that point to endocarditis, if they do not indicate it, which have
been, in a few instances, the precursors of murmur. It will be suffi-
cient if I simply name them. They are — 1. Loud heart sounds, the
first being sharp, the second ringing ; or both sounds may be ringing.
2. Healthy sounds with powerful action of the heart. 3. Boughness
of the first sound. 4. A humming noise over the right ventricle, and
in one case at the apex, where it was associated with murmur.
5. Doubling of the first sound (over the ventricle), which occurred in
two cases associated with a prolonged first sound, which was not
followed by a murmur in one of those cases. 6. Feeble first, loud
second sound, followed by tumultuous action of the heart and mitral
and aortic murmurs. 7. Extensive presystolic murmur (rrrp) present
in one case for five days, followed in succession by loud heart sounds
(6th day), doubling of the second sound (15th day), and a faint mitral
murmur, not limited to the apex. 8. Loud "plunging" first sound
over both ventricles, present on the 4th day, followed by prolongation
of the first sound on the 6th, and mitral murmur on the 8th ; and
9. muffling of the first sound, which in one case succeeded the murmur,
which was extinguished by an attack of pain in the heart, followed by
fainting.

All the above varieties in character of the first sound were, in the
instances referred to, followed within a veiy few days by a mitral
murmur.

The only one of these varieties of the first sound that I would speak
of is the last : the peculiar " plunging " sound. I call it so for want
of a better name. The sound is something like what I have heard in
the working of a steam-engine. It was as if the piston made a
peculiar plunging sound when it dipped down and reached the bottom
of its play. I have heard this sound in at least three cases. One of

ENDOCARDITIS. 475

them was attacked afterwards with delirium, long torpor, almost coma,
extreme depression, and pericarditis, but no murmur. In all the
cases, the constitutional symptoms more or less threatened endocarditis.

Besides these peculiarities of the first sound preceding mitral
murmur, there is one other affection of the sounds of the heart that I
would name ; and that is a complete silence of both sounds ; which
occurred in one case threatened with endocarditis, in which a mitral
murmur did not appear. In that case there was tenderness over the
heart, fighting for breath, a piercing pain between the chest and back,
and great depression, lasting for some days. On the 8th day she looked
more bright, on the 9th the sounds of the heart were audible, on the
14th its impulse had returned and was gaining power, and on the 26th
day the sounds were of natural loudness, and there was no murmur.

In most of the cases of endocarditis with mitral murmur there is
undue, but not great, strength of the impulse of the right ventricle,
which may be seen and felt between the cardiac cartilages to the left
of the lower sternum. This is found even in the earlier stages, and
before the appearance of the mitral murmur.

It is evident from what has just been stated, that while in some
cases that murmur bursts into full play at the commencement of the
attack, being audible on admission, and on the 3rd, 4th, 5th, 6th, or
7th days after the seizure ; in others it is not audible until a period
varying from the 8th to the 30th day, although there is unequivocal
evidence that the inflammation in the left side of the heart was present
before and at the time of admission. This evidence consists in the
existence of a tricuspid murmur, or a prolonged first sound, or pain
in the region of the heart or in the chest, with great or considerable
general illness.

The inflammation of the valve cannot cause regurgitation until
perfect adaptation is prevented by the formation of small prominences,
•covered with a deposit of fibrin upon the surfaces or lines of contact
of the margins of the valve, or by the softening and yielding of its flaps.

In three of the cases tricuspid or mitral murmur became audible
after admission, when the patient's illness increased. In ten other
cases, however, it was the reverse, for in all of them the murmur came
into play when the patient's health began to improve.

We are therefore, I conceive, warranted in assuming that in a con-
siderable number of the cases, the active stage of the endocarditis is
passing away at the time of the appearance of the murmur.

Progress of Cases of Endocarditis with a Mitral Murmur. — Cases
-with a mitral murmur from endocarditis affecting a valve previously
healthy, may usually be readily distinguished from those in which the
murmur is due to established disease of the mitral valve by the
character, seat, and area of the murmur, its changes, duration, and
transition, its cessation or establishment ; by the size of the heart and
the force, extent, and position of its impulse ; and by the nature of the
£rst and second sounds over the right ventricle, the pulmonary artery,

476 A SYSTEM OF MEDICINE.

the aorta and great arteries in the neck. The mitral murmur is always
situated over the apex and body of the left ventricle, and the ventricular
septum. The centre of the murmur and its point of greatest intensity
and purity is usually just below the left nipple. Sometimes it is limited
to tliis point, but in general it covers a larger area, spreading inwards
towards the right ventricle, outwards and upwards towards the axilla
and over the lung, and downwards over the stomach. This area is
rarely extensive, being usually limited by a diameter of from two to
three inches.

When the heart is high, owing to the elevation of the diaphragm, and
when the left ventricle is exposed in consequence of the shrinking of
the overlapping portion of the left lung, the murmur extends upwards
towards the axilla, and even above the mamma, and a little outwards,
rather than downwards. The direction of the murmur upwards
towards the axilla is peculiar to the mitral murmur of endocarditis,
for when disease of the valve is established, the lungs expand down-
wards to an unusual extent, and so muffle or arrest the murmur in
its course towards the axilla.

The extent of the area of the murmur depends much upon its
character. A smooth, soft, bellows-murmur, especially if it is rather
feeble, is in general limited to the apex and left ventricle ; so also is a
weak, grave murmur. But when it is vibrating, loud and almost
musical, and especially if a thrill is felt by the finger over the apex —
then the area of the munnur is extensive. Sometimes, indeed, it is so
all-pervading that it may be heard over the whole cage of the chest,
front and back, and even upwards into the neck and downwards over
the abdomen.

It is only in established mitral disease, or in very rare cases of
endocarditis with extensive mischief to the valve, that we find this
pervading vibrating murmur with perceptible thrill.

In cases of established mitral disease the munnur is usually
audible to a greater or less extent over the region of the stomach, often
coming quite down to its lower boundary: The vibration in the left
ventricle, which rests immediately upon the stomach, the diaphragm
alone interposing, awakens a corresponding vibration in the stomach,
and as this takes place in a hollow sac, its tone is often metallic, and it
thus sometimes imparts a musical character to the murmur at the apex.

In cases of endocarditis with mitral regurgitation, the murmur is often
so feeble that it is limited to its birthplace, and is unable to generate
corresponding vibrations in the adjoining organs. In these patients
the murmur is inaudible over the stomach ; but in other cases of endo-
carditis, according to the loudness and penetrating quality of the tone,
the murmur makes itself heard over a greater or less portion of the
stomach, at that part of it nearest to the apex of the heart.

The murmur was heard over the lower part of the back of the
chest in only two of the fifty cases of endocarditis with mitral
murmur of the first series, and in one of the twenty cases of the
second series. In one of these cases the murmur was audible

ENDOCARDITIS. 477

over the lower part of the back, the lungs being condensed, on the
4th day, but it was not again heard in that position. In another
such case the murmur was heard over the back of the chest
from the 27th to the 34th days after admission, but ceased to be so on
the 30th ; and in fche third case the murmur was heard below
the shoulder blades for the first time on the 18th, and for the last
time on the 42nd day. After that date the murmur Wcis less loud,
and its area was correspondingly lessened.

I have to add to these, one case of death with inflammation of the
mitral valve ; the anterior flap was softened and enlarged, its edge and
that of the posterior flap were covered with lymph or fibrine, and the
valve permitted extensive regurgitation through the mitral aperture.
The patient, a young man previously in good health, had been ill a
fortnight with acute rheumatism ; when admitted, he had an anxious
expression, hurried and difficult breathing, and sickness. A loud
mitral murmur, beginning with a sharp shock and followed by the
second sound, extended forwards almost to the sternum, where the
heart sounds were healthy, and backwards to below both shoulder
blades. From the 9th day to the 11th he raised phlegm tinted with
blood, he was propped up in bed, and there was dulness and fine crepi-
tation over the left lower lobe. On the 14th he sat forward in bed in
great distress, breathing with difficulty. In the course of that day he
died, and on dissection he presented the inflammation of the .mitral
valve and the extensive pulmonary apoplexy that were evidenced during
life.

The patients usually lay flat in bed, their pain being increased
by movement, and as the back was not examined, some of these
might have presented a murmur over the lower lobes of the lungs
behind ; but when we regard the limited area over which the murmur
was usually heard in front and at the side, it is evident that it could
scarcely have been audible behind. I think it probable that three
cases, in addition to those just named, may have been exceptions to this
rule, and perhaps two others, for in them the murmur was loud, while
in the first three it was vibrating in tone.

The mitral murmur at the time of its first appearance, or of its
transition from prolongation of the first sound, is as a rule either
weak and grave; or it is a soft, feeble, bellows murmur, and is there-
fore limited in area.

The mitral murmur invariably begins with an accent or shock, which
corresponds with the shock of the impulse, and it generally ends
with the second sound. It fills up, in fact, the space between the
first and second sounds, that space being often lengthened so as
to admit of greater prolongation of the murmur, with the effect of
altering the rhvthm of the heart. Sometimes the murmur does not
quite fill up this space, so that there is a distinct silent pause between
the end of the murmur and the second sound. The presence of the
accent or shock at the beginning of the first sound distinguishes an
endocardial murmur from an exocardial or friction murmur.

478 A SYSTEM OF MEDICINE.

The pressure test conies in to settle the difficulty of distinguish-
ing one condition from the other. If the noise be endocardial, the
sound may become louder from the closer application of the stetho-
scope, when pressed upon the walls of the chest ; but the quality of
the noise is unaltered, it is rhythmical with the heart sounds, it
retains its accent or shock, it fills up the space between the first
and second sounds, and it ends exactly with the second sound.

But if the noise be frictional, it usually loses its murmur-like tone
when the pressure is made— and becomes rustling or grazing, grating or
creaking in character ; it extinguishes the first and second sounds of
the heart, which were previously heard side by side, but not incor-
porated with the murmur ; it brings out a double sound where there
was but a single one before, a sound to-and-fro in character, or a
noise not unlike that made by the sharpening of a scythe, with a
single down-stroke during the beat of the heart, and a double up-stroke
during its pausp . Sometimes the mitral murmur is masked or confused
at the apex by the co-existence of a vibrating systolic noise. The
interposition of a piece of paper or cloth between the stethoscope and
the surface of the chest annihilates this vibrating noise, and the mitral
murmur is then heard with perfect purity and clearness. The interposi-
tion of the lung effects the same end — for this vibratoiy noise is heard
only where the heart is in direct contact with the walls of the chest ;
and hence, when using the naked stethoscope, we meet with cases in
which the murmur is more smooth and bellows-like just to the left of
the apex or towards the axilla, than it is over the apex itself. For
this effect, however, the layer of lung must be thin and the tone of the
murmur must be penetrating. In cases of endocarditis with mitral
regurgitation, the murmur is often muffled by a rumble, or a com-
paratively feeble vibration. The interposed paper or the intervening
lung extinguishes this vibrating noise, and brings a pure, soft, bellows
murmur into play.

The changes that the mitral murmur of endocarditis undergoes
during the progress of the case are remarkable, and they vary in
almost every instance. These changes consist in alterations of its
tone, loudness, and area ; in its transition from a true murmur to
prolongation of the first sound ; in the substitution of a tricuspid for
a mitral murmur, or the reverse, or the companionship of the two
murmurs ; in the suppression and reawakening of the murmur ; and
frequently in its final extinction, either directly or by passing again
into prolongation of the first sound, which precedes the restoration of
the healthy sounds of the heart.

In one-fourth of the cases (18 in 70) the mitral murmur was only
heard on one occasion.

Of 50 cases, in all of which the mitral murmur was heard more
than once, that murmur was of equal loudness during the successive
observations in one-fifth (11); became gradually weaker in one-third
(17), but in six of these it passed through a double oscillation and
increased and lessened a second time ; became gradually stronger in

ENDOCARDITIS. 479

one-fifth of the cases (11), in one-half of which it again gradually
declined ; was suspended and then renewed for a time in one-fourth
of the cases (12), when the murmur again faded away ; and it some-
times yielded to the healthy sounds of the heart, and sometimes to
prolongation of the first sound. In two instances, already included
in the abstract just given, there was a double disappearance and
reawakening of the mitral murmur, which in. one of them met with
final extinction, while in the other it became established.

The changes in the area of the murmur corresponded in a considerable
degree to the changes in its loudness, the former widening as the latter
increased and narrowing as it diminished.

In the great majority of the cases, and especially in those in which
the murmur disappeared, the tone of the murmur underwent but
little change. It became progressively louder and feebler, more clear
and more obscure in almost every instance, but it usually retained its
original character.

The murmur was observed to be soft and smooth, approaching
to the character of a bellows sound, in less than one-half of the first
series of the cases of endocarditis with mitral regurgitation, and in
less than one-third of the second series ; the cases in each series in
which the murmur was not characterized amounting to fully one-third
of the whole.

In a small proportion of the first series and a large proportion of
the second series of cases, the murmur was grave in character, being
in some of them feeble, and in a few, loud and almost vibrating.

Musical, sawing, and rasping murmurs formed but a small
proportion of the total number of cases, and these were they that
passed through a series of changes in tone and character.

One case, a youth, was a notable and rare instance of the variety of
changes in tone through which the mitral murmur may pass. He had
been ill a fortnight and had suffered from pain in the heart. On
admission he presented a tricuspid murmur. To this a loud mitral
murmur was added on the 3rd day, when he was very ill. On the
8th he was better, and from that day to the 15th the murmur was
weak, soft, and smooth. On the 21st it was louder and on the 29th
it altogether changed its tone and became musical. After this,
without apparent cause, it underwent two variations, having first
the character of a sawing and then of a bellows sound. The tone
of the murmur then again altered, and it became grave, and finally
on the 52nd day it had regained its lost musical character.

We must now answer the important practical questions suggested
by these observations, what are the rcharacter and progress of the
murmur, when the attack tends to end in perfect restoration of the
efficiency of the valve ? and what, when it tends to become per-
manently incompetent, owing to the establishment of mitral disease ?

The answer may be already almost gathered from what has gone
ljefore. When the murmur is permanently feeble, soft, and smooth,
with an approach to, or even the formation of, a gentle bellows sound ;

4#0 A SYSTEM OF MEDICINE.

or when it is feeble and grave, the complete restoration of the efficiency
of the valve may be anticipated. In illustration of this statement we
fiud that the murmur was feeble, soft, and approaching to a bellows
sound in 14 of the 25 cases of the first series that ended in recovery
of the valve ; and in 4 of the 10 that left with a lessening murmur,
the corresponding number in the two like classes of cases of the second
scries being 5 in 17, while of the 17 cases that ended in established
valve disease out of a total of 71, the murmur was feeble in none, and
-was smooth or soft in 6, most of which presented a definite bellows
murmur.

The feeble grave murmur was more frequently developed in the
later than in the earlier series of cases, but in both its presence was
almost always followed by the restoration of the function of the valve.

When the loudness of the murmur steadily diminished, or when it
first rose and then fell, or when after disappearing it reappeared and
again faded away, the integrity of the valve was generally regained.

When the murmur was loud, its area being extensive; when it
presented a sharply-defined loud, bellows, musical, sawing, or rasping
sound ; when it was vibrating in tone ; when it steadily increased in
loudness, or only slightly rose and fell to rise and fall again, without
a temporary disappearance ; then valvular disease was, as a rule, though
not invariably, permanently established. One patient, a nurse in the
Hospital, left with a loud mitral murmur, but after a time, when she
resumed her work, the murmur had given place to healthy heart sounds.

Condition of the Heart and the Cheat Vessels in Cases of Endocarditis
affecting the Mitral Valve. — In these cases there are, as I have already
illustrated, many affections of the heart besides imperfection of the
mitral valve with its attendant murmur. When inflammation affects
the great central cavity of the heart, the pivot of its action, the whole
organ is involved, and every part of it becomes, in succession, modified
in its action ; and in the force, movement, and sounds by which it
makes that action known.

Inflammation of the fibrous structure of the left side of the heart is
as essentially a part of acute rheumatism, as is inflammation of the
fibrous structure of the joints. The inflammation may commence
in the heart at the same time that it commences in the limbs. It
attacks that part of the heart that is working with the greatest force,
just as it attacks those parts of the limbs that are subjected to the
greatest labour. The increasing inflammation of the joints calls forth
increasing force in the action of the left ventricle, and so stirs up and
adds to the inflammation that may have already existed in that cavity
from the commencement of the attack.

This inflammation of the ventricle, like the inflammation of eveiy
other organ, lessens the power of the muscular cavity to expel its
contents, and to propel the blood round the vessels of the system.
This imperfect transmission of blood to the system, the demand for
which is increased by the inflammation in the limbs, causes distension
of the left auricle, and impedes the transmission of the blood through

ENDOCARDITIS. 481

the lungs. This induces distension of the pulmonary artery and its
branches, with, as its effects, accentuation — or loudness and sharpness,
or shock — of the second sound, with relative feebleness, or even
absence, of the first sound over that artery ; and distension of the
right ventricle, with increase in the action of its walls and in the
force and extent of its impulse.

We have, thus, two ventricles beating side by side, the left one, the
seat of the inflammation, beating with lessened power ; the right one,
with increased force.

The increased fulness and force of the right ventricle tend, when
they pass certain limits, to reverse the flow of a portion of the
blood, and to send it from the right ventricle back into the right
auricle ; with the effect of relieving the distension of the arteries of
the lungs, increasing the fulness of the veins of the system, and
producing a tricuspid murmur.

After a time, the wrhole volume of the blood is diminished, and the
proportion of its red corpuscles is lessened ; and then appear as later
and secondary effects, a murmur over the pulmonary artery, and some-
times a murmur over the aorta and its great branches — murmurs that
are due to the lessening of the contents, and relaxation of the walls
of those vessels.

Such murmurs in the great arteries appear, however, also in the
early stages of the affection, in the aorta more frequently, owing
evidently to the lessened power of the inflamed left ventricle, and the
diminished supply of blood that is therefore sent into the aorta, the
walls of which are thus relaxed ; and in the pulmonary artery occa-
sionally, for reasons that have yet to be ascertained.

The close study of the condition of the heart and great vessels
generally throws more light upon the degree of the inflammation of
the heart, and its effect on the vital powers of the organ, than does
the simple observation of the mitral murmur.

I shall now rapidly review the conditions of the heart and great
vessels as they presented themselves in the cases of endocarditis with
incompetence of the mitral valve — that valve being previously in the
virgin state and uninjured.

The Impulse of the Heart. — I find that I have taken notes of the
state of the impulse in one half of the cases with mitral incompetence,
or in 25 out of 50 of the first series, and 9 out of 20 of the second.

The beat of the heart was, as a rule, not extensive or strong. It
showed itself rather in the higher than the lower cardiac inter-
costal spaces, being present in only one instance below the fifth
space, less frequently in that space than in the fourth, and sometimes
even in the third space. While the impulse at the apex was in general
feeble or absent ; that of the right ventricle, though rarely powerful,
was usually somewhat increased in strength, being present in the
third and fourth, and even the fifth spaces between the cartilages.
This impulse of the right ventricle was not as a rule marked or strong,
but it could be felt diffused over those spaces when the ball of the

482 A SYSTEM OF MEDICINE.

palm of the hand was applied over them, or when the fingers were
pressed gently into the spaces.

In a few instances the action of the heart, and especially the
impulse of the right ventricle, was strong and diffused or powerful, or
even tumultuous and violent, soon after admission ; and then the size
of the heart, which was not in general notably affected, became
enlarged, the chest over the cardiac region being more prominent than
over the corresponding space on the right side.

In one or two patients the impulse presented a peculiar shock.

But the distinctive feature with regard to the impulse in a fair
proportion of the cases was its variation during the successive periods
of the disease. Thus, in one instanoe, it was feeble on the 1st day in
the fourth space, very strong on the 3rd day, moderate in strength
in the fifth space on the 8th day, and in the third and fourth
spaces on the 12th day. In another patient the impulse was felt
in the second and third spaces on the 2nd day, when there was
pain in the heart; on the 5th, the pain still continuing, the heart
beat violently ; from the 6th to the 18th the pulsation was strong
in the second space, and from the 28th to the 34th it was diffused
from the third to the fifth spaces. In this case mitral disease was
established, and the gradual extension of the impulse of the right
ventricle told with precision the story of the increasing valvular
disease in the left ventricle.

The study of the impulse conveys the most important lesson in all
cases of endocarditis. Its absence may tell of the want of vital power ;
and its excess in the right ventricle, while it is wanting in the left, shows
lessened power from inflammation in the latter cavity, and consequent
increased labour in the former. Its gradual increase in force, and
enlargement in area, with persistence of mitral murmur towards the
period of the termination of the attack of endocarditis, and after its
cessation, mark advancing and established valvular disease : and its
extent and force point out the amount of the back-flow^of blood from
the left ventricle into its auricle, and the obstacle to the on-flow of blood
through the lungs induced thereby. The impulse of the right ventricle
is, in short, a measure of the extent of the injury to the mitral valve,
and of the consequent resistance to the circulation through the lungs.

The impulse of the right ventricle was diffused and strong, extending
out to the nipple, in a considerable proportion of the cases in which
there was a tricuspid murmur.

In a few instances the impulse of the right ventricle was so high
as to be present in the second space ; but generally the pulsation felt
in that space was due to the presence there of the distended pulmonary
artery, when that pulsation was double, the second impulse being
more smart and shock-like than the first. In these cases the pul-
monary artery was distended, the first sound was feeble or absent,
while the second was unusually loud and strong, penetrating the ear
with a shock.

The apex beat is, in cases of endocarditis with mitral regurgitation,

ENDOCARDITIS. 48&

usually slight, sometimes absent — during the early period, before the
mitral murmur is developed, owing to the weakened muscular power
of the inflamed left ventricle ; and — after the appearance of the murmur,
owing to the relief afforded to the organ by the greater ease with which
its surcharge of blood is sent backwards into the auricle than forwards
into the aorta.

There are, however, certain exceptional cases of great interest,
several of which have come under my observation, in which the left
ventricle beats with great force, and unduly to the left.

In three of these cases there was extensive pulmonary apoplexy, or
pneumonia of that type, in the lower portion of the left lung.

One was a youth, with hurried and difficult breathing, tinted
phlegm, and dulness over the lower portion of the left lung, which
was solid and lessened in size owing to pulmonary apoplexy. The
condensed and solidified lung shrank away from its natural position
between the walls of the chest and the apex of the heart; and
the apex was therefore completely exposed, beating with all its force
upon the fifth space more than an inch beyond the left nipple. At
that time there was no mitral murmur, but as soon as the lung began
to recover itself, the murmur came into full play. When the lung
again expanded, it covered the apex of the heart, and its beat was
no longer perceptible. The whole heart in this case was displaced
to the left ; and its displacement was still greater in the sister case,
in which the apex beat was situated three inches beyond the nipple
line ; the impulse of the right ventricle was placed to the left of the
costal cartilages ; and the double pulsation of the pulmonary artery,
with a strong second shock, was present in the second space above
the mamma.

A fourth case, when admitted, had pain in the region of the heart,
and the apex beat was situated an inch and a half to the left of the
nipple. Five days later the extreme limit of the impulse hqd shrunk
one inch, being seated half an inch to the left of the nipple.

Accentuation of the Second Sound, with Silence, Feebleness, or Pro-
longation of the First Soimd over the Pulmonary Artery. — Accentuation
of the second sound over the pulmonary artery, in the left second
space, is a well established sign attendant upon mitral regurgitation,
and it may be present in every degree.

The second sound may be more or less loud and sharp or ringing —
or it may penetrate and strike the ear with a loud shock ; when a
double impulse is to be felt over the pulmonary artery, the first being
gentle and gradual, while the second gives to the hand a smart shock.

This increase in loudness and sharpness of the second sound is due
to distension of the pulmonary artery, owing to the difficulty with
which the blood travels through the vessels of the lungs.

Whenever the blood thus accumulates in the lungs, whatever be
the cause, the same effect is induced. In cases of phthisis, and
notably when there is haemorrhage from the lung and shrinking of its
tissue, the pulmonary artery, enlarged and tense, displaces the lung

484 A SYSTEM OF MEDICINE.

superficial to it, and presses against the second space ; where there is a
double impulse the first gentle, the second felt and heard as a shock.
In bronchitis, emphysema and pneumonia, there is the same disten-
sion of the pulmonary artery, but greater in degree. The interposition
•of the lung, enlarged owing to the disease, screens the pulmonary artery
from the hand and the ear, so that over it the second sound is often not
unduly loud ; but it is so in some instances over the right ventricle.

Whenever the tension of the pulmonary artery is thus so great as
to cause a strong and loud shock with the second sound, the first
sound is either almost silent, or feeble, or faintly prolonged.

When the blood is sent into a tight and full artery, it makes but
little, often no sound, either in the shape of shock or murmur ; but the
second sound caused by the smart and strong reflux of the blood upon
the walls and closed valves of the artery, makes a loud, sometimes a
ringing or metallic sound. The same occurs in the aorta when it is
enlarged and rendered tense owing to the difficulty with which the
blood leaves the arterial system in advanced cases of contracted granular
kidney. When you listen over the aorta a single sound is often heard,
a loud ringing metallic second sound, the first being almost or abso-
lutely silent Sometimes in these cases the artery is so large and
tense that it presses against the second right intercostal space, pro-
ducing there a double pulsation, the first gentle and gradual, the second
.smart and with a shock.

I find that I have described the second sound as being loud or sharp
or ringing in about one-half of the 50 cases of the first series and 9
of the 20 of the second series of cases of endocarditis with mitral
murmur, and in 5 of 13 of those of the first series with an uncom-
plicated tricuspid murmur. This does not of course include all of
this class.

It was noticed that the second sound was sharp or loud in the
early period in a large proportion of the cases in which that sign was
observed, or in 13 out of 25 of the first series, and 7 out of 9
of the second series.

In all but six of the patients in whom it was noticed that the second
sound was intensified, it continued to be loud down to a late period,
to the time in fact of approaching recovery.

Loudness of the second sound may be associated with each of
the signs, singly or in combination, that are habitually found in
cases of endocarditis with inflammation of the mitral valve. It
accompanied a mitral murmur, either alone or in combination
with a tricuspid murmur in 22 of the cases ; in about 15 cases it
was allied with prolongation of the first sound over the left and
sometimes the right ventricle; and in 8 cases it was joined to
tricuspid regurgitation, which was however combined with other
important signs in every instance but one. The first sound of the
pulmonary artery was affected, when the second sound over that
artery was loud or sharp, on ten occasions, in different patients :
in 4 of these there was a pulmonic murmur, in 4 the first

ENDOCARDITIS. 485

sound was prolonged, being generally free from shock, and in 2 it
was silent or scarcely audible.

These numbers, however, taken by themselves give a very inade-
quate idea of the relation of the first to the second sound of the
pulmonary artery in cases when that second sound is intensified.
Thus, as we have just seen, pulmonic murmur was followed by a
sharp second sound in four instances, but there were altogether 32
cases in which a pulmonic murmur was heard, and in only four of
them was it stated that the second sound was thus affected at the
time when the pulmonic murmur was audible. In one of the cases
in which there was a pulmonic murmur on admission, the second
sound was free from accent ; while on the 3rd when the pulmonic
murmur had disappeared, that sound was slightly accentuated over
the pulmonary artery. Again, in only two of the cases is it noted
that the first sound of the pulmonary artery was silent or scarcely
audible when the second sound was loud. Since, however, my atten-
tion has been drawn to the relation of the first to the second sound
of the pulmonary artery, in every instance that I have observed
accentuation of the second sound, especially with, but even without
shock, the first sound has been either very feeble, being occasionally
prolonged, or almost or even quite silent. This condition was signally
marked in a case of chorea under my care in the hospital, a boy, who
on admission, presented no mitral or other murmur over the heart.
After gaining ground steadily he became rather worse, his temperature
rose., he had pain in his chest, and the second sound was loud, the
first feeble over the pulmonary artery ; and six days later a mitral
murmur came into play. At the same time the right ventricle,
previously quiet, beat with great force, and a strong shock was felt
over the pulmonary artery with the second sound. On listening over
that vessel, a loud second sound penetrated the ear and struck it as
it were with a shock, and the first sound was silent, the second sound
being alone audible to all who listened. After a short time he
became very ill, and for two days he passed his evacuations involun-
tarily in bed. He kept both hands fixed on his wrists, and his fingers
on his hands. He soon began to improve, and gradually as this boy
gained strength, speech, power to move, and freedom from irregular
movements; and as his lungs enlarged, the mitral murmur being
still audible, the second sound though still loud lost its shock, the
second impulse ceased to be felt over the pulmonary artery, and the
first sound, though feeble, became more and more audible.

In a fair proportion of the cases in which the second sound was
sharp and loud at the early period of the disease, that sound retained its
character unaltered through all the surrounding changes in the sounds
of the heart. Let us take one case. At first there was a tricuspid
murmur, the second sound being sharp ; on the 6th day there was a
mitral murmur, and the second sound was loud ; next day the murmur
was less marked, but the second sound was still loud ; and on the
11th the murmur had given place to prolongation of the first sound

4B4 A 8Y8TEM OF MEDICINE.

superficial to it, and presses against the second space ; where there is a
double impulse the first gentle, the second felt and heard as a shock.
In bronchitis, emphysema and pneumonia, there is the same disten-
sion of the pulmonary artery, but greater in degree. The interposition
of the lung, enlarged owing to the disease, screens the pulmonary 'artery
from the hand and the ear, so that over it the second sound is often not
nndnly loud ; but it is so in some instances over the right ventricle.

Whenever the tension of the pulmonary artery is thus so great as
to cause a strong and loud shock with the second sound, the first
sound is either almost silent, or feehle, or faintly prolonged.

When the blood is sent into a tight and full artery, it makes but
little, often no sound, either in the shape of shock or murmur ; but the
second sound caused by the smart and strong reflux of t lie blood upon
the walls and closed valves of the artery, makes a loud, sometimes a
ringing or metallic sound. The same occurs in the aorta when it is
enlarged and rendered tense owing to the difficulty with which the
blood leaves the arterial system in advanced cases of contracted granular
kidney- When you listen over the aorta a single sound is often heard,
a loud ringing metallic second sound, the first being almost or abso-
lutely silent. Sometimes in these cases the artery is so large and
tense that it presses against the second right intercostal space, pro-
ducing there a double pulsation, the first gentle and gradual, the second
smart and with a shock.

I find that I have described the second sound as being loud or Bharp
or ringing in about one-half of the 50 cases of the first series and 1'
of the 20 of the second series of cases of endocarditis with mitral
murmur, and in 5 of 13 of those of the first series with an uncom-
plicated tricuspid murmur. This does not of course include all of
this class.

It was noticed that the second sound was sharp or loud in the
early period in a largo proportion of the cases in which that sign was
observed, or in 13 out of 2r> of the first series, and 7 out of 9
of the second series.

In all but six of the patients in whom it was noticed that the second
sound was intensified, it continued to be loud down to a late period,
to the time in fact of approaching recovery.

Loudness of the second sound may be associated with each of
the signs, singly or in combination, that are habitually found in
cases of endocarditis with inflammation of the mitral valve. It
accompanied a mitral murmur, either aloi
with a tricuspid murmur in 22 of the cases
was allied with prolongation of the first sound i
sometimes the right ventricle ; and in 8 cases it I
tricuspid regurgitation, which was however combinj
important signs in ever)' instance but one. TIic- fii
pulmonary artery was affected, when the second a
artery was loud or sharp, on ten ~—
in 4 of these there was a pul

ENDOCARDITIS. 486

sound was prolonged, being generally free from shock, and in 2 it
was silent or scarcely audible.

These numbers, however, taken by themselves give a very inade-
quate idea of the relation of the first to the second sound of the
pulmonary artery in cases when that second sound is intensified.
Thus, as we have just seen, pulmonic murmur was followed by a
sharp second sound in four instances, but there were altogether 32
eases in which a pulmonic murmur was heard, and in only four of
them was it stated that the second sound was thus affected at the
time when the pulmonic murmur was audible. In one of the cases
in which there was a pulmonic murmur on admission, the second
sound was free from accent ; while on the 3rd when the pulmonic
murmur had disappeared, that sound was slightly accentuated over
the pulmonary arteiy. Again, in only two of the cases is it noted
that the first sound of the pulmonary artery was silent or scarcely
audible when the second sound was loud. Since, however, my atten-
tion has been drawn to the relation of the first to the second sound
of the pulmonary artery, in every instance that I have observed
accentuation of the second sound, especially with, but even without
shock, the first sound has been either very feeble, being occasionally
prolonged, or almost or even quite silent. This condition was signally
marked in a case of chorea under my care in the hospital, a boy, who
on admission, presented no mitral or other murmur over the heart.
After gaining ground steadily he became rather worse, his temperature
rose, he had pain in his chest, and the second sound was loud, the
first feeble over the pulmonary artery ; and six days later a mitral
murmur came into play. At the same time the right ventricle,
previously quiet, beat with great force, and a strong shock was felt
over the pulmonary artery with the second sound. On listening over
that vessel, a loud second sound penetrated the ear and struck it qk
it were with a shock, and the first sound was silent, the second sound
being alone audible to all who listened. After a short time he
became very ill, and for two days he passed his evacuations involun-
tarily in bed. ( le kept both hands fixed on his wrists, and his finders
on his hands. He soon began to improve, and gradually as this bov
gained strength, speech, power to move, and freedom from irregular
movements ; and as his lungs enlarged, the mitral murmur being
still audible, the second sound though still loud lost its shock. :fce
second impulse ceased to I* felt over the pulmonary anorv. and :bt
Although feeble, became more and more audible.
Z apportion of the cases in which the seco&d sous: **
t at thriftily period of the disease, tha: sousd n:^»i- *
Q all the snrroundiik: ih-i:-.^;~ in :i? *"■"*"*
At firs;' ihervVi* * =*^*~
ing sharp; on &g ;:i. .Uy ;' -""■*'
d sound wa$ !osi
Mid sound ita? ;;■;; :.W" ■

486 • A SYSTEM OF MEDICINE.

over the right ventricle, and yet the second sound still remained loud.
In another instance on the 9th day there was an obscure mitral murmur,
on the 16th there was mitral, tricuspid and direct aortic murmurs, on
the 19th these had all vanished, and on the 23rd the tricuspid and direct
aortic murmur had returned ; and yet on each occasion there was the
same sharp second sound over the pulmonary artery. I could give
several instances of this kind and would refer to four cases. In these
instances the sharp second sound went on drumming, like the tom-
tom in the streets, whatever was the variety of the surrounding
noise, or even when there was freedom from murmur or prolongation
of the first sound.

The intensified second sound is, however, by no means always so
unvarying in its note. Thus, in one very interesting case on the 11th
day the second sound was very loud over the pulmonary artery, the
first being scarcely audible; on the 34th both sounds were loud
over the ventricles, the second being very loud ; and next day all the
sounds were natural

I must refer to one other case, in which on admission the first
sound was faint, the second loud over the pulmonary artery, the
first sound being prolonged over the ventricles ; on the 13th day the
two sounds were equal over the artery and there was a feeble
murmur at the apex ; on the 27th the second sound was again louder
than the first ; and on the 40th a singular change took place, the first
sound being louder than the second over the pulmonary artery — while
over the aorta it was the reverse, and on the 50th day the natural
standard was regained, the second sound being louder than the first.

The close study of the second sound and of its relation to tbe
first over the pulmonary artery, is of practical importance in
cases of endocarditis affecting the mitral valve. It may foretell
the coming murmur in the early, and betray the recently extinct
murmur in the later, period of the disease ; and during its progress,
it points by the degree and force of its accent to the amount of the
resistance to the pulmonary circulation, the intensity of the internal
inflammation of the ventricle, and the extent to which the function
of the ventricle is impaired. It is, in short, a tell-tale sound pointing
to the agency in the central cavity of the heart which gives it birth.
The intensified second sound of the pulmonary artery, or that of the
aorta, is associated as we have seen with a corresponding feebleness,
or even silence, of the first sound of each of the vessels respectively.
The observation of the one sound demands a corresponding observation
of the other sound. When the artery is distended, it enlarges, lengthens,
and advances, and comes gradually into contact with the second
intercostal space, displacing the intervening lung from before it. You
can then feel the double pulsation of the great artery ; the first move-
ment is gentle, gradual, barely perceptible to the touch ; the second
strikes the walls of the chest and the applied hand with a sudden
smart shock or tap. When you listen to it the ear takes in the same
offect through another sense ; the first sound is in extreme cases silent,

ENDOCARDITIS. 487

or i3 soft and gentle, feeble and perhaps somewhat prolonged ; while
the second penetrates and strikes the ear with a loud shock, often
ringing and metallic. Over the pulmonary artery, as I have just
said, that subdued sound or even silence, and this shock, betoken
tension of the artery, and obstacle to the flow of blood through the
vessels of the lungs ; whether that obstacle be caused by a back flow,
due to inflammation or disease, with incompetence, of the mitral
valve ; or directly to disease of the lung itself, whether from phthisis,
contracted lung, pneumonic bronchitis, or emphysema; the shock being
in these last cases shielded from the hand and muffled to the ear by the
interposition of a couch of lung, thickened by the undue expansion
of the air cells induced by the disease.

When the aorta is thus distended, pushing aside the lungs, beating
with a double pulsation upon the second right intercostal space, over
the ascending aorta, the first gentle and gradual, the second, a smart
shock, the first feeble or even silent, the second, a loud ringing, metallic
shock, you know that the blood forces its way with difficulty through
the fine vessels of the system, and that the cause of this is the con-
tamination of the blood, induced by advanced granular contraction of
the kidney.

Two conditions are needed forthe production of this double effect, one,
that just spoken of, the obstacle to the onflow of the blood; the other,
the force with which the pulsating ventricle sends its blood into the
artery. Lessen that force, and the supply of blood is lessened, the pro-
portion of blood in the vessels and the power to pass it on is brought
more into equipoise ; the tension of the blood being relieved, the first
sound becomes again audible, and the shock of the second sound is
subdued, so that it becomes merely unduly sharp or loud.

Additional observations are wanted on this important practical
point of the relative loudness of the first and second sounds over
the pulmonary artery and aorta ; combined with information as to the
poisoning and accumulation of the blood, structural change in the
walls of the arteries, and vital power. The two sounds must be
listened to, and their relative intensity noted, which I do by the ready
method of figures of varying size written on a diagram of the body
on which the outline of the ribs is traced. The size of each figure
denotes the relative intensity and actual loudness, judged of by the
ear, of the two sounds. When the first sound is silent, and the
second is loud and with a shock, I mark it thus, c/2; when two
sounds are equal, thus, 1/2 ; when the first is louder than the second,
thus, l/2 ; and when the second is louder than the first, thus, */2.
Every shade can be thus rendered. Combined sphymographic and
cardiographic tracings, some of which I have made, in these cases,
will give positive and scientific accuracy to our knowledge.

Doxibling of the Second Sound. — In two of the cases of endo-
carditis with mitral murmur, there was doubling of the second
sound. One of these came in with doubling of the first sound, or
almost a murmur at the apex, on the 4th day a peculiar plunging A

488 A SYSTEM OF MEDICINE.

first sound, with scarcely any second sound, appeared over the
ventricles. On the 6th day there was doubling of the second
sound. On the 8th day mitral and pulmonic murmur appeared,
followed by a tricuspid murmur, and on the 10th these murmurs
had all vanished. In the other case the doubling of the second
sound appeared late and was very tenacious. There was a mitral
murmur up to apd on the 23rd day, when the second sound was
prolonged over the pulmonary artery. On the next day there was
doubling of the second sound over that artery. The second second sound
was louder than the first — and this proved that the later sound was the
pulmonic, the earlier the aortic sound. In this instance the doubling
of the second sound, which lasted to the 60th day, disappearing on
the 69th, was due, I consider, to the longer time occupied by the right
ventricle than the left in emptying itself, owing to the resistance to
the flow of blood through the lungs.

Pulmonic Murmur. — Symbol ^. — A systolic murmur over the pul-
monary artery, at the second left space, was heard in a considerable
number of the cases of endocarditis with mitral murmur. This
number amounted to one-third of the first series, or seventeen in fifty-
two, and to one-half of the second series, or ten in twenty. This
murmur was present also in one-third of those cases of endocarditis
affecting the left side of the heart, in which there was tricuspid, but
not mitral, murmur. In more than one-half of those cases the pulmonic
murmur appeared towards the close of the attack, when all the acute
symptoms had gone by, when the period of convalescence was
approaching or established, when the patient was pale and thin,
having lost a large proportion of the red corpuscles from the blood,
and was weak from the exhausting nature of the disease. In nearly
one-half of the remaining cases this murmur appeared at the middle
period, and in one in four of the whole number it was audible soon
after the admission of the patient.

The murmur almost always occupied a well-defined limited area
at the edge of the sternum in the second space, just over the pulmo-
nary artery. It never extended as far as the right edge of the sternum,
but it could be heard very feebly in the first space, and occasionally
in the third. When the position of the pulmonary artery was unusually
low, the murmur moved downwards, being then heard strongly over
the third space, and feebly over the second and fourth spaces.

The pulmonic murmur rarely presents a smooth soft bellows sound,
but is usually grave and superficial, without however being large in
character or very loud. The murmur appeared as a peculiar scratching
noise in one-half of the cases, or 4 out of 8, in which the sign appeared
soon after admission, and besides these in one on the 8th and in another
on the 21st day. The scratching nature of the sound when I first
observed it (I found it noticed in one case as early as the year 1852) was
very puzzling. It strongly suggested friction sound. But it differed
in these respects : it was always systolic, being never to-and-fro ; pres-
sure sometimes highly intensified, but never altered it in tone ; it clung

ENDOCARDITIS. 489

to one spot ; and it gradually disappeared without passing into a wide-
spread double friction sound. Its noise was exactly like that made by
scratching slowly and gently with a pin on a deal table.

The cause of the pulmonic murmur is exactly the same as that of
the aortic " anaemic " murmur, which is audible only during the sys-
tole. It is due to the blood being very thin and lessened in quantity,
and propelled into the vessel when its walls are relaxed, with undue
force, by the ventricle.

When the pulmonary artery is flaccid, its contents have free room
to vibrate as they move onwards in the current of the circulation, and
therefore pulmonic murmur is engendered. The pulmonic murmur
thus indicates that there is relaxation of the pulmonary artery, or a
condition the opposite to that of tension of the artery. The second
sound following the murmur may be loud, but it is usually feeble. It
is loud if, during and towards the end of the contraction of the right
ventricle, the pulmonary artery becomes tense ; its walls then recoil
with force upon their contents and propel them with equal pressure in
two directions, forwards into the vessels, and backwards upon the
ascending pulmonary artery, its sinuses, and valve, where the
back-stream strikes with a sudden shock, the shock of the loud
second sound. The second sound is, on the other hand, feeble if
the flaccid artery does not become distended during the systole;
when the recoil of the walls is therefore weak, and when the back-
wave breaks with only moderate force upon the roots of the artery.

Silence or feebleness of the first sound is the opposite in char-
acter and cause to pulmonic murmur. If the artery is distended
when the ventricle begins to contract, the column of blood moves
steadily forwards, the walls of the vessel and its contents are not thrown
into vibration, and the first sound is either absent or feeble. The
extreme tension of the pulmonary artery thus induced, leads, when
the blood has ceased to enter it, to the recoil of its walls with excessive
force upon their contents, which are driven with a strong back-stroke
or shock upon the walls, sinuses, and valve of the artery. When
the lung is displaced from before the pulmonary artery, thus distended,
this si lock is felt by the hand and heard striking against the ear with
a loud metallic sound.

Pulmonic murmur, as we have just seen, came into play most
frequently when the disease was passing away. It was therefore
rarely, or only once or twice, associated with a mitral murmur when
at its zenith, and uncomplicated with other murmurs. In fully one-
half of the cases (13 in 24) it accompanied prolongation of the first
sound, or a feeble mitral murmur ; in nearly one-half of them (9) it
appeared with a conjoint mitral and tricuspid murmur ; and in one-
fourth with a simple tricuspid murmur, a companion sign that was
therefore present in three-fourths of the cases. In one-fourth of the
cases (6) it was traced side by side with an anaemic murmur over the
aorta or carotid artery ; and thrice it was unaccompanied by any
murmur. Nearly all these instances point to a state in which the

vol. iv. K K

482 A SYSTEM OF MEDICINE.

palm of the hand was applied over them, or when the fingers were
pressed gently into the spaces.

In one or two patients the impulse presented a peculiar shock.

But the distinctive feature with regard to the impulse in a fair
proportion of the cases was its variation during the successive periods
of the disease. Thus, in one instance, it was feeble on the 1st day in
the fourth space, very strong on the 3rd day, moderate in strength
in the fifth space on the 8th day, and in the third and fourth
spaces on the 12th day. In another patient the impulse was felt
in the second and third spaces on the 2nd day, when there was
pain in the heart; on the 5th, the pain still continuing, the heart
beat violently ; from the 6th to the 18th the pulsation was strong
in the second space, and from the 28th to the 34th it was diffused
from the third to the fifth spaces. In this case mitral disease was
established, and the gradual extension of the impulse of the right
ventricle told with precision the story of the increasing valvular
disease in the left ventricle.

The impulse of the right ventricle was diffused and strong, extending
out to the nipple, in a considerable proportion of the cases in which
there was a tricuspid murmur.

In a few instances the impulse of the right ventricle was so high
as to be present in the second space ; but generally the pulsation felt
in that space was due to the presence there of the distended pulmonary
artery, when that pulsation was double, the second impulse beiug
more smart and shock-like than the first. In these cases the pul-
monary artery was distended, the first sound was feeble or absent,
while the second was unusually loud and strong, penetrating the ear
with a shock.

The apex beat is, in cases of endocarditis with mitral regurgitation,

ENDOCARDITIS. 48&

usually slight, sometimes absent— during the early period, before the
mitral murmur is developed, owing to the weakened muscular power
of the inflamed left ventricle; and — after the appearance of the murmur,
owing to the relief afforded to the organ by the greater ease with which
its surcharge of blood is sent backwards into the auricle than forwards
into the aorta.

There are, however, certain exceptional cases of great interest,,
several of which have come under my observation, in which the left-
ventricle beats with great force, and unduly to the left.

In three of these cases there was extensive pulmonary apoplexy, or
pneumonia of that type, in the lower portion of the left lung.

Accentuation of the Second Sound, with Silence, Feebleness, or Pro-
longation of the First Sound over the Pulmonary Artery. — Accentuation
of the second sound over the pulmonary artery, in the left second
space, is a well established sign attendant upon mitral regurgitation,
and it may be present in every degree.

This increase in loudness and sharpness of the second sound is due
to distension of the pulmonary artery, owing to the difficulty with
which the blood travels through the vessels of the lungs.

484 A SYSTEM OF MEDICINE.

superficial to it, and presses against the second space ; where there is a
double impulse the first gentle, the second felt and heard as a shock.
In bronchitis, emphysema and pneumonia, there is the same disten-
sion of the pulmonary artery, but greater in degree. The interposition
of the lung, enlarged owing to the disease, screens the pulmonary artery
from the hand and the ear, so that over it the second sound is often not
unduly loud ; but it is so in some instances over the right ventricle.

Whenever the tension of the pulmonary artery is thus so great as
to cause a strong and loud shock with the second sound, the first
sound is either almost silent, or feeble, or faintly prolonged.

When the blood is sent into a tight and full artery, it makes but
little, often no sound, either in the shape of shock or murmur ; but the
second sound caused by the smart and strong reflux of the blood upon
the walls and closed valves of the artery, makes a loud, sometimes a
ringing or metallic sound. The same occurs in the aorta when it is
enlarged and rendered tense owing to the difficulty with which the
blood leaves the arterial system in advanced cases of contracted granular
kidney. When you listen over the aorta a single sound is often heard,
a loud ringing metallic second sound, the first being almost or abso-
lutely silent. Sometimes in these cases the artery is so large and
tense that it presses against the second right intercostal space, pro-
ducing there a double pulsation, the first gentle and gradual, the second
-smart and with a shock.

In all but six of the patients in whom it was noticed that the second
sound was intensified, it continued to be loud down to a late period,
to the time in fact of approaching recovery.

Loudness of the second sound may be associated with each of
the signs, singly or in combination, that are habitually found in
cases of endocarditis with inflammation of the mitral valve. It
accompanied a mitral murmur, either alone or in combination
with a tricuspid murmur in 22 of the cases ; in about 15 cases it
was allied with prolongation of the first sound over the left and
sometimes the right ventricle; and in 8 cases it was joined to
tricuspid regurgitation, which was however combined with other
important signs in every instance but one. The first sound of the
pulmonary artery wTas affected, when the second sound over that
artery Mas loud or sharp, on ten occasions, in different patients :
in 4 of these there was a pulmonic murmur, in i the first

ENDOCARDITIS. 485

sound was prolonged, being generally free from shock, and in 2 it
was silent or scarcely audible.

These numbers, however, taken by themselves give a very inade-
quate idea of the relation of the first to the second sound of the
pulmonary artery in cases when that second sound is intensified.
Thus, as we have just seen, pulmonic murmur was followed by a
sharp second sound in four instances, but there were altogether 32
cases in which a pulmonic murmur was heard, and in only four of
them was it stated that the second sound was thus affected at the
time when the pulmonic murmur was audible. In one of the cases
in which there was a pulmonic murmur on admission, the second
sound was free from accent ; while on the 3rd when the pulmonic
murmur had disappeared, that sound was slightly accentuated over
the pulmonary artery. Again, in only two of the cases is it noted
that the first sound of the pulmonary artery was silent or scarcely
audible when the second sound was loud. Since, however, my atten-
tion has been drawn to the relation of the first to the second sound
of the pulmonary artery, in every instance that I have observed
accentuation of the second sound, especially with, but even without
shock, the first sound has been either very feeble, being occasionally
prolonged, or almost or even quite silent. This condition was signally
marked in a case of chorea under my care in the hospital, a boy, who
on admission, presented no mitral or other murmur over the heart.
.After gaining ground steadily he became rather worse, his temperature
rose., he had pain in his chest, and the second sound was loud, the
first feeble over the pulmonary artery ; and six days later a mitral
murmur came into play. At the same time the right ventricle,
previously quiet, beat with great force, and a strong shock was felt
over the pulmonary artery with the second sound. On listening over
that vessel, a loud second sound penetrated the ear and struck it as
it were with a shock, and the first sound was silent, the second sound
being alone audible to all who listened. After a short time he
became very ill, and for two days he passed his evacuations involun-
tarily in bed. He kept both hands fixed on his wrists, and his fingers
on his hands. He soon began to improve, and gradually as this boy
gained strength, speech, power to move, and freedom from irregular
movements; and as his lungs enlarged, the mitral murmur being
still audible, the second sound though still loud lost its shock, the
second impulse ceased to be felt over the pulmonary artery, and the
first sound, though feeble, became more and more audible.

In a fair proportion of the cases in which the second sound was
sharp and loud at the early period of the disease, that sound retained its-
character unaltered through all the surrounding changes in the sounds
of the heart. Let us take one case. At first there was a tricuspid
murmur, the second sound being sharp ; on the 6th day there was a
mitral murmur, and the second sound was loud ; next day the murmur
was less marked, but the second sound was still loud ; and on the
11th the murmur had given place to prolongation of the first sound

494 A SYSTEM OF MEDICINE.

the heart. The face is anxious and dusky ; there is sometimes pain
in the heart ; the breathing is quickened and oppressed ; the impulse
of the left ventricle is weak, while that of the right is unduly strong ;
the circulation through the lungs is impeded ; the pulmonary artery
is distended, its first sound is silent or feeble, and its second is accen-
tuated ; a tricuspid murmur is often present, sometimes alone, some-
times conjointly with a mitral murmur ; prolongation of the first sound
precedes and follows the mitral and tricuspid murmurs ; and anaemic
murmurs are often heard botli over the pulmonary artery and the aorta,
during the early and also the late period of the disease, but rarely
during its acme ; the pulmonic murmur being more frequent at the
period of convalescence, the aortic murmur during the early stage of
the disease.

III. Cases of Rheumatic Endocarditis with Aortic Regurgitation.
(1) Not Accompanied by Mitral Murmur. (2) Accompanied
by Mitral Regurgitation.

Symbol ^.

(1) Aortic Regurgitation, not accompanied by Mitral Regurgitation.
— Incompetence of the aortic valve is much less frequent in rheu-
matic endocarditis than incompetence of the mitral valve. There
was a diastolic aortic murmur not accompanied by a mitral murmur
in ten ; and there was a mitral murmur without a diastolic murmur
in fifty of the first series of cases — while there was mitral regurgi-
tation in twenty, and aortic regurgitation in none of the later series
of cases. This brings up the cases of mitral in relation to aortic
regurgitation to the proportion of seventy of the former to ten of the
latter. Besides these, eight of the first series and one of the second
presented both mitral and aortic incompetence. This makes the total
number of cases in which there was aortic regurgitation eighteen, and
the total number in which there was mitral regurgitation seventy-nine.

In more than one-half of the cases of endocarditis with aortic
regurgitation, there was no mitral murmur (10 in 18). The mind
naturally infers that in these patients the inflammation was limited
to the aortic valve, and did not extend to the mitral. The close
examination of the cases, however, leads I consider to the conclusion
that in all of them there was inflammation of both the mitral and the
aortic valves.

A mitral murmur appeared in one of the ten cases for a single
day and was not again heard. That was the only case in which this,
the central and immediate sign of mitral endocarditis, was noticed. In
the others, however, the more important secondary signs of inflamma-
tion of the interior of the left ventricle were present.

In five of the cases a tricuspid murmur was audible over the right
ventricle. In three of these that murmur was heard before the murmur
of aortic regurgitation came into play ; in one, the two murmurs were

ENDOCARDITIS 41)5

present on the day of admission ; and in the fifth case, the tricuspid
murmur appeared a week later than the aortic, but the aortic murmur
was preceded by prolongation of the first sound, which was present
on the day of admission.

The first sound was prolonged over one or both of the ventricles in
six of the cases ; in three of which there was, and in three there was
not a tricuspid murmur. In two of the three in which there was no
tricuspid murmur, prolongation of the first sound preceded the aortic
murmur.

Thus eight of the ten cases of endocarditis with aortic incom-
petence, without mitral murmur, presented either a tricuspid murmur,
or prolongation of the first sound over the ventricles, or both
signs. In six of them, one or other of those signs preceded the
appearance of the aortic incompetence ; in one other the patient came
in with both aortic and tricuspid regurgitation murmurs ; and in the
remaining one only did the aortic murmur precede by three days the
prolongation of the first sound. The ninth case was admitted with
aortic regurgitation, and he suffered from pain in the region of
the heart.

The tenth case, a female patient, was an anomalous and doubtful
one. She was very ill when admitted, when she had pain in the left
side, and the sounds of her heart were rough. On the 12th day a
soft double murmur was audible in the second left space which was
probably due to aortic incompetence.

(2) Cases of Rheumatic Endocarditis with Aortic Regurgitation ac-
companied by Mitral Regurgitation. — In eight cases mitral and aortic
incompetence were combined, and in six of these the mitral murmur
preceded the aortic. Both murmurs were present on admission in
one of the two remaining cases, and they appeared together in the
other one on the seventh day after admission.

These illustrations, and the considerations that I have just advanced,
appear to me to render it conclusive, that the inflammation always
commences in the interior of the left cavities, affecting primarily the
mitral valve ; and that it extends at a later period, and in a limited
number of cases to the aortic valve.

These facts lead us to expect that in cases of endocarditis the aortic
diastolic murmur appears at a later period than the mitral murmur.
In two only of the cases was the aortic murmur heard on the day of
admission. One of these had been ill a week, and that was the
earliest date of the appearance of the murmur. In three of the
patients the aortic murmur appeared from the 7th to the 10th days,
in one-fourth of them (5) from the 10th to the 15th days, and in more
than one-half (10) from the 22nd to the 88th days, after the beginning
of the attack of acute rheumatism.

We have seen that aortic regurgitation is preceded with rare excep-
tions by a mitral or tricuspid murmur, or a prolonged first sound
over the ventricle, or in other words by evidence, immediate or

496 A SYSTEM OF MEDICINE.

secondary, of inflammation of the left cavities of the heart and the
mitral valve.

In a small proportion of the cases, amounting to three in eighteen,
the murmur of aortic regurgitation was preceded by prolongation of
the second sound over the aorta or the carotid artery. This prolonga-
tion of the second sound over the aorta before the appearance of the
aortic diastolic murmur, has evidently the same relation to that
murmur, that prolongation of the first sound has to a mitral or tricus-
pid murmur. It is a transition sound, and is the immediate herald of
the coming complete murmur of regurgitation.

An anaemic systolic aortic murmur sometimes precedes the appear-
ance of the diastolic murmur made by aortic regurgitation ; but
it more often comes at the same time or later, when the two sounds
combine to form a true double murmur. This double murmur was
present, in eleven of the eighteen cases of endocarditis with aortic
regurgitation, in four of which the systolic murmur was audible
before the diastolic murmur, in five they appeared together, and in
two the latter murmur came first into play.

The situation of the aortic diastolic murmur of endocarditis is
ruled by the position of the aperture of the aorta, and the direction of
the back current flowing through it into the left ventricle.

The murmur is more loud and intense to the left of the middle
of the sternum, just over the root of the aorta, than elsewhere. It
takes there a direction downwards and to the left, and is audible to
the left of the lower three-fifths of the sternum, becoming feebler as
it descends, and is lost usually before it reaches the limit of the
lower end of the sternum. The murmur was heard also in five cases
as high as the lower end of the manubrium, and indeed over that
portion of the sternum. In rare cases it is audible at the apex.

In my cases of endocarditis with aortic regurgitation, the most fre-
quent position of the murmur was to the left of the lower portion of the
sternum, a space that extended from the middle of the sternum to its
lower end, and from the third left costal cartilage to the sixth ; a space
that is immediately in front of the right ventricle, where it is
denuded of lung. The murmur was audible over this space in thirteen
of the eighteen cases. In four others it was heard at or to the left
of the mid-sternum, a position that is included in the space noted as
being to the left of the lower sternum, and which is, therefore, the
position at which the aortic diastolic murmur of endocarditis is heard
most frequently and with the greatest intensity.

In two of the cases the murmur was audible just below, and in one
of these over the manubrium. In none of them is it stated that the
murmur was heard to the right of the upper portion of the sternum,
a position in which the direct aortic murmur was audible in five
of the cases. In the exceptional and doubtful case, the double
murmur was restricted to the left second space. There was certainly
no regurgitation in that case from the pulmonary artery into the right
ventricle, and we are therefore. I think, entitled to consider that it

ENDOCARDITIS. 497

was, like the others, a case of aortic endocarditis, with regurgitation.
In a patient under my care in St. Mary's Hospital an exquisite
musical plaintive diastolic murmur sprang up at a late period just
over and below the lower portion of the manubrium, and over the
pulmonary artery in the second space, and was limited to that region.
In this case the position of the heart was high and the murmur was
heard over a correspondingly high and limited area.

In four, and in four only, of the cases the diastolic murmur was
heard at the apex.

When we consider that the current of blood flows from the aorta
back into the left ventricle, it seems natural to expect that the murmur
of aortic regurgitation should be heard over the left ventricle, into which
the stream of blood falls ; and not over the right ventricle, which, with
its double wall and its full contents, is interposed between the stream
of return-blood and the ear. But the fact is the reverse of this. The
murmur is always heard in front of the heart, over the right ventricle,
and rarely over the left ventricle, to the left of the septum.

After a little reflection, the reason of this curious deviation of the
direction of the sound becomes apparent.

When the aortic valve is incompetent, two streams pour side by
side into the left ventricle. One of these conies do\vTn, in a large
volume of blood, from the left auricle, through the mitral orifice, into
the left ventricle ; and this large living stream of blood occupies and
completely fills the whole of the outer portion of that cavity, which
is the part that is in contact with the walls of the chest at and
beyond the septum, and at the apex. The other stream is that of
regurgitation from the aorta. It is a small and an active stream which
plays downwards into the innermost portion of the cavity, or that
portion of it which lies immediately behind the right ventricle. The
large living stream of blood that pours down from the left auricle
into the outer part of the left ventricle, through the mitral orifice,
cuts oft* the inner, deeper, and finer current flowing back from the
aorta into the left cavity, and so silences it. This answers the ques-
tion, why do you not hear the murmur of aortic regurgitation at the
apex and over the left ventricle ? The answer, however, to the second
question is still to seek, why do we hear that murmur through the
right ventricle, with its double walls, and its large volume of blood
entering freely through the tricuspid orifice ? When thinking out the
answer to this question, we must steadily come back upon the facts as
to the position of the aortic orifice, the nature of that part of the
ventricle immediately in front of the aortic aperture, the direction of
the return-current of blood into the right ventricle, the point of the
greatest intensity of the murmur, and the bearing of the fading away
of the murmur.

The aortic valve lies behind the middle of the sternum, at its left
edge ; in front of it is the conus arteriosus, which is the shallowest
part of the right ventricle, its cavity being there wider than it is deep,
and its posterior wall being there pushed forwards by the left ventricle

408 A SYSTEM OF MEDICINE.

and the root of the aorta and the aortic orifice through which this
back-current flows ; the walls of the conus arteriosus are here thin,
especially the front wall ; the blood contained in this part of the right
ventricle is not in lively motion during the diastole, for it is above
the current of blood from the right auricle into the right ventricle ;
and that current pours across from right to left, low down into the
larger, deeper, and lower portion of the ventricle behind the lower
part of the sternum and upper part of the ensiform cartilage. The
murmur rapidly loses loudness and intensity as it approaches the
lower part of the sternum in front of the tricuspid current, and it is
lost before we reach the top of the ensiform cartilage.

We now see that the murmur of aortic regurgitation has a shorter
way to travel, and passes through a less troubled blood, by passing
straight through the arterial cone of the right ventricle, immediately
in front of the aortic aperture ; than it would if it were to force its
way through the large and deep living current of blood that flows from
the left auricle, through the mitral orifice, into the left ventricle, and
that completely occupies the body and outer or left side of that cavity,
where it presents itself at and beyond the septum and at the apex.

When active endocarditis passes away and leaves the aortic valve
permanently incompetent, the murmur becomes more intense, and its
area more extensive. The diastolic murmur may then be present over
the whole length of the sternum, extending to the right of that bone
at its upper portion ; and slightly to the right, and to a great extent
to the left of that bone at its lower portion ; the area of the murmur
sometimes extending as far outwards as the region of the apex of the
heart.

The murmur of aortic regurgitation in cases of endocarditis is
usually soft, smooth, and like a bellows sound. Sometimes it is
musical, the note being fine and plaintive, limited in area to the
middle of the sternum, or a little above that point, not penetrating,
and easily obscured by the other sounds of the heart, and by respira-
tion. It was thus in one case — a very pale woman aged 49. On her
admission she presented tricuspid, carotid, and loud mitral systolic
murmurs, and a musical diastolic murmur over the middle of the
sternum. On the fourth day she was better, and all the murmurs
were less marked ; and on the sixth they were gone. Next day there
was an obscure musical diastolic murmur, which also disappeared in a
lew days. In one case, on the 101st day after admission there was a
double musical murmur to the left of the lower sternum. In another
case, already alluded to, an exquisite musical murmur appeared just
below the manubrium, extended to the left during the time of con-
valescence, was limited in area, and disappeared in about a week.

In another patient, a man, who came in with a mitral murmur,
which established itself, a distinct double murmur appeared for the
first time on the 69th day. Six days later the diastolic murmur
appeared as a long whistle, but it resumed its usual character on the
following day. One other patient that presented a peculiar musical

ENDOCARDITIS, 499

diastolic murmur was a woman, aged 40, ill with acute rheumatism for
four days, who came in with a faint blowing tricuspid murmur, which
went on the third day, when she had pain in the heart. On the tenth she
was better in every respect, but a peculiar diastolic murmur appeared to
the left of the lower sternum, like the twang of a harp-string, which was
still audible next day ; but this was soon replaced by an ordinary short
diastolic murmur to the left of the mid-sternum, which ceased after a
few days, when both sounds were a little prolonged. Dr. Broadbent
observed this case with me.

In another patient, a man affected with acute rheumatism and
endo-pericarditis, a loud, grave musical murmur sprang up in the
course of the illness, a vibrating murmur, with a perceptible thrill over
the aorta, in the second right space, where the murmur was most
intense ; but the sound was heard to a great extent over and even
below the chest. This murmur became established.

Of the remaining cases (14), in nearly one-half (6) the murmur was
soft, or like a bellows sound, and this was undoubtedly its predomi-
nant character in the rest, although in them the precise nature of
the murmur is not stated.

In about one-half of the cases of rheumatic endocarditis with aortic
regurgitation, the murmur disappeared when the patients were under
observation ; while in the greater proportion of the remaining half, the
murmur became fixed, being associated with established mitral regur-
gitation in two-thirds of those cases.

It was interesting and a source of anxiety to watch the progress of
the murmur, dwindling and disappearing in the former set of cases,
and ripening into permanent valvular disease in the latter set.

We have already seen that the fine musical diastolic murmurs with
a limited area disappeared, while the louder ones of that class became
established.

The character of the early murmur of aortic regurgitation gave
little ground for foreseeing whether the incompetence would be per-
manent or transient. Thus in three, if not four, instances, a diastolic
murmur, obscure, faint, feeble or confused at first, ripened later into
an established aortic valve disease.

The history of the murmur, its development or decay, the widening
out or contraction of its area, and the presence or absence, the increase
or diminution of the characteristic signs of aortic regurgitation
attendant upon the murmur ; give more information as to the actual
state, progress, and probable future of the patient than the exact
character of the murmur on any particular day.

A statement of the duration of the murmur, and of the attendant
secondary signs in the cases in which the valve completely regained
its function ; and a brief recital of the leading points in one or two of
the cases that ended by producing aortic valve disease, will illustrate
practically the probable future prospect of the affection in these
important cases.

The diastolic murmur was short-lived in all but three of those cases

500 A SYSTEM OF MEDICINE.

that ended in restoration of the function of the valve, its duration
being from one to eight days. In the three others the murmur, which
diminished steadily in loudness, or sometimes remitted, lasted from
fifteen to fifty days.

We shall be the better able to understand the extent to which these
cases depart from health, and approach to disease, of the aortic valve
with regurgitation, by rapidly reviewing the characteristic signs of the
established disease, so as to obtain a standard of comparison.

The characteristic signs of permanent aortic regurgitation are —
enlargement of the left ventricle, fulness over that ventricle, and
undue force of the apex-beat, which extends beyond and below the left
nipple ; strong visible pulsation of the carotid arteries ; sudden ham-
mering stroke and collapse of the pulse, especially when the arm is
raised, when the pulse is visible, and is audible with a loud shock that
gradually lessens and disappears when the arm is lowered beneath
the level of the heart; diastolic bellows murmur over the whole
sternum, its maximum intensity being to the left of the middle of the
bone; the murmur extending to its left at the lower portion of the
sternum, becoming more feeble downwards, and to its right at the
upper portion becoming more feeble upwards ; a direct aortic murmur,
generally audible over the manubrium, and to its right, where there is a
true double aortic murmur ; and a grave vibrating systolic murmur
in the neck, over the visibly pulsating carotid artery, which is not
followed either by a second sound or a diastolic murmur.

When the patient sits up, the extent of regurgitation and the
collapse of the artery increases ; and as a consequence, the diastolic
murmur often becomes louder and more intense and extensive over its
proper region ; and the systolic murmur becomes more grave over the
aorta and carotid artery, or is replaced there by a local and sudden
shock when the regurgitation is very great so as to empty the ascending
aorta during the diastole, the shock being occasioned by the blow
with which the advancing column of blood is impelled by the stroke
of the left ventricle upon the walls of the empty aorta and carotid
artery.

If the incompetence of the aortic valve is caused by great enlarge-
ment of the aperture of the aorta, owing to dilatation of the vessel
from atheroma, the artery extends to the right of the upper sternum,
displacing the lung, and may present there a thrill and a loud vibrating
musical murmur, heard, perhaps, at some distance from the surface,
and extending over the whole chest, front and back, the neck, and
even the abdomen.

My cases of endocarditis with aortic regurgitation ending in com-
plete restoration of the valve, presented, with the exception of
the double murmur, to a very slight degree the characteristic signs
of disease with incompetence of the aortic valves. The diastolic
murmur was present at the mid-sternum, and a little higher, and
extended downwards, and to the left, becoming gradually feeble;
but it was never heard upwards, over and to the right of the upper

ENDOCARDITIS. 501

sternum, unless it was joined to a mitral murmur. The area of the
diastolic murmur was thus limited ; and it was feeble, very soft, and
like a bellows-sound, or plaintively musical.

A systolic murmur was present over the aorta, or the carotid artery,
or both, in two-thirds of the cases, this being an anaemic murmur, and
not one caused by obstruction. It was due, in fact, to the flaccid state
of the aorta, caused primarily by the comparatively small amount of
blood sent into it by the inflamed and weakened left ventricle, and in-
creased by the reflux of a portion of that blood sent back again into the
left ventricle through the inflamed and insufficient aortic valve. This
flaccid state of the aorta allowed the blood contained in it to play
freely to and fro in a series of noisy vibrations, with the effect of
inducing a grave systolic aortic murmur.

The impulse was rarely notably strong. It was observed in four of
the nine cases of this class. The apex-beat was felt close to the
nipple in one of these patients ; and in another, in whom the
murmur lasted long, it was present on admission in the fifth space,
outside the mammary line, and was stronger than usual on the 7th
day ; but it retreated within the nipple line from the 12th day,
varying in position from the fourth to the fifth space.

The second sound, which is usually lost over the carotid artery in
disease of the aortic valve, was audible in the neck in seven out of
the nine cases of endocarditis in which the incompetence of the aortic
valve was only temporary. In several of these cases the second sound
was at one time or other less clear than natural over the neck, being
feeble in two, grave in a third, and in a fourth, first prolonged, then
silent, and afterwards natural, but feeble.

Although, then, in these cases, the second sound is still audible,
perhaps, over the aorta, and certainly over its branches, the innominate
and carotid arteries, it is often palpably modified in character. The
presence of a second sound over the great arteries at the root of the
neck, and over the ascending aorta, where it is, however, rendered
doubtful by being blended with the transmitted presence of the
pulmonic second sound, is due to the slight degree of the imperfec-
tion of the aortic valve. The shock of the second sound is therefore
caused over those parts by the recoil of the walls of the distended
arteries after the end of the systole, which sends the blood not only
forwards into the arteries, but with a pressure equal in every
direction, also backwards with a return-stroke upon the inner walls of
the ascending aorta, including its sinuses, and slightly imperfect yalve.
The aortic second sound, although present, is often modified in tone
and blunted, owing to the force of the back-stroke of the blood being
impaired ; (1) by the reflux of a small portion of the blood into the left
ventricle through the inflamed and slightly insufficient valve ; and (2)
by the lessened supply of blood to the aorta and arteries from the left
ventricle, the action of which is weakened by the inflammation of its
inner surface. The degree to which the second sound over the neck
is rendered feeble, blunted, prolonged, or almost or quite silenced, is a

602 A SYSTEM OF MEDICINE.

key to the knowledge of the amount of regurgitation, and of the defective
supply of blood from the left ventricle. This important element of
diagnosis is farther illustrated by what is found in cases of Bright's
disease with contracted granular kidney, when the aortic valve is
rendered slightly insufficient by the great distension and enlargement
of the aorta. Here the blood is sent by the powerful left ventricle
into the aorta and the arteries, already rendered tense by the difficult
onflow of the poisoned blood through the small vessels; and the relief
afforded to the tension by the reflux through the insufficient valves is
so slight, that the back-stroke of the blood caused by the recoil of the
arterial valves is still made with so much force, that the second sound
usually retains the metallic ring, and the first sound the feeble note,
so characteristic of aortic tension from Bright's disease.

Some of the cases of endocarditis with aortic regurgitation, ending
in disease of the aortic valve, acquired step by step the characteristic
signs of the permanent affection.

One case of this class, a man, ill a week, came in with quick breath-
ing, a slightly prolonged second sound, and a rather extensive impulse.
On the 5th day a soft mitral murmur appeared, which was loud on
the 7th, when a diastolic murmur was also audible over the sternum,
which extended next day slightly both to the apex and the neck. A
week later there was a combination of mitral, tricuspid, and double
aortic murmurs, and an obscure second sound was heard in the neck.
At the end of the third week the disease was settling into its perma-
nent form, the impulse being extensive, the carotid pulsation visible,
and the second sound absent from the neck. The diastolic murmur,
feeble on the 24th day, was loud on the 34th, when it was combined
with a mitral murmur, and the apex-beat was strong.

Another patient, a labourer, ill eight weeks, was admitted with
profuse perspiration, tremulous hands, rather quick breathing, and a
double murmur to the right of the upper half of the sternum. On
the 4th day the murmur was louder, and was audible over the right
ventricle ; but on the 6th he was faint, and the murmur was again
limited to the aorta. On the 8th day he felt better, and the aortic mur-
mur was again audible to the left of the lower portion of the sternum, as
well as to the right of its upper portion. Variations followed, renewed
diminution of the aortic murmur over the right ventricle being joined
to renewed illness ; but after this the systolic murmur became rasping,
especially over the third right cartilage, and the diastolic bellows
sound became again widened in area.

The third case of this class, a woman, ill a week, came in with pro-
longation of the first sound, but no murmur. On the 3rd day an
obscure diastolic murmur was audible at the left nipple, and on the
7th this murmur was present along the whole sternum, especially
from below the manubrium, and to the right of its upper portion.
The second sound was heard in the neck, and the pulse was not dis-
tinctly audible at the wrist. On the 15th the diastolic murmur,
smooth and prolonged, was more extensive downwards ; the second

ENDOCARDITIS. 503

sound, feeble at the apex, was audible in tlie neck ; and a mitral
murmur was present for the only time. On the 29th day the pulse
was visible at the wrist, and on the 52nd, when she was almost well,
there was some fulness over the region of the heart, its impulse being
stronger over both ventricles, and especially at the apex. The
diastolic murmur was most intense at the fourth cartilage, but was
audible along the whole sternum, except its summit. The second
sound was still present in the neck, and the pulse was not audible.

In these three cases of endocarditis, the affection of the aortic valve
advanced steadily, but with variations, under my notice, and during
the evolution of the disease its characteristic signs came into play one
by one.

The next case, a man, stands alone ; the aortic regurgitation, after
being suspended for a time, returned, and again lessened, without
disappearing.

In the last group of four cases of endocarditis with aortic regurgita-
tion, ending in disease of the aortic valve, the murmur appeared at a
late period of the disease.

In one of these patients, a man, the murmur appeared suddenly
without warning and in full force on the 88th day, being heard
loud along the lower sternum. He had previously presented a vari-
able mitral and an occasional tricuspid murmur. This mitral murmur
was suspended during a period when the patient was ill with enteric
fever, and when prolongation of the first sound was its temporary
substitute.

A second case of this class, a boy, ill a week, came in with pain in
the heart, a friction sound, and a mitral murmur, which was still present
on the 5th day. After this there is a gap in the narrative until the
49th day, when there was still a mitral murmur. On the 69th
day a double aortic murmur suddenly appeared for the first time,
and already the pulse at the wrist was audible when the arm
was raised. This diastolic murmur varied, increased, and ex-
tended to below the ensiform cartilage, but not to the top of the
sternum ; was once a long whistle, but generally a bellows sound ;
was accompanied by a mitral murmur at the apex, probably by a
tricuspid, and certainly by a direct aortic murmur, there being no aortic
second sound. The impulse of both ventricles became extensive,
strong, and peculiar, pointing to adherent pericardium ; it presented
a double shock, one during the systole, and the other at the commence-
ment of the diastole.

In the third case, a woman, one of remarkable interest, a faint
diastolic murmur appeared to the left of the lower sternum on the
47th day, having been preceded and accompanied by varying mitral
and tricuspid murmurs. In this case the thyroid gland became very
large on the 64th day ; was a good deal smaller on the 74th, and
finally resumed its natural size. There was a distinct double murmur
on the 101st day.

The last case presented healthy heart-sounds on the 17th day after

504 A SYSTEM OF MEDICINE.

admission, and on the 22nd a soft diastolic murmur came into play
to the left of the lower sternum, and a double aortic murmur just
below the manubrium. The pulse was audible when the arm was
raised, and the impulse was normal in extent.

These interesting cases of aortic regurgitation, coming on by sur-
prise at a late period in cases of endocarditis, usually with a persistent
mitral murmur and extensive and deep-seated inflammation of the
interior of the left cavities ; show that the aortic valve, though it
suffers rarely and slightly when compared with the mitral valve, may
silently and without warning, and when the patient appears to be well,
break down in its functions by the steady and long advance of a
latent inflammation.

When we consider how remote the aortic valve is from the focus
of the inflammation, how passive and rigid the structures at the outlet
of the left ventricle are in which that valve is embedded, how gently
the flaps of the valve come together, how comparatively slight is the
force exerted upon the valve by the back-flow of the blood in the
artery, due to the recoil of the walls of the aorta — that vessel being
imperfectly supplied with blood by the inflamed and weakened left
ventricle — a force that spends itself mainly in driving the blood
forwards, and secondarily in impelling it backwards on the valve, it
is only natural that the aortic valve should be rarely incompetent
during the attack of endocarditis, and more rarely permanently
crippled. These cases perhaps point to a gradual extension of the
inflammation on the ventricular surface of the valve, and to the gradual
yielding of the inflamed and softened valve ; which at length gives way
suddenly at its margin, and so admits of regurgitation from the aorta
into the left ventricle.

IV. — Cases of Rheumatic Endocarditis with Prolongation of

the First Sound.

The examination of the cases of endocarditis in which there was
tricuspid, mitral, or aortic murmur, alone or in combination, show, I
think conclusively, that prolongation of the first sound at the apex
or over the right ventricle points to actual or imminent endocarditis.

Thus prolongation of the first sound both preceded and followed a
temporary tricuspid murmur in three cases, preceded the appearance
of that murmur in two other cases, and followed its disappearance in
two additional ones. The first sound was therefore prolonged in one
half of the cases (7 in 13) in which a tricuspid murmur was present
without a mitral murmur.

Again, a mitral murmur when present without aortic regurgitation
was preceded and followed by prolongation of the first sound in seven
cases ; and was preceded by it in nine, and was followed by it in twenty
other instances. The first sound therefore was prolonged in fully
two-thirds (36 in 50) of the cases of endocarditis with mitral murmur
in which there was no aortic regurgitation.

ENDOCARDITIS. 505

Finally, the first sound was prolonged in six of the ten cases of endo-
carditis with aortic regurgitation in which there was no mitral murmur;
and in four of the nine in which there was both aortic and mitral
regurgitation, or in more than one-half (10 in 19) of the cases of
endocarditis with aortic diastolic murmur.

If we combine the three series of cases with tricuspid, mitral, and
aortic regurgitation, we find that in a little more than three-fifths of
the whole number (53 in 82) the first sound was prolonged over one
or other or both of the ventricles, and that this proportion held its
ground in each of the three classes of valvular murmur from endo-
carditis. If we deduct from the 29 patients in whom there was no
prolongation of the first sound, those who both came in and went out
with tricuspid or mitral murmur, amounting to fully twelve cases,
and who could not therefore present prolongation of the first sound
preceding or following a murmur, we naturally increase the proportion
in which the first souud was prolonged ; and this proportion would
necessarily be still further increased if we could deduct the unknown
quantity of cases in which the prolongation of the first sound escaped
observation.

It is evident then that prolongation of the first sound is a sign of
transition; that it tends to expand into a mitral murmur when situated
over the apex, into a tricuspid murmur when over the right ven-
tricle, and occasionally into a systolic aortic murmur when situated
over the aorta ; and that when either of these murmurs passes away, it
naturally glides into prolongation of the first sound over the region of
the lost murmur.

Prolongation of the first sound over one or both of the ventricles in
a case of acute rheumatism is in itself then a sign, actual, probable, or
threatening, of endocarditis affecting the left cavities of the heart.
If it is present when the face is covered with a diffused flush, or is
dusky and anxious, when the breathing is quickened or oppressed,
or when pain is seated in the region of the heart, and the second
sound is intensified over the pulmonary artery, we may at once
conclude that the patient is affected with endocarditis.

I have included among the cases of endocarditis two of the patients
affected with acute rheumatism, who had prolongation of the first
sound without murmur, but in both of whom that sound was murmur-
like ; and who had also several important symptoms pointing to internal
inflammation of the heart, including pain over the heart in one, pain in
the chest in the other, and very great general illness. I have ranked
seven of these cases with prolongation of the first sound apart, among a
class in which endocarditis was probable, and I may say almost certain.

In more than one-half, or five, of these nine cases, including both
those in which endocarditis was present, and those in which it was
probable, the prolongation of the first sound was murmur-like in
character. In six of these cases there was a pulmonic murmur ; in
four the face was dusky ; in three there was restlessness or delirium ;
in two others the sleep was bad; in three there was pulmonary

VOL. IV. l L

606 A SYSTEM OF MEDICINE.

apoplexy, or cough, with phlegm ; in one there wcs pain in the heart ;
and in two there was pain in the chest.

It is more difficult to settle the exact position of those cases with
prolongation of the first sound that I have ranked among those
threatened with endocarditis. Among the cases of this class
belonging to the first series, amounting in the whole to 63, almost
one-half (30) presented prolongation of the first sound ; and in five
more there was a double murmur ; while in nine others the sounds of
the heart were affected, the first sound being very loud in three, and
doubled in one ; while both sounds were feeble or indistinct in five.

Of the 30 patients in whom there was prolongation of the first sound,
in one half (14) there was great or considerable, and in 16 there was
slight, general illness. I think that we may consider that the fourteen
patients with great or considerable general illness, nine of whom had
pain in the region of the heart, were probably, or almost certainly,
affected with endocarditis. To these perhaps may be added the four
patients who presented an obscure murmur. Three of these,
however, had but slight general illness. If we add to the fourteen
with great general illness and prolongation of the first sound, the
case with an obscure murmur and also with great general illness, we
may conclude that fifteen of those who were threatened with endo-
carditis were almost certainly attacked with that affection.

Among the 79 cases that are ranked among those who had no
endocarditis, seven had prolongation of the first sound, and one had
an obscure murmur. All of these had but slight general illness, and
I think that they have been properly assigned to their present place.

If we examine the cases of the second series, or those treated by
means of rest, we find that out of twenty-two cases threatened with
endocarditis fourteen presented prolongation of the first sound. Of
these nine had pain in the region of the heart, or great general illness,
or both, while in one of them the general illness was slight. Eight
of these cases may therefore, I think, be almost ranked with the cases
of endocarditis.

In two of the remaining cases threatened with endocarditis there
was a transient murmur.

V. — Cases of Kheumatic Endocarditis with previous Valvular

Disease of the Heart.

Previous valvular disease of the heart was present in 22 of the 107
cases of endocarditis of the first series, and in 7 of the 28 of the second
series of cases admitted into St. Mary's Hospital under my care during
the years 1851 — 1869-70. Among the cases of the first series, ten had
mitral, five had aortic, and seven had mitral-aortic regurgitation, and
the seven of the second series had mitred incompetence. Sixteen
additional cases with previous valvular disease appear among my
325 cases with acute rheumatism of the first series ; and of these
eight had endocarditis combined with pericarditis, four had " probable "

ENDOCARDITIS. 507

•endocarditis, two were "threatened" with that affection, and only
two presented no sign or symptom of endocarditis. We thus see that
of the total number of cases of acute rheumatism with established
valvular disease (amounting to 38), 30 (or 79 per cent.) had endocarditis ;
in 6 (or 16 per cent.) endocarditis was probable or threatened ; and

2 (or 5 per cent.), had no endocarditis. Compare these cases broadly
with the rest of the cases of acute rheumatism in which there was no
previous valvular disease. Of the total number, amounting to 287, 161
(or 56 per cent.), had endocarditis, of which 54 had pericarditis also ; in
73 (or 25 per cent.) endocarditis was probable or threatened, including

3 with pericarditis; and in 83 (or 29 per cent.) there was no endocarditis,
including 6 with pericarditis. We thus see that previous valvular
disease of the heart, in cases of acute rheumatism, exercised an all-
powerful influence in exciting endocarditis. Nor can we wonder at
this important result. It has been the key-note, underlying the whole
of this long clinical history of pericarditis and endocarditis, that
whatever part, liable to be affected by the disease, was exposed to the
burden of labour, was exposed, in exact proportion to that labour, to
the attack of inflammation, the severity and extent of the inflamma-
tion being proportioned to the amount of labour.

The presence, then, of established valvular disease, which adds
very seriously to the labour of the heart in cases of acute rheumatism,
adds very seriously to the probability, the almost certainty, of endo-
carditis in such cases. We have just seen that the influence of
valvular disease, which tells with such force in the production of
endocarditis, has but little effect in exciting pericarditis. The reason
is, I think, obvious. The great extra work is thrown upon the interior,
and not upon the exterior, of the left ventricle, and especially upon
its mitral valve. A second local influence, in the altered apertures
and roughened surfaces of the mitral and aortic valves, and especially
at their margins, comes in to heighten the effect of the local labour in
the production of endocarditis.

The two conditions that prevailed through the whole series of cases
of established valvular disease with endocarditis are — the variability
of the murmur from day to day ; and great general illness. That chain
of signs distinguished every case, and that chain of symptoms affected
all but two of the whole series of instances of endocarditis with
disease of one or more of the valves of the heart.

The variability of the murmurs showed itself not only in their
greater or less loudness during the successive phases of the disease,
but also in their transformation from one tone to another quite
different ; their extinction, suspension, and reappearance ; and their
extended, contracted, and shifted areas. This variation in the nature,
character, and field of the murmur, is governed mainly by three
leading influences : — (1) the changes to which the valves themselves
and the interior of the heart are subjected by the inflammation ;
(2) the varying power of the heart under the influence of increasing
general weakness, and returning strength ; and (3) the tumultuous

L L 2

608 A SYSTEM OF MEDICINE.

action of the heart owing to local pain, or the struggle to pass the
blood onwards through the obstructed orifices; or its intermission
and failure from the exhaustion of previous overwork.

I shall illustrate the variable character of the murmur in these
cases of endocarditis with previous valvular disease by the brief notes
of a few cases, first selecting from among those with mitral regurgita-
tion, then those with aortic, and finally those with mitral-aortic
valvular disease.

The first instance with mitral disease that I shall quote was a young
woman who had left the hospital four days previously with a mitral
murmur, due to a primary attack of acute rheumatism. She came in
suffering from a fresh attack, with a distressed, anxious look, a dusky
face, rather livid lips, and accelerated breathing. She had pain over
the heart, its action being rapid and tumultuous, and an indistinct
murmuT. On the 3rd day there was a loud systolic murmur at the
apex, and the second sound was sharp over the pulmonary arteTy :
and on the 4th she had agonizing pain in the heart, its action was
tumultuous, and its sound could not be defined ; she struggled violently
and perspired profusely. Next day a loud systolic murmur, tricuspid
as well as mitral, was audible over the whole region of the heart. On
the 1 0th day the tricuspid murmur was audible along the sternum,
and a second impulse, with a loud second sound, were present over
the pulmonary artery in the second left space. On the 18th she was
bright and cheerful, but a cough was still present, and the murmur
was softer. On the 23rd day she walked about the ward, but on the
29th there was a return of pain on movement, and the murmur was
louder. After this she did well, there was a thrill over the heart, the
murmur was loud over the apex, and was heard over the left scapula.
Here the mitral murmur was obscured when the heart was tumul-
tuous ; and was loud and smooth, and joined by a tricuspid munnur,
when the health improved and the heart was steady in its action.
Another case, with previous mitral regurgitation, had, when admitted,
tightness of the chest, pain over the heart, and a loud systolic murmur.
Three days later, with less pain, the murmur was almost musical at
the apex, and quite so below it over the stomach ; two days later she
looked better, and the murmur presented a third change, being not
nearly so loud ; but next day, with returning tightness of the chest,
there was a fourth transformation of the murmur, which was rasping
or almost musical over the heart; the 10th day, however, with
renewed improvement, showed a fifth variation in the murmur,
which was no longer rasping ; but on the following day there was
a sixth change, and the murmur was musical around the apex ; after
this, on the 13th day, the murmur was grave, this being its seventh
variation ; its eighth occurring on the 18th day, when it was again
musical over the stomach, and when it was joined by a systolic mur-
mur over the aorta. After this, with steady improvement, the munnur
was no longer variable. A third case illustrates the variations of the
murmur during the convalescent period.

ENDOCARDITIS. 509

These two cases are typical, but their successive snatches of ever-
varying murmur, contrast with the murmur, now swelling, now
dwindling, that is found in other and more simple cases. I will just
quote one of these. A youth, a carpenter, came in with pain in
the chest and a prolonged musical systolic murmur at the apex.
This murmur was persistent, but it varied in tone, being grave on
the 8th day, when pain was present. The heart's beat was strong.

Each of the remaining seven cases presented features of its own ;
the variations of the murmur being great and complicated in four of
them, and in three of them comparatively simple. In four cases, if
not five, the mitral murmur was associated with a tricuspid murmur,
in one with a pulmonic, and in one with a direct aortic murmur ;
while in one the first sound was prolonged over the right ventricle.
In one of the cases just enumerated, a diastolic aortic murmur
appeared and disappeared, reappeared, and was finally extinguished,
the mitral murmur being permanent throughout.

The aortic murmurs of established valvular disease scarcely vie with
the mitral murmur in variety of tone, loudness and area, and alternate
extinction and return, in cases of rheumatic endocarditis ; but I may
state that the study of the five cases that I can cite shows that in all
these points the diastolic-aortic murmur presents frequent variation ;
though the systolic murmur of aortic contraction is much less subject
to change.

In one case with aortic regurgitation, probably of some standing,
tricuspid and mitral murmurs were added temporarily to the diastolic
murmur, which varied much and was not always audible during the
attack of endocarditis. At the cessation of the illness a double aortic
murmur was alone audible. In the other case a double aortic
murmur, which went and came again during the illness, was apparently
joined on the 28th day by a tricuspid murmur, which had departed
on the 34th, leaving a double aortic murmur.

The remaining seven instances had previous mitral-aortic valvular
disease. Two of the cases belonging to this last group were admitted
twice with mitral aortic endocarditis, so that the actual number of
patients belonging to it is reduced to five. One of those two patients
that were thus admitted twice with endocarditis, had left the hospital six
months previously, after an attack of rheumatic endocarditis, and came
in with double aortic, and mitral murmurs ; which varied somewhat in
loudness and extent, but were substantially unchanged during this
illness. Four years later she returned with severe acute rheumatism
and endocarditis, and died after a very long illness, albuminuria
having been finally added to her ailments. The murmurs underwent
several oscillations, sometimes the mitral, sometimes the aortic
diastolic murmur, being very loud, while at other times one or other
of those murmurs was almost or quite extinguished at the heart ; the
mitral murmur being however generally distinctly though feebly
audible over the back of the chest.

In the three remaining cases the variations in the murmurs were

510 A SYSTEM OF MEDICINE.

ratter in loudness and extent of area, than in the tone and character
of the sounds.

The extent and strength of the impulse, and their variation during
the attack, are among the most decisive tests of the previous presence
of valvular disease in cases of rheumatic endocarditis. As a rule, the
impulse in such cases is unduly diffused, strong, and propulsive ; and
this applies more in degree to cases with mitral aortic, than to
those with simple mitral regurgitation. The extent of the impulse
in a case of valvular disease without endocarditises a test of the undue
amount of labour to which the heart has been put to overcome the
obstacle to the circulation of the blood caused by the affection of the
valves. The supervention of endocarditis sometimes, by rendering the
heart's action tumultuous, increases the impulse ; but sometimes its
effect is the reverse, and by lowering the power of the heart, it lessens
the impulse.

Among the ten cases of endocarditis with previous mitral incom-
petence, including one in which aortic incompetence sprung up
temporarily during the attack, in five the impulse was strong, in one
it was diffused, in two it was moderate, in one it was feeble, and in
one it was not described. In three of those cases the impulse was
stronger during the attack of endocarditis than after it, and in two
it was the reverse. The impulse of the left ventricle was usually
increased in the cases of established mitral incompetence, but
that of the right ventricle was, in proportion, more affected in those
cases.

Among the five cases of previous aortic incompetence with endo-
carditis, including the two that were joined during the attack, one
by mitral, the other by tricuspid incompetence, in three the impulse
was strong and extensive, especially towards the apex ; in one it was
diffused but rather feeble ; and in one it was of moderate force and
extent. The impulse was more extensive during the attack of endo-
carditis than after it in one case. The impulse was strong, extensive,
and unduly far to the left, in five of the seven cases of previous mitral-
aortic incompetence with endocarditis; it was diffused but rather feeble
in one; and in one it was feeble. The impulse appeared to be
strengthened during the period of the endocarditis in four instances,
while in one case it was the reverse.

Pain was present over the region of the heart in four of the ten
cases of endocarditis with previous mitral incompetence, in four of the
five with aortic incompetence, and in four of the seven with mitral-
aortic incompetence. There was pain in the side or chest, or tightness
of the chest, not including those with pain in the heart — in four
of the ten with mitral; in one of the four with aortic ; and in three of
the seven with mitral-aortic valvular disease. - There was no pain either
in the heart, chest, or side, in two of the ten cases with mitral; in none-
of the five with aortic ; and in one of the seven with mitral-aortic
valvular disease, or in only three of the twenty-two cases under con-
sideration. We have seen that pain in the heart, side, or chest, occurs.

ENDOCARDITIS. 511

in by far the largest proportion of such cases ; and that pain in the
parts named is much more frequent in cases of endocarditis in which
the heart was previously affected with valvular disease, than in those
cases of endocarditis in which the heart was previously healthy.

The respiration was seriously affected in a very large proportion of
the cases of valvular disease with endocarditis. This condition in such
cases is inevitable, for the effect of all the diseases of the valves is to
interfere with the efficient onflow of the blood towards the system, and
therefore to throw the blood backwai*ds upon the lungs. This applies
of course with primary and immediate force to incompetence of the
mitral valve, which throws a portion of the blood just received back
again upon the lungs, with the effect of overcharging the pulmonary
vessels. The return of the blood back again from the aorta, owing to
aortic incompetence, into the left ventricle from which it has just been
sent, is, however, only one short stage forwards from the seat of
mitral incompetence ; and the almost immediate effect of the aortic
incompetence is to produce a back-flow of blood upon the pulmonary
vessels, and to delay the blood in those vessels and congest them.
The presence of this surplus amount of blood in the lungs, which
upsets the healthy balance of the circulation through the lungs and
the body, compels the respiratory organs to exert themselves to
the top of their power, so that they may, if possible, expel forwards into
the body the weight of blood that oppresses them. Hence result
laborious, difficult, and rapid breathing, pulmonary apoplexy, pleurisy,
catarrh, and bronchitis.

The respiration was rapid in four, the chest was painful or tight in
two, and cough with pulmonary apoplexy occurred in another of the
cases with mitral valve-disease; while in two of those cases there is no
note of the state of the lungs, and in one they were healthy in function.
The breathing was quick, or there was cough, or pain in the chest, in
four of the five cases with aortic, and in six of the seven with mitral-
aortic valvular disease. More than three-fourths, therefore, of the
cases of valvular disease with endocarditis had serious disturbance
of the respiratory functions.

CLINICAL HISTORY OF ENDOCARDITIS IN CASES OF CHOREA.

The association of chorea with endocarditis has long been known,
both clinically and from examination after death ; and it has already
received illustration in this volume, at pages 290, 291, where two
important cases of chorea are alluded to that have been published by
Dr. Broadbent and Dr. Tuckwell, in both of which there was endo-
carditis, and minute cerebral embolism ; and in one of which there
was acute rheumatism as well as chorea. I had also occasion, in this
article on endocarditis, to give at page 485 a case which illustrates
the association of chorea with endocarditis. I shall now give a brief
account of the cases of chorea treated by me in St. Mary's Hospital,
with especial relation to their association with endocarditis.

51-2 ■ A SYSTEM OF MEDICINE.

Clinical History of the Cases of Chorea, in relation to the presence of
J.tdocarditis, observed by the Author in St. Manfs Hospital. — I find
notes of 40 cases of chorea that were under my care in St. Mary's
Hospital, and in 34 of them the signs of the heart are noted, while in
(5 of them they are not so.

CASES OF CHOREA IN RELATION TO THE PRESENCE OR ABSENCE

OF ENDOCARDITIS.

1.— Cases in which there was no endocarditis, heart sounds healthy . 10

2. — Cases in which there was probably no endocarditis : —

a. Slight prolongation of the hrst sound .... 5

b. Anaemic murmur over the pulmonary artery ... 1

8. — Cases in which there probably was endocarditis : -

a. Prolongation of the first sound 3

b. Murmur, tricuspid or pulmonic 2

4. — Cases in which there was endocarditis : —

a. With mitral regurgitation — >

<C^ Ending in restoration of valve 2

1> Lessening of murmur on recovery .... 2

Z£ Mitral regurgitation established on recovery 8

b. \\ With aortic regurgitation \ 1

34
Cases in which the heart was not observed 6

Total 40

Association of the Cases of Chorea with Rheumatism. — The well-
established association of chorea with articular rheumatism, renders
the study of the connexion of rheumatism with these cases of chorea
necessary before we consider the occurrence of endocarditis in chorea.
Acute rheumatism, as we have just seen, is so very frequently ac-
companied by endocarditis that we must be careful, when ascertaining
the frequency of endocarditis in chorea, not to attribute the internal
inflammation of the heart too readily to chorea, when it may be caused
by the rheumatism associated in certain cases with that affection.

Articular rheumatism, in a subacute form, was definitely present
during the attack in six of the forty cases of chorea. In five of these
cases the rheumatic affection immediately preceded the occurrence,
and continued for a short time after the supervention of the attack
of chorea. In one of the cases, in which there had been no previous
rheumatic attack, the joints became inflamed in the course x>{ the
choreal affection.

In addition to these six cases of chorea with pronounced articular
rheumatism, there were five cases of chorea in which there was pain in
all the limbs (in 1), or in the shoulder and hips (in 1), or in the legs

ENDOCARDITIS. 513

(in 1), or in the hands (in 1), or there was stiffness of the arms and
legs, and of the left ring-finger (in 1). In none of these cases, however,
was there swelling or redness over the joints ; but this does not apply to
the redness which affected the wrists, elbows, and face in one patient
from violent friction. There were also five cases of chorea that were
free from rheumatism during the attack, that gave a liistory of ante-
cedent acute rheumatism, occurring from two years to two or three
months, and in one instance for an uncertain period, before the
occurrence of the chorea.

The proportion in which endocarditis appeared in those cases will
be given presently.

Proportion of Gases of Chorea in which Endocarditis was 'present. —
In nearly one-third (10 in 34) of the cases of chorea in which the
sounds of the heart were observed, those sounds were healthy ; in
one-sixth of them (5) there was slight prolongation of the first sound,
and in one case there was a pulmonic murmur. I have classed the
six latter cases among those in which there was probably no endo-
carditis, and I think we may infer that those sixteen cases, amounting
almost to one-half of the whole, were free from inflammation of the
interior of the heart.

In three cases in which there was marked, almost murmur-like,
prolongation of the first sound, and in two with a tricuspid or
pulmonic murmur, amounting to almost one-sixth of the whole (5
in 34), the presence of endocarditis was probable.

The remaining cases, amounting to fully one-third of the whole (13
in 34), gave complete evidence of the existence of endocarditis, in the
presence of a mitral murmur in twelve instances, and of a diastolic-
aortic murmur in one.

I think it probable that the majority of the six cases of chorea in
which the heart was not observed, ought to be added to those in
which there was no endocarditis.

Cases of Endocarditis with a Mitral Murmur. — The cases of choreal
endocarditis with mitral regurgitation, considering the comparatively
small number of those cases, offered as great variety in character,
mode of commencement, course, and result, as the cases of rheumatic
endocarditis with mitral regurgitation.

Endocarditis with mitral regurgitation ended more than twice as
often in established mitral disease in chorea, than in acute rheumatism.
Mitral regurgitation became permanently established in two-thirds
of the cases of chorea with mitral murmur (8 in 12) ; and in less than
one-third of the cases of acute rheumatism with mitral murmur of
the first series (14 in 49), and in only one-sixth of those of the second
series treated by rest (3 in 20). The integrity of the valve was
restored in one-sixth of the cases of chorea with a mitral murmur (2
in 12), and in another sixth of them, the murmur was becoming feebler
when the patient left the hospital (2 in 12).

The mitral murmur in fully one-half of the cases (7 in 12) was
situated in the region of the apex, and was not described as extending

514 A SYSTEM OF MEDICINE.

beyond that region; but was simply entered as a systolic mitral
murmur, or a systolic murmur at the apex.

The five remaining cases, compared with those just dismissed,
presented greater breadth of area ; variety in intonation and volume
of sound ; and individual life.

In two of these cases the mitral murmur was very extensive, being
audible over the back of the chest, above and below the scapulae, and
the greater part of the left side. One of them, when admitted, had
been ill with chorea in a severe form for some weeks, but the affection
was now but slight. A loud systolic murmur centred itself at the
apex ; and was audible along the sternum, and far to the right of
its lower portion, though feeble at its upper part ; from the third to
the seventh left costal cartilages ; in front of the epigastrium and
the liver ; and all over the dorsum, especially on the left side. The
impulse of both ventricles was immoderately strong and extensive, the
apex-beat being present an inch to the left of the nipple-line. These
signs underwent little change after the admission of the patient, and
it was evident that the endocarditis had ceased.

The other case came in with acute endocarditis, a mitral murmur
being audible at the apex and over the right ventricle. A few days
later it could be heard towards the axilla, and over the back, as
high as the upper part of the scapula. At the end of the seventh
week the murmur was grave and musical, and a fortnight later it
appeared as a prolonged bellows sound. After this it was hardly
so loud, but towards the end of the fourth month after admission it
was grave and vibrating.

This case had an interest much broader than the simple relation of
chorea to endocarditis ; for it had interwoven with it from its com-
mencement, and throughout an important part of the early period of
its course, the relation of acute rheumatism to chorea, and of acute
rheumatism to endocarditis also. It began with inflammation of the
ankle, conjoined with chorea. Six weeks later, when admitted, the
knee was inflamed, chorea being the most pronounced disease, and
the two affections being accompanied by endocarditis. Was this endo-
carditis the direct offspring of the subdued attack of acute rheumatism,
or of the chorea, or of the two conjoined affections, each taking its
part in giving a combined birth to endocarditis ?

During the third week the arms were slightly Theumatic, as well
as the lower limbs, and the patient lay motionless in bed, apparently
stilled by the affections of the limbs and joints, the chorea being
almost or quite latent After this the rheumatism insensibly dis-
appeared, the chorea insensibly reasserted itself, and for the remainder
of the patient's long history, the chorea, modified in form and
severity, was the only apparent affection; accompanied throughout,
however, by endocarditis.

The other three instances of which I have to speak were cases of
chorea, unalloyed, during the attack, by rheumatic arthritis ; but two
of them had suffered some time before from acute rheumatism.

ENDOCARDITIS. 515

One of them, a girl, had been long ill with chorea, and had gone
through a rheumatic attack two years before. She came in with
a loud, smooth, systolic murmur at the apex, which was audible over
the right ventricle. After this the murmur underwent minor transfor-
mations, being like a bellows sound on the 4th day, and almost musical
on the 8th, when the apex-beat extended further outwards, the murmur
being faintly, if at all, audible below the angle of the left scapula.
The apex-beat extended a little beyond the nipple. This case came in
with endocarditis, which was evidenced by the varying character of
the murmur; but there is nothing to show whether or not this
patient had acquired mitral disease from the old attack of acute
rheumatism.

This last question does not [complicate the next case, for though
this patient, a girl, had twice been affected with acute rheumatism,
yet she had no murmur, but a prolonged first sound, on admission. A
murmur, however, appeared at the apex on the 4th day, which was
grave on the 6th and the 8th, and was loud on the 14th day, when it
extended towards the axilla. The apex-beat was strong on the 6th
day, three-and-a-half inches from the sternum; but on the 8th it
could scarcely be felt.

The last case, a boy, was free from rheumatic taint, and presented
no murmur during the first six weeks ; but at the end of that time
he had pain in the chest, and a week later a smooth bellows murmur
appeared at the apex, which three weeks later spread upwards
towards the axilla, and downwards over the stomach. After this,
during a long period, extending from first to last over five months, the
murmur underwent various changes, being a very smooth bellows
murmur on the 62nd day, audible upwards towards the axilla, and
downwards over the stomach. On the 76th the murmur was very
loud and superficial, being heard towards the axilla, but for a very
short way below the heart. The first sound was very feeble, while
the second was very loud over the pulmonary artery, in the manner
already related at page 464. After this the mitral murmur under-
went various modulations, being moderately loud on the 102nd day,
very loud at the apex on the 105th, but scarcely audible over the
lung to the left, or towards the axilla ; much weaker on the 126th ;
but on the 135th day it was loud below, especially on expiration, and
was not heard outwards during inspiration. On the 146th day, and
the last report, there was very slight fulness over the heart, the
impulse of the right ventricle, which seven weeks previously was
strong, extending from the third cartilage to the sixth, and from the
sternum to the nipple, was on the last observation less strong to the
right of the lower sternum, and extended from the second to the
fourth cartilages. The mitral bellows murmur was not so smooth
as before, and was again heard up to the axilla. The double im-
pulse of the pulmonary artery, previously marked, was no longer
perceptible. There was no murmur over tie back. He went out
comparatively well, being free from choreal movements.

516 A SYSTEM OF MEDICINE.

In this case, as in that just related, during the attack of endocarditis,
when the patient lay speechless in bed, the heart became enlarged,
and the lung shrank away from before the heart, exposing its increased
impulse over a large area ; and the mitral murmur was heard exten-
sively over the region of the contracted lung, and that of the stomach.
At a later period; however, with returning health, strength, and exercise,
the lung expanded freely, and interposed itself between the greater
part of the heart and the walls of the chest, so as to cut off the
extended border of the area of impulse, and to lessen that of the
murmur by damping and silencing its sound.

Case of Endocarditis with a IHastolic-Aortic Murmur. — This
patient, a boy, came in with a second attack of chorea, which began
three weeks previously with pain in the legs of a rheumatic cha-
racter, followed, a week later, by choreal symptoms, which became
gradually more severe. On his admission the heart sounds, so far
as they could be made out, were healthy, but on the 3rd day a
diastolic murmur was audible over the centre of the sternum. Ten
days later this murmur wa3 heard, very prolonged and loud, over
the whole length of the sternum ; being audible to the right of the
upper part of the bone, aud to the left of its lower portion,
but becoming weaker towards the apex of the heart. On the
86th day the diastolic murmur was still loud, and maintained its
ground everywhere; and it was joined by a systolic murmur,
loudest at the sternum and not mitral Three weeks later the
diastolic murmur was inaudible at the middle of the sternum, and
was feeble at its upper and lower portions ; but on the 79th day, the
last observation, it had apparently resumed much of its loudness
and extent, and the systolic murmur was silent

In this case, as in one of those just told, the question must be
put, Was the endocarditis caused by the primary articular rheuma-
tism, or by the resulting chorea, or by the combined influence of
the two affections ?

ENDOCARDITIS IN PYEMIA.

There was pnly one instance among the 71 cases of pyaemia or
secondary inflammation examined after death in St. Mary's Hospital
in which the appearance of endocarditis was observed and reported.
That case, a man, who was under my care, presented a spot in the
right lung, an inch long, consisting of pus, and apparently broken
down lung-tissue, and superficial to this a patch of dry fibrinous
deposit on the pleura ; and numerous spots, similar but smaller,
through the back of the middle and lower lobes of that lung. There
was also a large globular and fluctuating tumour on the upper and
inner part of the left kidney three inches in diameter. On cutting
into it highly offensive blood-like fluid escaped, and on laying it freely
open there was a clot of blood and a little pus. The sac was lined with
a delicate, highly organised, chorion-like membrane, with numerous
prominent blood-vessels ramifying on its surface. There was a large

ENDOCARDITIS. 517

black spot of apoplectic effusion in the substance of the kidney near
the membrane. The structure of the kidney was healthy.

The heart was of natural size, and there was a patch of recent
roughness on the surface of the left auricle. Several nodules, from
the size of a split pea to that of a millet-seed, were situated on the
free margin of the mitral valve. The corpora Arantii of the aortic
valve were enlarged. The patient was admitted in a state of great
depression, his mind wandered, and mucous and sonorous noises were
audible over the chest. The state of the heart was not observed.

The attack of endocarditis was in this case the marked secondary
effect of the pyaemia, but the solitary occurrence of this instance
with endocarditis in 71 cases of pyaemia shows that the inflammation
of the interior ot the heart, so common, as we have seen, in acute
rheumatism and chorea, is rare in pyaemia, though less so, as we
shall see, than in the fatal stage of Bright's disease.

The signs of the heart affection were not observed in this case of
pyaemic endocarditis. I have had, however, frequent opportunities
of examining a patient affected with pyaemia, in the course of whose
very serious illness the signs of endocarditis appeared and held their
ground. Pleurisy first showed itself, and the evidence of inflamma-
tion in both lungs; and after a time a systolic murmur became
audible at the apex. This murmur was constant, but it varied in
loudness, tone, and area during the course of the illness. After this
patient's recovery a mitral murmur was established.

ENDOCARDITIS IN BRIGHT'S DISEASE.

I have only been able to find one instance with evidence after
death of endocarditis in the whole of the cases of Blight's disease
described in the post-mortem records of St. Mary's Hospital
amounting to 207, excluding those in which there was regurgitation
through the mitral or the aortic valve, or through both valves, or ob-
struction of the mitral orifice. That case was one of fatty disease of the
kidney in a man, aged 41, who was under my care. His heart was
rather large, weighing 12£ ounces, and was dilated and flabby. The
structure of the valves was healthy, with the exception of a patch
of white deposit on the anterior flap of the mitral valve, which did
not appear, after death, to interfere with the function of the valve.

This man, when admitted, presented a yellowish pallor and puffinesa
of face. He had been a healthy man until he took cold, nine
months previously, after which he became gradually weak and pale,,
and had palpitation and frequent vomiting, symptoms with which he
was still troubled. There was some albumen in his urine. The right
veins of his neck was rather swollen and pulsating, and there was
pulsation of the temporal artery. The heart's impulse was very
feeble, and diffused over the cardiac space during expiration only,
but it could be felt between the ensiform cartilage and the left seventh
costal cartilage. The liver was firm and low, and presented a diffused
pulsation in the epigastric space.

518 A SYSTEM OF MEDICINE.

A soft systolic bellows murmur was audible at the apex, and a
peculiar short double murmur between the nipple and the sternum,
which was obscured by the natural heart sounds. These murmurs
varied considerably from day to day, but they were generally audible,
though the diastolic noise was more or less obscure. About a week
after his admission a peculiar humming venous murmur was heard
to the right of the sternum when he sat up, but not when he lay
down , which, sometimes, disappeared without apparent cause, when
it could be brought back by pressure over the jugular vein.

On the 42nd day he presented considerable general dropsy, and
for the first time the murmurs were very faint and obscure, and two
days later they were lost. After this the mitral murmur was some-
times audible, but was generally not so, and the diastolic murmur
was only heard once, corresponding with a thrill near the apex. The
last observation was made on the 77th day, when a faint systolic
murmur was heard over the seventh cartilage, and feeble doubling of
the first sound over the sixth cartilage. The urine was then scarcely
albuminous, and it had been so during a considerable period of the
history of this patient, who died on the 98th day.

I have ranked this case as one of endocarditis, because of the
presence of a white deposit on the mitral valve, which was other-
wise healthy, and of the history of varying murmurs, pointing to
changing affection of the mitral and aortic valves. The long duration
of the case, and the small amount of change to which the valve had
been subjected, make it doubtful whether the endocarditis was
present in more than its effect, the white deposit on the mitral
valve, at and before the time of death ; but if we take that appear-
ance, and the varying signs of double regurgitation into account, I
think we may infer that this case was one of endocarditis. It is
true that both mitral and aortic regurgitation may be present in
Bright's disease when there is very great tension of the arteries,
and great hypertrophy, with dilatation of the left ventricle ; that in
such cases those murmurs usually vary in character, according to the
varying intensity of the causes that gave them birth ; that they may
be suspended, restored, and again lost, even permanently ; but this
case did not present those conditions, for the heart, though dilated,
was not greatly enlarged, and was not hypertrophied, since it only
weighed 12} ounces.

Admitting, then, that this was a case of endocarditis occurring in a
patient affected with Bright's disease, it is evident, that as this was
the solitary instance of that kind that was noticed among so many
cases of Bright's disease without disease of the valves, that although
endocarditis may occur in that disease, yet that it is rare. This
becomes more marked when we compare the cases of acute rheumatism,
and of chorea, with those of Bright's disease ; for in the two former
affections, from one-half to one-third of the cases were affected with
inflammation of the interior of the heart.

The frequent presence of thickening of the mitral valve, and

ENDOCARDITIS. 519

occasionally of the aortic valve ; and the large proportion of cases of
valvular disease without a previous history of acute rheumatism ;
perhaps point to the occurrence of endocarditis in those cases during
the earlier period of their history. If so, endocarditis, and pericarditis,
behave very differently from each other in Bright's disease, for while
pericarditis is common towards the fatal period of this disease,
especially when the kidney is granular, and is rare during its
earlier history, endocarditis is very rare towards its fatal period,
but is not very infrequent during its earlier history; that is — if
the thickening of the valves, and especially of the mitral valve, and
complete valvular disease, have their origin in the Bright's disease
itself.

CLINICAL HISTORY OP ENDOCARDITIS OCCURRING IN CASES OF

VALVULAR DISEASE OF THE HEART.

The influence of previous valvular disease in rendering endocarditis
more frequent and severe in cases of acute rheumatism has been
already seen at page 507. We then observed that the presence in
that affection of disease in the valves of the heart, by adding to
the labour of that organ, and by rendering its internal apertures
more rough and irregular, increased the danger of the occurrence of
internal inflammation of the heart, and intensified that inflammation
when established.

So great, indeed, is the influence of valvular disease in exciting and
intensifying inflammation of the diseased valve, that we find that
endocarditis is apt to occur in such cases, even when free from acute
rheumatism, chorea, or any other general disease.

I would refer here to some interesting remarks by Dr. Moxon on
this important subject.

The accompanying table (p. 520) will show at a glance the proportion
in which endocarditis was present at the time of death in the cases
of valvular disease of the heart treated in St Mary's Hospital.

Pathological Evidence of Endocarditis in cases of Valvular

Disease of the Heart.

It is difficult, even impossible, in every case to say, from the appear-
ances presented after death, whether or not endocarditis is present on
the affected valves, and the adjoining surfaces of the ventricle and
auricle. This is due to the readiness with which, in certain cases, a
deposit of fibrin from the blood as it streams backwards and forwards
through the mitral and aortic apertures, attaches itself to the surfaces
of the imperfect valves, roughened by disease. This is equally the
result, whether those surfaces be roughened by the slow degeneration
of the diseased fibrous tissues, which, although they may nave been
generally inflamed at the starting point of the disease, yet they may
have long ceased to be so ; or whether the surfaces of the valve w

620 A SYSTEM OF MEDICINE.

inflamed by a recent and renewed attack of local endocarditis. In
many instances, however, it is self-evident that inflammation actually
affects the valve, for the appearances presented are precisely those
that are found in cases of recent endocarditis, owing to acute rheuma-
tism, chorea, or pyaemia. Those appearances in these cases are to be
confided in, for the diseased valves have been described, without, how-
ever, as a rule being defined as being inflamed, by a succession of able
and careful pathologists, including the distinguished names of Dr.
Markham, Dr. Burdon Sanderson, Dr. Murchison, Mr. Gascoyne, Dr.
Charlton Bastian, and Dr. Payne.

Table showing the number of cases with established valvular
disease, among those not affected with acute rheumatism, in which
endocarditis was present at the time of death. Affected

with Bright's
disease.
I. — Cases with established mitral regurgitation : —

a. Cases with endocarditis, not affected with Bright's disease . 9 5

b. Cases with fibrinous concretions on the valve, probably not

affected with endocarditis 2 3

c Cases in which no description of the valve was found ... 1 2

d. Cases without endocarditis or concretions 22 19

I.— Total 84 l 29 l

II. — Cases with aortic regurgitation : (A)— from disease of the aortic valve : —

a. Cases with endocarditis, not affected with Bright's disease . 5 I

b. Cases with fibrinous concretions, endocarditis doubtful or absent 5 5
c Cases in which there was no description of the valve ... 2 2
cL Cases without endocarditis or concretions 13 12

Total 25 20

(B) — From great dilatation of the aorta, the flaps of valve being healthy

but insufficient 5 I

II. — Total with aortic regurgitation . 30 21

III. — Cases with mitral-aortic regurgitation: —

a. Cases with endocarditis, not affected with Bright's disease . . 5 3

b. Cases with fibrinous concretions, endocarditis doubtful or absent 4 0

c. Cases in which there was no description of the valve ... 3 0

d. Cases without endocarditis or concretions . . . . .16 16

III.— Total 28 19

IV. — Cases with obstruction of the mitral orifice : —

a. Cases with endocarditis, not affected with Bright's disease . 1 1

b. Case with roughness and ulcer at edge of valve .... 0 1

c. Cases with vegetations or concretions on valve, endocarditis

doubtful or absent 2 1

d. Cases without endocarditis or concretions 18 6

IV.— Total 21* 9*

1 I am not certain that these numbers include the whole of the cases with mitral
regurgitation, since most of tho original copies of those cases have been lost or mis-
placed, and I have taken them from a detached tabulated abstract of those cases.

This note applies also to the cases of mitral regurgitation given in the Table at
page 512.

* In 5 of these cases the size of the mitral aperture is not described ; in 5 it was
contracted to a moderate extent, and in 19 to a great extent ; and in 1 it was almost
closed by a ball of organised fibrin.

ENDOCARDITIS. 521

Among the cases of mitral regurgitation^ five presented " fringes "
aud one a ring of small papillary elevations or granulations around
the free edges of the valve, and two others had warty or rough
excrescences, and another had nodules of lymph on those free edges ;
and in one of these, the auricular surface of the valve was roughened.
One of those instances described, I think, by Dr. Payne, presented
also yellow succulent elevations, almost resembling a false membrane,
but seated under the epithelium. I have also included among the cases
of endocarditis four instances with vegetations on the auricular surface of
both flaps of the mitral valve, and one with extensive ulceration of
its anterior flap, in which case the adjoining surface of the ventricle
was inflamed ; five other cases presented large excrescences, or concre-
tions and smaller vegetations, but these I have not included among
those with endocarditis, although some of them may have had that
affection. This mav be said also of a doubtful case in which the
posterior flap of the valve was attached to the wall of the ventricle by
adhesions readily separated.

Five of the fourteen cases that I have classed among those with
endocarditis wrere affected with Bright's disease, and nine of them
were not so.

Forty-one cases with mitral regurgitation were free from vegetations,
and of these, nineteen had Bright's disease, and twenty-two were free
from that affection.

The cases with awtic regurgitation presented comparatively few
instances or severe, with endocarditis, but these presented great variety
in their features. One of them showed deposits of red vegetations
towards the edge and centre of each flap of the aortic valve. In
another, the flaps of the valve were cemented together, and then free
margins were roughened, by fibrinous deposit. In a third the aortic
aperture was converted into a mere chink by adhesions ; and there
was an irregular deposit of lymph, forming vegetations, about the basis
of the conjoined flaps, some being hard, some cheesy, and others
apparently quite recent. The united flaps projected like a funnel
into the aorta in the fourth instance, and a little above the valve, and
therefore on the inner surface of the aorta, was an oval patch, half an
inch long, with a red highly vascular flocculent surface. The aortic
valve, in the fifth case, was enlarged but soft. One of the flaps had
ulcerated away at the sides, and a large nodular mass was appended to
its sesamoid body. The sixth case was one of great interest, with
contraction of the descending aorta below the subclavian artery so as
scarcely to admit a probe, and embolism, blocking up the left brachial
artery. The valve was universally red, soft, pulpy, and formless, and
the aperture was contracted. I had originally only ranked five of
these cases as being affected with endocarditis, but I think that the
whole six may safely be so classed. Only one of these six cases with
endocarditis had Bright's disease, the remaining five being not so
affected. Ten other cases presented concretions of various size, some
being large, one like an alpine strawberry, attached to the aortic valve ;

VOL. iv. M M

522 A SYSTEM OF MEDICINE.

these cases being affected, and unaffected, l>y Bright's disease in equal
numbers. Twenty-five of the cases with aortic regurgitation were free
from concretion, and of these, thirteen had Bright's disease, and twelve
were free from that affection. In six cases, aortic regurgitation was
due to great enlargement or dilatation cf the ascending aorta, the
flaps of the aortic valve being healthy in structure, but of insufficient
size to close the widened orifice of the aorta.

It will I think be sufficient if I state the proportions in which the
cases with mitral aortic regurgitation were affected with endocarditis,
presented concretions, without distinct evidence of endocarditis, and
were free from concretions, -without entering into details. I consider
that eight of those cases had endocarditis, five being free from, and
three being affected with, Bright's disease ; four of them had con-
cretions on the valves, none of which1 had Bright's disease ; and in
thirty-two there was no concretion on the valves, one half of these
being free from, and the other half affected with, Bright's disease.

I shall deal with the cases with obstructed mitral orifice in the
manner that I have just dealt with those having mitral-aortic re-
gurgitation. Two of them had endocarditis, one being free from, and
one affected with, Bright's disease, and another case having that disease
presented roughness and ulceration of the edge of the contracted
mitral valve; three had vegetations, one of those only having
Bright's disease, and twenty-five of them had neither endocarditis nor
concretions in any form on the obstructed mitral orifice, only seven of
which cases had Bright's disease.

It is evident that while cases with mitral regurgitation are affected
in a rather large proportion, or nearly one-fourth (14 in 63), with
endocarditis, only one, or at most two, in twenty-nine of the cases
with obstruction of the mitral orifice gave evidence after death of that
affection. Cases with aortic regurgitation occupy a middle position
between the two classes just considered, 6 in 51 (or 1 in 9) of these
cases being affected with endocarditis. The cases of aortic regurgita-
tion that were free from Bright's disease were much more frequently
affected with endocarditis (5 in 30 or 1 in 6) than those that were
affected with that disease (1 in 21).

Cases with mitral-aortic regurgitation have endocarditis rather
more frequently (8 in 47 or 1 in 6) than those with aortic regurgita-
tion (G in 51 or 1 in 9), and less frequently than those with mitral
regurgitation (14 in 63 or 1 in 4$).

Valvular disease was less frequently attacked with endocarditis in
those cases that were affected with Bright's disease (11 in 78 or 1 in
7) than those that were free from that affection (20 in 105 or 1 in
52) ; and, as we have seen, this tendency in Bright's disease to lessen
the frequency of the occurrence of endocarditis in cases affected with
valvular disease, prevailed through the whole of the varieties of
disease of the valves that we have been investigating, excepting in
cases with mitral obstruction.

ENDOCARDITIS. 523

The Signs and Symptoms of Endocarditis affecting Cases with

Valvular Disease.

The signs and symptoms of endocarditis when it occurs in cases of
valvular disease of the heart, not affected with acute rheumatism, do
not differ essentially from the signs and symptoms of endocarditis,
when it attacks cases of acute rheumatism affected with valvular
disease of some standing. I have already given a brief clinical history
of a series of cases of that class at pages 507-511, and it will, 1 think,
be sufficient if I here refer to the narrative and risumi of those cases.
As in those cases so in these, the two great distinguishing features of
the supervention of endocarditis upon valves already affected with
regurgitant or obstructive disease are (1) the great variability of the
valvular murmurs, and of the size of the heart, as indicated by the
alternate extension and contraction of the area of the impulse, and
the alternate increase and diminution of its force ; and (2) the great
general illness with which the patient is affected, an illness not
marked by dropsy, but by elevation of temperature, over-action or
failing power of the heart, and pain in the cardiac region, side, or
chest, hurried, difficult, and laboured respiration, connected often with
a congestive affection of the lungs, showing itself sometimes in the
form of bronchitis or of pulmonary apoplexy with its attendant
pleurisy. I would again refer to the illustrations I have given with
regard to those vital symptoms in a previous part of this article.

I would here remark that the occurrence of a special fever, such as
enteric fever, may, as we have already seen, suspend a mitral or an
aortic regurgitant murmur for a time ; but this occurrence proclaims
itself by its own distinctive symptoms.

I have not given any account of the temperatures of the body in the
above clinical histories of pericarditis and endocarditis ; for the ther-
mometer was only employed in the later cases, and therefore in an
insufficient number to enable us to arrive at general results.

Endocarditis affecting the Tricuspid Valve.

Endocarditis and structural disease of the tricuspid valve are
admitted to be so rare in the adult, that there are few clinical or
pathological records describing affections of that valve.

I have examined the whole of the cases of valvular and other
diseases of the heart, and of Bright's disease, contained in the post-
mortem records of St. Mary's Hospital, from 1851 to 1869-70, with
the special object of ascertaining the frequency, extent, and character
of any affection of the tricuspid valve that might occur in those
cases, and the result is given in the accompanying Table.

M M 2

524 A SYSTEM OF MEDICINE.

Cases with Affection of the Structure of the Tricuspid
Valve, not including instances in which the valve was incompetent
owing to the great size of the tricuspid aperture ; but including
all those in which the edges of the valve were thickened, but the
function of the valve was unaffected.

a. Cases with endocarditis, not affected with B right's disease

b. Case with fibrinous concretion on valve

e. Case with contraction of mitral valve . . . .

d. Oases with thickening and corrugation, or roughness of valve

(1 with mitral-aortic reg., 1 with mitral ob3tr.) .

e. Cases with thickening of valve, valve not incompetent

Affected

with Bright')

disease.

ll1

7»

14 10

The tricuspid valve wa9 affected with endocarditis in two instances;
one of these patients was a woman, aged 40, who had been subject to
acute rheumatism when a child, and had palpitation on slight exertion.
She had been a patient in the hospital ten months previously with
dropsy, ascites, albuminuria, and a mitral murmur. The ascites and
dropsy disappeared, but they were greater than before when she was
readmitted, when the lips and nose were blue; and the urine was
scanty and very albuminous. The mitral murmur was louder than
before, and dyspnoea appeared in paroxysms. The heart was rather
large (12 inches), and presented patches of lymph on its surface ; the
walls 'of the right ventricle were half an inch thick, being thicker
than those of the left ventricle. Warty, rough, irregular fibrous
excrescences were present around the margin of the mitral orifice;
looking towards, and being entirely in, the left auricle ; the ventricular
surface being free from deposit: and there was a smooth fibrinous
deposit on the (auricular) surface of the tricuspid valve.

The other case with endocarditis of the tricuspid valve, was a
woman aged 42, who had contraction of the mitral orifice, which
allowed of the passage of but one finger. The heart was of very
great size, and its cavities contained twenty ounces of blood, although
it only weighed 13£ ounces. The tricuspid valve had all its flaps
thickened with excrescences along their margins, but the valve itself
was competent. She became subject to palpitation twelve months
previously after a shock or fright. Three days before admission, she
raised half a pint of bright blood. The legs and feet were swollen,
she had pain in the chest, the heart's action was violent, and there
, was a confused rumbling sound at the apex. There was no albumen
in the urine. She became gradually worse, and finally palpitation and
dyspnoea were superseded by drowsiness.

In both of these cases, the right side of the heart was excited to

1 O the 1 1 without Bright's disease, 2 had mitral, 2 aortic, 8 mitral-aortic regurgi-
tation ; 2 mitral obstruction, and 1 had no valvular disease.

1 Of the 7 with Bright's disease, 2 had aortic regurgitation, and 5 had no valvular
disease.

ENDOCARDITIS. 525

excessive and continuous labour by the diseased condition of the mitral
valve, which in one instance was affected with regurgitation, and in
the other with great obstruction.

In one remarkable case a large concretion was attached to the
tricuspid valve. This patient was a man, aged 69. The heart was
large, weighing 16 ounces, the tricuspid valve was universally thickened,
and a fibrinous deposit, the size of a nut, was present on the anterior
surface of one of the flaps. The tendinous cords were hypertrophied
and atheromatous. One of the valves of the pulmonary artery was
converted into a hard concrete mass. There is no account of the left
side of the heart.

These were all the instances that I can find in which there was
endocarditis of the tricuspid valve, or the presence of concretions on
its flaps ; but the inquiry into the number of other cases in which the
tricuspid valve was affected may throw some light on the probable
frequency of antecedent endocarditis of the tricuspid valve, as a pro-
bable cause of disease of the valve.

I may briefly state that in one case there was contraction of the
tricuspid orifice, so as barely to admit two fingers ; and thickening
round the margins of the valve ; and although the other valves were
stated to be healthy, a mitral murmur was audible during life. In
another case, with mitral obstruction, the edges of the tricuspid valve
were thick and corrugative ; and in a third patient, who had been
affected with acute rheumatism six months previously, which was
followed by mitral-aortic regurgitation, the tricuspid valve, which was
not seen, felt rough and thick. These are the only cases that permit
definite evidence that in them the tricuspid valve had been previously
affected with endocarditis. There were however eighteen other cases,
as may be seen in the Table, in which there was some thickening of
the tricuspid valve, in two of which it was stated to be atheromatous ;
but in none of these cases did it appear that the tricuspid valve was
incompetent. Twelve of those cases had mitral, aortic, or mitral-aoytic
regurgitation or mitral obstruction; and of the remaining six cases that
were free from valvular disease, five had Bright's disease.

It does not appear to me that any of these cases present definite
evidence of the previous existence of endocarditis of the tricuspid
valve as the cause of the thickening of its flaps, although it is pro-
bable that in some of them the valve had been originally inflamed
and especially in those cases that presented aortic, mitral, or mitral-
aortic regurgitation, or mitral obstruction.

TREATMENT OF ENDOCARDITIS.

Endocarditis is so completely an affection associated with those
important diseases, acute rheumatism and chorea, in which it is rare,
with pyaemia and Blight's disease, in which it is common, and with
established valvular disease, that the proper treatment of the parent

626 A SYSTEM OF MEDICINE.

affection must in all such cases be the proper treatment of the associated
inflammation of the valvular structure of the heart. The treatment of
those diseases, however, should be modified in the form of additional
precautions when endocarditis appears ; and the general treatment of
acute rheumatism and chorea must, from the first, be mainly governed
by the consideration that in both of them endocarditis is the most
serious natural complication of the general disease. What I have
said with regard to the treatment of acute rheumatism in relation to
the prevention of pericarditis, applies also to the treatment of acute
rheumatism in relation to the prevention, if possible, and the alleviation
of endocarditis. We have already seen that one-half of the first series
of cases of acute rheumatism are affected with endocarditis (165 in
325) ; and that in one-half of the remainder (79 in 164) the occurrence
of endocarditis is either threatened (in 63) or probable (inl3). This
treatment may be summarized in the brief but effectual rules of (1)
the absolute rest of every limb and joint, and of the whole body,
during the attack of acute rheumatism ; and the maintenance of this
absolute rest, especially in the limbs and joints that have been most
recently affected, for a period of several days after the complete dis-
appearance of the local inflammation ; and (2) the application of the
belladonna and chloroform liniment, sprinkled on cotton-wool, over
the affected joints, and the support of those joints by the application
of flannel over the affected parts so equally adjusted as to give relief
and comfort to the patient. We have already seen that the great
cause of the inflammation affecting the interior of the left ventricle
is the powerful exercise and over-work of that ventricle in maintain-
ing the circulation through the vessels of the inflamed parts, which
at the same time call for a greater supply of blood. The fibrous
structures of the heart, in common with the fibrous structures of the
joints, are prone to inflammation in acute rheumatism ; and in the
struggle to which the left ventricle is subjected, the valves of that
ventricle readily become inflamed at their surfaces and lines of
contact. When endocarditis threatens, or first discloses itself, and
especially if there be pain in the region of the heart, the application
of three or four leeches over that region may be of essential service in
lessening the inflammation, and so perhaps permanently saving the
valve. It will be well also to cover the region of the heart with
cotton-wool, sprinkled with the belladonna and chloroform liniment.

The influence of the treatment of acute rheumatism by means of
rest, and the employment of soothing applications and comfortable
support to the joints, on the occurrence, severity, and permanent ill
effects of endocarditis, will be best illustrated by comparing the
clinical history of the 74 cases treated by rest,1 with that of the 325
cases not so treated.

There was endocarditis alone, or combined with pericarditis, in
one-half (161 in 325) of the first series of cases that were not treated

1 See the Author's Address on Medicine ; a copy of which will be given by the Publisher
of this work to any reader applying for it.

ENDOCARDITIS. 527

upon a system of absolute rest ; and in two-fifths (34 in 74) of the
series that were so treated.

Valvular disease became established in 43 of the 127 cases (or 1 in
31, or 34 per cent.) of endocarditis, with a cardiac murmur, including
those with pericarditis also (18 in 46), but excluding all those that
had previous valvular disease, of the series not treated by rest ; and
in 3 of the 24 (or 1 in 8, or 12*5 per cent.) of the same kind of cases,
of the series that were treated by rest If we extend the comparison
to the whole of both series of cases, excluding those that had previous
valvular disease, we find that 43 in 281, or 1 in 6*6, of the series that
were not treated by rest, and 3 in 61, or 1 in 20, of the series that
were treated by rest, had established valvular disease, indicated by a
permanent murmur after their recovery from acute rheumatism, and
at the time of their last examination.

There was no murmur, and therefore no valvular disease, when the
patient recovered from the attack of acute rheumatism, in 60 of the
127 cases with endocarditis, and without previous valvular disease (or
1 in 21, or 44*4 per cent.), that were not treated by rest ; and in 17
of the 24 (or 1 in 1*4, or 71 per cent.) of the cases of the like kind
that were so treated.

The murmur was lessening in intensity at the time of the last
observation, when the patient had recovered from acute rheumatism,
in 24 of the 127 cases just spoken of (or 1 in 5*4) that were not
treated by rest ; and in 4 of the 24 (or 1 in 6) of the analogous cases
that were treated by rest.

We here find that, in the series of cases of acute rheumatism that
were treated by a system of absolute rest, the proportion of those that
were attacked with endocarditis was slightly less than that of those
that were not so treated. Thus far the comparison is but slightly in
favour of the treatment of ajcute rheumatism by a rigid system of
rest ; and this would seem to suggest that a certain, and a very large
proportion of cases of acute rheumatism are habitually and intrin-
sically attacked by endocarditis. "When, however, wre extend the
comparison, and ascertain the proportion in which those cases of
endocarditis, not previously so affected, acquired permanent valvular
disease, so as to injure health during the remainder of life, and to
shorten life itself, we discover that the series of cases not treated by
a system of absolute rest wrere thus permanently injured in a far
larger proportion of cases, amounting to more than twice as many, or
in the ratio of 8 to 3, than in those that were treated by rest.

If we pursue the inquiry further, so as to discover the relative
extent to which the interior of the heart was inflamed in the two
series of cases, we discover that there was but one instance, or 1 in 24,
of those with endocarditis and without previous valvular disease,
of the series treated by a rigid system of rest, that gave definite
evidence of inflammation of both the aortic and mitral valves ; while
in 19 instances in 127, or 1 in 6*7, of the same kind of cases that
were not treated by a rigid system of rest, there was direct evidence

528 A SYHTXat OF MEDICIXX.

of aortic regurgitation. In nine, or rather ten, of those cases that
were not treated by rest, there was a mitral murmur, and therefore
direct evidence of inflammation of the mitral valve; but in the
remaining nine cases there was also evidence of mitral endocarditis
in the shape of a tricuspid murmur, or prolongation of the first sound,
with intensification of the pulmonic second souud, and obstacles to the
flow of blood through the lungs. The whole chain of evidence points
then, I think, irresistibly to the conclusion that the extent, severity,
and permanent ill effects of the endocarditis were much greater in tiie
series of cases that were not rigidly treated by rest tlian in the series
that were so treated.

Pericarditis, also, attacked a much larger proportion of the cases
not treatsd by a system of rest, or 03 in 325, or I in 52, than of
those that were treated by rest, or 6 in 74, or 1 in 122. ThuB more
than twice as many of the former series of cases, that were not
treated by a rigid system of rest, were attacked with pericarditis,
than of the latter series of cases that were treated by a rigid system
of rest.

1 am of opinion, however, from a careful revision of the clinical
history of those cases, that the treatment by opium, which was pur-
sued in a considerable proportion of the first series of cases that were
not treated by rest, had some influence in increasing the frequency
and severity of inflammation of the heart, and especially of its
exterior. Taking this into account, however, I consider that the
clinical evidence here afforded shows, that the severity and permanent
ill effects of endocarditis, and the frequency and severity of pericarditis,
are greatly lessened by a system of treatment by re3t absolutely
maintained; and combiued with the use of local means in the shape
of the application of the belladonna and chloroform liniment, and oi
equal and comfortable support to the affected joints, and the employ-
ment of leeches applied over the region of the heart, when that organ
was attacked by inflammation, and especially on its exterior, and when
accompanied by pain.

The clinical evidence in favour of the treatineut of acute rheuma-
tism by rest is conclusively supported on the pathological grounds
stated at the commencement of this article (see page 457), and in
Dr. Moxon's very striking, important," and convincing lecture on
endocarditis, to which I have there referred. We have there seen
tliat the surfaces or lines of contact, pressure, and friction of the valves,
and chiefly of the mitral valve, are the parts that are especially
affected with endocarditis. Thus the over-work of the left ventricle
of the heart, and the resulting friction, pressure, and tension of ii
valves, in cases of acute rheumatism and choivn. tend to augment Ii
primary influence of the parent disease, and to excite and inte
the inflammation of the interior of the heart, and especially "
mitral valve.

CARDITIS. •
By W. R. Gowkrs, M.D.
Synonyms. — Myocarditis; Interstitial Myocarditis.

Definition. — An acute affection of the walls of the heart, consisting
in interstitial serous exudation or cell-infiltration, and degeneration of
the muscular fibres. The latter may occur without any change in the
interstitial tissue. This has been regarded as a " parenchymatous myo-
carditis." But this change, when general throughout the heart, occurs
as the result of some general blood state, and is unassociated with
other evidence of inflammation in the heart or remaining organs.
Without denying the possibility of the occurrence of a general paren-
chymatous inflammation of the heart, it seems more consistent with
the relations of the process to consider these cases as examples of
acute degeneration. (See Art. " Fatty Degeneration. ")

Yakikties. — The inflammation may be general, affecting all pails
of the heart ; or it may be partial, being limited to a small area. When
general it may be diffused uniformly through the heart ; it may affect
the superficial layers only (when secondary to pericarditis) ; or it mav
result in scattered foci of suppuration. Circumscribed inflammations
may result in the formation of an abscess in the wall of the heart,
lastly, the varieties have been distinguished of primary and secondai v
inflammation; the former occurring apart from, the latter in consequence
of, pre existing disease, general or local.

Etiology. — Tn the consideration of the causes of the disease, the
variety which is due to the extension of inflammation from the peri-
cardium may be excluded from consideration, since it owns the yum*;
causes as the pericarditis to which it is due, and is commonly the
consequence of acute rheumatism. Other forms of carditis orrur in
the male much more frequently than in the female m,x ; and at all
ages, but rather more frequently before than attar thirty years of age-
As a primary affection, carditis is extremely rai-e : a f v lW /,f the record
cases have been ascril>ed to exposure to old after .sew-M- i-xt-jtion, °r
J^-Wows on the precordial region. In other ea.-e.s Ul) f.xrjtiii» c&£
3 discovered. As a secondary affection it ha, of-cum-d ii*'*'
icute rheumatism, apart, it is said, from cm Jo- 0j pvri'&C
i various septicemic affections, Jt.s chiV-l" ]»./-.i| muht^
fldocfUTditisin«rec«,ises,e/ijhoIiVmJ;,jjrj n^mh-in* -

AxATom'.— The inflamed ]uu^uhrf^

kted, and then swollen and Mi/twied. r*&i
m mattered Uirough it; the f ;.,,„. btfy |
I tfz^and may break down in:,, a pulpy

630 A SYSTEM OF MEDICINE.

the acute degeneration and destruction of the muscular fibres, and
partly owing to their separation by an interstitial infiltration of serum,
blood-corpuscles, and corpuscular inflammatory products, derived from
the interstitial connective tissue-elements or from the blood. These
may be in the form of pus cells, which may be disseminated through
the heart in the tracts of connective tissue, or may be aggregated in
minute abscesses. In the localised form of inflammation, softening
and breaking down of tissue may occur without actual pus formation,
and a pseudo-abscess may result. If pus cells are formed, a true
abscess of the heart is the consequence, and the destruction of the
muscular fibres may be so complete that only pus may be found in
the cavity. The adjacent tissue is, however, softened and degenerated.
Such an abscess may attain the size of a hazel-nut. This local
inflammation is much more common in the wall of the left than isi
that of the right ventricle, and is very rare in the auricles. It is most
common in the left ventricle near the apex, in the posterior wall,
or in the septum. When softening, purulent or non-purulent, has
occurred, the wall is bulged at the spot, and secondary pericarditis
may be produced. When the inflammation is adjacent to the inner
surface, it may invade the endocardium, and spread to an adjacent
valve. Ultimately, in most cases, the outer or inner wall of the abscess
or pseudo-abscess gives way, and the contents escape into the pericar-
dial cavity or into the ventricle; causing, in the former case, purulent
pericarditis, in the latter, an " acute aneurism of the heart " and septi-
caemia, usually fatal in a few hours. Both walls have given way at
the same time, and " rupture of the heart " has occurred. An abscess
in the septum has burst into both ventricles ; from the upper part of
the septum it has burst into the aorta behind the aortic valves, or into
the right auricle. In this way a fistulous communication has been
established between the two ventricles, between either or both ven-
tricles and the aorta, or between the left ventricle and the right
auricle. If the inflammation subsides without the formation of pus,
the cellular products may develop into fibrous tissue. This often occurs
in the superficial layers of the heart after pericarditis, and it may
occur in the localised form of carditis, a circumscribed patch of fibrous
tissue resulting. Less commonly caseation takas place, even after pus
has been formed, and the caseated mass may shrink and calcify.

Symptoms. — The symptoms of acute inflammation of the heart are
sometimes distinct enough, but are in other cases obscure or mis-
leading. The local signs are those of cardiac weakness, suddenly
developed, after, it is said, a transient stage of excitement. The impulse
is weakened or imperceptible ; the first sound toneless. A systolic
murmur has been heard in some cases, due, perhaps, to incapacity of
the papillary muscles. The cardiac dulness is normal, or sometimes
widened, from acute dilatation. The pulse is feeble, frequent, and may
be irregular. Uneasiness about the sternal or cardiac region has
been an early symptom in several cases, increasing in some to acute
pain. The general symptoms are those of heart failure, and those

CARDITIS. 531

which depend on cerebral anaemia may be so pronounced as entirely
to obscure the real nature of the case. Dyspnoea is the most constant
symptom, continuous or felt on the slightest exertion. Nausea and
vomiting, collapse, with coldness of extremities, and clammy perspira-
tion occur. Convulsions, delirium, and coma have been prominent
symptoms in several cases. The central temperature is raised ; in one
recorded case it reached 107°. The symptoms of collapse rapidly
increase, and death occurs usually in a few days. Friedreich found
the average duration to be four days, the minimum being a few hours,
the maximum a week.

Localised inflammation of the heart may be attended by similar but
less urgent symptoms, or may run an entirely latent course until the
occurrence of the grave symptoms which proclaim the rupture of an
abscess, such as, on the one hand, those of acute pericarditis, or, on the
other, those of systemic or pulmonary embolism. In one case a pustular
rash occurred, it is conjectured from embolism of the cutaneous arteries.

Diagnosis. — The diagnosis is a question rather of theory than of
practice, for the disease is extremely rare, and its symptoms are pro-
duced by many other causes. The sudden onset of symptoms of
cardiac weakness and failure, less sudden than in cases of rupture,
more sudden than in cases of acute degeneration, if coupled with
considerable elevation of temperature, and especially if occurring
in the course of a disease such as pyaemia, may give rise to a
suspicion of the existence of carditis. Abscess of the heart is even
more equivocal in its symptoms. The rupture of an abscess may be
suspected if sudden symptoms of systemic or pulmonary embolism or
of pericarditis, supervene on less urgent symptoms of cardiac failure.

Prognosis.— General carditis has hitherto only been diagnosed after
death, and it is doubtful whether recovery has ever taken place. In
the circumscribed form it is probable that subsidence of the inflam-
mation has, in a few cases, permitted the continuance of the heart's
action and the disappearance of the symptoms. The prognosis in the
form which is secondary to pericarditis is much less grave, since a large
proportion of the muscular tissue is not damaged, and, with the sub-
sidence of the adjacent inflammation, recovers good functional power.

Treatment.— The treatment of carditis is necessarily symptomatic.
Its existence can rarely be ascertained, and, if known, no meaus of
direct treatment exists. Rest to the heart is the first point to be
secured. Cold to the precordial region has been recommended ; warm
poultices would perhaps give more relief. Warmth should be applied
to the extremities, to equalise the circulation and lessen the tendency
to correlated congestion of internal organs. The heart's action must
of necessity be sustained by stimulants which, with the recumbent
posture, constitute the best treatment for the cerebral symptoms.
For the cardiac failure in septicaemia, full doses of the perchloiide of
iron have seemed to the writer to be of distinct service.

532 A SYSTEM OF MEDICINE.

HYDROPERICARDIUM.— HYDROPS PERICARDII.

By J. Warburton Begbie, M.D.

The occupation of the pericardial sac to a greater or less extent
by serous fluid, a condition known under both of the terms men-
tioned above, or simply as Dropsy of the Pericardium, is not of
unfrequent occurrence. Laennec indeed speaks of this condition as
being very common. " Uhydro-p^ricarde," he says, " ou Taccumu-
lation d'une quantity plus ou moins grande de s^rositoS dans le p6ri-
carde, est un cas extr§mement coininun;"1 but he qualifies this
statement by the remark, that idiopathic effusion into the peri-
cardium is very rare, that ordinarily but a few ounces of serum are
found in the sac, and that this quantity is effused shortly before
death, sometimes at the very moment of dying, or even immediately
thereafter. The causes of dropsy of the pericardium are various,
and some of them most obscure. Dr. Wakhe recognises an Active
and Passive Hydropericardium ; also, a third form dependent on
mechanical obstiniction.2 The first of these three varieties is very rare.
Dr. Walshe, however, refers to certain instances of Bright's disease,
in which he has known the pericardium fill with fluid, the symptoms
indicating an irritative state, while the signs of pericarditis were
wanting. Examples of a precisely similar kind are familiar to the
writer, in connection with the dropsy of scarlet fever. He has seen a
sudden and copious effusion into the pericardium occur at the same
time that dropsical swelling manifested itself in the more ordinary
situations , and in such cases, found no evidence whatever of plastic
formations either upon or within the heart.

Passive Hydropericardium is seen in connection with other dropsies,
with anasarca and ascites, but especially with hydrothorax. The
relation of the latter, however intimate, as in some cases it is, to
pleural dropsy, is by no means constant. On two occasions we have
fonnd a very large Hydropericardium in cases of primary cardiac
disease with great anasarca, bnt with little, if any, hydrothorax.

Mechanical Hydropericardium.-r-Ari effusion of serous fluid into
the cavity of the pericardium has been found in connection with
aneurism of the aorta, with cancerous disease seated in the anterior
mediastinum, exerting injurious pressure on the great venous trunk,
and thus preventing the due return of blood through the coronary
and pericardial veins, and certain morbid states of the heart itself, in

1 Traits de r Auscultation. — Des Maladies du Coeur, chap. xxii. : De PHydro-pencard.
* Diseases of the Heart, p. 266.

HYDROPERICARDIUM. 633

which the venous circulation is greatly embarrassed In such instances
the dropsy, evidently due to direct obstructions near its seat, may
with great propriety be called mechanical.

The serous fluid which occupies the pericardial sac is sometimes
colourless ; at other times, although quite limpid, and without any
admixture of albuminous floculi, it presents a lemon yellow, or even
rose-coloured tints ; rarely is it sanguinolent. The quantity of fluid
varies greatly. Usually it is not excessive, but, on the contrary,
moderate. In Passive Hydropericardium, Dr. Walshe has stated the
amount to be from eight to twelve ounces; more than the latter
quantity he has never seen. Instances, however, are on record in
which a very large accumulation of serous fluid has been found in
the pericardium. Benisart has related one, in which there existed
four pints, or eight pounds {huit livres). From twelve to eighteen
ounces of fluid can be injected into the healthy pericardium of an
adult, but there can be no doubt that the pericardium, contrary
to what is stated in certain anatomical treatises,1 is extensible ; the
fibrous, as well as serous nature of the membrane may impair, but
does not prevent its extensibility. In all probability, those cases of
enormous distension of the sac by fluid, which are described by
Corvisart, Avenbrugger, and others, were examples of pericarditis. It
is apparently when altered by inflammation that the pericardium
becomes most capable of distension.

Dr. Stokes refers to a case published by Sir Dominic Oorrigan, in
which the heart was covered with a pulpy lymph, and there was a
vast effusion of liquid into the sac,2 and Dr. Graves, in describing a
most interesting case of Hydropericardium, connected with malforma-
tion of, and recent deposition of lymph upon the pulmonary valves,
makes the remark, " the pericardium was distended with straw-
coloured fluid, so abundant that we expected to find pericarditis ; " 8
implying that this distinguished physician regarded pericarditis as the
usual determining cause of large pericardial effusions.

The most important and reliable indications of the existence of
Hydropericardium are furnished by percussion and auscultation, but
independently of these, there are other particulars, the value of which
is by no means small. A sensation of discomfort in the region of the
heart is frequently complained of, and even a sense of weight — a
symptom of pericardial effusion to which Lancisi attached great sig-
nificance. Senac describes the undulatory movement of the fluid as
visible between the third, fourth, and fifth ribs ; and Corvisart, the
sense of fluctuation in the same situations, as distinguished by touch.
Dyspnoea, more or less urgent, is usually present in cases of Hydro-
pericardium. It must, however, be admitted that there exists no small
amount of difficulty in assigning the true share in the production of
this symptom to the effusion within the pericardium, seeing that it may

1 E.g. Holden's Illustrated Manual of Anatomy, p. 98.

1 Diseases of the Heart, p. 20.

* Clinical Lectures : Pericarditis, p. 678.

534 A SYSTEM OF MEDICINE.

in most cases be in part likewise attributed to the visceral disease, on
which this form of dropsy depended, or possibly to the hydrothorax, by
which it is so likely to be accompanied. A feebleness of the pulse, and,
not unusually, an intermittent or irregular condition of the pulse exists.
By auscultation, the heart-sounds are feebly audible, and appear to be
distant or remote. On percussion there is extended pericardial dulness,
for the most part not rising so high, nor passing to the same limits
laterally, as is the case in chronic, and even in some instances of acute
inflammatory effusion within the pericardium. The dilatation of the
precordial region, or even of the left lateral region, as noticed by
Louis, the epigastric tumour described by Corvisart, and the ex-
tension of the left lung upwards, of which Dr. Graves and Dr. Stokes
have written, are rare but striking phenomena connected with large
pericardial effusions, dependent, however, on inflammatory action.
Besides the general symptoms to which reference has been made, it
must be held in view that others of the same nature will be likely
to show themselves, the latter, however, having a more distinct
relationship with the visceral disease on which the dropsy depends.
The Hydropericardium, moreover, will in all probability be connected
with some other dropsical effusion, hydrothorax or anasarca, or it
may be ascites.

The remedies most useful in the treatment of dropsies are seldom
effectual in relieving the dropsy of the pericardium. The writer has
known the repeated application of blisters over the region of the heart
to produce a decided impression in one case. The stronger diuretics
and hydrogogue cathartics, " will," as Dr. Walshe observes, " be tried,
were it only for the removal of the usually concomitant dropsies." Para-
centesis pericardii, which has been repeatedly performed in the treatment
of pericarditis attended by large effusion, and in some instances success-
fully performed, is of course an available means for affording temporary
relief in the truly dropsical affection, temporary because, although
the heart be freed by the operation from the surrounding fluid, unless
the disease giving rise to the dropsy be removed, the fluid must neces-
sarily re-accumulate.

ANGINA PECTORIS AND ALLIED STATES ;
INCLUDING CERTAIN KINDS OF SUDDEN DEATH.

By Professor Gairdner, M.D.

The phenomena of the disease, or group of symptoms, termed Angina
Pectoris by Heberden, are perhaps the most interesting in themselves,
and the most deserving of study in relation to other forms of cardiac
disorder, of any which we shall have to consider in this section. In
treating of this difficult subject we must separate with great care
the essential facts of the disease from the various speculations, or
associated ideas, that almost inevitably force themselves into the mind
in considering the facts. And this separation is by no means easy ;
for in this instance the facts themselves are apt to be more or less
withdrawn from exact observation ; the phenomena characteristic of
the disease being mostly subjective, i.e. present to the consciousness of
the patient only, and only through his description of them made known
to the physician. It may even be said with truth, that no one fact
in a typical case of angina pectoris is necessarily other than subjective,
with the exception of the awful terminal fact of sudden death. And
when this is wanting, or when it is delayed, there is hardly any
combination of the remaining symptoms that may not vary in
individual cases, or be differently presented by the sufferer, according
to the exactness and concentration of his habits of thought, the
vividness and power of his imagination, or the degree and kind of
his individual sensitiveness to morbid impressions.

Still, the fact of sudden death, superadded to the evidence of certain
sensations preceding death, may be considered to afford the nearest
approach we have to an accurate definition of this disease. What
these sensations are we shall endeavour to indicate, in so far as the
inadequacy of language will allow, from the consideration of such
individual instances as have been minutely and carefully recorded
either by the sufferers themselves, or by physicians simply giving
expression to the spontaneous testimony of their patients. By
following the ideal descriptions of those who have allowed themselves
to be guided by theories of the disease rather than by the facts, we
might easily add to the fulness, without increasing the value, of our
description.

First on the list of symptoms, according to Heberden and the
majority of authors who have followed him, is pain.1 How far pain,

1 In his Commentaries (1796), Heberden treats of this disease under the general title "De
dolore pectoris " (Sec. lzx.). In his first communication on the subject to the College

636 A SYSTEM OF MEDICINE.

in the ordinary sense of the word, is essential to the idea of angina
pectoris, we shall afterwards consider; for the present it may be
sufficient to observe that pain, or at least a sensation of local distress
amounting in certain cases to pain of a peculiarly overwhelming
character, is in this disease closely associated with the symptoms
immediately preceding death.

This peculiar anguish, or, as it might justly be called, agony of
suffering, is paroxysmal; it frequently reaches its climax within a
few minutes, and is relieved or disappears entirely within a like period
of time, or at most within an hour or two ; it recurs at uncertain
intervals, sometimes without any obvious exciting cause, at others
manifestly determined by exertion, and especially by too rapid
walking up-hill, in which case it often ceases, especially in the earlier
attacks, almost immediately on standing still: it is instinctively
associated in the mind of the patient with the idea of a particularly
severe form of oppression or suffocation; or rather, to be more
exact, with some indefinable sense of impending danger, to which he
is unable to give expression, and which he endeavours to convey to
others by similitudes that do not satisfy his own mind. A frequent
expression is that recorded by Dr. Latham in the case of a very
eminent man of the highest intellectual power ; after an attack he
said he " could scarcely bear it if it were as severe as it had been ;"
and shortly afterwards, " One can bear outward pain ; but it is not
so easy to bear inward pain." x This essential wnbearableness of the
suffering is most characteristic of angina pectoris, and it is quite
independent of the degree of severity of the pain in other respects.
And further, it is to be observed that the intolerance here alluded
to is not the mere impatience of the nerves, which can be mastered
by a strong will and a calm heroic self-restraint ; it is the sense that
the very springs of life are implicated, and that under a prolongation
or increase of the pain the whole machine must suddenly give way.2
It is from this sense of impending death (rarely thus expressed in
words by the patient), and from the fact that sudden death actually
occurs during the paroxysm in a certain number of cases, that the
pain, or special sensation, of angina pectoris derives almost all that it
has of a distinctive character ; and therefore Dr. Latham has justly
elevated this most important but almost indescribable symptom to a
co-ordinate rank with the pain itself, in his description of the disease
as a whole. Angina pectoris, according to his admirably succinct
definition, "consists essentially of pain in the chest and a sense of

of Physicians in 1768 (Medical Transactions, vol. ii. p. 5P), he merely terras it "A
Disorder of the Breast. " The two descriptions do not differ in essentials, but a few
details of difference which seem to be of more or less importance will be noticed below.
The eminently careful and exact use of language by Heberden in his singularly con-
densed clinical studies, whether in Latin or in English, tends to invito attention to even
the minutest discrepancies between his earlier and later statements.

1 Latham, "Diseases of the Heart," vol. ii. pp. 376-6. It is no secret, that the caso
was that of the late Dr. Arnold, of Rugby.

* " Qui hoc raorbo tenenhir, occupari solent . . . ingratissimo pectoris angore, vil« ex -
tinctionem intentante, siquidem augeretur, vel perseveraret." — Heberden, CVmra.loc. cit.

ANGINA PECTORIS AND SUDDEN DEATH. 537

approaching dissolution." "The subjects of angina pectoris report
that it is a suffering as sharp as anything that can be conceived in
the nature of pain, and that it includes, moreover, something which
is beyond the nature of pain, a sense of dying." l

Such, then, are the most important or essential facts which clinical
observation teaches in reference to angina pectoris. Let us now
consider them separately, and more in detail.

The pain of angina is usually felt at the lower sternum, but some-
times also under the middle or upper sternum, inclining, however,
towards the left side.* Sometimes the pain extends to both sides of
the chest in front, and perhaps more frequently into both shoulders,
and into the back. Very specially characteristic is a " pain about
the middle of the left arm," 8 sometimes present in the right, or in
both arms, which, according to Dr. Heberden, occasionally precedes,4
but more commonly follows the pain in the chest. This, together
with a degree of numbness of the left arm, may be described as
present in the majority of cases in which the pain extends beyond
the thorax.6 The pain and numbness together, or the pain alone,
may extend down to the fingers, or may 3top short at the elbow,
usually at the inner side of the arm ; and painful sensations, more or
less definite in character, may be felt also in the neck, or in one or
both lower extremities ; but these are exceptional, and there is reason
to think that in some cases the local symptoms connected with
aneurismal tumours implicating the nerves may have been confounded
with those more specially characteristic of angina pectoris.6 At all
events, these local varieties of pain are not to be regarded as essential

1 Op. cit. pp. 366, 364.

9 "Always inclining moro to the left side." (Heberden, Med. Trans.) "Nonraro
inclinatior ad sinistrum latus." — Comment.

s Hel>erden, Med. Trans, uti supra. " Dolor saepissime pertinet a pectore usque ad
cubitum lsevum. ... In nonnullis vero ... ad dextrnm pariter ac laevum cubituin
pertigit, atque etiam usque ad raanus ; sed hoc rarius evenit ; rarissimum autom est, ut
orachium simul torpeat ac tumeat." — Comm. loc. cit.

4 Med. Trans, vol. iii p. 3.

5 The group of symptoms here alluded to, though first clearly indicated by Heberden
as characteristic, was described long before by Morgagni in the case of a woman, forty-
two years of age, who died suddenly during a paroxysm, and was found to have a dilated
and ossified aorta. The description is worth quoting, from the fact that it is probably
one of the first clinically exact records existing in medical literature of a case of this
kind. The patient had been "diu valotudinaria, diuque obnoxia paroxysmo cuidam ad
hunc modum se habenti. A concitatis corporis motions ingruebat molestus quidam
angor intra superiorem thoracis sinistram partem, cum spirandi difficultate, et sinistri
brachii stupore : quae omnia, ubi motus illi cessarent, facile remittebant. Ea igitur mulier,
cum circa medium Octobrem A. 1707 Venetiis in continentem trajecta, rheda veheretur,
he toque esset animo, ecee tibi ille idem paroxysmus ; quo correpta, et mori se, aiens, ibi
repeute mortua est." The examination after death showed disease of the aortic orifice
and aorta, and Morgagni regards the sudden death as due to the sudden excitement of
carriage exercise (" insolitum in Veneta foemina rhedre motum ") operating upon a circula-
tion weakened and obstructed by chronic disease, as co lead to ultimate failure in the
power of the heart to propel the blood ("ut sanguis restitans promoveri amplius non
poterat "). — Dc Scdibus ct Causis Morborum, ii. Epist. xxvi. 31 et seq.

8 As, for instance, in several of the cases recorded by M. Trousseau in his interesting
chapter on the subject. (Clinique de l'H6tel-Dieu, vol. ii. p. 434 et scq. deux i em e
edition; Paris, 1865.) English Translation, 1868, vol. i. p. 596, etseq.

VOL. IV. N N

638 A SYSTEM OF MEDICINE.

elements of the disease, although from their occurrence and their
distribution they may lead to more defined conceptions of the nervous
plexuses involved, and thus occasionally to the detection of an organic
cause, or of something tending to throw light upon the peculiarities,
or to guide the treatment of an individual case.1

Local tenderness on pressure is an occasional but by no means a
constant symptom of angina pectoris. Sometimes, on the other hand,
the pain is decidedly relieved by pressure, or by rubbing, as well as
by counter-irritation of the parts affected. The pains are aggravated
by movement of the whole body, and especially by severe or even
moderate exertion in walking, which indeed becomes impossible
during a severe paroxysm. Very marked relief is often afforded by
the eructation of wind from the stomach, whether spontaneously or
under the influence of carminatives. Rest of body, and warmth to
the extremities, are among the more obvious of the physiological
conditions which have been observed to have a well-marked effect in
relieving the pains of angina, in their less extreme varieties.

The peculiar sensation which culminates in the sense of impending
death, has been very variously described,2 and indeed seems from its
very nature to be almost indescribable. Among the uninstructed, or
in the case of persons unaccustomed to observe and analyse their own
sensations, nothing is more common than to find the term " breath-
lessness," or "want of breath," applied to every kind of thoracic
oppression, and the sense experienced in angina pectoris of constric-
tion, or in other cases of repletion in the chest, accompanied as it
usually is by gasping or irregular respiration, is undoubtedly often
called a "want of breath," or "suffocation," by persons who are simply
feeling about, as it were, for an expression whereby to represent an
uncommon and intensely oppressive sensation. A similar confusion

1 In one very exceptional case, recorded by Heberden in the "Commentaries," there was
no pain complained of in the chest, bnt only in the left arm, having, however, in other
respects the characters of angina. After fifteen years of occasional and increasing suffer-
ing, the patient died suddenly at seventy-five years of age.

2 It is difficult to judge from Heberden's descriptions how far the "angor pectoris,
intentans vita; extinctionem," was regarded by him as a simple pain. In his first memoir
he speaks of the "sense of strangling, and anxiety with which it (the disorder of the
breast) is attended, " and applies the name Angina Pectoris on account of these characters
rather than on the ground of pain. The anonymous patient who described his own case
in the third volume of the "Medical Transactions," apparently discriminates very sharply,
on the one hand between the pain in the left arm and chest, coming on tl when walking,
always after dinner, or in the evening ; " and on the other, the "sensations which seem
to indicate a sudden death;" which he describes as being like "a universal pause
within me of the operations of nature for perhaps three or four seconds," and afterwards
"a shock at the heart, like that which one would feel from a small weight fastened to
u string to some part of the body, and falling from the table to within a few inches of
the floor." This distinction of the sensation of impending death from the pain was
unfamiliar to Heberden, who says he does not remember to have heard it mentioned by
any other patient ; and thinks that the sudden death of this patient, which came to his
knowledge afterwards, was connected more with the pain than with this j)eculiar sensa-
tion. Dr. Parry speaks of the first symptom in angina pectoris as "an uneasy sensa-
tion, which has been variously denominated a stricture, an anxiety, and a pain." Dr.
Latham was probably among the first to define the sense of impending death as being
distinct from the pain.

ANGINA PECTORIS AND SUDDEN DEATH. 539

lies latent even under the more technical language of Heberden, in
his use of the Greek term Angina,1 which, according to its etymology,
signifies a strangling, and according to its actual and primitive use
was applied chiefly to certain affections of the throat, occasionally
leading to sudden death by laryngeal suffocation, and giving rise to a
sense of choking, or of constriction in the fauces. Yet Heberden, in
using this term, had thoroughly realised the fact that angina pectoris
is not really a suffocation or a breathlessness, in the ordinary accepta-
tion of these terms. At most it is a sensation which by its urgency
and oppressiveness recalls the impression of suffocation, and which
may in certain cases be associated with true dyspnoea, or still more
frequently with orthopncea. In many instances, however, careful
examination shows, and the patients themselves may be easily con-
vinced, that respiration is really not impeded ; that inspiration and
expiration are alike free and noiseless ; that the air is taken into the
chest in full measure, and (in so far as the evidence of stethoscopic
examination goes to prove the fact) that the mechanical renewal of
the air in the vesicles of the lungs is perfectly accomplished. In this
sense, the observation of Heberden is profoundly exact, that in the
beginning of this distemper the patients "nulla tenentur spirandi diffi-
cultate, a qua hie pectoris angor prorsus est diversus." 2 And yet it
might possibly be maintained that in a more transcendental sense
respiration, i.e., the chemistry of respiration, is usually impeded ; that
the transit of the blood through the pulmonic capillaries is for the
time suspended or impaired, that the right heart is perhaps unduly
loaded, and that the sensation of " breathlessness " is therefore not
without a physical equivalent in the state of the blood, for the time
restricted in its supply of oxygen. In the more advanced stages of
angina pectoris, indeed, especially when in connection with organic
disease, it rarely happens that some positive evidence of real dyspnoea
does not exist, at least as a complication, if not as a part of the disease.
Even in such complicated cases, however, it is usually easy for the
experienced clinical observer to detect a difference of habit and aspect
from cases in which the breathing is primarily impaired, e.g. as in
aggravated cases of emphysema with bronchitis, or of double pneu-
monia, or extensive pleuritic effusion unconnected with a cardiac cause.
We are obliged, therefore, under these circumstances, to accept the
necessary limitations of ordinary language in conveying extraordinary
or almost indescribable impressions. It is certain that the patient in
angina pectoris has a sense of obstruction in the thorax so over-
whelming and so full of apparently imminent danger that he in-
stinctively likens it to a suffocation ;3 yet it is equally certain that in

1 From &yxw, straagulo, whence also the compound words Cynanche and Synancho,
and the Latin verb angerc, which acquired the secondary sense of undefinable distress
••onveyed also by anxkUis, and still more by our English word anguish.

-Heberden, Comment, loc. cit. "Have no shortness of breath." {Med. Trails, uti
supra. )

* •* A sense of dissolution, not a fear of it," said one of the most gifted men I ever
knew, and one most competent to analyse sensations. — J. U.K. Editor.

N N 2

640 A SYSTEM OF MEDICINE.

many cases impeded respiration, in the ordinary sense of the term, is
not present. This remarkable sensation, which is sometimes repre-
sented as a tightness or constriction, sometimes, on the other hand, as
a fulness or over-distension of the chest, contributes even more than
the pain to the indescribable anguish of angina pectoris; and it is
this sensation especially which gives to the pain its peculiar character
of " unbearableness " already noticed ; this also, which carries with it
in its graver forms that impress of immediately impending death, by
which the real danger, and the ultimate probable event, are rendered
so vividly present to the consciousness of the patient.1

The other symptoms of angina pectoris have been variously
described ; so variously, indeed, as to lead to a suspicion of inaccu-
racies of detail on the part of individual observers of the paroxysm.
On all hands it is agreed that in the intervals the patient may have
all the appearances of perfect health; his colour may be good, his
appetite unimpaired, his breathing apparently natural, the action and
sounds of the heart perfectly normal. It is equally certain that the
paroxysm itself is unattended by fever, and that in uncomplicated
cases it has none of the characters, as it has none of the consequences,
of an inflammatory seizure.2 But it is difficult to accept without hesi-
tation the statement of some authorities, that throughout the attack
the pulse may be entirely undisturbed either as to its rate of frequency,
or as to its characters.8 In most of the cases in which details have

1 A recent medical observer, himself a sufferer from angina, whose case will be
referred to again in the section on treatment, has contributed what is perhaps the only
really exact description in medical literature of one form of the constrictive sensation :
"The front of the chest seemed to be bulged out in a convex prominence, wliich sud-
denly terminated at the lower end of the sternum in a sharp and deep depression
towards the spine. This was a purely subjective phenomenon. There was no contrac-
tion of the diaphragm, and no retraction of the abdominal walls. But though the hand
laid upon the parts convinced my mind of their normal condition, it in no way modified
the sensation. (Dr. "W. Hemes Madden, in the Practitioner, vol.ix. 1872, p. 834.)
In the case of John Hunter, to be cited below (a case full of instruction in detail as to
many phases of disease included in the present article), the sense of thoracic constriction
in one attack was preceded for a fortnight by symptoms of " nervous irritation " in the left
side of the face and head, as well as down the left arm. The special sensation in the
chest in this case was a "feeling of the sternum being drawn backwards towards the
spine, as well as of oppression in breathing ; although the action of breathing was attended
with no real difficulty. (See infra, p. 563.) The special character of the breathing in
Hunter's case, elsewhere alluded to, will be found to be a most exact anticipation of
what has since been called "ascending and descending," or by some, " suspirious "
repiration ; a form of disturbance frequent in cases of angina, though it seems to have
escaped Heberden's observation. See also the remarks on the case of Seneca, below :
and at page 563, note.

1 Dr. Latham has admirably modernised Heberden's arguments on this point. (Op. cit.
vol. ii. p. 383. )

3 "The pulse is, at least sometimes, not disturbed by this pain." (Heberden, Med.
Trans.) " Arteriai eoium, qui in hoc dolore sunt, naturaliter prorsus moventur. ... In
ipsa accessione pulsus non concitatur. " (Comment, loc. cit. ) Several authors have followed
Heberden here without observing that his real meaning is not that there is no alteration
of the pulse, but that there is no excitement of it, i.e. that the pulse is not quickened
("non concitatur") as in inflammation. Dr. Parry, regarding the disease as a syncope,
speaks from another point of view, and has no difficulty in showing that the pulse,
though not always greatly disturbed, " becomes more or less feeble according to the
violence of the paroxysm." Such personal experience as I havo on the point leads me to

ANGINA PECTORIS AND SUDDEN DEATH. 541

been carefully given, the pulse, at the height of the seizure, has been
found small, often imperceptible or irregular in rhythm, but not neces-
sarily accelerated, and sometimes morbidly slow ; the countenance has
been pale as death, the features pinched and anxious, the extremities
cold ; there has been often a cold sweat on the brow, sighing or inter-
rupted respiration, and other signs of approaching syncope. On the
other hand, it must be admitted that in a few instances the heart has
been heard beating in the very midst of a paroxysm without appre-
ciable alteration in the character of the sounds and impulse, and the
pulse has been also said to be regular, and neither rapid nor weak.
The senses and the consciousness have also been observed to be fre-
quently quite entire in the midst of the paroxysm, though this fact
also, like some of the others above mentioned, must be held as subject
to numerous exceptions. On the whole, the strict analogy between
the phenomena of angina pectoris and ordinary syncope cannot be
unreservedly maintained, notwithstanding the arguments of Dr.
Parry,1 who, however, has undoubtedly marshalled a strong array of
facts and reasonings in favour of this view of the case. The paroxysm
of angina pectoris remains, after all, a mode of morbid function sui
generis, although in some instances the manner of death in the
paroxysm is more or less allied to syncope.

The condition of the nervous system, and especially of the brain
and spinal cord, in angina pectoris, opens up many very difficult, and
at present even insoluble problems connected with its ultimate patho-
logy. For practical purposes it is sufficient to state the facts estab-
lished by clinical observation. While it is quite certain, as stated
above, that integrity (in a practical sense) of the nervous functions
may be maintained up to the very instant of death in certain cases of
angina, it is equally well ascertained that in other instances giddi-
ness, vertigo, disorders of the special senses, spasms, tonic and clonic,
and almost every kind of disorder of the general sensibility and
consciousness, may occur, and may also be the distinguishing features
of particular paroxysms in persons in whom at other times paroxysms
may occur devoid of all such phenomena. It is probable that in some
of these forms of the disease the cerebro-spinal complications may be
determined by special derangements of the circulation within the

agree with Dr. Parry. The recent experiments and sphygmographic tracings of Dr.
Lauder Brunton will be discussed in connection with the pathology of the disease
further on.

1 His expressions are as follows : — " From the preceding observations, I think it
evidently appears that the Angina Pectoris is a mere case of syncope or fainting,
differing from the common syncope only in being preceded by an unusual degree of
anxiety, or pain in the region of the heart, and in being readily excited during a state of
apparent health, by any general exertion of the muscles, more especially that of walking."
(Inquiry into the Symptoms and Causes of the Syncope Anginosa, commonly called Angina
Pectoris, Ac. r>. 67). To the points of difference here noted must be added the persistence
of the sensibility up to the very instant of death in many cases of angina pectoris, and
the incomplete extinction of the pulse ; while in ordinary syncope (as for example from
emotion, or from hot rooms) the most absolute temporary insensibility, with a radial
pulse which cannot be felt, and respiration just sufficient to maintain life, may occur as
symptoms and be maintained for some minutes, with almost no danger to life.

542 A SYSTEM OF MEDICINE.

cranium, or even by disease of the arterial system extending to the
brain ; but there are very rarely any permanent changes, either of
structure or of function, tending to throw light on these attacks. On
the other hand, it seems premature to infer, with Trousseau, the
existence of any distinct relation between epilepsy as a predisposing
cause, and angina pectoris ; still more premature to affirm that " in
certain cases, and perhaps in a considerable number, the angor pectons
is one expression of this formidable and cruel disease, a phase of its
vertiginous form, or in two words an epileptiform neuralgia''1 The
extreme rarity, on the one hand of true angina pectoris among the
countless multitudes of confirmed epileptics, on the other of genuine
and well- formed epileptic attacks among the subjects of angina
pectoris, seems to oppose a considerable difficulty in the way of
accepting M. Trousseau's hypothesis. That the relation, however,
between the occasional cerebro-spinal symptoms in these cases, and
the cardiac disorder, is more than a coincidence, is shown by the fact
that a veiy similar series of symptoms is observed in some cases ot
fatty heart ; and the author of this article has in more than one
instance observed like phenomena in connexion with large aneurisms
within the thorax.

In certain cases of angina pectoris, more especially when perfect
rest cannot be obtained during the attacks, they are apt to be
attended by more or less of sickness, and even of vomiting ; but these
symptoms are rarely obstinate. Flatulence has been already noticed
as a frequent accompaniment of the paroxysm, the discharge of the
imprisoned air by the mouth usually giving marked relief. In some
instances the close of the paroxysm is accompanied or followed by a
copious discharge of watery urine, as in hysteria. In one case Dr.
Walshe has observed tetanic spasms, with complete opisthotonos,
followed by local tonic spasms continuing for some hours after the
paroxysm.

The diagnosis of angina pectoris is not very difficult in severe
cases, except in so far as difficulties may arise from the inability of
the patient to express his sufferings in words, or on the other hand
from the too fluent and misleading descriptions of comparatively
insignificant pains referred to the heart, by persons either unduly
frightened or unduly sensitive. Persons who have lost near relative?
or even intimate friends, by sudden death of cardiac origin, are
extremely apt to be terrified by nervous symptoms of this kind ;
gouty and rheumatic sufferers are frequently a prey to flying pains
which now and then occupy the habitual seats- of angina pectoris,
and which sometimes give rise to alarms not justified by the event,
all the more when suspicion has been once aroused, and when, as
happens not unfrequently, the physician as well as the patient may be
for some time in doubt as to the cause of the symptoms. Disorders

1 Clroioue MR d» l'HftteMHeo, t. ii, p. 444. Paris, 1865; and in the English trans-
lation, vol. L p. 602;

ANGINA PECTORIS AND SUDDEN DEATH. 543

of the stomach, aud still more notably of the uterus, frequently
lead to pains in the left side, which may pass for cardiac angina.
Intercostal neuralgia may have many causes, and not unfrequentiy
radiates towards the left arm. In hysterical and romantic girls, pains
about the heart are often associated with palpitation and irregular
sighing respiration, sometimes also with well-marked irregularities of
cardiac rhythm, or with murmurs requiring care in their discrimi-
nation, though not, on the whole, very apt to lead into serious error.
Each of these cases requires its own special diagnosis, with reference
to the cause of the symptoms ; and it should always be remembered
that the number of persons presenting themselves on account of such
symptoms immensely exceeds that of the sufferers from genuine and
dangerous angina pectoris. Moreover, the urgency of the symptoms
is usually far less in these affections than in the true angina. The
pains, in the milder disorder, are usually much less defined iu
character, and are never, or hardly ever, accompanied by so grave a
sense of impending dissolution. The diagnosis requires tact and
judgment rather than any elaborate rules of investigation, to save
the physician from error.

A much more difficult diagnosis, and one in which in many cases it
is impossible to arrive at more than a proximate conclusion, is the
determination of hoto far any organic disease, and what kind of
organic disease, may have had to do with the symptoms present in any
particular instance of angina pectoris. Clinically speaking, it may
be said that, as a question of pure experience in the living patient, the
formidable prognosis of true angina is not necessarily relieved by the
knowledge that after careful examination no organic disease can be
discovered ; for, in the first place, organic disease may exist with-
out the possibility of discovery ; and, secondly, they are precisely the
forms of organic disease most difficult of discovery that have been
shown to be most frequently associated with death from angina
pectoris. Given, therefore, a very perfectly characterised instance of
angina in repeated paroxysms nearly fatal, and tending to increase in
severity, it cannot be said that the special diagnosis of organic
associated lesions has any very immediate practical significance.
The prognosis in such cases is emphatically grave in the highest
degree, and remains so even after the most careful examination of the
organs of circulation has given only a negative result. In cases of
minor urgency, however, and in cases where the diagnosis of the
angina paroxysm is not perfectly clear and well defined, or where one
or two such paroxysms only have occurred at long intervals, it
becomes a very important question for the physician, and still more
for the patient, whether or not there is any organic lesion of the chest
forming a barrier to ultimate recovery, and in case any such lesion
exists, whether it is of a kind likely to be rapidly and inevitably
fatal, or the contrary. These considerations give an importance to the
details of diagnosis in angina pectoris which at first sight they might
not seem to possess, as bearing on prognosis and treatment.

544 A SYSTEM OF MEDICINE.

Dr. Latham lias very truly said that in this respect at least the
paroxysm of angina bears a certain resemblance to the paroxysm of
epilepsy. In the attack itself we are obliged to act by routine, and
are unable to discriminate. It is in the intervals that the physician
tries to advance beyond the mere name that has guided him in dealing
with the most urgent symptoms, and by careful examination of every
OTgan and every function to discover how the whole organisation can
be most effectually strengthened against the enemy that is at the
gates — nay, that is threatening the very stronghold of life itself.
Such a complete investigation, and no other, constitutes diagnosis.

It needs scarcely be said that in the first instance the attention of
the physician must be concentrated upon the heart, arteries, and
great veins. He will inquire with the utmost care into the whole
details connected with the circulation, both during the paroxysm and
during the intervals. He will carefully look for evidences of hyper-
trophy, dilatation, valvular disease. But above all, and even in the
absence of these, he will endeavour to estimate the probabilities of
structural disease in the fibre of the heart itself, or of disease in the
coats of the arteries leading, it may be, to induration and obstruction,
or to aneurism.

Dr. Jenner, the discoverer of vaccination, was the first to make a
decided advance in the pathology of angina pectoris. He did not
himself publish anything on the subject, but communicated his
information to Dr. Parry,1 by whom his views were substantially
adopted and brought before the public. A very remarkable series of
facts appeared to these observers to show conclusively that angina
pectoris was dependent in many, if not in most cases, on "ossification,"
or some other form of obstruction by disease, of the coronary arteries
of the heart. Subsequent researches have proved that this view
cannot be exclusively maintained, although according to Lussana 2 this
condition has been found present in twenty-one out of thirty-six fatal
cases. The statistics adduced by Sir John Forbes3 show that in
twenty-four out of forty-five cases examined after death there were
found diseases and degenerations of the aorta ; in sixteen cases the
coronary arteries were diseased, and in a like number the valves of
the heart ; while in ten cases there was positive disease, and in twelve
cases preternatural softness, of the heart itself. Many authors, from
Morgagni downwards, have recorded cases of thoracic aneurism
having in a more or less perfectly developed form the characteristic
symptoms of angina pectoris; and we have already alluded to M.
Trousseau as confirming by his large and carefully- watched experience
the view that such cases may very closely resemble, and may, in
fact, for a lengthened period, and after careful observation, be
indistinguishable from what he regards as the truly idiopathic

J 1 Op. cit. p. 3.

2 Gazzetta Med. Lombard. 1858-9 (ref. by Friedreich in Virchow's Handbuch, vol. ii.
! p. 422).

5 Cyclop, of Pract. Med. ; art. Angina Pectoris.

ANGINA PECTORIS AND SUDDEN DEATH. 545

forms of angina. The author of this article is able from personal
experience to say that no organic disease has appeared to him more
frequently to assume the symptomatic characters of angina than
aneurism ; and he is also prepared to state as the general result of
inquiries pursued over many years, and particularly directed to this
subject, that even small aneurisms, arising very near the heart, and
especially such as project into the pericardium, or compress in any
degree the base of the heart itself, are much more apt to give rise to
angina-like symptoms than much larger tumours in more remote
positions. The attention of the physician in cases of supposed angina
pectoris should therefore always be very minutely directed to the
state of the arterial system as a whole, and more especially to any
evidences that may exist of irregularities in the sounds or impulse of
the arteries near the heart, or of the aorta in its ascending portion.
The careful examination by percussion of the substernal region, and
especially of the upper sternum; the comparison of the sounds of the
heart with the arterial sounds, as heard at different points of this
region ; the detection of even slight traces of abnormal impulse, or
of evidences of arterial obstruction at the root of the neck ; the
comparison of the radial pulses, and the thorough investigation even
of remote parts of the arterial system, may lead to inferences favour-
able, or the contrary, to the idea of an organic cause for the symptoms
of angina pectoris.

Not less important, could it be obtained with reasonable precision,
would be the evidence, in any case of angina, of a permanently
weakened or disorganised state of the muscular fibre in the heart
itself. We have seen that in twelve of the forty-five dissections col-
lected by Sir John Forbes, there was found preternatural softness, and
in ten positive disease of the heart, apart from valvular lesions. That
many of these must have been cases of fatty degeneration of the ulti-
mate texture of the organ is rendered extremely probable, if not
absolutely certain, by the results of later inquiries,1 which show that
in a large proportion of cases of sudden death such changes in the
tissue of the heart have been revealed by the microscope. On the
other hand, it must be admitted that fatty heart has been often
observed to be present to a very great degree when no symptoms at
all resembling angina pectoris have been recorded during life, and
when death, too, has not been sudden, but has occurred in the course
of ordinary and sometimes of acute disease, having no apparent con-
nexion with the state of the heart. This subject will come under
consideration hereafter, but in the meantime it may be stated in
general terms that while a degenerated state of the cardiac muscular
fibre is with great probability to be inferred in angina pectoris, there
are few positive criteria which can be applied so as to ascertain the
fact of the degeneration, much less its pathological character, or the

i Dr. Quain has stated the argument with reference to the older observations of soft
flabby heart, with great force and conciseness in his paper on " Fatty Diseases of the
Heart ; " Medico. Cnir. Trans, vol. xzxiii p. 129.

546 A SYSTEM OF MEDICINE.

extent of fibre involved in any particular case. Only after careful
and repeated examination of the heart under various conditions of
activity and comparative repose, will a careful physician venture an
opinion as to the soundness of the organ in this respect, and even then
it will be prudent to express his opinion with some degree of reserve.
The practical inferences, moreover, which can be safely founded on
such an opinion, either in relation to prognosis or treatment, are far
from being clearly established.

Having as far as possible investigated the condition of the heart
and arteries, it will be the duty of the physician to complete his
diagnosis by a survey of the condition of the other organs and
functions. Although in many of the most extreme cases of angina
pectoris the lungs seem to be perfectly healthy, yet a certain amount
of pulmonary congestion or obstruction may attend the disease in par-
ticular cases, especially in those complicated with dilatation of the
heart, or with valvular disease. Such cases usually present more or
less alteration of the complexion in the direction of lividity, and are
also attended by cough, or by true dyspnoea. And it must not always
be concluded that the effect of a pulmonary or bronchial complication
is to give a more dangerous or hopeless character to the symptoms of
angina. On the contrary, the pulmonary disease being frequently of
a manageable kind, the application of the proper treatment will some-
times extricate the patient from a state of the greatest apparent danger,
and allow of the return of the heart to a state either apparently
normal, or nearly so. The author has a most vivid recollection of one
case in particular, where, on numerous occasions during five or six
years, he had to attend a patient manifestly suffering under complex
diseases of the heart and lungs, with distinct paroxysms of angina,
and physical signs of dilatation of the heart. In the worst attacks
there was always a nearly or absolutely complete disappearance of the
pulse at the wrist ; the complexion was livid, and the expectoration
was of the character usual in hemorrhagic condensation of the lungs,
which was also indicated by dull percussion at both bases ; yet from
this formidable state the patient again and again rallied under careful
treatment of the pulmonary disease, and although the state was
evidently one of hopeless character as regards the ultimate termination,
he was able in the intervals to pursue a rather laborious occupation.
In other instances, the symptoms of angina pectoris are associated
with enlargement or disease of the liver, and it is not easy to say
whether the hepatic disorder is of primary or of secondary origin ; but
here also the cautious use of remedies is often very effective in
removing the obstruction to the portal circulation, and thereby in
restoring the heart to a comparatively sound condition, in which the
threatening symptoms of angina may disappear.1 Renal disease forms

1 It occasionally happens that the very intense ami sickening pain of biliary calculus
presents a degree of resemblance to angina in its accessories ; and the author has even
observed cases in which the diagnosis remaiued doubtful until the yellow tinge of the
conjunctiva, appearing after an interval of hours, relieved the apprehensions of tin*

ANGINA PECTORIS AND SUDDEN DEATH. 547

a very serious and often unmanageable complication, attended by
most distressing sickness, or by violent dyspnoea or orthopncea, and
requiring great caution in the use of internal remedies, but perhaps
not altogether beyond the scope of treatment. Dyspeptic complica-
tions are usually of secondary importance, and cannot be said to
be characteristic. They are most frequently associated with gouty
angina.

Among constitutional states, gout is unquestionably the one which
is most frequently related to angina pectoris ; indeed, it would
scarcely be too much to say that a large proportion of the suddenly
fatal endings of gout in its irregular and atonic forms, more especially
in the forms popularly termed " gout in the stomach," or "gout in the
heart/' are of this character.1 No doubt the pathology of the states
indicated by these terms is very uncertain, and the terms themselves
vague and unsatisfactory to the last degree ; but enough remains after
every deduction to show — 1. That gouty persons, and especially those
who have had regular gout, degenerating after repeated attacks into
the irregular and atonic forms, are subject, in an unusual degree, to
the causes of sudden death ; 2. That not only is death in such persons
apt to be extremely sudden, but, further, the course of the disease is
apt to be disturbed by violent paroxysms of internal pain ; 3. That in
certain cases the pain has distinctively the character of angina, while
in other instances it seems to be associated with dyspeptic suffering,
and with disorders of the liver and kidneys — the latter, at least, dis-
tinctly represented by a special form of disorganisation which can be
discovered and recognised after death ; 4. That in gouty subjects the
heart and arteries are very prone to become disorganised, and that the
disorganisation is specially apt to assume the form which other obser-
vations show to give a predisposition to angina, viz., calcareous de-
generation of the aorta, especially of its commencement, and of the
coronary arteries ; 5. That cerebral disorders of various kinds in the
gouty have often a like origin in disease of the arteries of the brain.
From these various observations, which will be found amply supported
by the experience of physicians, and illustrated in the treatises of best
authority upon gout, it may be inferred that the so-called metastasis
of gout to the heart is the result of gradual degenerative changes
operating more or less throughout the organism, which, if not so dis-
tinctly related as has sometimes been supposed to the gouty par-
oxysm in its ordinary form, are at all events closely associated with
the causes of gout, and therefore form part of its history as a disease
of the constitution. So much may be fairly asserted here, without
involving us in this article in a discussion of the complicated

physician. The remarks in the text, of course, apply not to this condition of pseudo-
angina, but to the combination of true angina with hepatic congestion. But the
admission of the existence of such a combination is not to be taken as a confirmation
of the view of Brera, and of the elder Latham, that angina pectoris may be simply a
disorder of the liver and nothing more.

1 On this subject see Dr. Brinton's thoughtful dissertation on "Gout in the Stomach,"
in the second edition of his work on Diseases of the Stomach, p. 354, 1864.

648 • A SYSTEM OF MEDICINE.

questions of pathology and diagnosis, as well as of treatment, which
arise out of the general question of gouty metastasis.

As regards other constitutional states associated with, or tending to
produce, angina pectoris, nothing is known of sufficient importance
to find place here. But the careful physician will always endeavour
in each case to discover all the causes of deranged general health
which may be interfering with the normal state of the functions ; and
thus, with each new observation thoroughly and scientifically recorded,
the diagnosis of the disease, and with this many questions bearing on
its pathology and treatment, will probably be rescued from the
obscurity that at present surrounds the whole subject.

What has to be said here about the causes of angina has been to
a considerable extent anticipated in the preceding sketch of the
diagnosis. All the associated diseases may be regarded as causes
or on the other hand, and sometimes with greater probable truth, as
conjoined effects of one or more common causes. Thus, to take the
last-mentioned instance, gout may be more or less directly a cause
of the angina paroxysm ; or gout and angina pectoris, each of them
separately considered in relation to previously existing states of the
constitution, may have grown out of like proclivities in respect of
age, sex, inheritance, habits of life, &c. In following out this obscure
subject, there is great danger of running into over-refinements, which
may mislead, and at all events may not be supported by sound
practical observation. A few facts, however, remain to be stated as
to the predisposing causes.

In his classification of cases according to age, Sir John Forbes
found that only one-seventh of the cases recorded (12 out of 84)
were below the fiftieth year of age ; and in respect of sex, only
one-eleventh (8 out of 88) were in women. It is just possible,
indeed, that these apparent facts may be greatly biased by the
mode of collection of the instances.1 In a disease the symptoms
of which are so purely subjective, the deaths of men of eminence,
or men of a certain force and decision of character, leading to clear
and precise statements as to their symptoms and morbid history,
will culminate, as it were, in the minds of physicians, and will be
recorded prominently when others would pass unobserved, or at
least unrecorded ; and in this point of view it is worth while to
remark that the Registrar-General's returns, bearing on sudden
death, do not show anything approaching to this remarkable disparity

1 Sir John Forbes, in giving the numbers in the text, expressly states that it 'is
necessary to "make some allowance for circumstances connected with these recorded
cases, before they can be received as grounds for fixing the statistics of the disease, taken
without reference to its degree of severity." His iaca is that the "more severe cases,
particulaily such as depend on organic disease of the heart and great vessels/1 occur
chiefly in males ; the milder in females. " The very severe cases naturally attract more
attention, more particularly if they have been terminated by a sudden death, and
followed by a dissection; and these are the cases that are usually recorded and published."
Art. Angina Pectoris, Cyclop, of Medicine, vol. L p. 88.)

ANGINA PECTORIS AND SUDDEN DEATH. 549

of males and females, nor even the marked if not exclusive proclivity
of the advanced ages to this form of death. On the other hand, the
Kegistrar's returns no doubt include under the term " sudden death "
a great mass of utterly heterogeneous cases, some of which have no
natural alliance with the disease now under consideration ; and the
convictions of individual physicians of large experience tend more
or less in the direction of Sir John Forbes's averages.1 Another fact,
of importance if correct, and so far corroborated by Dr. Walshe, is
to be found in certain tables by Sir Gilbert Blane,2 showing the rarity
of Angina Pectoris in hospital practice. Both in hospital and private
practice, however, perfectly typical instances of the angina of Heberden
are rather rare ; and Sir G. Blane's figures, supported as they seem to
be by an appeal to so large a number of miscellaneous cases (3,835
hospital, 3,813 private), probably mean only that Sir G. Blane was
too busy to know much about the internal sensations of his hospital
patients, and knew only a little about a very few of his more distin-
guished private patients. Medical statistics are altogether perverted
from their legitimate use when statements of this kind are put
forward without qualification, as if numerically exact. It is certain
that conditions at least closely allied to angina pectoris are not very
rare in hospital practice, and the author of this article has seen
enough even of typical instances in hospitals to neutralise the force
of Sir G. Blane's remark. Still, it may be conceded as at least
probable, that in the higher ranks of society cases of extremely
sudden death, associated with the symptoms described by Heberden,
and not of aneurismal origin, or connected with valvular disease
of the heart, bear numerically a higher proportion to the whole field
of disease than among the classes usually treated in hospital. The
subject, however, is one still open to investigation, and one on which
a really adequate contribution of carefully and impartially observed
facts would be of great advantage to science. The facts above
recorded, so far as they may be trusted in leading towards a con-
clusion, tend to support the theory of the gouty origin of true angina
pectoris. It cannot fail to be remarked that the disease seems to
be dominated by the same proclivities of age, sex, and condition in
life as gout. And there is further a very general impression among
physicians and among the public, not supported by exact statistical
evidence, but not on that account to be disregarded, that sudflen
death from heart disease is frequently hereditary, or at least is found
to cling as a tolerably well-marked characteristic to certain families,
sometimes for several generations. On the other hand, it should be
stated, in qualification of this impression, that there are numerous
instances of eminently gouty families in which no such tendency
has been observed.

1 Among authorities of the first class, Trousseau is almost singular in disputing this
position. "I do not think it proved," he says, "that males are more subject than
females to this singular affection." Op. cit, Eug. Transl. p. 603.

a Med. Chir. Trans, iv. 133.

550 A SYSTEM OF MEDICINE.

The general result of the inquiry into predisposing causes has
been stated by Sir John Forbes in terms which may well receive the
assent of physicians, at least as a provisional conclusion, till further
and more exact analysis of the facts becomes possible. " Like many
other diseases," he writes, " angina is the attendant rather of ease tod
luxury than of temperance; on which account, though occurring
among the poor, it is more frequently met with among the rich, or
in persons of easy circumstances." l To this it must be added, that
the influence of sedentary occupations is remarkably apparent in
Dr. Quain's collection of cases of fatty heart, in many of which the
death was sudden, and with symptoms more or less allied to angina.
Thus, in twenty-four of the cases in Dr. Quain's memoir,2 in which
the habits of life were noted, they were found to be " sedentary " in
twenty-two, "active" only in two cases; and in several cases the
sedentary habits were obviously determined by injuries which had
restricted the power of exercise, or by accumulations of external fat
amounting to excessive corpulency. In some cases also, the disease
itself has produced an aggravation of the tendency, by still further
limiting the capacity for physical exertion, and thus allowing of
fatty accumulation. Thus, in the well-known case of John Hunter,
who certainly was not chargeable with any original sins of lazi-
ness, and who died of angina, it is recorded that after the tendency
had been clearly declared, "the want of exercise made him grow
unusually fat."

Thus far we have treated of Angina Pectoris as a distinct morbid
form or group of phenomena, in which disorders of the circulation
tending to sudden death are associated with local pain and other
symptoms in the chest of a more or less definable character. But it
must be added that many cases of sudden death, in which there is
reason to attribute the ultimate result to disease of the heart, have
occurred apparently without pain, sometimes without any, even the
slightest, previous evidence of cardiac uneasiness, and certainly
without any of the more characteristic and special symptoms of
angina pectoris. It remains to consider these cases before proceeding
to discuss the pathology of the whole subject.

Dr. Latham has justly remarked, in reference to the present
subject, that " cases of sudden death often present themselves as
mere fragments to our observation. Individuals are found dead.
The mode of their dissolution and the circumstances preceding it
are unknown." It can only be inferred remotely, as it were, and that
only in some instances, from some casual and often very imperfect
observation, that in these individuals the symptoms might possibly
have been shown, had they been fully ascertained, to " hold a patho-
logical kindred " with angina pectoris.

1 Loc. cit., vol. i. p. 83.

2 Med. Chir. Trans., vol. xxxiii. p. 194.

ANGINA PECTORIS AND SUDDEN DEATH. 551

But again : cases not infrequently occur in which the symptoms
observed during life resemble angina pectoris, but where certain of
the characters attributed to that disease are either, entirely wanting
or imperfectly developed. It may be the pain that is wanting to
the completion of the picture ; it may be the sense of impending
death, or it may be that sudden death does not actually occur, although
most of the other symptoms of angina are present. Can we, with
any degree of security, bring out of these nosological " fragments "
such new combinations as may tend still further to throw light
on the pathology of angina ?

In this difficult inquiry, in which we are reduced to the study of
" broken lights " and " fragments " of truth, we feel more strongly than
ever the inadequacy of language, as between man and man, in treating
of the mysteries of life. We are engaged upon what ought to be a
strictly inductive clinical investigation ; but the very elements of the
induction are in great part withheld. Many patients, when threatened
with death, refuse to speak about it, and remain, up to the very last,
silent as to what is passing within. Many other patients throw out
hints and indications, but are either unable or unwilling to enter into
a detailed analysis of their sensations. A few describe their sensations
with great minuteness, but in terms which are almost sure to mislead.

From these various causes it happens that sudden death may appear
to occur absolutely without previous warning, or with very imperfect
previous warning, and yet there may have been in reality a very
decidedly abnormal state, fully present to the consciousness of the
patient, but not spoken out by him ; either because the symptoms were
unspeakable, or because from one cause or other he was indisposed to
speak. On the other hand, sudden death may not occur, and yet
a patient may have lived days, or months, or even years, in the
apprehension of sudden death, being warned by such internal sensa-
tions as have been described in reference to the paroxysm of angina.
When, indeed, pain is the culminating symptom, the patient rarely
omits, or refuses to speak out; he is then sufficiently explicit as
regards the pain, but in many cases he leaves the other and less
definable sensations to be inferred. But where pain is not the cul-
minating symptom, we are often reduced to inference altogether ; and
it is only in the case of persons whose outward lives and inner
thoughts are much before the public, that an inferential diagnosis can
be arrived at. Two cases of tliis kind, occurring in different ages of
the world, and under very different circumstances, appear to afford in
some degree the means of access to some of the information we are
in quest of. One of these is the case of the Eoman philosopher
Seneca; the other that of the Christian divine Dr. Chalmers. The
former case has been often referred to (though with some hesitation,
the source of which will be immediately apparent) as one of angina
pectoris ; the latter has been recorded expressly as a case of sudden
death from fatty heart.

The case of the philosopher Seneca was as follows : —

552 A SYSTEM OF MEDICINE.

In early life he was apparently of delicate constitution. It is
recorded of him by Dio, that but for the apparent probability of his
early death spontaneously, Caligula would have bad him destroyed.
The supposed disease at this time was a tabes. He himself records
that he was nursed with difficulty through a long illness by his aunt
(Consolatio ad Helviam, 16). He further speaks in one of his epistles
of having been extremely subject to catarrhal fluxes (destillationes), and
in another he §ays that almost every form of bodily disturbance had
affected him at one time or other.1 It seems, therefore, extremely
probable that Seneca was one of those martyrs to tubercular disease
in early life, who, after a more or less protracted period of ill-health
became somewhat more robust in constitution towards the middle
term of life. He was, however, to the last more or less delicate, and
at the time of his violent death at the instigation of Nero, he is said
by Tacitus to have been " emaciated in body from scanty nourish-
ment."2 The peculiar symptoms, however, which have specially
attracted the attention of writers as indicating angina pectoris, seem
to have been confined to the last two years of his life, according to the
opinion of Lipsius, who considers the epistles to Lucilius as having
been written when he was sixty-one or sixty-two years of age. What
gives a peculiar interest to the description, and at the same time may
possibly make necessary a qualification of some of its expressions, is
the somewhat affected and pretentious tone in which in these letters
Seneca, a disciple of the Stoic philosophy, congratulates himself on
the ease and freedom with which he could look death in the face, and
maintain under severe illness, and in the prospect of sudden death,
the calm, self-possessed, and cheerful spirit of the sage. His philo-
sophy, under these circumstances, has in its details no important
relation to the present inquiry ; but the fact that his mental condition
was such as is here described is important.

After a long truce from suffering, he says,3 his bad health has
returned upon him suddenly. He is as if given over to one disease,
as regards which he adds : " I know not why I should give it a Greek
name, for it may fitly enough be called Suspirium — a sighing, or want
of breath." The attack is very brief and like a hurricane — it is over
almost within an hour. As compared with any other disease it is like
the difference between being sick merely, and giving up the ghost — so
that the physicians themselves call this disease meditatio mortis; and
sometimes death, which is always threatening in it, actually occurs.
Knowing these things Seneca adds that he is by no means confident
of recovery, even when relieved from severe symptoms. He con-
siders only that he has got a respite ; he is perfectly prepared for

1 Omnia corporis aut incommoda aut pericula per me transierunt. Epist. ad. Lucilium,

54.

* The scanty nourishment here spoken of was not starvation, but probably deficient
power of assimilation ; for Seneca, as is well known, was enormously rich, and there is
no reason whatever to suppose that his stoicism ever took the form of asceticism, or of
voluntary fasting such as to injure bodily health.

3 Epist. ad Lucilium, 54.

ANGINA PECTORIS AND SUDDEN DEATH. 553

death ; he does not at any time count even upon seeing out the day.
He is, however, buoyant and cheerful, entertains himself with glad-
some and strong thoughts, even in the midst of the stifling (in ipsa
suffocations). Death is, after all, not to be dreaded by the wise man;
death may take him unawares, but he is nevertheless always ready to
go. Even at the best, he adds, reverting to his own precarious condition,
his state is not one of entire comfort ; the breathing1 is not quite natural;
he feels always a degree of impediment (hasitationem quandam ejus et
moram). " Be that as it may be," he adds, " provided my sighing is not
in sad earnest" (dummodo nisi ex aniino suspirem). He holds him-
self as in the condition of one likely to be soon ejected, but yet not to be
ejected, inasmuch as he is willing to go. c Nihil invitus facit sapiens;
neccssitatcm effugit quia vult qv-od ipsa coactura est.' 2

In this case of Seneca we have, in a highly developed form, the
sense of impending death, associated wth something which he himself
calls a " suffocation," occurring in paroxysms, and causing daily and
hourly uncertainty as to his tenure of life. But we have not the
severe and peculiar pain of the angina of Heberden, nor have we the
actual fact of sudden death, at least in the usual sense of the word ;
for, as is well known, Seneca was put to death by Nero, or rather was
invited to put himself to death ; and what we are able to gather from
contemporary history as to his last moments would lead us to infer
that death came by no means easily, but after a rather long and tedious
struggle. Much doubt has been expressed accordingly, since this
narrative was suggested to Dr. Parry by "a learned physician " as
a case of angina pectoris, whether the symptoms will bear that con-
struction. Dr. Parry himself inclines to consider it " rather a disorder
of respiration than angina pectoris."3 Sir John Forbes, on the other
hand, says that " the case of Seneca, as described by himself, has been
generally considered a case of angina, and we think most justly." * It

1 u Non ex naturfl. fluit spiritus." The double sense of 8piritn* in Latin, as of the
Oreek tvcu/xo, must be kept in view in interpreting this expression.
8 Loc. cit. Compare also Epist. 01.

3 Op. cit. p. 36.

4 Loc. cit. p. 81. The opinion of Dr. Stokes, published in 1854, and founded mainly
on the character of the respiration as implied in the word " suspiriuni, " (which, as we
shall hereafter see, ho had himself occasion to describe as characteristic of fatty degenera-
tion of the heart) is too important for its details to be omitted here. We therefore giro
it entire, as it occurs in " The Diseases of the Heart and Aorta," p. 530. "We must agree
with Dr. Parry in the opinion that the symptoms here detailed are not those of angina
pectoris. It is remarkable that the occurrence of pain is not alluded to. But their
similarity to that abnormal respiration, already described as the attendant on the fatty
heart, is too obvious to be overlooked. For in this affection we sec that special form of
dyspnoea which may be described as a paroxysm of sighing. Seneca's words, 'Satis enim
apte dici suspiriuni potest,' and again ' Brcvis autem value, et procellte similis, impetus
est," are singularly expressive of a severe case of the cardiac signing observed in persons
labouring under fatty heart, for which, when the highest point of suspirions breathing has
l>een reached, we can have no better comparison than that of a storm. And the words
' Deinde paullatim suspiriuni iUudquod esse jamanhelitus croperat, intervalla majora fecit
et rttardatum est et remansit,' well expresses the gradual ascent from what we may term
the apnoeal period to the extreme point of the paroxysm, and its subsequent decline." It is
important to observe, that Dr. Stokes, in the chapter on Deranged Action of the Heart,
expresses himself as follows with regard to angina pectoris in general : — " The respiratory

VOL. IV. 0 0

554 A SYSTEM OF MEDICINE.

is evident that materials fail us in attempting to decide the question ;
and they fail precisely at the very point where materials always must
fail, unless the fact of actual death, and of sudden death with
symptoms and signs referrible to the heart, comes in to decide the
point in favour of angina. True, the absence of recorded pain on the
one hand, and the presence of something like a record of dyspncea on
the other, have been regarded as additional circumstances in favour of
the view that Seneca's disease was spasmodic asthma. But in spas-
modic asthma, however severe, there is rarely that vividly present
sense of impending death so much dwelt upon by Seneca. Moreover,
the noisy paroxysms of asthma would probably have provoked some
more distinct allusion to the wheezing as a feature of the attack.
Having regard to the idiom of the Latin language, indeed, the question
as between some form of cardiac suffering and asthmatic dyspncea
must remain doubtful ; but while the allusions to the breathing are of
a very indefinite character, it must be remarked that the sense of
impending death is the one obvious fact in the description.1

f Turning now to the case of Dr. Chalmers, we find in almost every
point the converse of that of Seneca. We have here the awful fact
of sudden death in all its solemnity and mystery — not only without
any adequate clinical history of chronic disease, but without any
evidence of angina, or any other form of acute attack preceding the
fatal event. And what adds to the mysteriousness of the result is,
that the death took place, not amid any exciting crisis of passion, or
of physical exertion, but in the darkness and stillness of the night,
when body and mind alike had been undisturbed for hours. One
indeed, who knew him,2 has said of his conversation and manner the
evening before his death : — " I had seen him frequently in his most
happy moods, but I never saw him happier.,, But this is not all.
The narrative of Dr. Chalmers's death, and of the last weeks of his
life, has reached us from two particularly well-informed sources. Dr.
Hanna, who was his son-in-law and perhaps his most intimate friend,

phenomenon which belongs to angina is some form of tho sighing respiration so im-
portant a symptom in the fatty or weakened heart. . . . Upon the whole we may
■conclude that the special group of symptoms described as angina pectoris by Hebcrdeii,
Parry, Percival, and Latham, is but the occurrence, in a defined manner, of some of the
symptoms connected with a weakened heart." Op. cit.t p. 487. These remarks of one
of the greatest masters of modern medical observation will be found to have a very
special importance in connection with what we have ventured to call, in a subsequent
paragraph, Angina sine Dolorc.

1 Seneca particularly notes that the physicians called his disease meditatio mortis ;
a very unlikely and unusual form of medical expression for a disease so well-known
as ordinary spasmodic asthma. On the other hand it must be admitted that sits*
pirium was sometimes used as synonymous with asthma. Compare Cael. Aurel.
Morb. Chronic. L. iii. 1 ; and Plin. Nat. Hist, xxiii. 7, 63, § 121. Celsus makes use of
difficult™ spirandi, and spiritus difficultas, but not of suspirium. The noise of
the breathing is specially noticed by Celsus— "snirare aeger sine sono et anhelatione
nonpossit" (L. iv. 8); and also by Cael. Aurel. "stridor, atque sibilatio pectoris."
Loc. cit.

9 The Rev. Mr. Gemmel who was living in his house at the time. See Hanna's Life
of Chalmers, edition of 1854, vol. ii. p. 775.

ANGINA PECTORIS AND SUDDEN DEATH. 555

Las given us the facts as known to his domestic circle. Dr. Begbie,
who was his medical attendant, has recorded them with special refer-
ence to the observation, made after death, that the heart was in an
advanced state of fatty degeneration, soft and friable, the muscular
fasciculi barely traceable, without visible striae, and everywhere con-
taining fatty granules ; the ventricles unusually thin, the " coronary
artery loaded with calcareous deposit, much contracted, and in one
place obliterated, presenting considerable resistance to the knife."1
It is in the presence of these pathological data (given on the authority
of Dr. Bennett) that we have to explain, if we can, the known facts
of Dr. Chalmers's later life, and of its sudden and mysterious close.
And the peculiar interest and value of the case in relation to our
present inquiry consists in the following statements, which are
carefully condensed from the two narratives above referred to.

Dr. Chalmers was a man not only of great genius and devotion,
but of the most incessant and absorbing occupations. During a life
•extending nearly to the term of " threescore years and ten," he was
scarcely ever withdrawn from public observation. He was eminently,
in the highest and best sense, aval; avhp&v — a leader and ruler of men ;
the " care of all the churches " was upon him, as on St. Paul, and the
earnest and ceaseless labours of a life devoted to noble ends, were
•continued up to the very day before his death, in 1847, in his sixty-
eighth year. In 1834, it is true, on the 23rd of January, he had
suffered a rather alarming attack of hemiplegia, from wThich, however,
he soon recovered ; and in June of the same year there was again a
threatening ; but with these exceptions his health appeared to have
been always good, and equal to every ordinary exertion whether of
mind or body. " He was hardly ever incapacitated by infirmity or
loss of health, from prosecuting his enterprise; and from early
manhood to green old age, even up to his latest hour, he toiled, and
spent his energies and strength." Probably no man in Scotland in
the present century, with the doubtful exception of Sir Walter Scott,
had led a life of such persistent literary activity, combined with so
much and so various intercourse with men of -all ranks in society.
In his later years he retired more than previously from public
business, but, as Dr. Begbie writes, " he was firm and robust. With
accumulating years came a disposition to obesity; and with the
silver-grey on the massive forehead came also the pallid and somewhat
sickly look of fading health. Yet he seldom complained ; or, if indis-
posed, it was only by some trivial ailment arising from indigestion.
He was sometimes sick at stomach, but he was never faint, nor ever
swooned away. ... He had no precordial pain, or distress in breath-
ing; no palpitation of the heart, or intermission of the pulse. He
ascended heights with wonderful facility ; he slept on either side, and

1 Edinburgh Monthly Journal of Medical Science, vol. xii. 1851, p. 205. There
were also traces of very chronic disease of the membranes of the brain, but probably
not of such amount and character as to have much clinical importance as regards the
.fatal event

oo 2

556 A SYSTEM OF MEDICINE.

his rest was calm and refreshing." Such was his state apparently,
according to his physician, up to a period indefinitely near the fatal
close.

It so happens that of the last month of Dr. Chalmers's life we have
very exact records, including many memoranda, letters, &c, from his
own hand. It was a month fraught with unusual excitement and
exertion for a man in his sixty-eighth year. On Thursday the 6th
of May, 1847, he set out for London to attend a committee of the
House of Commons on a subject in which he was very deeply
interested. He preached * in Marylebone Church on the 9th, and on
the 12th submitted to a long, searching, and fatiguing examination,
wherein Sir James Graham tried to " heckle " him (as lie expresses it)
for an hour together ; but, he writes at the close of a lengthened
description of the day's proceedings, " we concluded in a state of great
exhaustion, but with an erect demeanour and visage unabashed."
Such was his own humorous account of an event which obviously
gave him much anxiety. In London, also, he made many visits and
saw many sights, not sparing himself at all, or complaining in any
way. On the 15th he went to Brighton, where he preached on the
16th, returning to London on Monday. On Tuesday he went to
Oxford, seeing the sights of the place and then going on to Bristol ;
the remainder of the week he spent there in excursions with great
enjoyment, and among friends. He preached on Sunday at Bristol,
and on Tuesday the 25th was at Darlington. In this interval he
wrote a long and carefully considered note on the Education Question
for Mr. Fox-Maule ; and took a most affectionate leave of his sister,
Mrs. Morton, with many effusions of pious feeling, but apparently
without any despondency or personal misgiving as to the future ; on
Friday the 28th he returned home, as Dr. Hanna records, " bearing
no peculiar marks of fatigue or exhaustion."

The next day (Saturday) was fully occupied in preparing a Report

for the General Assembly, which he was to read on the following

, Monday. On Sunday morning (30th of May) he did not rise to

1 It may be worth while to remark here that preaching, with Dr. Chalmers, was some-
thing very different from the mere delivery of written words in an audible tone of voice.
It was, in truth, a work into which he threw all his great energy of mind and body, and
in its effect fully justified the remark of the old Scotchwoman who found it necessary to
apologise for her favourite preacher reading his sermon, "Ay, but its fdl reading
iSum. " That Dr. Chalmers preached on every Sunday during this excursion is therefore
a noteworthy fact, and the more so as he appears at this time to have been little in tin-
habit of preaching when at home. — In a more recent case, where death from heart disease
was not sudden, but on the contrary very lingering, and where the very earliest symp-
toms, twenty-seven years before, had been such as to give warning of an impending
danger, preaching had to be abandoned almost from the first ; and although afterwards
resumed, it became, in a second attack of ill health, the first duty that had to give way,
from its manifest tendency to overstrain the weakened organ. (See the Autobiography arnl
Memoir of the Rev. Dr. Guthrie, recently published; especially vol. ii. pp. 201-41, 215,
16, 18, 406-11.) It is to be observed that a very active use of the pen, and a great deal
of work and enjoyment of life, continued possible to Dr. Guthrie for eight or nine years
after the formal closure of his career as a preacher. He died in 1873, in his seventieth-
year.

ANGINA PECTORIS AND SUDDEN DEATH. 557

breakfast, but, in answer to inquiries, said — "I do not by any means
feel unwell ; I only require a little rest." He conversed " with the
greatest clearness and vigour;" attended church, and walked some
distance afterwards with a friend on his way homewards ; spent the
evening in apparent good health and spirits, and among other occupa-
tions wrote to his sister at Bristol a hopeful and affectionate letter,
expressive of perfect contentment and satisfaction. He retired to rest
at the usual time, and next morning was discovered dead and cold.

The separate accounts given by Dr. Hanna and Dr. Begbie leave no
doubt that death took place long before the morning light, but at what
exact period it was impossible to say. The body had an attitude of
calm repose. " The bed-clothes were scarcely disordered ; on them
rested a basin which had received the contents of the stomach."1
This was the only evidence of anything like a death-struggle. Had
it not been for this, it might have been supposed that Dr. Chalmers
died in his sleep.

Cases like that of Dr. Chalmers (in respect to the suddenness of the
fatal close) have often been recorded ; but in very few of those in
which the fatal result has been most sudden and startling have there
been any such records of the incidents preceding death as are given
above. In not a few of the cases observed personally by, or more or less
intimately known to, the author of this article, there has l>een reason
to believe that considerable suffering, or sense of disability, though
not always of one and the same character, has been present; and in
some of these it might easily, perhaps, have escaped attention had the
individual been extremely reticent, or not surrounded by anxious
friends, intent upon everything that appeared to affect the comfort of
one dear to them, or the well-being of a family. In several instances,
the first note of real alarm has been sounded on the discovery of an
irregularity in the pulse ; in one such case, sudden death took place
within a fortnight, or at most three weeks, after this discovery.2 In
other cases there has been an indefinite distress felt on exertion, or on
going up a hill ; in a few, the more regular form of angina pectoris.
One patient, who had more or less of angina-like pain and (so-
called) breathlessness on exertion for at least some years, died at
the last in bed, in the night, and at the side of his wife, who was not
even awrakened, or in any way made aware of his being at all uneasy,
but found her husband motionless and half-cold, probably some hours
after the event.8 It therefore becomes exceedingly probable that the

1 Monthly Journal, ubi supra, p. 205.

8 Iu the case of Dr. Guthrie, above mentioned, a similar irregularity, with symp-
toms not very dissimilar in other respects, appeared to threaten sudden death in 1846,
while death did not actually take place till 1873.

3 This case was recorded with additional details, in Gout : Its History, Causes, and
Cure, by William Gairdner (first edit. 1849, pp. 88 — 42), as a case of fatty degeneration
of the heart, liver, and kidneys. The narrative there given of the symptoms is by my
father, but I have a most distinct personal recollection, even at this distance of time, of
all the essential facts, which both from intimate friendship, and from early professional
studies, had more than usual interest for one who was just then engaged for the first time

558 A SYSTEM OF MEDICINE.

actual death was either painless, or at least that the duration of the
suffering was so brief, as not to have given an opportunity for any
expression of it. Thus a person may have been affected with angina
pectoris once or oftener, and he may die suddenly, and yet it may not
be at all clear that he has died in a paroxysm of angina. On the
other hand, symptoms of a different order from the genuine, painful,
angina pectoris, may become associated with angina-like paroxysms at
a subsequent period; and yet, even then, the death may not be
strictly sudden (in the sense above described), or even unexpected as
to its occurrence, but rather the gradual culmination of days or weeks
of sleepless agony. It is notorious among physicians that in valvular
diseases of the heart, and even in aneurisms, in which the popular
impression, derived from a few startling instances, is to the effect
that sudden death is always to be expected, this mode of termina-
tion is in fact exceptional. One or two cases, widely reported, and
taking possession of the imagination by their peculiar and mysterious
close, become the types of a whole series, in which the incidents are
only slightly or not at all removed from the ordinary course of fatal
disease, as to the fact of the end being to a certain extent expected
and foreseen. But even here we are beset by anomalies of experience
arising from the extreme difficulty of realising facts depending so
much upon subjective impressions. For example, a young man in-
timately known to the author of this article went to Edinburgh many
years ago to study medicine, it being known to himself and some
of his friends that there was some internal flaw or weakness, in regard
to the precise nature of which he always maintained a strict reserve.
It was reputed (as in the case of Seneca) to be more or less of the
character of " asthma ; " but no regular asthmatic paroxysm was ever
brought under notice. This young man pursued all his medical
studies and took his degree without apparent difficulty; living in
the main carefully, but often visiting the hospital at night and doing
all the miscellaneous work of a hardworking student. He afterwards
went to the Crimea and served through the whole campaign, up to
the taking of the Eedan fort, as an assistant-surgeon attached to a regi-
ment ; his letters at this time giving most minute descriptions of all
his personal impressions of the scenes and great events around him,
but being almost entirely silent as to his own physical sensations, if
he had any, of chronic disease. He was afterwards affected with
some of the current diseases of the service, and had also an attack
of rheumatic fever, after which he was sent home, but continued with
his regiment on its return, and finally died at Chichester in a time
apparently of profound tranquillity, and with such startling suddenness
that he had barely time to use some of the most familiar remedies

in minute pathological research ; especially as occurring only a few months after the
death of Dr. Chalmers. The patient became subject to the first symptoms of car-
diac disease in 1841 ; had a smart attack of regular gout in 1846, followed by giddiness
and cardiac pains, which were rarely altogether absent afterwards. He died suddenly,,
as described, in September 1847, in the 63rd year of his age. — "W. T. G.

ANGINA PECTORIS AND SUDDEN DEATH. 559

and common external appliances before he was called away, his fellow-
officers having had no previous note of warning whatever. A subse-
quent inquiry led to the discovery that the local applications which
he had himself directed in the moment preceding his death were
precisely those which he had learned in the Edinburgh Eoyal Infir-
mary to apply in several cases of angina pectoris, in the study of
which he had interested himself. He had also, it appeared, confided
to his mother the idea that he might possibly die suddenly, owing
to some imperfection of which he was sensible at the heart He died
in his twenty-seventh year. The pericardium was found to be firmly
adherent, and the heart rather small, its muscular fibres pale, and
apparently altered in texture. In this instance it would seem pro-
bable that symptoms of an appreciable, but still of a tolerable kind,
may have existed for many years, unreported, undescribed, and
perhaps not even distinctly-realised by the patient himself, though he
was one carefully instructed in all that relates to this subject, and
known to have taken a special interest in it from the point of view of
medical observation.1

The cases adverted to above have been, with one or two exceptions,
cases of sudden death in which the symptomatic history of the facts
leading up to the fatal result is either imperfect, or altogether
mysterious ; and in which also the picture of angina pectoris as drawn
by neberden fails at some point or other to apply to the facts. But
in cases of true angina of the most typical kind, and especially ia
those associated with a distinct organic lesion, such as calcification or
other disease of the coronary arteries or fibre of the heart, it might
easily be argued that the fact of a sudden, as opposed to a more
ordinary mode of death, is not less mysterious than in any of those
cases in which it has been preceded by no such typical symptoms.
For, after all, what we know in cases of true Angina is simply the fact
that pain of a certain order and of a certain degree of severity often
brings death in its train; how the death occurs, and what precise
conjunction of phenomena or pathological causes determines its
occurrence at a particular moment, we know as little apparently in
the painful as in the comparatively painless cases. It is plainly out
of the question to suppose that a chronic, and in its very nature

1 For additional details see the Edinburgh Medical Journal, vol. v. 1859, p. 95.
Heberden's remarks in his first paper (1768) as to the association of angina with sudden
death are important. He had at tnat time seen about twenty cases (four years later he
notes fifty, and in his Commentaries about a hundred cases) ; of the twenty cases first observed
he had knovm six to have died suddenly ; and perhaps more may have so perished, with-
out the fact being known. " But," he argues, " though the natural tendency be to kill
suddenly, yet some of those afflicted may die in anotner manner" (unless such persons
could be considered as exempt from all the other diseases proper to advancing age) " since
this disorder wiU last, as I have known it more than once, near twenty years. ' Heber-
den had first become aware of the tendency to sudden death in angina, on mentioning
the peculiar symptoms to a physician of great experience, who had told him that most
of these cases had in his cxDcrience been suddenly fatal. The careful manner in which
Heberden's own experience had been matured (so to speak) for publication appears very
clearly in these incidental remarks.

560 A SYSTEM OF MEDICINE.

gradually advancing lesion, like fatty degeneration or disease of the
coronary vessels is the direct and immediate determining cause of
a death which occurs in a moment, or of spasmodic seizures which
come on in the midst of comparative health, and pass away in many
instances in a few minutes, or at most in an hour or two, leaving the
patient with a quiet pulse, free from serious complaint, and (apart
from certain forms of exertion) able for many of the ordinary duties
of life. The cardiac fibre which carried Dr. Chalmers safely over the
last three weeks of his life, with its harassing duties and active exer-
tions in various places, cannot be reasonably supposed to have become
suddenly so much more diseased (physically speaking) that it. must
needs be disabled to the extent of ceasing to act altogether, in the
absolute quiet of an undisturbed night, after a day peacefully and
happily spent in his own home, and an evening closed in a state of
radiant satisfaction and joy, without any apparent trace of morbid
misgivings. A like argument would probably apply to many or most
of Dr. Heberden's cases of angina pectoris ; to all cases, indeed, in
which the element of spasm (so-called) is a prominent feature ; and in
the elaborate argument, so well rendered and modernised by Dr.
Latham, in which Heberden vindicates for his "dolor pectoris" a
place among the spasms, as opposed to inflammation or organic disease,
we are only seeking, with him, for a mode of reasoned description or
of generalisation for facts which are confessedly mysterious. The
whole of the argument that has been raised since Heberden's time as
to whether death in these cases is caused by spasm or by paralysis of
the heart, and the small amount of actual information or real science
which has emerged from the somewhat fruitless controversy, shows
strongly how much we may deceive ourselves with the idea that in
describing a mere association of symptoms with certain pathological
lesions, we have fully explained the nature of the connection of the
one group of facts with the other. From this point of view one more
instance of sudden death, with all its preceding life-history, may be
regarded as having a sufficient interest for us to be cited here with
some detail.

The great comparative anatomist and profound physiologist John
Hunter died, as is well known, with startling suddenness in the year
1793 ; and from all that has been transmitted to us of the circum-
stances of his fatal illness, and of the symptoms from which he
suffered for twenty years before his death, it is evident that the
opinion of one, at least, of his most intimate and confidential friends,
as well as probably the secret convictions, in the end, of the dis-
tinguished sufferer liimself, pointed in the direction of the angina
pectoris of Heberden as the true nosological interpretation of his
morbid state. The detailed posthumous narrative of the symptoms,
coming as it does, almost from the very lips of Hunter,1 and charac-

1 "Each symptom," writes Sir Everard Home, "was described at the time it
occurred, and either noted by himself, or dictated to me when Mr. Hunter was too ill to

ANGINA PECTORIS AND SUDDEN DEATH. 561

terised by all his restless activity of mind in the search after truth,
forms unquestionably one of the most instructive chapters in the whole
history of medicine. There is hardly a sentence in this wonderful
narrative which will not repay the careful study of the physician ; and
although the substance of the whole is here faithfully preserved, the
need for condensation will compel the sacrifice of many of the vivid
touches which reveal the mind of genius intent, even amidst physical
suffering, upon the mysteries of its own being.

How far these descriptive touches had been reasoned out into clear
conceptions in the mind of Hunter himself does not appear from the
narrative ; it is certain, however, that his most intimate and congenial
friend, Edward Jenner, postponed for many years the publication of
certain highly original observations on angina pectoris (afterwards
adopted and in part published by Dr. Parry), from the fear of compro-
mising the feelings of John Hunter by a too obvious reference to his
case.1 Tt is well established, also, that the case, did, in fact, fulfil the
anticipations of Jenner, both as to the fatal event, &nd as to the ap-
pearances observed after death. It has rarely happened, surely, that
two minds so keenly alive to theoretic truth, and yet so observant of
detail, have been applied to any, even the most indifferent obscure
case in medicine ; for in this instance it is the author of the " Treatise

write ... As the statement is made up fiom detached notes which were not written
with a view to publication, it will appear in point of language extremely deficient ; it
was thought, however, best to leave it in its present form, lest by altering the language
the effect of some of the expressions might bo diminished, or misunderstood." — Life of
Hunter, prefixed to the Treatise on Inflammation, 1794, p. xlv.

1 The circumstances, as delivered in writing by Jenner to Dr. Parry, are curious, and
specially interesting as bearing on the early symptoms in John Hunter's case. "The
first case I ever saw," writes Jenner, "of angina pectoris was that in the year 1772,
published by Dr. Heberden, with Mr. Hunter's dissection. There, I can almost positively
sav, the coronary arteries were not examined. Another case of a Mr. Carter, at Dursley,
fell under my care" (date not given); but in this case "the coronary arteries were
become bony canals." " Soon afterwards Mr. Paytherus met with a case" . . . "At this
very time, my valued friend Mr. John Hunter began to have the symptoms of angina
pectoris too strongly marked upon him ; and this circumstance prevented any pubU-
cution of my ideas upon the subject, as it must have brought on an unpleasant conference
between Mr. Hunter and me. I mentioned both to Mr. Cline and Mr. Home my notions
of the matter ; but they did not seem to think much of them. When however Mr. Hunter
died, Mr. Home very candidly wrote to me, immediately after the dissection, to tell me
I was right." In 1778, Jenner wrote a distinct statement of his fears about Hunter's
case, and of his views on the pathology of angina pectoris, intending it as a commu-
nication in private to Dr. Heberden ; but, probably from the fear that it might lead to
publication, the letter never was sent (See Life of Edward Jenner, by Dr. Baron,
vol. i. p. 39). It is, moreover, certain that Hunter, in a fatal case recorded by Dr.
Fothergill ("Medical Observations and Inquiries," vol. v. p. 254), had actually observed
disease of the coronary arteries in connection with sudden death from angina pectoris as
early as March, 1775 ; so that the presumption is exceedingly strong that Hunter not only
was intimately acquainted with Jeuner's views on the subject, but also had in part sug-
gested them. There is thus a chain of evidence of no ordinary consistency tending to
show that Hunter, who never formally identified his own symptoms with those of the
angina pectoris of Heberden, was nevertheless cognisant of their real nature and probable
termination, at least as early as Jenner's suspicions took origin, which, as we shall after-
wards see reason to believe, was in 1777. The death of Hunter, in 1798, was in fact
almost an exact reproduction of the very circumstances of FothergilPs case, viz. "in a
sudden and violent transport of anger ; and the appearances on dissection were also
strikingly similar.

562 A SYSTEM OF MEDICINE.

on the Blood, Inflammation/' &c, who is both sufferer and narrator,
while it is the clear-sighted and eminently truth-loving discoverer
of vaccination who forms and announces to us the diagnosis.

John Hunter " was a very healthy man for the first forty years of
Ms life, if we except an inflammation of his lungs in the year 1759.
In the spring of 1769, in his forty-first year, he had a regular fit of the
gout, which returned in the three following springs, but not in the
fourth." In the spring of 1773 (rather more than twenty years before
his death) he had the first appalling attack of what may, from our
present point of view, be fairly regarded as angina pectoris, though
the pain (perhaps from some association of ideas with " gout in the
stomach," the regular attack having, as stated above, not appeared at
the expected time) was in this instance referred to the region of the
pylorus. "While he was walking about the room, he cast his eyes
on the looking glass, and observed his countenance to be pale, his
lips white, giving the appearance of a dead man ; this alarmed him,
and led him to feel for his pulse, but he found none in either arm ;
the pain continued, and he found himself at times not breathing.
Being afraid of death soon taking place if he did not breathe, he
produced the voluntary act of breathing by working his lungs by the
power of the will.,,1 The " sensitive principle " was not affected ; for
three quarters of an hour he continued in this state, when the pain
gradually lessened, and in two hours he was completely recovered.

The next attack was in 1776 ;2 it was distinguished, however, by
a very decided amount of vertigo, which was not present, apparently,
in the first attack ; he felt as if he had drunk too much, and was a
little sick; on lying down it seemed as if he was suspended in the air;
motion in a carriage gave the uneasy " sensation of going down, or
sinking;"3 motion, either of the head or foot, was insufferable, from
the idea it gave of ranging through vast distances. " The idea he had
of his own size was that of being only two feet long." The special
senses were extremely acute; the appetite indifferent; the pulse about

1 In this and other passages the mind of Hunter is very apparent. The speculations
which follow may possibly be those of Sir Everard Home, and at all events they are not
of much value as regards the present narrative.

* This date is prooably a mistake, either of Hunter or the copyist ; the true date was
1777, as appears from a letter to Jenner on May 11th, in which Hunter writes— " Not two
hours after I saw your brother, I was taken ill with a swimming in the head, and could
not raise it off the pillow for ten days ; it is not yet perfectly recovered." During his
convalescence Hunter went to Bath for three months, on the advice of his friends, who
took a much more serious view of his case than he himself appeared to do. It was during
hia residence at Bath, apparently, that Dr. Jenner saw Hunter personally, and formed the
strong views as to the character and probable issue of the case which he ever afterwards
retained, and which he wrote out, as above mentioned, for Dr. Heberden in 1778.

8 There is a characteristically Hunterian note here given in Home's narrative, which
is valuable as showing how much these details of subjective phenomena interested John
Hunter as a physiologist, while as mere personal matters he gave all his own suffer-
ings extremely little consideration, " It is very curious that the sensation of sinking is
very uneasy to most animals. "WTien a person is tossed in a blanket, the uncomfortable
part is falling down ; take any animal in the hand and raise it up, it is very quiet, but
bring it down, and it will exert all its powers of resistance, every muscle in its body is in
action ; this is the case even with a child as early as its birth."

ANGINA PECTORIS AND SUDDEN DEATH. 563

sixty, and weak. In this state he continued for about ten days;
bleeding was of no service, purging and vomiting (by medicine) " dis-
tressed him greatly ; " nothing appeared to be of the least use. From
this severe illness he gradually recovered, but only after a long con-
valescence; and he does not seem to have been ever again perfectly
well, having, it is said, grown much older looking in the interval
between this and his next severe attack, which was in 1785.

The illness of April 1785 may be said to have commenced with
an ordinary attack of gout, followed by a great variety of anomalous
nervous sensations which are minutely described, but over which it is
not necessary to detain the reader.1 Suffice it to say, that from this
time onwards Hunter became increasingly subject to paroxysmal
attacks, which assumed more and more the characters of typical
angina pectoris. The nervous disturbance appears to have been at
first peripheral, e.g., " a sensation of the muscles of the nose being in
action," an unpleasant sensation in the left side of the face, jaw, and
throat, which seemed to extend into the head on that side, and down
the left arm as low as the ball of the thumb, where it terminated all
at once." After a fortnight these symptoms of nervous irritation
" extended to the sternum, producing the same disagreeable sensations
there, and giving the feeling of the sternum being drawn backwards
towards the spine, as well as that of oppression in breathing, although
the action of breathing was attended with no real difficulty ; at these
times the heart seemed to miss a stroke, and upon feeling the pulse,
the artery was very much contracted, often hardly to be felt, and
every now and then the pulse was entirely stopt." He had also pains
in the heart itself, "as well as the diaphragm and stomach, attended
with considerable eructations of wind, " a kind of mixture of hic-
cough and eructation." In the most severe attacks " he sunk into a
swoon or doze, which lasted about ten minutes, after which he started
up, without the least recollection of wrhat had passed, or of hia
preceding illness." The agonies he suffered were dreadful,2 and when
he fainted away he was thought to be dead.

As in other instances of angina, these attacks were at first brought
on chiefly by motion, " especially on an ascent, either of stairs or of
rising ground." The affections of the mind that were chiefly injurious
were anxiety and anger ; " it was not the cause of the anxiety, but
the quantity of it, that affected him ; the anxiety about the hiving of

1 Dr. Pitcairn elicited on this occasion, by special inquiries, that Hunter's mind had
been much harassed, in consequence of his having opened the body of a person who had
died of the bite of a mad dog, about six weeks before ; in doing which he had wounded
his hand. For a fortnight, it is added, his mind had been in continual suspense, from
the idea that he might be seized witli symptoms of hydrophobia ; and it certainly seems
very probable, as it was supposed, that the nervous symptoms alluded to may have been
in some measure, at least, determined or produced by this accident.

* This is the personal testimony of Sir Everard Home, who witnessed this attack,
having become Hunter's regular assistant in his practice, and acted for him during his
illness. It is probable, but not expressly stated, that Home also was a witness
to the first attack of illness in 1773, as he was then a young man living in Hunter's,
house.

64 A SYSTEM OF MEDICINE.

a swarm of bees, the anxiety lest an animal should escape before he
could get a gun to shoot it," brought on an attack ; " anger brought on
the same complaint, and he could conceive it possible for that passion
to be carried so far as to deprive him of life; but what was very
•extraordinary, the more tender passions of the mind did not produce
it ;" compassion, admiration, &c. might be carried to the extent of
tears, " yet the spasm was not excited." " He ate and slept as well as
ever, and his mind was in no degree depressed ; the want of exercise
made him grow unusually fat."

Mrs. Hunter, in writing to Jenner, called the disease, even at this
stage, " flying gout." * We have already seen what Jenner thought of
it several years before. Hunter himself was probably familiar with
Heberden's description, and at all events had assisted in Heberden's
inquiry by performing the examination of the very remarkable case
recorded in the " Medical Transactions " in 1772. He himself began
to suffer in 1773. That he had realised in some degree the danger of
his position, therefore, can scarcely be doubted. He had indeed no
unmanly fear of death, and was far too busy to occupy himself with
what he would have regarded as weak sentimentalisms about himself.
He probably avoided the subject deliberately,2 and felt himself able
to pursue all his various occupations with the same ardour as ever, in
the intervals of suffering. But he was deeply sensible of the risk to
which he was sometimes exposed by over-exertion, and still more by
his uncontrollable temper ; he was accustomed to say, that " his life
was in the hands of any rascal who chose to annoy and tease him ; "3
a remarkable expression, and a sad anticipation of the actual ending.

The close of 1789 brought with it a new set of complications, which
may be briefly summarised as loss of memory, and various kinds of
visual disturbance, especially the apparent deflection of objects from
their true direction ; some of the former subjective sensations, men-
tioned in the attack of 1776, returned upon him. " Dreams had the
strength of reality, so much so as to awaken him ; the disposition to
sleep was a good deal gone, an hour or two in the twenty-four being
as much as could be obtained. Neither the mind, nor the reasoning
faculty, however, were affected ; " indeed he reasoned most acutely in
regard to his own visual derangements, and pursued the questions
suggested by them in physiology with a keenness, which was quite
characteristic.

At last the busy, ever active mind was to cease from its labours,
and the strong, much-enduring bodily frame, wearied out and spent
in the service, was to give way. His recovery from this indisposition
was much less perfect than from any of the others ; he never lost
entirely the oblique vision ; his memory was in some respects evidently
impaired, and the spasms became more constant ; he never went to

1 Palmer's Life of John Hunter, p. 96.

8 In all his published correspondence there is only one brief allusion to Lis owu
illnesses, the one given above from a note to Jenner.
3 Palmer, ut mpra, p. 119.

ANGINA PECTORIS AND SUDDEN DEATH. 565-

bed without their being brought on by the act of undressing himself;
they came on in the middle of the night ; the least exertion in conver-
sation after dinner was attended by them. Even operations in surgery
if attended with any nicety, now produced the same effects.

The end is well known. There is reason to think it was almost
foreseen by himself. A dispute of a painful, but not, after all, of a
very serious or overwhelming character, had embittered his relations
with the governors of St. George's Hospital. On the 16th of October,
1793, he determined to be present at a meeting, where, however, he
apprehended a personal dispute. He expressed to a friend the feeling
that such a dispute might be fatal to him, but went nevertheless.
Something that he said in the Board-room was noticed, and flatly con-
tradicted. He stopped, left the room in a silent rage, and had just
time to gain the next room, when " he gave a deep groan, and fell
down dead."

The appearances in the dead body were complex. The pericardium
was very unusually thickened ; the heart very small, its muscular sub-
stance pale ; the coronary arteries were converted into open bony
tubes ; the valves of the left side of the heart also were involved in
a similar degeneration ; the aorta was dilated, in its ascending part,
to the extent of one-third. The carotid and vertebral arteries within
the cranium were also bony, and the basilar artery " had opaque white
spots very generally along its coats." The structure of the brain
itself was normal.

To these observations of what may be almost called historical cases,
bearing upon the fact of sudden death and its associated symptoms, I
will add only a few details gathered from a long and close observation,
of cardiac diseases in general.

Apart from what has been variously termed cardiac asthma^
dyspnoea, or orthopncea, which in many cases receives its clear ex-
planation from the associated states either of the pulmonary circula-
tion, or of the lungs, bronchi, and pleurae, as disclosed by physical signs,
there is often an element of subjective abnormal sensation present in
cardiac diseases which, when it is not localised through the coincidence
of pain, is a specially indefinable and indescribable sensation, almost
always felt to be such by the patient himself. I make this remark
deliberately, as the result of experience, and well knowing that it is
liable to be brought into question in particular instances ; that, in
fact, a large part of what has been described under the titles given at
the commencement of this paragraph, has been inextricably confounded
by systematic writers with the sensation, or group of sensations,,
to which I refer.1 To this group of sensations, when not distinctly
accompanied by local pain, I have, in various instances, given the

1 " In considering this subject we must not forget," writes Dr. Stokes, "that under
the name angina pectoris, physicians have included, and still include, many examples of
diseases which vary in their nature and combinations. "Well marked instances of the
affection as described by Dr. Latham, are rarely met with ; and the same may bo said of

566 A SYSTEM OF MEDICINE.

name of Angina sine dolore, recognising, thereby, what I believe to be
its true diagnostic and pathological significance, and its alliance with
the painful angina of Heberden ; the pain in which, however, as we
have already seen, is an exceedingly variable element, both in degree
and in kind. This painless, or at least not definitely and locally
painful, angina, is found in connection with every kind of cardiac
lesion which ends in death (whether sudden or not) in varying pro-
portions ; often associated with the other phenomena which make up
the picture of a confirmed case of organic heart disease tending to
death, but not rarely also under circumstances which admit of its
being separately described. Among the valvular lesions of the heart,
incompetency of the aortic valves is the one which most frequently
gives rise characteristically to this peculiar form of suffering ; and in
the majority of the cases in which it arises early in the course of
aortic valvular disease there is neither dropsy, or lividity, nor haem-
optysis ; very often there is no disease of the lungs ascertainable by
physical signs, and in particular no wheezing, even in very severe
paroxysms of this truly cardiac anguish or indefinable distress. But
there is, in variable degrees, a sensation which can only be called
anxiety, or cardiac oppression ; the patient acquires a haggard, almost
a frightened look4 and from his habitual attitude and manner, as much
as from anything he distinctly declares in words, it becomes evident
that he is suffering from a sense of insecurity which he cannot pos-
sibly express. In the more aggravated cases the loss of sleep is a
serious part of the suffering, and patients will sometimes declare that
they are afraid to sleep, lest some other and greater evil than the loss
of sleep should come upon them ; obviously an experience actually
acquired, that sleep is, in this state, sometimes the precursor, and
apparently the cause, of a formidable increase in the symptoms. An
intelligent patient in this condition recently put the question to his
medical attendant, with respect to a very moderate dose of hydrate of
chloral, proposed to be given after many sleepless nights, whether it
would not be " dangerous," i.e. (as he afterwards explained to me),
whether the sleep artificially induced might not be the means of
determining an attack which might prove fatal. When sleep is
obtained, it is brief and easily disturbed, often by frightful dreams ;
and when these occur they are mixed up with the sensations of an ap-
proaching paroxysm, so that the dream may appear to be the actual
cause of the paroxysm. An assertion of the patient just alluded to
was that he "woke up with the peculiar sensation on him, and
it was too late to check it." In very extreme cases, which are often,
however, complicated with true orthopnea, dropsy, and other more
recognised cardiac and respiratory symptoms of secondary origin, the
patient may for weeks together be unable to lie down or to take

the purely nervous cases noticed by Lacnnec. I have never seen citiicr oj these forms.
The disease which in this country (Ireland ?) "most often gets the name of angina
pectoris might be more properly designated as cardiac asthma. " Op. cit. p. 488.

ANGINA PECTORIS AND SUDDEN DEATH. 567

•ordinary rest, and on the other hand may he almost continually half-
asleep ; in such cases accidents are apt to occur, from the patient fall-
ing forwards in a fit of sheer exhaustion, or getting hurned or otherwise
injured while in a state of insensibility. Nor are more distinctly
cerebral symptoms wanting. In some of these cases I have seen
attacks closely resembling epilepsy, without any subsequent paralysis ;
when however, hemiplegia or aphasic symptoms occur, it is most
probable that they are due to more distinctly organic changes in the
nervous centres ; and usually to cerebral embolism. It would be vain
to indicate the verbal expedients by which patients endeavour to
describe their sensations, when found in an attack of this paroxysmal
suffering. Palpitation, and breathlessness are often alluded to, sepa-
rately or together ; but still more often it is a sense of " oppression,"
or of " pressure," which is sometimes described as if the chest were
actually being compressed from before backwards ; one patient de-
scribed it as a " kind of surging up," which came, as he thought, from
the bowels, and was attended with the feeling of wind, and also, I
suspect, with a degree of hysteric globus, rising, as he described it,
to his throat, and causing him to pant for breath. The respiration is
by no means necessarily or invariably disturbed in these cases, though
it is frequently more or less quickened, and sometimes the opposite ;
in certain cases the respiration is alternately frequent and infrequent ;
several rapid panting or gasping respirations are continued over half-
a-minute together, and are gradually succeeded by a corresponding
period of comparative quiescence, which at times culminates in a
positive arrest or suspension, for a time, of a respiratory act (see the
narrative of John Hunter's case above cited).1

This peculiar type of tt suspirious," or irregularly sighing, respira-
tion (as it has been termed), is so far characteristic of the " angina

1 It is very remarkable that Dr. Stokes, who is undoubtedly entitled to the credit of
having first distinctly realised, and clearly stated, the importance of this type of respi-
ration as indicating cardiac disease (especially weakened action, or fatty degeneration, of
the fibre of the heart) should have so completely overlooked the case of John Hunter, while
fixing upon the symptoms described in Seneca's case as characteristic (see note, p. 553).
The same remark applies to all the now numerous dissertations, in Germany as well as
in this country, on the " Cheyne-Stokes respiration," as it has been called on the con-
tinent. " It consists," says Dr. Stokes (op. tit. p. 324), "in the occurrence of a series
of inspirations, increasing to a maximum, and then declining in force and length, until
a state of apparent apncea is established. In this condition the patient may remain for
such a length of time as to make his attendants believe that he is dead, when a low in-
spiration, followed by one more decided, marks the commencement of a new ascending
and then descending series of inspirations." Probably the first really exact description
of this phenomenon was by Dr. Cheyne, in 1818 (Dublin Hospital Reports vol. iL, p. 216).
The peculiar interest and value of Hunter's case, however, for us consists in its giving
the personal impressions, or subjective sensations, of that great physiologist in a way
that no merely objective description could effect, and wholly apart from hypothesis. It
is curious to observe how completely Hunter's description of his own sensations corre-
sponds with Galen's commentary on a notable passage in Hippocrates, where a certain
kind of "rare and large " respiration is described as "like a person who forgot for a
time the need of breathing, and then suddenly remembered." See the very interesting
account of the most ancient observations on this subject by Dr. Warburton Begbie, in
his recent Address in Medicine (British Medical Journal, August 7, 1875, p. 166) in
which there will also be found a brief but exact account of the more modern theories as
to this kind of respiratory disorder.

568 A SYSTEM OF MEDICINE.

sine dolore," that I cannot but regard it as being in some way related
to lesions involving the respiration through the cardiac nerves.
Whether dependent necessarily on cardiac causes or not, however, it
is certainly not necessarily associated with any organic lesion of tlie
lungs or air-passages ; it occurs, as Dr. Stokes has recorded, " without
any rdle or sign of mechanical obstruction." Frequently the irregu-
larities of respiration do not go beyond a few quick gasps, or deep
sighing inspirations, at a time, and the period of apna?a, or of rare and
slow respiration, is correspondingly shortened ; but when tliis condi-
tion of the respiration, even in its minor degrees, is associated with
the peculiar look of indescribable anguish, the head thrown back, the
arms extended or tossed about, and the whole frame showing by sheer
muscular restlessness the terrible character of the agony (indicated
often by cries, even when without local or positive pain), it scarcely
requires the aid of a verbal description to make the diagnosis of
angina clear to the observer. It is, however, important to remark that
the character and peculiarly altered rhythm of the breathing are
essentially distinct from the laborious but more regular and at the
same time noisy respiration of true spasmodic asthma and of asthma-
tic bronchitis. I have also observed that organic and valvular deformi-
ties of the right side of the heart, even when complicated with great
cyanosis, are only slightly characterised by the symptoms I have now
endeavoured to indicate ; and, on the whole, the diseases of the
mitral valve are less apt to be accompanied by this form of angina
than those of the aortic, and the obstructive lesions less than the
regurgitations. Dilatation of the heart in its more aggravated forms,
however caused, and aneurisms (as already indicated) arising very
near the heart, or projecting into the pericardium, are apt to be
accompanied by considerable degrees of angina, as above described.
And some of the worst cases I have seen have been those, in which
the only lesion that could be fairly presumed to exist was fatty or
other degeneration of the fibre of the heart, sometimes with, some-
times without, direct evidence of moderate or slight dilatation of the
left ventricle.1 As in the case of the locally painful, or neuralgic

1 In one case of this kind, a much valued friend and a distinguished clergyman of the
Church of Scotland, who died at the age of forty-one, after a gradually progressive illness
watched with the greatest anxiety, and with full fore-knowledge of its character and
probable termination, the beats of the heart frequently numbered as low as 22-24 in the
minute ; and I have counted them as low as 18, without any marked irregularity. The
radial pulse was at these times exceedingly soft and small, but although the suffering was
at times intense, it was not usually accompanied by positive definable pain, at least until
the last few days or weeks of the disease, when (tno patient not being at the time under
my own immediate observation) I had the testimony of a well-informed medical friend
as to the really angina-like character of the paroxysms. The suspirious respiration was
always present in tnc more considerable paroxysms of suffering, and was usually not alto-
gether absent. There were on several occasions very alarming pseudo-apoplectic or
slight epileptic attacks, without permanent disorder either of the intellectual functions or
of voluntary movement. Although this truly noble-minded and self-denying man pur-
sued the work of liis life up to the very verge of sudden fainting or death in the pulpit,
yet his death in the end was by no means sudden, but rather a lingering agony. Thc-
cntire duration of his fatal illness was under two years, and he continued at his post,
with some interruptions, until about eight months before his death, which happened in.

ANGINA PECTORIS AND SUDDEN DEATH. 569

angina, the relation of the symptoms to the organic lesion is by no
means constant, even when the latter can be shown to be present, and
to be presumably, in a certain sense, the cause of the symptoms.
And it may further be affirmed, that the essentially paroxysmal
character of this angina is such as to lead us inevitably to look for an
explanation of it beyond the positive and permanent organic lesion of
the heart or aorta, whatever that may be in the particular case.

We are now in a position to discuss, with such assistance as can be
had both from clinical observation and from physiological pathology,
the extremely obscure subject of the mode in which the innervation
of the heart is affected in Cardiac Angina — in other words, the ulti-
mate pathology or pathogeny of tlie affection. We have seen that
the dolor pectoris, or angina pectoris, of Heberden was specially
distinguished by him from all those pains in the chest which were
regarded as due to inflammation, accompanied or followed by
organic changes corresponding with the extent and severity of the
inflammatory process. In other words, the essential pathology of
angina, according to Heberden, was that of a neurosis. This we
believe to be the only just rendering of the argument of this great
physician, when he assigned to angina pectoris a place among the
distensiones, or spasms. Later observers and pathologists have been
much exercised in the attempt to resolve the question, whether
sudden death, occurring under such circumstances, is from spasm, or
from paralysis, of the heart ; but we may safely conclude that no such
question was, otherwise than remotely, involved in Heberden's
argument. That argument was directed towards a very practical and
real conclusion, and was not at all, we may well suppose, intended to
foreclose questions of physiological pathology, which, according to
all the evidence before us, were not before his mind, or, at least, not
matured for discussion at the time at which he wrote. Angina
pectoris had to be placed carefully apart from the pyrexia and the
phlegmasia: ; had any doubt been left open on this subject, the dolor
pectoris would have been considered as demanding the treatment of
all so-called inflammatory pains in that day — large and repeated
bleedings, vomitings, purgings, &C1 Hence the anxious care with
which Heberden insisted on the paroxysmal and non- febrile character
of the pain, and on the collateral circumstances which led him to
bring it into the great group of the spasms ; e.g. u suhito acccdit, et
rcccdit " — " in ipsa accessione pulsus non concitalur" &c. It is need-
less to pursue the argument in detail ; possibly, indeed, the details

January, 1865. Up to a few days before death be maintained bis pastoral connection
with liis congregation by means of letters, some of which have been published, and
show all the power of a robust mind under the guidance of Christian principle and
hope. Dr. Walshe, who saw this case with me in consultation, agreed with me in con-
sidering it one probably of fatty degeneration of the heart ; but there was no post-moi'tcm
examination.

1 Angina pectoris, quantum adhuc illius naturam intellexi, ad distensionem, non nutcm

ad iiiflammationem, videtur pertinere Sanguinis missio, vomitus, et purgHiitia

jnihi visa sunt aliena^— Cowwt. uti supra.

VOL. IV. P P

570 A SYSTEM OF MEDICINE.

might be open to question in some instances. But on endeavouring,
as Dr. Latham has done, to grasp the essential principles of the argu-
ment, as seen through a somewhat obsolete phraseology, we majr
readily assent to them, even if we should suppose th&t Heberden, in
his desire to prove angina pectoris a neurosis, may have somewhat
neglected the evidence of its being often associated with organic
disease.1 He found in the suddenness of the paroxysms, in the
apparent good health of the intervals, in the relief often afforded by
stimulants and by opium, the basis of his pathology of angina ; and
we may easily admit that some cases, at least, of the typical angina
of Heberden must have been fairly open to the construction of being
cases of spasm, and nothing more. But we now know that this
typical angina is only the culminating form of a group of symptoms,
which, in their less pronounced, less definitely painful, and more
complicated forms, are found to permeate the whole field of cardiac
pathology and diagnosis. The angina which consists purely of a
paroxysm of pain, and of a paroxysm which kills suddenly and
instantaneously, is rare ; but the angina which consists of a tendency
to paroxysmal aggravations (not always purely of pain), superinduced
upon, and complicating, the other symptoms and sequelae of cardiac
organic diseases, is matter of every-day experience. In both forms
there occurs occasionally a paroxysm which ends in death ; but in the
second form death is less frequently instantaneous and unexpected, both
because the paroxysms are individually less intense, and because the
fatal result, when it arrives, is brought about in part by other causes
than the immediate causes of the paroxysm. And even if we should
maintain that fatal angina is always more or less dependent upon
organic changes,2 there would still remain to be explained these
unquestionable facts, viz : — 1. Pain, suddenly coming and going ; 2.

1 He refers, however, to several cases which seemed to him to imply the existence of
organic change ; and to one only, in which "a very skilful anatomist could discover no fault
in the heart, in the valves, in the arteries, or in the neighbouring veins, excepting soma
small rudiments of ossification in the aorta. Nor were any indications of disease found
in the brain." There is no doubt that Heberden's personal experience of angina was
almost purely clinical, not pathological ; but it has the advantage, for us, of being stated
in language singularly terse, exact, and free from the suspicion of prejudice. Heberden
claims, in his Commentaries, to have seen nearly a hundred cases of angina pectoris, of
which three were in women. One was a boy twelve years old, " who had something
resembling this affection." All the rest were in men near or past the fiftieth year of
their age. At the time of his first paper, in 1768, Heberden had " never seen one opened,
who had died of it. Most of those,' he adds, " with whose cases I had been acquainted
were buried before I heard that they were dead. " The case specially alluded to above-
was almost certaiuly that of the "Unknown," who, in April 1772, wrote to Heberden a
minute account of his symptoms, and dying suddenly about three weeks thereafter, was
found to have left in his will express instructions that Heberden should be informed of
his death, with the view of having his body examined. This was accordingly done by
John Hunter, and it is this case to which Dr. Jenner alludes, when he says that he can
almost certainly affirm that the coronary arteries were not examined. The case was.
recorded in the third volume of the Medical Transactions.

a Eulenburg refers to Desportes, in Lartigue— " De 1'Angine do Poitrine," p. 78,
Paris, 1846 ; Surmay, L'Union Medicale, XXXI, No. 80, p. 34 ; for evidence of angina
without disease of the heart. Anstie, in his Treatise on Neuralgia, pp. 69, 70, details,
briefly, a fatal case, in which " not the slightest organic heart mischief could be detected,
either during life or after death." Latham has aJso recorded cases where the appearances

ANGINA PECTORIS AND SUDDEN DEATH. 671

The paroxysmal character of the symptoms, other than pain; 3.
Absolutely sudden death in a few cases. On these grounds, now as
in the time of Heberden, we may assuredly claim for angina pectoris
a place among the neuroses, even while the admission is freely made
that the element of neurosis is often superinduced upon organic, too
often indeed incurable, disease in the heart itself, or in its nutrient
vessels, or in the first part of the aorta.

Certain authorities have treated of angina pectoris as a form of
visceral neuralgia, or "hyperesthesia"1 (Eomberg) of the cardiac
plexus. The latter term (as Dr. Anstie has well pointed out) is
essentially a bad one ; the former, in the case of typical angina, is
perhaps admissible, viewing the disease from the side of the pain
alone ; but it errs both by excess and by defect, inasmuch as, on the
one hand, pain of the severe form implied in the term neuralgia is not
always the central or exclusive phenomenon, even of the cases ending
in sudden death ; while, on the other hand, a form of cardiac pain, or
pseudo-angina 2 (as it has been termed) is not infrequent, which ihas
most of the attributes of a neuralgia in the highest possible degree,
and which, though eminently paroxysmal, is by no means apt to lead
to sudden death, or to any grave consequences whatever. This admis-
sion, which is very candidly and fully made by the late Dr. Anstie s
in his interesting dissertation upon the subject, appears to me a very
cogent reason for maintaining, rather than consenting to forego, the
now well-known term angina pectoris, for which he entertains so
strong an aversion, but which is, nevertheless, quite indispensable to
us, as carrying the impress of a long line of personal observations,
extending back to that " molestus quidam angor," which Morgagni
has described as having suddenly terminated the life of a Venetian
woman in 1707. And if it must be admitted that the name "angina,
pectoris " has sometimes been used in ignorance, or rather (from dis-
regard of purely clinical experience) in a way really objectionable
and tending to confusion, it is equally certain that the term " neuralgia"
is beset with theoretical interpretations which tend to bias both

after death were, at least, of very questionable and doubtful character. But it is difficult
to prove a negative by isolated instances which arc opposed to the general results of
pathological research.

1 " Pain has been described by some of the most distinguished writers on nervous
diseases as a hyperesthesia. Yet there is really very little difficulty in convincing our-
selves, if we institute a thorough inquiry into the matter, that pain is certainly not
a hyperesthesia, or excess of ordinary sensory function, but something which, if
not the exact opposite of this, is very nearly so." — Anstie on Neuralgia, p. 2, et. seq.

2 " Genuine angina pectoris is undoubtedly a very rare affection. On the other hand, 1
utmost daily meet with a form of complaint combining in a minor degree many of the
characters of angina ; and to this imitation of the true disease I propose to give the-
name of pseudo-angina. I believe that herein lies the explanation of Lacnnec s notion
(so discordant with the experience of English observers) that angina pectoris is of very
frequent occurrence." — Walshe, Diseases ot the Heart and Great Vessels, 4th edit, 1873,.
p. 208. Compare the observations on Diagnosis in p. 542, of present chapter.

3 On Neuralgia, and the Diseases that resemble it, by F. L. Anstie, M.D., 1871 ; pp.
63, 64. The first sketch of this most valuable treatise, contributed by the mucn-
lamented author to the present work in 18C8, contains no detailed refeience to
angina pectoris.

pp2

572 A SYSTEM OF MEDICINE.

clinical and pathological research. We have endeavoured in tl
preceding pages to give an impartial statement of a wide range
phenomena, into which a neuralgic element enters in various propo
tions. A consistent theory must take account of that element, b
will not allow it to take possession of the entire field.

Another question that requires consideration is, the nature of tl
disorders in connection with motor nerves which unquestionab
occur in angina pectoris. Here, again, we find ourselves in the pr
seuce of vague and often quite fruitless discussions, indicated by tl
general terms spasm, paralysis, hyperkinesia, &c, and, among tl
older authors, asthma convuHivum, stenocardia, syncope anginosa, >S

A third department of the inquiry, leas generally cntertaine
inasmuch as the phenomena to which it refers are less constant,
the nature of the connection between the cardiac symptoms in angii
pectoris, and those cerebrospinal manifestations which sometim
occur, and which we saw well illustrated in the case of Jol
Hunter.

Is it possible to give any account of these three orders of pb
nomena which shall be consistent and intelligible, which shall 1
founded on positive facts and well-ordered experiments, and shi
thus fulfil the purposes, even provisionally, of a reasonable theory
angina pectoris ? In endeavouring to answer this question, it will 1
necessary to refer to physiological researches which are still ve
incomplete, and even to clinical facts whicli have not as yet be
tested by a sufficient number of independent observers. But
certainly seems as though some large and fruitful lines of resean
had recently been opened up amid much darkness and confusion.

We owe to Dr. Lauder Brunton * the clinical observation of a fa
which, besides its therapeutic consequences (to be afterwards co
sidered), may be regarded as shedding a new light upon the patholoj
of angina pectoris. In investigating a case of rheumatic disease
the aortic valves (obstruction and regurgitation), with dilatation of tl
aorta, and considerable hypertrophy of the heart, he found th
during the angina-like paroxysms of pain to which the patient w
subject, the sphygmograph invariably showed a great diminution
the amplitude of the pulse-wave, with blunting of the apex, slow
greatly postponed recoil, and obliteration of the dicrotic wave ; t
ordinary pulse of the individual (at least in the right radial arter
being characterised by a very ample and instantaneous upstroke,
pointed apex, a rapid recoil, and a distinct though not exaggerat
dicrotic wave. Repeated experiments convinced Dr. Brunton th

1 lancet, July 27, 1867, p. P7 ; Journal of Anatomy anil Physiology, vol. v. p. £
Trulls, of the Clinical Society of London, vol. iii. p. 191. The cose, which is fu
recorded m the ( 'linL-al Society'* Transactions, whs that of a man iiged twenty-j
admitted into the Royal Infirmary of Edinburgh under Professor Maclngan, on Dec.
1668; and sphygmograpliic observations, begun at his instance, were continued under Pi
Bennett, to whom the case was transferred on Feb. 1, 1S87. There were palpitation
the heart, and violent throbbing of the carotids, l*Bidcs the angina-pain. The aeon
and digitalis were ordered by Professor Maclagan; the small bleedings by I'rofes

ANGINA PECTORIS AND SUDDEN DEATH. 573

these altered characters of the pube were due to an increased tension
in the systemic arteries during the paroxysm, and that this increased
tension was chiefly, i£ not solely, owing to " contraction of the small
systemic vessels, so sudden and so great as to deserve the name of
spasmodic."1 Following up this line of observation, and being
aware that Dr. B. W. Richardson 2 and Dr. Arthur Gamgee 8 had per-
formed numerous experiments which showed that nitrite of amyl,
when inhaled in small quantities, had the effect of remarkably
lessening arterial tension by diminishing the contraction of the
arterioles, Dr. Brunton was led to employ this substance for the
purpose of relieving the symptoms in this case, and had the great
satisfaction not only of finding that almost immediate ease was given
in the severer paroxysms, but that the observations previously made
on the relation of the paroxysm to increased vascular tension, were
emphasised (so to speak) by the action of the nitrite of amyl. For
when in the severest paroxysms the pulse was almost annihilated to
the finger (though still regular and somewhat accelerated), thirteen
drops of the nitrite of amyl inhaled from a cloth produced, in one minute
and twenty seconds, a decided effect at once on the sphygmographic
tracing and on the pain ; while one or two smaller doses, repeated
over sixteen minutes, restored the amplitude of the pulse-wave, and
entirely removed the pain. It is, perhaps, unnecessary to multiply
details, especially as regards doubtful points.4 The experiment was
repeated sufficiently often to show that, in this patient at least, increased
arterial tension and angina-spasm were constantly associated, and that
agents which produced diminution of the arterial tension always re-
lieved the paroxysms. Among these agents, it is to be noted (though
none was nearly so powerful as nitrite of amyl), small blood-lettings
(of four ounces) were found to exercise a notable influence. Digitalis,
on the other hand, appeared rather to aggravate the pain, and both
digitalis and aconite made the pulse intermit, which was never the

1 Clin. Soc. Trans., vbi supra, p. 199. A lithograph, with eleven tracings in different
states of the patient, is given, on which the description in the text is founded.

1 Dr. Richardson's numerous and valuable reports of experiments on anaesthetic
vapours, and on nitrite of amyl, from 1863 onwards (brought in successive years before
the Brit. Association of Science), determined the power of this substance as an anti-
spasmodic and paralysing agent, and made numerous suggestions as to its probable
curative value in tetanus, asthma, and other spasmodic diseases. Dr. Richardson also
repeated, and investigated scientifically, Guthrie's accidental observation in 1859, as
to its effect in dilating the capillaries ; and he inferred that this effect was due to its
paralysing the arterioles through the vaso-motor nerves.

3 Dr. Gamgee's (unpublished) experiments were made with the sphygmograph and
hfemodynamometer, and led directly to Dr. Brunton's trials of the nitrite of amyl
in angina, by demonstrating in animals and in man its action in lessening arterial
tension.

4 There is an ingenious attempt to show that a partial restoration of the original form
of the pulse-tracing, which was shown to correspond to a remission, but not cessation,
of the mroxysm under nitrite of amyl, was due to the persistence of abnormal tension in
the pulmonary circulation, after the systemic had been relieved. The pain, under such
circumstances, "disappeared from the greater part of the cardiac region, the neck, and
the arm, but remained persistent at a point about two inches to the inside of the
right nipple .... So long as this condition remained the pain was almost certain
to return. — Clin. Trans, iu. p. 199.

674 A 8Y8TEM OF MEDICINE.

case with the nitrita On the whole, it must be admitted, that not-
withstanding certain unavoidable deficiencies, the experiment is as
complete as can reasonably be expected in the evidence it affords of a
correlation of some kind between angina-paroxysms and increased
arterial tension, in at least one clearly-defined case of organic
cardiac disease.1

Many other experiments, both on man and on animals, have been
performed, which amply confirm the action attributed to the nitrite of
amyl in this case. The therapeutical part of the subject wiE receive
consideration afterwards ; in the meantime it is sufficient to say, that
the relaxing effect of the vapour on the arterioles, and its efficacy, in
some cases at least, in greatly and instantly relieving the breast-pang,
have been placed beyond reasonable doubt.

The points still open to further investigation seem to be these : — It
is as yet not piwod that all the forms, and all cases of angina, axe
characterised by increased arterial tension during the paroxysm. If,
indeed, there be cases corresponding exactly with the original descrip-
tion of Heberden, cases in which (the heart being to stethoscopic ami
physical examination normal) "the pulse is not disturbed by the pain,"
it would be extremely desirable to have sphygmographic observations
of such apparently uncomplicated angina-paroxysms. But we have
already expressed doubts of the existence of such cases ; at all events,
the one recorded by Dr. Brunton is not such a case, but rather one in
which the phenomena of the arterial tension must be regarded as
wholly abnormal, being influenced by the fact, of aortic regurgitation,
a strictly mechanical cause of permanently and morbidly' lemand
blood-pressure in the arteries.

But again : Supposing it proved that a suddenly-developed and
decided increase in the arterial tension is a characteristic, or even an
essential feature of the true angina-paroxysm, we may still regard it
as an open question whether the change in the blood-pressure is to
be attributed entirely in such cases to contraction of the arterioles, or
partly also to changes in the innervation of the heart itself, which
would account at once for the pain and for the sudden death which
sometimes occurs during the attack? Dr. Brunton has himself
pointed out a fact which tells in this direction, notwithstanding the
^elaborate reasonings by which he supports the theory of vaso-motwr
derangement ending in spasm of the arterioles as the starting-point
of the paroxysm. The experiments of Marey and others have shown
that the effect of high blood-pressure in the arteries, per se, is to
retard the pulse ; while diminished arterial tension arising from relax-
ation of the arterioles (as in fever, or in capillary congestion from the

1 It is to be observed, that although the diagnosis actually made was that of aortic
-obstruction and regurgitation without aneurism, and although this was quite in* accord-
ance with the physical sign*, and particularly the murmurs, described ur the report}, tin
remarkable difference in the sphygmographic tracings of the two radial, pulses ctannottet
"be regarded as leaving a doubt open as to the negative part of the diagnosis. On the- other
hand, aneurism, if present, may have been responsible in part for the definite chmraotan
of the pain, which is usually not so well-marked in cases of aortic regurgitation simply.

ANGINA PECTORIS AND SUDDEN DEATH. 575

•effect of external warmth) increases the frequency of the heart's con-
tractions. Now in the case alluded to, what actually took place was
exactly the reverse of what might have been expected on the theory
Above mentioned. During the severest paroxysms, when arterial ten-
sion was at its height, the pulse was small and rapid, and when the
pain and spasm had been subdued by the inhalation of the nitrite, the *
pulse diminished in frequency while regaining strength and volume;
Dr. Brunton considers these phenomena as indicating " a derange-
ment of the cardiac regulating apparatus) producing quickened instead
of slowed pulsation." Further observations, therefore, seem to be
required before it can be safely assumed that either vaso-motor
derangement on the one hand, or disorder of the cardiac innervation
on the other, is the primary or essential phenomenon of true angina
pectoris; although we may probably take it as provisionally esta-
blished that some law of intimate relation exists between increased
blood-pressure in the arteries and certain forms, at least, of the angina-
paroxysm.

The peculiar interest of Dr. Brunton s observations, for us, consists
not in his having finally settled the nature of this relation, but in his
having shown that a remedy which has the remarkable power of
instantly diminishing arterial tension has also a corresponding and
almost equally instantaneous control over those paroxyms of angina in
which increased arterial tension is known to occur. We shall recur
to this subject when speaking of treatment

Meantime it seems necessary to observe that Dr. Brunton had been
anticipated, in several quarters, in the merely speculative attempt to
connect the symptoms of angina pectoris with vasomotor changes;
Thus Traube1 had argued that the diminished volume and increased
tension shown in the arteries in many attacks of stenocardia axe to be
viewed, in connection with the increased rate of the pulse and the
feeling of anxiety (angstgefiihl), as related to* an increased! stimu-
lation of the nerve-centre of the vaso-motor system. Cahen2 had
treated at length of various neuralgic affections (including trifacial
neuralgia, and various painful affections of the pelvic organs) as- affec-
tions of the vaso-motor system of nerves attended by congestion ; and
he referred angina pectoris to the same category, and indicated
arsenic as a valuable remedy for such oasee, without, however, adding
any tiling important to the symptomatology of angina. Landois8 had
made a somewhat similar generalisation as to some cases- of excessive
nervous palpitation, which he regarded as being a vaso-motor anginal
pectoris. Finally, Nothnagel, in a very ingenious and interesting
contribution to the clinical study of the " vaso-motor neuroses/1 devotes
an entire article4 to the special consideration of " Angina* Pectoris

1 Die Symptoms der Krankheiten des Respirattons-trnd Circulations-apparatus, p. 41:
(lief, in Nothnaael's article, infra.)

8 Archives Generates de Medecine, 1S63, vol. ii. p. 664*

,: Correspondenz-Blatt fur Psychiatrie, 1866 (quoted by Nothnagel).

4 Deutsche* Arohiv. fur Klinische Medizin, yol. 3, xiv. p. 309. Compare abo Tol. 2;
p. 190, Case VII.

576 A SYSTEM OF MEDICINE.

vasomotoria," upon the basis of five detailed cases (without special
8phygmographic observations). But the details of Nothnagel's cases
will show that, however closely some of the subjective symptoms of
angina pectoris may be simulated by a purely vaso-motor lesion, there
are some very striking differences between the disease so induced and
# the true angina pectoris of Heberden. For — 1st, in the greater
number of Nothnagel's cases the disease yielded easily to very simple
treatment, and in none was there a fatal issue, or even, apparently,
much real apprehension of immediate or urgent danger ; 2ndly, the
sensations in the extremities (deadness, coldness, formication, not
pain) were usually present in all the extremities indifferently, and
preceded the palpitations and the cardiac uneasiness by some minutes ;
3rdly, the specially cardiac or other internal sensations were, a very
distressing sense of palpitation, attended by anxiety, and sometimes
by vertigo, or incipient faiutness ; 4thly, in one of these cases only
was the pulse-rate decidedly altered, and in that case it was dimin-
ished from 84 to 64 — 60 during the attack ; 5thly, pain was either
absent, or assumed little prominence among the symptoms ; 6thly,
the sensation of impending death was evidently connected with, and
probably caused by, the palpitation (in Heberden's most characteristic
case above quoted,1 as also probably in John Hunter's case, the very
opposite of this was the fact ; the feeling was of " a pause in the
operations of nature for perhaps three or four seconds"). 7thly,
Several of the cases recorded were below the typical age (30, 38, 39,
46), and one only above it (63) ; that one being a woman, The les-
son, therefore, taught by Nothnagel's cases is not, properly speaking,
that typical, still less that fatal, angina pectoris is always to be re-
garded as due to vaso-motor spasm, but rather that, under certain
peculiar conditions of the system, a sudden check to the circulation in
the extremities, determined by vaso-motor spasm, may become the
cause of an increased action of the heart, palpitation, and pseudo-
angina ; the disease so induced, however, being devoid of the charac-
teristic pains and the more aggravated phenomena of fatal angina ;
and that in such cases heat, and mild counter-irritation of the surface,
have almost complete power to control both the external and internal
manifestations ; the prognosis being (according to N.) entirely favour-
able. At the same time, although we cannot admit that Nothnagel's
cases were genuine cases of Heberden's angina, they are very instruc-
tive, and may, no doubt, afford some insight into the pathology of the
true disease.

Leaving, for the moment, the line of inquiry suggested by these
observations, we may revert to the pain of angina, which has been
commonly regarded as a neuralgia of the cardiac plexus ; the impres-
sions of pain in the severer cases being radiated outwards through the
numerous connections which are known to exist between the special
ganglionic system of the heart, and the spinal nerves entering into
the cervical and brachial plexuses through the cervical ganglia. It

1 Seo page 538, note 2.

ANGINA PECTORIS AND SUDDEN DEATH. 577

is difficult, from the very nature of the case, to prove this proposition ;
but there is no inherent improbability in it, unless, indeed, we should
assume that the cardiac nerves of the ganglionic system are incapable
of giving rise to acute pain ; an assumption not in accordance with
the facts of medical experience in the cases of gallstone, colic, &c.
Holding in view, moreover, the proved association of angina pectoris
in many cases with disease of the coronary arteries of the heart, and
with other lesions" exclusively within the range of the ganglionic
system of the heart and aorta, it is difficult to resist a bias in favour
of the view that the nervous system of the heart itself is the origin
or the chief seat of the pain, in the great majority of the cases. To-
these arguments it may be added that in most cases the internal sen-
sations (whether distinctly referred to the heart or not by the patient)
are obviously first in the order of time and of degree ; the brachial,
intercostal, or cervical pains being sometimes altogether absent, and
usually present only in the more severe and protracted attacks. It
has, however, been plausibly maintained, notwithstanding these facts,
that the spinal nerves are the true seats of the apparently cardiac-
pains of angina, and that all the apparently reflected sensations in the
limbs, &c, are transmitted, like the external neuralgia, through a
spinal centre. Dr. Anstie, who holds this view, adduces the unilateral
character of the brachial pain in at least four cases out of five (?), as
an almost irresistible argument against the radiation of pain outwards
from the cardiac ganglia, through the peripheral nerves of communi-
cation. " It appears greatly more probable," he writes, " that angina
is essentially a mainly unilateral morbid condition of the lower cervical
and upper dorsal portion of tlve cord ; liable of course to be seriously
aggravated by such peripheral sources of irritation as would be fur-
nished by diseases of the heart, and especially by diseases of the
coronary arteries." The question is one which can scarcely be made
less obscure by any arguments falling within the scope of this article.
We have already indicated some of the difficulties that have to be
encountered in extending the group, or order, of the neuralgias so as
to include angina pectoris ; meaning by that term, of course, the for-
midable and fatal disease we have been chiefly describing, and not
the very numerous, or rather innumerable, instances of pains referred
to the heart, by hysterical women and others, which have no such
significance. Referring chiefly to fatal cases of angina pectoris, Sir
John Forbes and all the more considerable authorities from Heberden
downwards concur in giving an immense preponderance to the male
sex. Without insisting too much on the numerical details, which for
reasons formerly indicated may perhaps be considered as somewhat
biased by the mode of collection, it may be well to compare this
overwhelming proportion of males who fall victims to cardiac angina
(an excess on the male side greatly exceeding the greater proclivity
of males to organic disease of the heart in general) with the numerical
statements given incidentally in Dr. Anstie's work as regards the
liability of the two sexes to neuralgise in general. " Eulenburg saw

578 A SYSTEM OF MEDICINE.

a hundred and six cases of neuralgia of all kinds, of which seventy-
six were in women, and only thirty in men : my own experience is
very similar ; viz., sixty- eight women and thirty-two men out of a
hundred hospital and private patients." * A difference so extreme as
this is not to be accounted for " by supposing that as men take a much
larger amount of strong physical exercise than women, they will furnish
a much larger proportion of subjects in whom an ill-nourished heart
will break down under its work, and be seized either with paralysis
or cramp ;" 2 and it seems scarcely necessary to do more than place
these facte before the reader, in order to make it apparent that many
of the arguments by which analogies drawn from the study of neuralgia
in. its more familiar forms are applied to angina pectoris, are ques-
tionable, if not altogether unsound. And yet I would by no means
be understood to deny that persons hereditarily predisposed to neurotic
diseases, and especially to those of advanced life, may be specially:
liable, ccvteris paribus, to angina in its more painful forms. Much care,
however, is necessary in sifting facts and details of symptoms when.
recorded with a view to make good a general theory of this kind ; and
when we are called upon to accept a narrative of epidemic angina
pectoris in a ship's crew, in which " numbers of men were simulta-
neously affected," while others were seized with '* other forms of
neuralgia, and severe colics," 3 I cannot but infer that the limits of a
safe induction have been considerably exceeded. In like manner,
" remarkable " cases of " hysteria, the paroxysms of which were always
accompanied by stenocardiac attacks/1 can only serve to give a doubt-
ful cliaracter to the theoretic interpretations which Eichwald has
obtained from such a field of experience.4 And even Eulenburg*
notwithstanding the sobriety of his tone in general, and the great im-
portance of his work as a magazine of valuable information and research,
has shown how much a sound clinical observation has been subordinated
to theoretical ideas, when he pronounces dogmatically that the disorders
of respiration in angina are merely " consequences of the pain ; the
patient is afraid to inspire deeply, but if induced to do so, can generally
accomplish it" 6 It may be doubted, I think, on the whole, whether

i Op. cit. p. 156'.

2 Ibid. p. /2. This might be a valid hypothesis were it possible to affirm that the
subjects of fatal angina arc chiefly drawn from the class of men that take the greatest
amount of strong physical exercise. The opposite, however, is notoriously the fact. We
have already alluded to the generally received statement of Sir John Forbes, that angina
pectoris is " the attendant rather of ease and luxury than of temperance ; " and that

laborious el

it is comparatively rare (in its simple and typical form), amon^ the
8 Ibid. p. 74. The authority given is Guelineau, Gaz. des Hopitaux, 1862.
4 See Isulenburg, infra, p. 438. Ferhaps the same remark applies to the presumed
relationship between angina peotoris and spasmodic asthma, as indicated by Kneelaaad^
Amer. Journal of Med. Science, Jan. 1850, and Anstie, op. cit., p. G8. It is to 1»
remarked that Trousseau, in his vast and varied experience, has not recorded anything
tending to confirm the relationship of these two neuroses, except in a case where bot£
of them were dependent on aneurism of the aorta. See his Clin. Med., Kngliah trauaW
tion, voL L p. 634.

* Med. Times and Gazette, March 26, 1870, p. 329. We have seen how emphatically
this idea- is contradicted by the specific statements in John Hunters case, as well as by
all the most exact clinical observations from Heberden downwards.

ANGINA PECTORIS AND SUDDEN DEATH. 579

much real knowledge has been gained by the classification of angina
pectoris among the neuralgise ; to which, nevertheless, the character
of its pain shows a remarkable affinity.

Proceeding now to consider the motor derangements which form a
part of the angina-paroxysm, and especially those which, affecting
the heart itself, determine the fatal termination, it. is impossible to
overlook the facts brought to light by physiology as regards the
influence of certain nerves on the movements of the heart. In parti-
cular, the remarkable inhibitory influence of the efferent nerves pro-
ceeding to the heart through the pneumogastrics, demonstrated by the
brothers Weber x in 1846, and in L856 shown by Waller2 to be due to
filaments from the spinal accessory nerves joining the pneumogastrics
near their origin, has a peculiar interest for us in connection with this
subject. It has been. conclusively shown that by a galvanic current
transmitted outwards through these filaments, or by galvanisation of
the centre in the medulla from which they are derived, the heart's
action may be controlled, or even stopped, so that a true cardiac
paralysis is tbe result of a strong current, while weaker galvanio action
produces an indefinite retardation in. the rate of the cardiac pulsations.
Whatever theory be adopted as regards the so-called inhibitory influ-
ence, its results are too closely allied to the phenomena of syncope,
pure and simple, to escape attention in treating of sudden death from
angina. But it has been further shown by Cy on and Ludwig,3 that a
reflex influence may be: so transmitted through newes arising from the
pneumogastrics, (viz., the so-called depressor-nerves), as at once to
control the cardiac pulsations through the inhibitory efferent nerves,
and to diminish muscular tension through the vaso-motor system.
As we have already seen reason to. believe that in angina pectoris the
vascular tension is usually increased rather than, diminished, it may
be inferred with great probability that if the pneumegasfeic nerve be
implicated at all in the anginal-paroxysm, it is probably more as an
inhibitory or efferent, than as a reflex or afferent nerve. It must not
be forgotten, however, that paralysis of the. sympathetic nerve has the
effect also of enfeebling and retarding, though not, apparently, of
stopping, the heart's action ; which, in a. certain sense, may be regarded
aa not essentially dependent upon influence transmitted from any nerve-
centre, though subject, as we have just seen, to control through the
inhibitory or efferent, cardiac filaments of the pneumogasfcric.

If we endeavour now to determine, in the light of these facts, what
is the particular mode, in which the heart's action is. suddenly arrested
in. a paroxysm of angina, it must, be confessed that no ultimate de-
cision seems possible. Almost all. the vague and. unsatisfactory specu-
lations formerly alluded to, as to whether spawn or paralysis is tbe
prevailing condition in the fatal paroxysm, have proceeded on the
assumption, that these two conditions are essentially contrasted,, or

1 Wagner, Handwbrterbuch der Physiologic, BcL iii.,. 2te Abtheilung, S. 42.

8 Gazette M^dicale, Paris, 1856, t. xi. p. 420.

\ Journal de PAnatomie, Paris, 1867, t iv. p. 472.

580 A SYSTEM OF MEDICINE.

rather opposite to, and inconsistent with, one another; the former
representing undue strength, the latter undue weakness, or absolute
annihilation of contractile energy. Now this assumption can by no
means be regarded as a legitimate, *or even a probably correct one.
At least it may be fairly affirmed, as a probable result both of phy-
siological and pathological inquiries, that spasm (i.e., irregular or
abnormal contraction, whether painful or not) in a voluntary muscle
is much more allied to weakness, or to deficient innervation, than to
absolute excess of normal energy. And the frequency of the associa-
tion of rigid or tonic spasm with paralysis, in the voluntary muscles,
would tend to show that there is no absolute inconsistency, at least,
in the supposition that both spasm and paralysis may, in varying
degrees, be present in the heart's arrested action which leads up to
sudden death in the angina-paroxysm. As far as observation goes, in
the case of spasm of the involuntary muscles (other than the heart),
it seems as though abnormal, or painful, disturbances of rhythmic
action were almost always an indication of weakened innervation,
rather than of superfluous energy in the contractile apparatus as a
whole. The spasm of colic, for instance, is associated with constipa-
tion, or deficient peristaltic action of the intestines ; the false pains, or
painful spasms, of the uterine muscles retard, instead of expediting,
the process of delivery. We might, therefore, not unfairly argue from
these analogies, that a painful spasm of the heart might be expected to
interfere with its rhythmic or normal action quite after the manner of
a paralysis, the abnormal being substituted for the normal action, and
the whole sum of disordered effort being less than the sum of normal
energy expended in healthy cardiac action. So that it might very
well be presumed that painful spasm is by no means unlikely to be
associated with a tendency to sudden stoppage of the heart's action,
or virtual paralysis, whether from inhibitory nervous irritation through
the pneumogastrics, or from disorders originating in the cardiac ganglia
themselves, and allied in character to true paralysis of muscular energy.
It must, however, be conceded to the advocates of the theory of para-
lysis, pure and simple, that nothing but the presence of severe pain in
the angina-paroxysm, and the absence of this symptom, as a rule, in
purely paralytic affections, tends to support the spasm-theory of angina.
Post-mortem examinations have generally shown that the heart is found
flaccid, rather than rigidly contracted ; and the lesions found in the
muscular substance of the heart itself are usually such as would con-
firm the idea of decidedly and permanently weakened energy, rather
than a disposition to abnormal contraction. Eupture of the muscular
bundles, so commonly observed in tetanus and other severe spasms of
voluntary muscles, has never been recorded in sudden deaths from
angina pectoris ; while anaemia, fatty degeneration, and fibro-tendinoua
substitution, have been the predominating lesions of the muscular fibre
itself. The question as between spasm and paralysis, therefore, is one
of great difficulty, if not indeed practically insoluble in the present
state of our knowledge.

ANGINA PECTORIS AND SUDDEN DEATH. 581

While dealing with hypotheses of which no absolute or experimental
proof can be obtained, we may remark that vaso-motor spasm, operat-
ing indirectly through the smaller arteries upon the muscular fibre of
the heart itself, may possibly give a clue to some of the pathological
changes which attend the paroxysm, and especially those which pre-
cede dissolution. Both Erichsen1 and V. Bezold2 have shown that as
a result of deligation or occlusion of the coronary arteries, the heart's
contractions become feeble or irregular, and ultimately cease ; the
normal action being restored again on removal of the ligature or of
the compression. Now apart from the obvious bearing of these facts
upon the case of organic obstruction or constriction of the coronary
vessels (perhaps the most clearly established of all the permanent
organic changes in connection with fetal angina pectoris), is it not
extremely probable that a similar effect, or an aggravation of a pre-
existing tendency to interrupted cardiac action, might occur, if in a
case of disease of the aorta or coronary arteries, cardiac anaemia were
aggravated for the moment by vaso-motor spasm of the smaller
arteries within the heart itself? Even without such preceding
organic disease it is conceivable that extreme vaso-motor spasm might
affect the cardiac circulation directly through its smaller arteries, and
so produce changes more or less similar to those observed in the
experiments above mentioned. What has been already stated, how-
ever, in regard to Nothnagel's observations would seem to show that
really fatal angina does not occur in this way ; and that the first
effects of general vaso-motor spasm upon the heart are more of the
nature of palpitation, or excited action, than of interrupted or sus-
pended pulsation.

On the whole, it must be admitted that the ultimate pathology of
the angina paroxysm does not admit of being reduced to any very
precise expression or definition ; but various more or less probable
conjectures may be made, in accordance with known facts and experi-
mental researches, as well as with clinical and pathological obser-
vation, to account for the facts. Viewing the paroxysm as a neurosis,
we might attribute its phenomena partly to vaso-motor spasm, and
partly to inhibitory influence transmitted through the vagus nerve
from the medulla oblongata. This latter influence would account
more reasonably and probably than any other for those cases of angina
in which mental causes and sudden shocks of any kind are known
to influence the production of the paroxysm, without the intervention
of peripheral changes such as can be attributed to vaso-motor spasm.
In cases, again, resembling in their symptoms those described by
Xothnagel, whether accompanied by organic disease or not — cases in
which coldness of the surface, deadness of the extremities, and per-
haps palpitation or increased rate of the pulse can be ascertained to
precede the cardiac pain, there would be reasonable ground for pre-
suming that the vaso-motor nerves were the earliest involved in the

1 London Medical Gazette, July 8, 1812,

* Centralblatt fur die Med. Wissensehafton, 1867, No. 23.

682 A SYSTEM OF MEDICINE.

morbid circle, though it is still probable that, if such cases ever end
in sudden death, it is through some more direct impression on the
cardiac nerves, or on the coronary circulation. It is very doubtful,
however, whether under any circumstances fetal angina pectoris can
be viewed as a pure neurosis. Much more probably, the paroxysm is
the expression in symptoms of sudden changes arising, indeed, from
neurotic accidents, but only assuming grave importance in respect
of their coincidence with a permanent cause of detriment to the cir-
culation. Either the heart's fibre is permanently weakened, or its
arteries are obstructed and diseased, or the general arterial circulation
is disturbed through disease in the first part of the aorta, aneurismal
or other. In certain cases it may be that the innervation of the heart is
directly implicated in organic disease ; at least in two cases of this
kind1 the cardiac plexus and cardiac branches of the vagus were
found to be compressed in connection with angina-paroxysms which
proved fatal ; though probably the inferences which have been drawn
from these rare instances may not be applicable to the general patho-
logy of the subject. But whatever be the nature of the permanent
change underlying the disease, its effect in the most characteristic
cases is not much felt when the circulation is in a moderately tran-
quil state. In some of the very worst cases, indeed, it has been
clearly ascertained that very shortly before a fatal paroxysm the
patient has been in a state of entire comfort and tranquillity, with a
regular and normally acting heart, and all the functions apparently
so well-adjusted as to involve no appearance of any disease tending
to shorten life. Usually there is an incapacity for sudden or severe
exertion, and a liability to grave disturbance imder strong emotion ;
but on the other hand, a patient has been known to say, within three
days of his death hi a paravtfsni, " I can walk with ease ten or fifteen
miles, after I have been stopped three or four times at intervals of a
hundred yards." 2 In such cases the paroxysms are plainly neurotic ;
but the disease is nevertheless not a pure neurosis. It is, on the
contrary, obviously of a complex character, involving a permanent
nucleus, so to speak, of organic change, together with a neuralgic
element, more or less pronounced, and, connected with this, perhaps
as a reflected neurosis in some cases, an element of motor disturbance
in the heart's action, which may in some cases be of vaso-motor
origin, while in others it may be more directly determined through
the inhibitory filaments of the vagus. It is probably in the former

J Heine, in Midlers Arehiv. 1S41, p. 236 ; and Lauccrcaux, in Gazette Medicale,
1867, p. 432. In the former case the heart was at times observed to cease beating for
several seconds, and at these times there was a feeling of indescribable auxiety, like that
of angina pectoris ; in the intervals of the paroxysms the patient felt perfectly well. Tho
right phrenic nerve, the nervus cardiacus magnus, and the pulmonary branches of th*
left vagus were all involved in, or compressed by, calcareous deposits. In lianeereaux's
ease, the cardiac plexus was found vascular, and compressed by exudation ; but the
coronary arteries were also obstructed, and the aorta was diseased. The patient died of
angina pectoris, in a paroxj'sm.

2 Walshe, Diseases of Heart and Aorta, ith edit, p. 190, >«>'<-.

ANGINA PECTORIS AND SUDDEN DEATH. 583

class of cases that the action of nitrite of amyl is most immediately
and surely productive of benefit.

There remains for remark only one obscure, and apparently non-
essential, part of the pathology of angina pectoris, viz., the nature of
the cerebral accidents we have indicated in the description of the
disease as sometimes coinciding, sometimes alternating, with the more
decidedly cardiac attacks. It is to be observed that among these
accidents spasms, giddiness, temporary attacks of coma, associated
with, or followed by, various disorders of the special and general
sensibility, are common ; while on the other hand, paralysis, either
spinal or cerebral, is rare. These facts point strongly in the direction
of a neurosis, and very probably a vaso-motoT neurosis, of the cere-
bral circulation ; and we know that in animals most of the symptoms
above referred to may be induced artificially, by cutting off the
arterial vascular supply of the brain and medulla-oblongata, as in the
well-known experiments of Sir Astley Cooper.

The Prognosis of angina pectoris is difficult to realise in individual
cases, in proportion to the absence of clear lines of distinction between?
this and the various affections resembling Heberden's angina, which
we have discussed in various parts of this article. Probably a
critically exact, or absolute, prognosis, could only be founded on a
kuowledge of the nature and extent of the organic changes under-
lying the paroxysmal neurosis ; and although we have already indi-
cated a doubt as to whether the latter ever terminates fatally in
the absence of such organic changes, yet it is beyond all question
that the amount of organic disease which can be detected in any
given case during life is a most insecure guide in estimating the
probabilities of death during a paroxysm in that particular case. " It
is accordant with my experience,,, says Dr. Walshe, " that fatal angina
is more to be dreaded in association with organic defects, either diffi-
cult or impossible to diagnose (such as slight fatty metamorphosis
and calcified coronary arteries), than with those grave forms of struc-
tural mischief that are readily discoverable by physical examination."1
Add to this that the mere inference from symptoms as to the gravity
of the prognosis is likewise extremely open to fallacy ; inasmuch as.
a series of comparatively mild or lessening attacks may sometimes
(under apparently unchanged conditions) be succeeded by the most
violent or dangerous, even fatal, paroxysms ; while on the other hand,
one or more attacks, very nearly fatal, may be followed by a long
interval of comparative, or nearly complete, freedom. From this
dilemma there is, in the present state of our knowledge, no escape ;
and all that we can do, therefore, towards the establishment of a
guarded and limited prognosis in any case, is to study carefully its
individual features, and particularly the relation of the symptoms to
particular causes of aggravation, or of relief. Generally speaking, a
form of disease which yields, gradually, to carefully pursued hygienic

1 Op. cit. p. 201.

4)84 A SYSTEM OF MEDICINE.

treatment, and in which the paroxysms are obviously under the con-
trol of the remedies about to be discussed, is relatively favourable ;
while the opposite indications justify the gravest prognosis. An
absolutely favourable prognosis could only be justified by circum-
stances tending to place the disease in the category of pseudo- angina,
as above indicated ; and indeed it may be generally observed that
the gravity of cases of angina in the experience of individual
observers is often found to be in an inverse proportion to their
estimated frequency, cases of hysteria, intercostal neuralgia, spas-
modic dyspnoea, &c, being admitted by some more freely than others
into the category of angina. There seems no reason to doubt, how-
ever, that a person affected with absolutely typical angina pectoris
may survive for years, even after repeated paroxysms ; and in some
cases, apparently of the most threatening kind at one stage of their
progress; the disease has been so far reduced in its frequency and
severity that we may even, perhaps, speak of such cases as cured, in
a practical sense. But cures of this kind are rarely, if ever, recorded
with such minute attention to details as to inspire confidence, apart
from the credit due to the reporters ; and perhaps even the statements
of Heberden as to the long survival of some of the cases mentioned in
his first paper (see p. 559, note) may require qualification on the ground
that clear evidence is wanting as to the absolutely typical character of
the symptoms referred to.1 Among cases actually ending by a fatal
paroxysm, it has not occurred to me personally to have been informed
of a longer duration than six or seven years, counting from the first
well-defined seizure ; but I have known more than one instance of
survival for much longer periods, after attacks bearing so much re-
semblance to true angina as only to have required death to have
occurred in a paroxysm, as a conclusive argumeut for considering them
to be typical instances of the disease. In John Hunter's case, as we
have seen (assuming the first attack of supposed gout in the stomach
to have been really identical in character with succeeding seizures) a
duration of rather more than twenty years, with numerous intervals
of tolerable health and great mental activity, may be regarded as well
established. Dr. Walshe has " met with an instance in which there
was the strongest evidence that the first paroxysm had occurred
twenty-four years prior to my interview with the patient." 2 And, in
the general experience of physicians who have had occasion to see
much of cardiac disease, it is by no means uncommon to find cases
of valvular or other very positive and well-defined organic disease, in
which symptoms of a dangerous or proximately fatal kiud, probably

1 It is at least worth noting (though the omission may be accidental) that in the
Commentaries these statements arc not repeated : and perhaps the language, though
carefully guarded, admits of the inference that thirty years of additional experience had
rather increased than diminished Heberdcn's sense of the gravity of the prognosis.
" Exitus hujut affectus est perquam memorabilia. Qui mini co tencntur, siquidem, nullo
citsu iiUerveniaUe, angina pectoris ad cucfiriv iKrrenerit, omncs rtpcnJte corruunt, etferr
niomento pcrtunty ..." Unicum vidi {/tgrum), id quo hoc malum spontc sud Jinttnm
est." 2 0p. cit., p. 200.

ANGINA PECTORIS AND SUDDEN DEATH. 565

more or less allied to angina, have preceded the fatal issue by an
interval of very many years ; sometimes, indeed (as in the 'case
of the Kev. Dr. Guthrie, already referred to1) for more than a
quarter of a century. Such cases, however, are rarely quite typical
instances of Heberden's angina, and accordingly only a small propor-
tion of them are characterised by the very sudden ending proper to
the disease as described in the " Commentaries." It is difficult to obtain
exact clinical histories of cases extending over so many years, but in
one, in which I was consulted in 1872, and which terminated fatally
some months ago, there was reason to suppose that the foundations
of the aortic valvular lesion of which the physical signs were apparent,
and of which the obvious symptoms had certainly existed many years
before 1872, had been laid as early as 1852, when the patient had
suffered from pulmonary haemorrhage. The threatening symptoms
present on that occasion had been popularly attributed to a consump-
tive tendency, but Dr. Christison, who was consulted, had evidently
detected some valvular lesion of the heart, and had carefully questioned
the patient as to its possible rheumatic origin. It is not, indeed,
certain, or even perhaps very probable, that well-marked and consid-
erable aortic regurgitation existed at this period, nor is it possible
now to ascertain at what precise interval after the first commence-
ment of the disease the angina-like symptoms, which were notably
present when I saw the patient, first became apparent. What I can
personally affirm is, that in 1872 the symptoms and physical signs
were those of old-established aortic regurgitation, with very consid-
erable hypertrophy of the left ventricle, and all the usual concomi-
tants ; and notwithstanding this, the patient assured me that so late
as 1870 he had explored the Aletsch glacier, and on other occasions,
from about 1865 onwards, had been able to carry out walking tours
in Switzerland, the Tyrol, and the Dolomite country, the character of
which may be inferred from his having walked over the Monte Moro
pass and the Gemini, visited the Mer de Glace, and gone nearly to the
Jardin, in addition to all the usual excursions about Chamounix.
Moreover, tliis gentleman was in 1872 performing the duties of a
parish clergyman in a populous place, sparing himself somewhat,
indeed, in visiting, but preaohing often more than once a day, and, as
he affirmed, without any apparent injury or physical exhaustion ; and
the question most urgently and repeatedly pressed upon his medical
advisers was as to his carrying out an engagement of marriage, entered
into several years before, and maintained with full knowledge on both
sides of the precarious condition of his bodily health. I need not say
that no medical encouragement to this step could be obtained ; but
the marriage, nevertheless, took place in about a year after I was first
consulted, and the death of this patient not long ago shows how real
was his danger, and at the same time what a terrible burden of
positive organic disease may be borne without apparently " giving in,"
by one whose objects in life are of sufficient importance to induce him

1 See ante, p. 568, note.
VOL. IV. Q Q

580 A SYSTEM OF MEDICINE.

to disregard the silent warnings of internal suffering. In yet anothei
case known to me, in which, however, the symptoms were far more
decidedly and typically those of angina pectoris, while the physical
signs were much less manifest than in the preceding case, the patienl
was able to make numerous long journeys to the Holy Land, Egypt
&c, and always felt himself the better for them. This patient in the
end perished suddenly.

The Treatment of angina pectoris resolves itself naturally into twe
departments, viz., that of the paroxysm, and that of the intervals
The former treatment is essentially palliative, and directed exclusively
to the urgent symptoms then existing: the latter aims at being
founded, in a wider sense, upon the diagnosis and prognosis of the
individual case, after a complete examination into the state of all the
bodily functions.

Heberden's views of treatment were limited to the first indicatior
— the control of the paroxysm. " Wine and cordials taken at going tc
bed will prevent, or weaken, the night fits ; but nothing does this sc
effectually as opiates. Ten, fifteen, or twenty drops of the tincture
Thebaica taken at lying down will enable those to keep their beds
till morning who had been forced to rise, and sit up, two or thret
hours every night for many months." * We have already seen thai
Heberden altogether repudiated the (so-called) antiphlogistic treat-
ment as inapplicable to this disease, which he considered as belonging
to the order of spasms, not of inflammations. In his later work he
repeats in general terms the above recommendations, and adds tc
them a single phrase in favour of rest and warmth. He has seen at
approach to a cure in one case, where the patient prescribed to him-
self the labour of sawing wood for half an hour every day. Beyonc
this, he has little or nothing to tell, and does not profess to have
greatly advanced the cure of a disease, " qui vix ad hue locum, aul
nomen in medicorum libris invenit." It may be fairly inferred fron
these expressions, that Heberden's views of the treatment of angim
remained almost stationary for at least thirty years ; and that here
as in the matter of prognosis, he does not appear to have gained con
fidence with his advancing experience. The treatment of tin
paroxysm by opiates and stimulants of various kinds has in fact beei
repeated by almost all the leading authorities, and is even now th(
only medical treatment which can be said to have received genera
assent. Latham, Stokes, and Walshe, among our more modern authors
concur in recommending from forty to sixty drops of laudamira
together with wine, brandy, or aromatic spirits of ammonia, repeats
according to the violence of the paroxysm. Hoffmann's anodyne, o
sulphuric ether in half-drachm doses, has been a favourite remed
with many ; and musk, camphor, and other antispasmodics, have als
been employed, though confessedly of less value than ether, whicl
lias also been followed by good results when administered by inhala

1 Med. Trans., vol. ii., ut snjira.

ANGINA PECTORIS AND SUDDEN DEATH. 587

tion. Of late years, opium has been given hypodermically, and, it is
stated, with more immediate as well as more successful results than
when administered by the mouth. In so far as the principle of the
treatment can be inferred from the success that has attended those
remedies in some cases, it would appear that a rapidly induced nar-
cotism, benumbing the sensory nerves and extending, perhaps, to the
centre through which painful sensory impressions are reflected in the
form of a paralysing or inhibitory influence on the heart, by the motor
fibres of the pneumogastric, is the first object to be accomplished in
the presence of overwhelming pain, while the second and not less im-
portant object is to stimulate the heart's action by all the known
excitants of the circulation. Warmth to the extremities and to the epi-
gastrium, sinapisms to the thorax, and sometimes between the shoulders
or at the back of the neck, may be regarded also as additional means
of fulfilling the latter indication, and of assisting the cardiac contrac-
tions by their influence on the vaso-motor nerves. In my own expe-
rience, no remedial agencies have appeared more powerful than warm
pediluvia with mustard, and fomentations applied at the same time to
the arms and thorax, as hot as they can well be borne. With these,
and with ether and other diffusible stimulants, I have often been able
to dispense with the use of large opiates, in doubtful cases, or incases
where they seemed to be in some respects contra-indicated. It is
well, if possible, to be informed of the condition of the kidneys, and of
the lungs before prescribing opiates. Dr. Stokes x evidently looks
upon large opiates as unsafe where fatty degeneration of the heart's
fibre is suspected ; and Niemeyer 2 discountenances narcotics altogether.
The use of opium, however, is too valuable in typical cases of Heber-
den\s angina, when apparently uncomplicated, to be readily given up.
It should be given with discretion, its effects being carefully watched ;
and it should probably be withheld, or given in extremely moderate
doses, wherever there is risk of uraemia, or of bronchial and pulmonary
sudden congestion or oedema, or of the cerebral accidents that accom-
pany angina in certain cases, especially those in which the cardiac
fibre is the seat of degeneration. In these cases, too, it is not usual
for the mere pain of angina to be so threatening, per se, as to suggest
opium in the same high doses as in the more typical instances where
the paroxysm occurs in the midst of apparent good health.

Hydrate of chloral, from its well-marked sedative and anodyne
powers, has been suggested as a substitute for opium in cases of
painful angina;3 but on the other hand, the depressing action of
chloral-hydrate in large doses has been supposed to be a fatal object-
tion to its employment in cases of weakened cardiac action. My
experience of this remedy in severe cases resembling angina pectoris
is limited to one case, but it is so remarkable as to deserve notice here.
John McN., aet. 35, was subject to paroxysms of intense cardiac

1 Diseases of the ITeart and Aorta, p. 489.

2 Text-book of Practical .Medicine, American translation, vol. L, p. 371.

3 Strange, Medical Times and Gazette, Sept 4, 1870.

QQ 2

588 A SYSTEM OF MEDICINE.

suffering, of a rather obscurely painful character, but with considerable
orthopnoea, palpitation, sleeplessness, and frightful dreams. His symp-
toms are more particularly referred to in an earlier part of this article,
and from a very careful consideration of them I arrived at the con-
clusion that they were essentially of the character there described as
angina sine dolore, with slight bronchitic complication, and slightly
albuminous urine^-sp. gr. 1013 — 20. The heart's action was irregular,
and the physical signs pointed unmistakably to hypertrophy of the
heart and liver, with valvular and (probably) arterial disease. The
details are too complicated to be introduced here, but my diagnosis
was — Aortic insufficiency, with aneurism. The case was certainly not
one in which extreme doses of any narcotic would have been regarded
as expedient ; but, guided by experience acquired before he applied to
me, I allowed this patient to have thirty grains of hydrate of chloral
to obviate the sleeplessness, and if possible to ward off the attacks.
It answered well the first night, and on a succeeding occasion the
same dose was ordered, and was to be given a little before midnight.
By a misunderstanding of the directions three drachms of hydrate
of chloral were sent instead of a like quantity of the usual syrup, and
this being in one dose, apparently to be given as a draught, the
patient took 180 grains at once of chloral-hydrate, from the hands of
a night-nurse, after a restless and disturbed evening, at 11.30 p.m.
Next morning I found him very drowsy, but not quite comatose, as
he could be roused to give rational answers as to his own condition ;
the breathing was quiet, and only slightly stertorous. The pupils
were, on the whole, contracted, but variably so ; the pulse, which had
been irregular in rhythm, was decidedly more natural than before ; the
face was a little congested, and the eyelids puffy, but the surftice gene-
rally warm, and the whole appearances not such as to justify any
very great alarm, especially as at the time it was supposed that only
thirty grains of chloral-hydrate had been given, the mistake being
found out afterwards. The patient gradually recovered from the effects
of the overdose, and it is very remarkable that he always continued
to attribute to this happy accident (as it might be called, speaking of
the result only) a comparative immunity afterwards from the angina-
like symptoms. The irregularity of the pulse recurred after the effects
of the overdose of chloral had passed off, but under repeated doses of
from thirty to sixty grains he became much better in all respects, and
a course of iodide of potassium, with careful hygienic management,
accomplished what, so far as the more immediately urgent symptoms
are concerned, may almost be called a temporary cure of a very peril-
ous condition. This man is now performing regulated duties as a
railway servant, and is still occasionally taking hydrate of chloral,
though warned not to allow it to become a regular habit. It is clear,
therefore, that in some cases, at least, of angina pectoris chloral-hydrate
might probably with advantage replace opium in the treatment, and
that irregularity of the heart's action does not always prove a contra-
indication to its use.

ANGINA PECTORIS AND SUDDEN DEATH. 589

Inhalations of chloroform have been proposed, and in some cases
employed, for the relief of painful angina ; but, from the supposed
tendency of deep chloroform-ana3sthesia to paralyse the heart, this
remedy has never been warmly supported or largely employed by
physicians in such cases. The inhalation of ether seems preferable
as attended with less risk ; and chloroform, if given at all, should be
in doses short of complete anaesthesia, whether by inhalation or by
the mouth.

Of all the more modern additions, however, to the resources of the
physician in the angina-paroxysm, the most important by far appears
to be the employment by inhalation of nitrite of amyl, as first re-
commended by Dr. B. W. Richardson, and successfully carried out
on a basis of careful clinical and experimental observation in angina
by Dr. Lauder Brunton. We have already indicated in this article
the nature of the scientific evidence on which this therapeutic sug-
gestion rests, and have now only to consider the details of purely
clinical experience in relation to this remedy, and the qualifications
and cautions required in its employment. On this subject our know-
ledge is still very incomplete, but it is none the less necessary to
place on record here whatever can be said to be well established as a
guide to the practitioner.

My own experience, I may remark in passing, is certainly favour-
able to the use of this remedy, not only in positive angina pectoris,
but also in many cases of cardiac asthma, and even of true spas-
modic asthma without cardiac complication. In the very few cases
of typical angina in which I have prescribed it, I have had dis-
tinct testimony as to the relief afforded, although my opportunities
of close observation of the actual paroxysms have not been such as
to enable me to add anything of real value to the statements of other
observers. Looking to the practical aspects of the question, there is
probably no single observation hitherto made which, as a simply
clinical narrative, can rank beside the history of his own case by Dr.
W. Herries Madden of Torquay.1 We shall therefore give here
some details of this remarkable personal experience.

Dr. Madden seems to have suffered from a temporary break-down
in health at 24 years of age, " with obscure heart-symptoms, and
threatened lung mischief.,, His father had died shortly before from
angina pectoris — " the organic cause in his case being atheromatous
obstruction of the coronary arteries." In the winter of 1859, at about
44 years of age, Dr. Williams detected slight mitral incompetency.
In the spring of 1871, Dr. Madden records that he suffered from an
attack of bronchitis, with great nervous prostration, but recovered in
autumn, and was able to perform all his usual duties during the next
winter and spring, in the midst of " a good deal of professional anxiety
and much painful worry of a different nature." On July the 8th,
1872 (at 57 years of age), he had his first attack of angina, which
occurred " suddenly, without the slightest warning," and was charac-

1 The Practitioner, vol. ix. 1872, p. 831.

690 A SYSTEM OF MEDICINE.

terised by " pain extending across the front of the chest, along the
inside of the left arm, and across the chin." In about ten days the
frequent recurrence and increased severity of the attacks compelled
him to desist from all professional duty. Notwithstanding the repose
so obtained, the attacks, after a few days' interval, continued to increase
in violence, lasting, for the most part, for a quarter of an hour or
twenty minutes, and recurring frequently at intervals of about three
hours. " Various remedies were tried, but with little or no benefit.
Hypodermic morphia was the most useful, but it was impossible to
employ it often enough without producing dangerous narcosis." At
this period Dr. Madden was led, after considerable hesitation, to give
a trial to the nitrite of amyl; which he had previously supposed to be
Buitable only for those cases in which the face was pallid during the
paroxysm. " As mine was flushed," he writes, " I dismissed from my
mind all thoughts of trying it, and paid the penalty of hasty conclu-
sions in the shape of a large amount of acute suffering." The result
of the first trial of five drops, inhaled during a severe attack in the
night, " was truly wonderful. The spasm was, as it were, strangled at
its birth. It certainly did not last two minutes, instead of the old
weary twenty. And so it continued. The frequency of the paroxysms
was not diminished for some time ; but then they were mere bagatelles
as compared with their predecessors. Under these improved circum-
stances, strength gradually returned ; the attacks became less and less
frequent, and finally ceased. At the time of writing these lines
(October 11, 1872) I have not had an attack for five weeks, and have
resumed my ordinary duties, of course with care." It is most satis-
factory to be able to add, from a private letter with which the author
has been favoured, from Dr. Madden, that his confidence in the remedy
continues unabated, but that at this date (August 1875) he has not
required to use it for a considerable time.

As regards the more obvious effects of the inhalation of nitrite of
amyl, Dr. Madden records that " the first effect was often bronchial
irritation, causing cough ; then quickened circulation ; then a sense
of great fulness in the temples, and burning of the ears ; then a violent
commotion in the chest, tumultuous action of the heart, and quick
respiration. The angina pain died out first in the chest, next in the
left upper arm, and last of all in the wrist, where it was usually
extremely severe. . . . When the pain had ceased there was generally
for some time a strong involuntary tendency to suspension of breath-
ing, each prolonged pause being followed by a very deep inspiration.
There was not at any time the slightest confusion of thought, or
disturbance of vision, but occasionally slight and transient headache."
The physical signs in Dr. Madden's case seem to have varied some-
what, and latterly had more the characters of aortic than of mitral
disease. The description of the peculiar subjective sensations con-
nected with the heart-pang in this case has been already quoted at
p. 540, note 1.

It can be but rarely that, in a disease so paroxysmal and uncertain

ANGINA PECTORIS AND SUDDEN DEATH. 591

in its characters as angina pectoris, the conditions of a therapeutical
experiment can be so perfectly attained as in this case. The heredi-
tary predisposition, the age and sex of the patient, the proved exist-
ence of positive cardiac disease, and the vivid and personal narrative
of the symptoms, combine in assuring us that the angina was of the
most formidable kind, and all but typical, if not indeed absolutely
so, in character. On the other hand, the relief was so marked, so
strikingly instantaneous, and so frequently observed in repeated
paroxysms, as to leave no doubt of the control exercised by the
remedy. And further, the ultimate relief amounts to something
more than a palliative remedial action ; something, indeed, closely
approaching the character of a cure. Further, as Dr. Madden has
remarked, the relief is shown not to have been contingent upon the
external evidences of vaso-motor disturbance during the paroxysm,
although closely associated (as in Dr. Brunton's case) with the physio-
logical action of the remedy in relaxing arterial tension. It is to
be remarked, however, that beyond the more obvious facts, no very
exact observations were made in Dr. Madden's case as to the con-
nection between the attacks of angina and vaso-motor changes. " The
presence of intense pain," he says, " is not favourable to the exercise
of calm, philosophic analysis, and I can only tell what I felt."

But although this case, and others more or less resembling it
which have been published, give the utmost assurance of the benefi-
cial action of nitrite of amyl in the angina- paroxysm as a fact ascer-
tained by experience, yet the moment we proceed beyond the mere
fact, we find the question of the modus operandi, indications, and
contra-indications of the remedy surrounded with difficulties which
have not as yet been resolved by scientific observation. It has been
commonly supposed that the action of the amyl-nitrite is purely
peripheral, i.e., on the vaso-motor nerves of the vessels only, apart
from the vaso-motor nervous centre ; and that the relief caused in
angina is in direct relation with the previously increased vascular
tension, as suggested by Dr. Lauder Brunton in his first experiment.
We had occasion to point out, however, when speaking of that
remarkable case in its relation to the theory of the angina-paroxysm,
that the state of the heart's action corresponding with the period of
increased vascular tension on the one hand, and with the relief through
amyl-nitrite on the other, was different from what could be attributed
to vaso-motor spasm and paralysis alone ; and that there remain
phenomena of the paroxysm which can be explained, in all proba-
bility, only through the innervation of the heart itself. A like
difficulty still surrounds the explanation of the physiological and
therapeutic action of the nitrite of amyl. Though unquestionably pro-
ducing some of its well-known effects through vaso-motor paralysis,
we are not quite able to affirm with confidence that its action is
purely peripheral, or even that it is quite uniform in all cases of
angina. Thus in Dr. Maddens case it seems to have produced, as a
primary result, "quickened circulation, tumultuous action of the

592 A SYSTEM OF MEDICINE.

heart, and quick respiration. " This is, in fact, the usual effect of
amyl-nitrite on healthy persons, in whom the pulse-rate may be
raised in a few seconds from a normal state of about 70 to 120
or 140 pulsations in the minute ; the flushing of the face, and the
other distinctly vaso-inotor effects following the rise in the pulse-rate.
In Dr. Brunton's case, on the other hand, the pulse became slower
when the spasm was being relieved. In a case published by Dr.
Haddon, which, though rather imperfectly reported, appears to have
been one of aortic incompetency with angina-like pain, the pulse was
jerking, and 80 per minute at the commencement of the. inhalation,
and after only three drops were inhaled " the pulse lost its jerking
character and became gradually slower/' but the face did not become
flushed, and the pain was not relieved. In the course of a minute,
" the pulse beat so slowly that I thought the heart would stop alto-
gether ; while the patient raised himself on his elbow, and with a pale
face moved his head about, as if for breath. At the same time he
seemed confused, and did not answer questions."1 Under brandy and
free ventilation the pulse recovered its former character and fre-
quency, and the patient fell asleep in half an hour. In another case,
which proved on post-mortem examination to be one of aneurism of
the first part of the aorta, pressing on the right ventricle and pul-
monary artery, and with universal adhesion of the pericardium, besides
a degree of compression of the left phrenic nerve by a diseased bron-
chial gland, the paroxysms of coughing, wliich were among the most
apparently dangerous symptoms in the case, were greatly aggravated
on one occasion by the inhalation of five drops of amyl-nitrite, and a
critical state of apnoea was induced. It is obvious that neither of
these cases was one of typical angina, and it is quite possible that
the phenomena may have been only accidentally connected with the
inhalation ; but Sander has recorded two cases, and Samelsohn one
case,2 in which alarming symptoms of collapse followed closely on
the inhalation of amyl-nitrite. In the latter case there was not even
a suspicion of internal disease, the inhalation being done experi-
mentally, with a view to test its effects upon spasmodic closure of
the eyelids in an anaemic young woman. The usual flushing
occurred, but was in an instant " replaced by a deadly pallor ; the
pulse became thread-like and slow, the skin cold and clammy, re-
spiration difficult, and gasping ; consciousness was retained." These
symptoms recurred again and again at intervals for an hour, and even
up bo next day the patient complained of feeling very cold. It is
stated that she was menstruating at the time, and that on subsequent
occasions she inhaled the nitrite without any such alarming incidents.
It is quite possible that the effects of fright, or agitation, or some
other accidental disturbing cause, may in these cases have complicated
the action of the amyl-nitrite; but still they form a warning, not
only that dangerous results may in certain circumstances follow its

1 Edin. Med. Journal, July 1870, p. 46.

2 London Medical Record, March 17, 1875, p. 168 ; and Aug. 16, 1875, p. 479.

ANGINA PECTORIS AND SUDDEN DEATH. 593

inhalation, but that the theory which regards its action as purely
vaso-niotor, and still more that which considers the vaso-motor
nervous centres, and the brain and spinal cord generally, as not
within the range of its direct influence, must be held in the mean-
time as subject to reservations to be afterwards ascertained by
experience.

Generally speaking, the administration of nitrite of amyl in angina
has been found to be free from danger, when used in doses of from two
or three up to ten minims on a cloth or handkerchief, abundant access
of air being allowed at the same time. The first effects of the remedy
in healthy persons are, as stated above, increased frequency of the
cardiac pulsations, with a feeling of palpitation, and throbbing of the
carotids, followed in the course of thirty to forty seconds after the
commencement of the inhalation by flushing of the face, warmth of
the head, face, and neck, with perspiration; the latter symptoms
beiug often general. Breathlessness and disposition to cough, giddi-
ness, headache, slight indistinctness of vision, lassitude, and a feeling of
intoxication, are among the variable after-effects. The actual ther-
mometric temperature of the body does not appear to be much, if at
all, affected ; and consciousness is always preserved.1 When given in
angina the effects are similar, with the exception of the discre-
pancy formerly alluded to as regards the cardiac pulsations. The
flushing of the face must be fully developed, in severe attacks of
angina, before any relief is to be obtained ; but in minor attacks the
pain and sense of constriction give way before a very few drops ;
almost immediately on the first inhalations, or even after merely
applying a bottle containing a little of the remedy to one nostril.
Three to five drops on a small piece of lint, or on a handkerchief,
may be said to be an ordinary, or experimental dose, as a commence-
ment. When the patient has become thoroughly familiar with the
effects of the remedy he may, if intelligent and conscientious, be
entrusted with a quantity sufficient for ordinary use at his own dis-
cretion. One patient mentioned by Dr. Jones 2 had used about thirty
ounces in six months ; but the large quantity was accounted for by
his belief that the remedy when kept in the pocket in a small stop-
pered bottle, became " flat," and required to be renewed. Dr. Jones
believes that he was right in this impression. This patient discarded
the lint, and always inhaled directly from the bottle, which he always
carried about with him, containing about half a teaspoonful of the
remedy. " One night his father found him sound asleep, with his

1 Compare Goodhart, Practitioner, voL vi. 1871, p. 12 ; and Talfonrd Jones, ibid,
vol. viiL 1872, p. 213. Dr. Wood (Amer. Journal of the Med. Sciences, new series,
vol. lxL 1871, p. 422) found that by poisonous doses in animals temperature was
lowered "to a degree which is almost unheard of in the history of drugs." He also
found that this substance has "the curious chemical property of checking oxidation."
It prevents the change of venous into arterial blood, produces gradual paresis, depresses
the action of the heart, and yet fails to affect consciousness and sensibility almost to the
very lust Some of these results appear to require confirmation.

J The Practitioner, vol viii. p. 219.

504 A SYSTEM OF MEDICINE.

hand hanging over the bed, and the bottle held firmly in its grasp."
He declared that " he would not be without ' his bottle of drops ' for a
hundred pounds." This was a most remarkable case of relief, in
what seems to have been aortic regurgitation, in a man of twenty-one
years of age. It shows, however, that this remedy, like all others of
the same class, is liable to abuse.

The remaining remedies of the angina-paroxysm are probably of
small account in comparison with those already mentioned ; but it is
desirable to add a few words with respect to some of them. Not-
withstanding the opinion of Heberden, blood-letting has been recom-
mended, and in some cases, perhaps, successfully practised ; the cases
being probably those in which evident signs of cardiac venous con-
gestion existed. In Dr. Brunton's case small blood-letting, of a few
ounces only, appeared to give relief. Dry cupping between the
shoulders is a more reasonable, or, at all events, less spoliative method
of unloading the heart, and might in some cases co-operate advan-
tageously with the use of warm stimulation of the surface as above
recommended. Laennec first suggested the transmission of a mag-
netic current through the chest; but this suggestion may be said to have
had no practical result, and the first apparently effective use of elec-
trical or galvanic currents in angina pectoris is due to Duchenne, of
Boulogne,1 who professes not only to have relieved, but to have
cured a typical case of severe angina of five months' duration, in a
currier, aged fifty, " of a stout build and sanguine temperament, rather
fat, and with a short neck," by treatment for a fortnight only with a
strong faradic current passed through the skin of the nipple and upper
region of the sternum. The description of the case is extremely
striking, but its phenomena being purely subjective, there is not any
absolute guarantee for its being more than a severe case of intercostal
neuralgia, in which the extremely violent action of the " induction-
apparatus graduated to maximum intensity, and working with very
rapid illtermissions,,, . produced the effect of a strong and sudden
counter- irritation. On any other supposition, indeed, the results
are almost too wonderful for belief. The first shock produced excru-
ciating pain, so that the patient uttered a loud shriek, and the current
had to be arrested. This artificial pain, however, completely and
immediately removed the angina pain, as well as the sensations of
numbness and formication which accompanied it ; and " the patient
felt at once in his normal condition." Succeeding paroxysms were
similarly arrested, and in a fortnight the patient was able to resume
his employment. Another case, communicated by Aran to Duchenne,
is specially cited by Trousseau (who records both cases in great detail)
as " giving more value to the preceding considerations ;" but this will
probably not be the judgment of the reader of the preceding pages,

1 De l'clectrisation localiseo et do son application a la pathologie et a la therapeutiquc.
3ieme. etJit. Paris, 1872, p. 808. See also note Sur l'inlluence therapeutique de.l'ex-
citation electro-cutauee dans l'angine de poitrine, Bulletin de T/tfrapcutique, 1853 ;* aud
compare note on next page.

ANGINA PECT0BI8 AND SUDDEN DEATH. 595

when he learns that the subject of Aran's therapeutical experiment
was a woman of thirty-two, who had been extremely hysterical, if
not cataleptic, from intense grief, and had been for a long time a prey
to a multitude of nervous disorders, the result of violently disturbing
emotions.1 Eulenburg has employed the constant current, up to a
strength represented by thirty elements of Siemen's battery, applying
the positive pole with a large surface for contact to the sternum, and
the negative to the side of the lower cervical vertebrae ; the successes
which he claims, however, are rather equivocal, and it may be inferred
from the method of his reasoning that he only employed the remedy
in cases regarded as of vaso-motor origin.2 I am not aware of any
case in which angina pectoris of obviously organic origin has been,
even temporarily, relieved by any form of electrical or galvanic appli-
cation ; but possibly further trials may still be desirable. Digitalis,
aconite, and veratrum, have all proved either useless or injurious.

The treatment of the inter-paroxysmal state in angina pectoris
depends essentially on the careful application to the individual case
of all the practical suggestions arising from a very complete diagnosis,
and from a consideration of the causes which have been observed or
supposed to be chiefly at work in predisposing to, or in actually bring-
ing on, the paroxysms. Generally speaking, tranquillity, both of body
and mind; especially the suspension of all occupations, or even
amusements, that tend to overstrain the heart, or hurry the breathing ;
very moderate daily exercise on level ground, and only to such an
extent as is requisite for preserving the bodily tone, or for good diges-
tion ; the avoidance of all manner of food tending to flatulence, and
the regular, but strictly moderate evacuation of the bowels, either
spontaneously or by the mildest laxatives, are measures of hygiene
so obviously suggested by simple prudence as hardly to require more
than a passing allusion. It is not by any means certainly ascertained
whether the subjects of angina ought to use alcoholic stimulants in
any measure liabitually, or to reserve them for the critical period of
the attack. I incline to the latter opinion. Venereal excitement is
probably in all cases an unfavourable influence. The use of tobacco

1 It is, perhaps, worthy of remark, that the experience of twelve years after his first
acquaintance with the facts of Duchenne's aud Aran's cases had not enabled Trousseau
to add anything of a more personal kind to his long citation from Duchenne's narrative,
first published in 1853. See the 2nd edition of Trousseau's " Clinique do l'Hotel
Dieu " (vol. ii. pp. 453-7), published in 1865, not mug before his death. Duchenno
himself, in the 3rd edition of his well-known work (referred to above) published in
1872, and called in the preface "presqueun nouveau livre," gives only one new case,
with scanty and unsatisfactory details, in which, moreover, after " partial amelioration "
under the method of electro-cutaneous excitation previously described, the patient died
suddenly when entering M. Duchenne's consulting-room. He refers, however, to a
case of cure by M. Boullet, and to "several cases of cure" communicated to the Aca»
demy of Sciences, in February 1869, by M. Ed. Becquerel. These last I have not been able
to discover. M. Becquerel simply reports M. Boul let's case without commentary, and
with such brevity and want of essential details as to deprive it of all real clinical value.
Evidently there is great inexactitude here, as well as a *' plentiful lack " of trustworthy
facts.

9 Med. Times and Gazette, May 7, 1870, p. 490.

096 A SYSTEM OF MEDICINE.

in great excess has been specially investigated as a cause of angina
by M. Beau ; * but although I have frequently observed palpitation
and intermission of the heart's action in smokers, it has not occurred
to me to observe true angina pectoris thus produced. It will be
obviously right, however, to discountenance any indulgence of this
kind which is even doubtful as to its effects upon the heart's action.
Beyond these simple measures of precaution, the treatment must vary
according to the circumstances observed in each case, and it may even
be said that there are cases in which no clear indication exists for any
treatment beyond that of the paroxysm. But if it be discovered that
gout, or congestion of the liver or lungs, or well-marked dyspeptic
symptoms, or renal derangement, has concurred with, or alternated
with, the paroxysms, or even that any of these disorders has been a
marked feature of the case, without any obvious relation to the
angina, it may be found that in undertaking the treatment of these
apparently intercurrent disorders the cure or alleviation of the par-
oxysms may follow in due course. It is said, indeed, by some that
gouty angina is peculiarly amenable to treatment, and therefore less
formidable in its prognosis than other kinds ; aud although this is pro-
bably only an imperfect statement of the fact that cures of angina-
like symptoms are sometimes obtained by remedies in the gouty
habit,2 yet as a practical question of duty there can be no doubt that
we are bound to treat the constitutional disease, as the best means
known of influencing the local symptoms. It will therefore be ex-
pedient to use all possible means for eradicating, or at least diminish-
ing, the gouty predisposition, in cases of angina so characterised, by
careful regulation of the diet and the use of anti-arthritic remedies,
such as the carbonates of potash and lithia, or even in some cases
small doses of colchicum ; though it is very doubtful how far a
well-marked attack of gout in the foot ought to be checked, either by
colchicum or any other disturbing remedy, in those who have had
angina and other internal manifestations of the disease. A holiday
at Carlsbad, Vichy, or Toplitz, or, according to the fashion of last
century, at Bath, may help to dispose of the remains of gout when
its regular form threatens to pass into irregular manifestations.
Fothergill and others have affirmed the cure of angina pectoris in
this way.3 If the urine shows persistently, or even frequently, a

1 De l'influence du tabac a fumer sur la production de l'angine do poitrine. — Gazette
des H6yilaux, 1862.

* On the other hand, a large proportion of the fatal cases of angina pectoris has been,
as already shown, connected with gout, and between these two opposite sides of the
question it is not easy to find a secure basis for the alleged relatively favourable prognosis
of gouty angina.

* The case here specially referred to was mentioned.by Fothergill in 1773, incidentally,
in a paper on angina j>ectoris, as " the first case apparently of this nature that occurred to
me, above twenty years ago." He adds, "the person is now, or lately was, living, and in

food health ... He was at that time about thirty years of age, and the youngest subject
have ever seen affected with this disorder." The symptoms are fairly described, con-
sidering the early date, and long interval between their occurrence and the publication,
but can scarcely be looked upon as thoroughly characteristic. He " went to Hath

ANGINA PECTORIS AND SUDDEN DEATH. 597

tendency to deposit litkic acid crystals, the treatment will of course
be guided by this indication : and if acid dyspepsia is present, it will
be necessary to use remedies at once antacid and tonic. If, on the
other hand, the neuralgic element is highly pronounced, more espe-
cially if it is hereditary, or has been manifested in the individual
patient in other forms, the angina pectoris being presumably a mere
form of a more extended constitutional neurosis ; we may probably
look in such cases for relief to nervine tonics, but especially to iron,
strychnine, and arsenic. I have seen in one or two cases very decided
good results from the last of these remedies, given in the form of
the ordinary Fowler's Solution, TT^v. for a dose, two or three times a
day over a considerable period ; and I can to this extent support the
statements of Dr. Anstie, who in this country has chiefly advocated
the use of arsenic in angina pectoris, and who refers to a case pub-
lished by Philipp,1 as having first strongly directed his attention to
the subject. Anstie begins with three minims, and increases the dose
gradually, if well tolerated, up to eight or ten minims three times a
day ; he has found, however, that some neurotic patients cannot tole-
rate arsenic from the irritability of their alimentary canal, and in such
cases it must be discontinued, or perhaps some other form of adminis-
tration might be devised. Anstie gives several striking cases, in one
of which, at least, there had been a few slight attacks of gout, and
a few small calculi ; another was that of a woman, aged forty-six,
who was still menstruating, though irregularly, and who certainly
seems to have had extremely severe symptoms of the order of angina;
she was cured by a six months' course of arsenic in doses gradually
mounting to 21 minims daily; after eight weeks the patient
abandoned the remedy, supposing herself cured, but had to recur to it
from experiencing a renewal of her sufferings, which again yielded to
a precisely similar treatment.2 Arsenic is specially adapted for
anaemic cases, and often exercises a favourable influence over the
function of hsematosis ; but in cases where anaemia is well-marked it
may be combined with iron, or the latter may be given with

several successive seasons, and acquired his usual health. This is the only instance that
has occurred to me," writes Fothergill, "of a perfect recovery from this obscure, and too
often fatal malady." We have seen that Heberden's experience also yielded only one
case of apparently perfect recovery. In one other case, witn distinct gouty complications,
Fothergill prescribed Bath waters, with good results as regards the gout, but with no
favourable effect on the angina. In another case the Buxton water appeared to be of
temporary service. Fothergill seems to have been strongly impressed with the necessity
of reducing exuberant fatty deposition in angina pectoris, and for this purpose recom-
mended vegetable diet ; though no did not anticipate in any respect later observations as
to the connection of sudden death with fatty degeneration of the fibre of the heart itself.
See Medical Observations and Inquiries, vol. v., 1776, p. 223, " Case of an Angina
Pectoris, with Remarks ; " and p. 252 of " Farther Account of the Angina Pectoris, by
J. Fothergill, M.D., F.R.S."

i Berliner Klin. Wochenschrift, 1865. See, however, Cahen (ut supra) Archives
G6n6rales, 1863 ; and a much older case by Alexander, of Halifax, 1790 (History of a
case of Angina Pectoris cured by the Solutio arsenici), Medical Commentaries, vol. xv., p.
373. This last case has, apparently, had very little effect on English practice, but is
referred to by Desgranges, Trousseau, and other continental authorities.

1 Anstie, op. cit. Compare pp. 78, 182-4, 226-7.

698 A SYSTEM OF MEDICINE.

strychnine (ten minims of the sesqnichloride tincture with TV gr.
strychnine three times a day). Phosphorus has lately been recom-
mended by Dr. Broadbent, in doses of from fa to fa gr. twice
daily, but has not as yet been adequately tested. Zinc, silver, and
most of the older remedies of this class, have been, on the whole,
found wanting in true angina pectoris, though sometimes useful in
pseudo-angina. A remarkable experience was that of Bretonneau
(detailed by Trousseau),1 who, following out a very crude chemical
theory of the calculous origin of angina, professed nevertheless to
have stumbled upon the practical result of treating cases of angina
successfully by large doses of bicarbonate of soda, combined in cer-
tain cases with belladonna. The directions given are very compli-
cated, but the essential part of the treatment seems to be as follows :
The alkaline treatment is begun with two scruples of the bicarbonate
of soda, daily, in divided doses, rising gradually to eight or ten
scruples, increasing and diminishing- the dose alternately over inter-
vals of ten days, and then suspending the treatment for fifteen or
twenty days together ; these various processes are repeated up to the
end of a year or more, after which a pause of several months is
allowed. At all stages of this lengthened treatment, belladonna may
be given in gradually increasing doses, up to the point of relief to
the spasms, or until symptoms of incipient poisoning occur, viz.,
"unpleasant dryness of the mouth, marked disturbance of vision,
accompanied by a very striking dilatation of the pupils." Notwith-
standing the great therapeutic reputation of Bretonneau, I have not
been able to learn that anyone else in France has personally suc-
ceeded with this treatment, and even M. Trousseau, his most distin-
guished pupil and follower, does not profess to do more than record his
master's opinions. The facts as stated may therefore probably remain
among the curiosities of medical experience ; but as they have been
generally referred to, it is necessary to make brief allusion to them here.
In cases of angina connected with positive organic disease, the
treatment must follow the lines of that of the cardiac or vascular
lesion which is discovered to be the cause of the symptoms. It is veiy
doubtful, however, whether in cases of fatty heart, or of calcareous
and other degenerations of the vessels, there is any positive special
treatment which can be recommended with confidence. In cases of
aneurism, on the other hand, the iodide of potassium, in large doses of
20 to 30 grains and upwards, will be found of great value in checking
all the painful sensations, and even, in some eases, arresting or sus-
pending the disease ; and the bromide of potassium, or of ammonium,
may be given in some cases along with the iodide, as a palliative.
A late American writer2 specially commends the bromide of am-
monium, and gives two cases in which, in doses of 15 to 20 grains,
it seems to have averted the paroxysms.

1 Op.cit., Eng. transl., vol. i. p. 610.

2 Dr. Ituf'us K. Hinton, Philadelphia Medical and Surgical Reporter, March 6, 1875.

ANGINA PECTORIS AND SUDDEN DEATH. 599

Note on the Literature of Angina Pectoris. — The leading authorities
have been mostly referred to in the preceding pages, and will be
found quoted much more numerously and in chronological order in
the two great French dictionaries mentioned below,1 under the head
" Angine de poitrine." I have not in the text of this article referred
to the letter of M. Rougnon to M. Lorry, in 17G8,2 which has been
set forth by M. Jaccoud and others as constituting a claim on the part
of France to priority, or at least to a simultaneous discovery of angina
pectoris with that of Heberden. From the accounts given of this
letter, as I have been able to read them, it is manifest that M.
Rougnon is in no just sense of the words a rival or competitor of
Heberden ; he is, however, probably entitled to the credit of having
independently described a single case of sudden death, with symptoms
more or less resembling Heberden's angina, as we have seen that
Morgagni had done a century before. Without in the least degree
desiring to detract from what is due on this account to Rougnon, it
must be here pointed out that Heberden's position is entirely dif-
ferent. Instead of describing only one case, and reasoning inaccurately
as to its pathology, Heberden founded a minute and exact clinical
description upon the observation of not less than twenty cases, of
which, he informs us, six had been known to him as having perished

i Nouveau Dictionnaire deMedecine etde Chirargic pratiques, tome 2Iwne- 1865, p. 509
(Art by Jaccoud). Dictionnaire Encyclopedique ilea Sciences Medicalcs, tome 5leTue
1866, p. 65 (Art. by Parrot). Consult also the Bibliography in Forbes, Cyclopaedia ot
Practical Medicine, vol. iv. ; the essay of Wichmann, Ueber angina pectoris und polypus
cordis (Ideen zur Diagnostic, vol. ii. 1801); Brera (Delia stenocardia ; saggio patologieo-
clinico, Modena, 1810) ; Desportes (Traite de l'angine de poitrine, Paris, 1811) ; Zecchi-
nelli (SiilP angina del petto e sulle morte rcpentine, Padova, 1814); J urine (M^moiresur
Pangine de poitrine, Paris et Geneve, 1815) ; Lartigue (De l'angine de poitrine, Paris,
1846) ; Lussana (Intorno all' angina pectoris, Gazette Medica Lombards, 1858-59),
besides the great and well-known works of Senac, Corvisart, Laennec, Testa, Kreysig,
Bouillaud, Hope, I^atham, Stokes, Walshe, Friedreich (in Virchow's Handbuch), Bam-
berger, ami others on Diseases of the Heart, the most recent being that of Dr. Hayden,
Dublin (1875), which reached me after the first part of this article was written, but to
which I have been indebted for several suggestions in the latter part of itf and some
valuable references. The works of Romberg and Eulenburg, on Diseases of the Nerves,
should also be consulted ; and the articles in all the older systematic treatises and dic-
tionaries, whether British or continental. With the exception of Rougnon, all the
authorities quoted in any of these sources up to 1778 are English. In that year Eisner
published at Konigsberg a monograph, entitled, "Abhandlung iiber die Brustbraune,"
which was followed in 1782 by Griiner (Spicilegium ad angina? pectoris . . ), and
Schafter (l)issertatio de angina pectoris, 1787). Several articles or treatises soon fol-
lowed in Germany, Denmark, and Holland ; but I do not know if angina pectoris is even
mentioned by name in French medical literature prior to the paj>er of Baumes in 1808,
" Rechcrchns sur cette maladie a laquelle on a donne" les noms d'angine de poitrine
et de syncope angineuse," (Annales de la Soci^te do Medecine pratique de Mont-
pellier, 1808). The first Italian monograph was that of Brera in 1810, cited above.
After this, the literature becomes much more copious ; but the well-known article of Dr.
Forbes, in the first volume of the Cyclopaedia of Practical Medicine, 1833, will always
remain, especially for the English reader, the chief source of exact information down to
a comparatively recent date.

2 Lettre a M. Lorry touchant les causes de la mort de M. Charles, ancien capitaine
de cavalerie, arrivee h. Besancon le 23 feVrier, 1768 (Besancon, 1768, 8vo.) Rougnon
described the paroxysms of pain, and ascribed these and the sudden death to ossifica-
tion of the costal cartilages. He did not give any name to the disease, or indicate
otherwise its pathological and clinical relations.

600 A SYSTEM OF MEDICINE.

suddenly. Hebcrden's account of the " Disorder of the Breast,"
v, accordingly, soon became known to medical men in various countries

^ as an accurate and comprehensive sketch of a new disease, while

Rougnon's case passed into oblivion, without even in France exciting
the attention that was perhaps due to it as an isolated observation.
The claim advanced on behalf of Rougnon is evidently an after-
thought, and cannot now be admitted. If sudden death from angina
is to be recognised in any sense at all as a discovery on the strength
of an individual case, the credit undoubtedly belongs to Morgagni
rather than to Rougnon. It is right, however, to add that I make
these remarks without having personally read Rougnon's letter,
which I have inquired for in vain in the medical libraries of this
country.

DISEASES OF THE VALVES OF THE HEART.

By C. Hilton Fagge, M.D., F.R.C.P.

The literature of diseases of the valves of the heart, as of all other
thoracic diseases, is necessarily divided into two periods ; that before,
and that after, the discovery of auscultation. The earlier period,
however, contains very few observations. Burns1 quotes two cases of
aortic obstruction, briefly related by Eiverius and Willis respectively,
towards the end of the seventeenth century. Dr. Gee 2 points out that
Vieussens in 1715 recorded a case of disease of the aortic valves, in
which the pulse was "fort vite, dur, inigal, et si fort que Vartbre de
Fun et de V autre bras frappait le bout de mes doigts autant que
Vauroit fait unc corde fort tendue et violemment 6branl4e."

Friedreich s is therefore not quite accurate in heading his list of
papers and works on affections of the endocardium with Meckel's
essay in the M(5m. de TAcad. Roy. des Sciences, published in Berlin in
1756. But it is in the second half of the eighteenth century that we
find the first detailed observations of diseased cardiac valves. Among
the most striking of these is one recorded by John Hunter, in his
"Treatise on the Blood, &c.," which originally appeared in 1794. It is
that of a Mr. Bulstrode,4 who had " almost throughout his life had an
irregular pulse and upon the least increase of exercise a palpitation at
his heart, which was often so strong as to be heard by those who were
near him. ... He of late years (about the age of thirty), took to
violent exercise such as hunting ; and often in the chase he would be
taken ill with palpitations and almost a total suffocation. Some of
these fits continued several days : at such times he became black in
the face. Sometimes an universal yellowness took place ; and then he
could not lie down in his bed, but was obliged to sit up for breath.
He consulted Dr. Heberden and Sir George Baker ; the palpitation I

1 " Observations on some of the most frequent and important Diseases of the Heart"
Edinburgh, 1809, pp. 175, 176.

* " Auscultation and Percussion," 1870, p. 260.

* "Krankheiten des Herzens," Virchow's Handbuch der speciellen Pathologie und
Therapie, 1867, p. 198.

4 The preparation from this case is still in the Hunterian Museum of the Royal
College of Surgeons, which also contains several other specimens of diseased cardiac
valves, preserved by Hunter himself. The passages cited in the text are from the
**' Catalogue of Path. Specimens," vol. iii. p. 197.

VOL. IV. K R

602 A SYSTEM OF MEDICINE.

suppose tliey thought either arose from spasm or was nervous, for they
ordered cordials. I was sent for on the same day to give a name to
the disease. My opinion was that there was something very wrong
about the heart, that the blood did not flow freely through the
lungs. . . That the means to be practised were rest, bleed gently,
eat moderately, keep the body open and the mind easy. . . Eight
ounces of blood were taken from him that day which relieved him. . .
At last he became yellow, and his legs began to swell with water. . .
and he died. The heart was very large . . . the valves of the aorta
shrivelled up, thicker and harder than common. The diseased
structure of the valves accounts for every one of what may be called
his original symptoms; the blood must have flowed back into the
cavity of the ventricle again at every systole of the artery. . . . We
. can easily trace the effects of this retrograde motion, which would only
be a stagnation of the blood beyond the left ventricle, first in the left
auricle, then the pulmonary veins, then the pulmonary arteries, next
the right auricle, and in all the veins of the body ; producing that
darkness in the face, &c." Even earlier than this, Senac, in his
Treatise on the Heart (the second edition of which appeared in 1783)
had related a case in which the auriculo-ventricular valves were
ossified, and remarked that the pulse was necessarily small, because
the blood did not all pass into the aorta, but some of it flowed back
into the auricle. Soon after the commencement of the present
century, three works on diseases of the heart were published, in which
valvular affections are treated of with considerable detail: that of
Corvisart,1 in 1806 ; that of Allan Burns,2 in 1809 ; and that of
Kreysig,8 in 1815.

The study of these works is of considerable interest. Corvisart
gives an admirable account of the anatomical appearances exhibited
by diseased valves, which he distinguishes as undergoing calcareous
or osseous induration, or as presenting excrescences (vegetations).4
It is remarkable, however, that he seems to have had no conception
of these diseases as causing regurgitation, or imperfect closure of the
valves.5 The tendency of valvular affections to cause dilatation of

i " fissai siir les Maladies et les lesions orgauiques du Coeur et des Gros Vaisseaux/' So
far as diseases of the heart arc concerned, however, this writer (who will always be
remembered as having popularized Avenbrugger's discovery of percussion) is better known
by his second edition, which appeared in 1811, and was translated into English by Mr.
Hcbb in 1813. a Op. cit.

3 " Die Krankheiten des Herzens. " Berlin.

4 The word " vegetation" is now commonly used in this country, but it may be inte-
resting to note that Mr. Hebb, the translator of Corvisart, never employs it as an
English term, but always incloses it between brackets, and uses "wart" or ** excrescence"
as its equivalent.

5 This must be borne in mind in estimating the claims of different writers to priority
in regard to the discovery of the presystolic thrill and bruit. Corvisart first mentioned
the sign afterwards known as frimisscmaU catairc. He speaks of it as " a particular
rustling, difficult to describe, perceptible to the hand when it is placed over the precordial
region, and which doubtless proceeds from the difficulty which the blood experiences in
passing through an aperture no longer proportionate to the amount of fluid to which it
has to give vent." It might thus appear that Corvisart associated thrill with mitral
stenosis. But it must be recollected tliat he summed up the effects of all valvular

DISEASES OF THE VALVES OF THE HEART. 603

the heart (or, as he terms it, " aneurism of the heart ") was well
known to Corvisart. By Burns and Kreysig considerable advances
were made. Both these writers recognize valvular lesions as pro-
ducing two distinct effects, " obstruction " and " regurgitation," and
trace many of the consequences of the latter conditioa Kreysig lays
special stress on inflammation of the endocardium as causing the
lesions in question. Burns may even be said to hint at the occurrence
of cardiac murmurs, for he speaks of regurgitation from the ventricle
into the auricle as producing not only a jarring sensation but also " a
hissing noise, as of several currents meeting. In all probability " (he
goes on to say) " it is something of this kind which is described as
audible palpitation in some diseases of the heart,"

The history of the subsequent literature of valvular affections is
involved in that of the auscultatory phenomena which they produce ;
and hereafter, when these are under consideration, I must endeavour
to deal with the most important parts of it.

Description and Anatomy. — The pathological changes met with
in the valves of the heart are naturally divisible into two groups ; 1.
Those which are acute : 2. Those which are chronic.

1. The acute affections are of an inflammatory nature, and come
under the general head of endocarditis. Indeed, it has long been
known that the membrane forming the valves is more liable to in-
flammation than any other part of the endocardium. And, as we shall
presently see, recent observations have shown that this is true in a
more absolute sense than had been imagined : and that when inflam-
mation of the linings of the heart's cavities is met with, it has almost
always been set up by a similar affection of one of the valves.

The microscopical anatomy of inflammation of the valves may,
therefore, be dismissed in a very few words, as being the same as that
of endocarditis in general. The minute blood-vessels, which recent ob-
servers have shown to exist in the valves, become gorged with blood, and
the cells of the external tunic of these vessels undergo proliferation.1 But
this change is quite subordinate to that which occurs in the proper
substance of the valve itself: in the connective tissue of which young
cells are formed in large numbers, while the intercellular material
becomes softened. The tissue is thus much swollen; and as the change
in question is not at first general, but is confined to certain spots,
the result is the formation of a number of small granulations,
projecting from the surface of the valve. These granulations are
very commonly limited, in the first instance, to a particular region
in each valve, namely, that which lies immediately behind the line
of closure. Thus, in a cuspid or auriculo-ventricular valve, the
earliest swelling is found on the auricular surface, and a little above

diseases in the contractions of the corresponding orifices which he supposed them to
cause. He had no conception that the presence of thrill was of any value as regards a
differential diagnosis of valvular affections.
*J Kindfleiseh, " Lehrbuch der pathologischen Gewebelehrc." Leipzig, 1871, p. 205.

B R 2

604 A SYSTEM OF MEDICINE.

the free edge ; in the case of the semilunar valves, it is on the ven-
tricular surface, and along the delicate curved line, limiting the apposi-
tion of the valves, that stretches on either side of the corpus Arantii. In
these positions the granulations are often pretty uniformly arranged,
like a row of minute beads. The remembrance of their seat may be
facilitated by imagining the valves to have been coated on their
apposed surfaces with a layer of some soft substance (such as butter),
which during closure of the valves would be forced into precisely the
positions that the granulations occupy. And according to the view
formeily entertained, that the granulations were formed of an exuda-
tion of plastic lymph, it was easy (with Sir Thomas Watson)1 to refer
their arrangement to this cause. But, as we have seen, the microscope
shows that they are swellings of the tissue t)f the valve itself, and this
explanation is, therefore, untenable. The granulations vary in appear-
ance ; being sometimes colourless, sometimes red (the latter perhaps
from imbibition). Their consistence is different in different cases:
sometimes they are so soft as to be detached from the valve by the
slightest touch ; sometimes they are so hard as to resist all attempts
to remove them. They are much more often seen on the valves of
the left, than on those of the right side of the heart : the former
being in fact much more subject to endocarditis than the latter.

When acute endocarditis occurs as part of a rapidly fatal general
disease, the presence of such a line of minute granulations is generally
the only sign that inflammation of the valves had existed : and if (as
is often the case) the affection be confined to the auricular surface of
the edge of the mitral valve, it may be entirely overlooked, unless
attention be specially directed to this spot.

But in certain cases, the changes are far more considerable. The
granulations are very much larger, and become confluent, so as to
form masses, which fairly deserve the name of vegetations. These
bodies, projecting into the stream of the blood, necessarily offer
a favourable surface for the reception of coagula ; and thus colourless
fibrin of firm consistence is deposited upon them, often in large quan-
tity. This so closely resembles in appearance the swollen tissue of
the valve itself, that it may be impossible to say where the one begins
and the other ends. Indeed (as has already been mentioned) the
older theorists (who thought that the valves, which were then supposed
to be non- vascular, were incapable of inflammation) believed even the
smallest granulations to have been thus deposited from the blood.
When this opinion was shown to be incorrect, its opposite prevailed ;
and it is only after repeated and prolonged discussions that patho-
logists have come to the conclusion that the larger masses have the
double origin just attributed to them. These, again, are often found
to be still further increased in size by the deposition of dark red clots
upon them, -vfrhile the patient is in the act of dying, or during the
post-mortem coagulation of the blood.

These vegetations necessarily float to and fro with the valve to which

1 " Trine, and Tract, of Physic," 4th edition, vol. ii. p. 294.

DISEASES OF THE VALVES OF TEE HEART. 605

they are attached, and thus they are almost always brought into con-
tact with the surface of another valve opposed to them, or with some
part of the endocardial lining of the heart's chambers. For it must
be added that they are not always sessile, but are often suspended by a
pedicle of some length, allowing them to swing backwards and forwards
through a considerable range of movement. The result is that the)'
frequently set up inflammation in the parts against which they rub.
This fact was, I believe, first pointed out by Dr. Moxon, who, in 1868
and 1869 exhibited to the Pathological Society several illustrative
specimens.1 My own observations have convinced me that his state-
ments are perfectly correct. A vegetation hanging from an aortic
valve is often thrown upon the wall of the aorta during the ventricular"
systole, and sets up there a little idcer, penetrating into the middle
coat, or even down to the adventitia : during the diastole the same
vegetation is carried downwards, and touches the anterior surface of
the mitral valve, or the endocardial lining of the ventricle, and the
spot touched is found, after death, to be precisely indicated by the
presence of a little fresh mass of vegetations. The opposed surfaces of
the aortic valves are often seen to be coated with vegetations, in such
a way as to suggest that the one was affected secondarily to the
other, although it may not be possible to say which was primarily
diseased. Or, again, a button-like mass of vegetations projecting from
one aortic valve has been seen to bore a hole right through the sub-
stance of the valve opposed to it. A cluster of vegetations growing
from the auricular surface of the mitral valve often sets up inflamma-
tion in the base of the opposed segment of the valve, where the
vegetations meet it during closure of the valve : and from this spot
the inflammation spreads into the auricle.2 Dr. Moxon has even
expressed the opinion that vegetations attached to the lining membrane
of the heart's cavities are scarcely met with, except as the result of
friction, in the way just described, the valves being first diseased.
And I would add my belief that there are few cases of acute inflam-
mation of the valves, in which secondary effects of this kind may
not be traced.

The rapid and extensive movements performed by these floating
vegetations have probably much to do with the frequency with which
portions of them become detached and carried with the blood-stream to
distant parts, producing effects which we shall hereafter have to consider.
But it must be added that they are also very liable to undergo a
finely granular metamorphosis (according to Rindfleisch, not fatty),
which renders them still softer than they originally were. In this
softening process the inflamed tissue of the valve itself takes part :
so that large portions of it often become disintegrated, and an ulcer is

1 Path. Trans, xix. p. H8, xx. p. 156. It will be shown further on that Dr.
Hodgkin long ago described the effects of friction in the case of valves affected with*
chronic disease.

8 These statements are derived from the detailed reports of the post-mortem examina-
tions at Guy's Hospital during the last few years, most of which were made by Dr.
Moyon, but suine by myself.

606 A SYSTEM OF MEDICINE.

.produced, which may destroy the whole thickness of the valve and
perforate it. Such ulceration, for instance, may separate one or both
edges of an aortic valve from attachment to the arterial wall ; or
eat away a large part of its substance. In the mitral valve, it is not
uncommon for a hole to be pierced right through its substance. In
this case, however, the edges of the aperture are always thick and
raised, and covered with large vegetations ; and these generally meet
across it, so that there is no reasoa to suppose that by such a perfora*
tion the physiological action of the valve is in any way impaired.
Indeed, these vegetations are often so massive, that the existence of a
perforation, and even of an ulcer, may escape notice unless it be specially
looked for. The records of post-mortem examinations at Guy's Hos-
pital contain only one notice of such a perforation in the course of six
years ; but I have little doubt that it had really occurred more often.
It must be added that the ulceration not rarely extends from the
valves themselves into the adjacent parts of the muscular substance
of the ventricle.

The same process of softening and ulceration, occurring in the
chordae tendineae of the cuspid valves, leads to their rupture. This
is by no means infrequent ; in six years I find it recorded sixteen
times in the reports of post-mortem examinations just referred to.
Clinically it would appear to be of far greater importance than
perforation of the valve : I imagine that it must invariably render the
valve incompetent. The changes which precede rupture of the chordae
would appear to consist in a swelling and thickening of their substance.
Generally they give way in about the middle of their length; but
sometimes they are torn away from the musculus papillaris, which
may then exhibit no trace of their original insertion into it. The left
and the right chordae of the mitral valve appear to be equally liable to
rupture. Sometimes the laceration is confined to a single chorda ;
sometimes it affects nearly all those that arise from one musculus
papillaris. The ruptured chordae float to and fro with the stream of
blood, which necessarily regurgitates freely into the auricle at each
systole. Once I saw such a loose end tied neatly into a knot, which
took some time to undo. In another instance three or four broken
chorda3 were twisted up spirally into a body resembling an uvula,
being matted together by a deposit of fibrin. In a third case, recorded
by Dr. Moxon, the free extremities of two such chordae seemed to have
become adherent to the surface of the mitral valve above, forming
loops, beneath which a probe could be passed. Large masses of fibriu
are whipped out from the blood, and deposited on the sides and
extremities of ruptured chordae, and often unite them together, so that
it is impossible to say how many of them may have been torn through,
until the superjacent mass of coagulum is removed.

Another effect of this process of ulceration, especially in the mitral
valve, is the formation of a so-called " aneurism of the valve." An
ulcer having formed on its ventricular surface, the base of this yields
before the pressure of the blood, and a pouch is formed, projecting from

DISEASES OF THE VALVES OF THE HEART. 607

the auricular face of the valve. Such an aneurism is generally very
small : I lately saw one which was of about the size of a percussion
cap ; it had on its summit a mass of small vegetations. This form of
aneurism must be distinguished from that described by Dr. Thur-
nam,1 which arises in the gradual yielding of all the coats of the valve,
and which may attain a much larger size.

2. In chronic diseases of the valves the appearances vary greatly,
not only in individual cases, but also according as one or another
valve is affected. But they may generally be summed up as depen-
dent on the growth of a firm connective tissue, which thickens the
substance of the valve, and by its contraction leads to great altera-
tion in its form, and more or less seriously impairs its functions.
Calcareous matter also is often deposited.

This " sclerotic " change, — if we may adopt the term sclerotic as
equivalent to the chronische sclerosirende Endocarditis of German
authors, — may either be primarily chronic, or arise out of an acute
inflammation of the valve. In the latter case, vegetations are some-
times found, showing that endocarditis had once occurred ; and these
may even be calcified. But they are not necessarily present. In
several cases of valvular disease, that had, in each instance, doubtless
arisen in attacks of acute rheumatism which the patient had had some
years previously, I have, on post-mortem examination, found that the
mitral valve exhibited no trace of vegetations : it was simply thickened,
with its chordae ; and its orifice was narrowed. Here the affection had
been of acute origin: but the appearances were undistinguishable
from those which are met with in disease that has from the first been
chronic. The difficulty of determining the way in which valvular
changes arise is further increased by the fact that thickened valves
are very liable indeed to the supervention of an acute process, identical
with that already described as belonging to acute endocarditis. It
would appear that the elements of the morbid tissue in chronically
diseased valves are apt to undergo a fatty change, analogous to that
which gives rise to atheroma in chronic arteritis. The result is that
the structure of the valves becomes softened and gives way, and thus
that a process of ulceration is set up, precisely as in acute endocarditis.
A very large proportion of the cases in which the autopsy shows the
chordae tendineae of the mitral valve to have been freshly ruptured
are cases of long-standing valvular disease, in which inflammation
has thus supervened. Another common result is that masses of
calcareous deposit, evidently of old formation, are found lying loose
in the floor of recent ulcers.

a. In the cuspid valves the effect of chronic disease is generally to
produce a stenosis or narrowing of the aperture. The wall of the
valve, especially towards its free edge, becomes greatly thickened, and
its segments cohere together. The morbid tissue is exceedingly dense
and hard, so that by the older writers such valves were described as
cartilaginous : it often contains masses of calcareous deposit, and

i Med. Chir. Trans., ser. ii. vol. iii. p. 250.

608 A SYSTEM OF MEDICINE.

these sometimes attain a very considerable size. The chordae tendineae
undergo a similar change and coalesce, so that sometimes each musculus
papillaris gives origin only to a single massive column, which may be
more or less fluted, or pierced with one or two slits, indicating the
lines of separation between the chordae of which it was made up ; at
the same time the chordae generally become much shortened, so that
the edge of the valve is drawn down; and thus with its small
aperture it has very much the appearance of a funnel, projecting far
into the cavity of the ventricle. Dr. Douglas Powell,1 has
endeavoured to distinguish two forms of stenosis of the mitral
orifice, iu one of which the valve presents this funnel shape, while in
the other it is stretched horizontally, like a diaphragm, between the
auricle and the ventricle. But it appears to me that no such distinc-
tion can be fairly drawn, and that in all cases a narrowed mitral
valve tends more or less to assume the form of a funnel, although
this is no doubt much more marked in some instances than
in others. The orifice at the bottom of the funnel is sometimes
circular : but in the case of the mitral valve it more often resembles
a slit, of which the axis corresponds with the line uniting the meeting
angles of the original segments of the valve. The latter variety has
long been known as the button-hole mitral. In either form the
aperture may be so contracted as hardly to admit the tip of the little
linger ; and cases are often met with in which only two fingers can be
introduced, instead of the three which can be passed through the
healthy valve.

But the effect of chronic disease of the mitral valve is not always
to produce stenosis. It may be the very reverse. It is said that
sometimes one of the flaps of the valve becomes adherent to the
ventricular wall, and so is rendered incapable of meeting its fellow.
But this is a very rare occurrence; indeed I doubt whether it is
ever met with. At any rate I have not been able to find a single
instance of it in the recent records of post-mortem examinations at
Guy's Hospital. These records, however, contain one case in which
Dr. Moxon found the edge of the anterior curtain of the valve turned
up on its ventricular surface, and adherent there, so as to form a ridge
on this surface,2 — a change by which the depth of the curtain must
of course have been diminished. It might be thought that the same
process of contraction which ordinarily causes stenosis of a thickened
valve might (if acting in a direction at right angles to that in which
it usually acts) draw up and shorten the valve without narrowing its
orifice. Writers have in fact described such an appearanca But it
is one which I have never myself seen, nor have I met with any
recorded instance of it : and I am not sure that it ever occurs. Not
uncommonly, however, some of the chordae tendineae become elongated,

1 Med. Times and Oaz., 1871, vol. i. p. 395.

1 This condition is analogous to one which is comnioidy seen in cases of perihepatitis,
where the anterior thin edge of the liver is neatly folded over on to the convex surface,
and bound down beneath the thickened capsule, the apparent rounded margin of the
liver being thus really derived from the under surface of the orguu.

DISEASES OF THE VALVES OF THE HEART. 609

and do not properly tether the membranous part of the valve, which
therefore becomes inverted into the auricle during the ventricular
systole ; and this result is often favoured by the conversion of the
corresponding muscularis papillaris into a dense fibrous tissue. Some-
times those chordae which are inserted nearest the centre of the
valve alone undergo this process of lengthening, and this part of
the curtain is then found after death to be bent on itself and flaccid,
having evidently been accustomed to yield before the pressure of the
blood. Sometimes, again, the chordae become shortened by disease,
instead of being elongated, and thus tether the valve too closely,
and prevent the apposition of its segments.

I believe that the preceding paragraph includes descriptions of all
the chronic changes in the cuspid valves, by which regurgitation is
produced, without obstruction to the onward current of blood. Each
of these, however, is of infrequent occurrence. In six years, during
which period sixty-seven cases of mitral stenosis presented them-
selves in the post-mortem theatre of Guy's Hospital, I find only
twelve recorded instances of what I may term pure regurgitant
disease of the same valve ; in six of which the edge of the valve is
stated to have been inverted into the auricle, in the manner above
described.

The fact just stated will doubtless surprise many readers, who are
aware of the frequency with which mitral regurgitant disease is clini-
cally spoken ot The question must be discussed in detail further
on ; but it may be well here to state that, in a large proportion of
cases, a reflux of blood into the auricle during the ventricular systole
is probably independent of disease in the valve itself, and due to
changes in the walls and cavity of the ventricle, destroying the due
proportion between the auriculo-ventricular orifice and the valve by
which it should be closed. It must be added that many cases are
placed after death under the head of mitral stenosis, which had before
been regarded as examples of regurgitant disease. For when mode-
rate obstruction and regurgitation co-exist, the latter is often clini-
cally more noticeable, and (as I believe) is often alone discoverable
before death ; while at the autopsy the appearance of the valve may
be exactly similar to that wlrich is found in another case, in which
during life obstruction had been the main feature.

fi. In the semilunar valves the morbid appearances resulting from
chronic disease vary much more than in the cuspid valves. First
may be mentioned the adhesion of the valves together. This begins
at the point where the corners of adjacent valves are inserted into the
aortic wall, and gradually creeps along their free edges, uniting them
together. All three valves may thus be fused into a single mass,
projecting into the arterial channel in the form of an inverted funnel,
with a central aperture, which is often of very irregular form, and may
be extremely small, being, in most cases, further narrowed by the
presence of rough calcareous nodules of greater or less size, deposited
in the substance of the altered valves. While this process is going

610 A SYSTEM OF MEDICINE.

on, the natural attachment of the corners of the valves to the aorta
often gradually becomes obliterated ; two of the pouches, or even all
three of them, become thrown into one ; and three slight projections
in the floor of the resulting funnel-shaped mass are often all
that is left to indicate the original lines of separation between the
different valves.

In other cases the effect of chronic disease of the semilunar valves
is, that they become puckered and shrivelled. Instead of forming
pouches, they often rather resemble flat, narrow shelves, projecting
a little way from the wall of the artery, the mouth of which they are
quite unable to close. The corpus Arantii, with the thin curved
borders on either side of it, disappears entirely ; and all that is left
is a thick, shapeless body, often with its rounded edge retroverted,
and perhaps torn away from its aortic attachment on one side, so as
to hang down like the lip of a jug, or a dog's ear. Or, again, the
valve may contract, and its free border thus become tightly drawn
across between its points of attachment, so that the open pouch is
converted into a deep pocket with a narrow entrance, into which the
tip of the finger cannot be made to enter. This result, however, is
not always due to changes in the valves themselves. Sometimes it
depends on chronic disease in the coats of the base of the aorta,
attended with yielding and dilatation of its walls, by which the
valves, although healthy, are unduly stretched. So considerable
may this yielding be, that in one case recorded in the reports of
post-mortem examinations at Guy's Hospital, the corners of adjacent
valves had become distant from one another a quarter of an inch at
their points of attachment.

When a valve, thickened or retroverted by chronic disease, comes
into contact with any part of the lining of one of the heart's cavities
during the movements of that organ, further morbid changes are
produced by the friction, as is the case in acute affections. There
is, however, this difference, that the endocardium does not become
ulcerated or covered with vegetations, but is thickened, opaque, and
slightly roughened. This was pointed out by Dr. Hodgkin as far
back as the year 1829.1 In the case of Dr. Cox, one of aortic disease,
in which a valve was stretched to upwards of an inch in length,
"the coats of the aorta for about an inch and a half above the
retroverted and distended valve, and against which it must have
been carried during the systole of the heart, were considerably
thickened, and presented an uneven surface. On the inner surface
of the heart there were some irregular spots of opacity at the part
where the diseased valve would have struck during the diastole."
Dr. Hodgkin adds that " the partial thickening on the internal sur-
face of the heart and vessels, in consequence of some unusual contact,
is a morbid appearance, which has not been particularly pointed out
by pathological anatomists, yet it does not appear to be a rare
occurrence." Except Dr. Moxon, I do not find that any writer

1 " On Retroversion of the Valves of the Aorta," Lond. Med. Gaz. vol. iii. p 489.

DISEASES OF THE VALVES OF THE HEART. 611

has since alluded to the appearauce in question. But in another
respect our knowledge has advanced greatly since the publication of
Dr. Hodgkin's paper; for we find him relying on these effects of
contact as proving that the blood had been subjected to two motions —
the one progressive, and the other retrograde — a fact with which, of
course, everyone is now familiar. According to Dr. Peacock and Dr.
Bristowe,1 it is not uncommon, in cases of disease of the aortic orifice,
for the endocardium below the valves to present a fibroid thickening
in the form of bands or reticulations, due probably to the impact of
the regurgitant stream of blood on that part. Of this I have lately
seen a striking instance. The same thing may also occur in the
auricle, as the result of mitral regurgitation.

It will be observed that in the semilunar, as in the cuspid, valves
the effects of chronic disease are twofold. It may either cause
obstruction to the onward flow of blood, or give rise to regurgitation
and to a backward current. All writers, in fact, insist on this dis-
tinction, while admitting that both effects often exist together. Dr.
Moxon, therefore, rather surprised me a short time ago by stating that
in his experience the occurrence of aortic obstruction, apart from
regurgitation, has been extremely rare. I at first supposed that he
was referring to fatal cases only, among which pure aortic stenosis
would naturally be infrequent, since this is generally said to affect the
prospect of life less than any other form of valvular affection, and
since, moreover, it is very apt to become complicated sooner or later
by the development of regurgitation. Thus, in looking through the
records of post-mortem examinations for the last six years — during
which time there have occurred sixty-eight fatal cases of aortic
regurgitant disease — I find only two, or perhaps three, of pure aortic
stenosis ; and in at least one of them the patient's death was due not
to this affection, but to co-existing mitral stenosis. But I afterwards
ascertained that Dr. Moxon believed aortic obstruction, independent of
regurgitation, to be rare clinically, as well as in the dead-house ; and
this opinion certainly appears to be confirmed by the fact that,
during part of the period in which I acted as Medical Begistrar at
Guy's Hospital (within which period seventy-one cases of aortic
regurgitation came under observation) I find only two recorded
instances of pure stenosis of the orifice in question ; and in one of
these regurgitation became developed before the patient's death.

The changes to which the aortic valves are liable are not all in-
cluded in the thickenings, and adhesions, and puckerings that have
hitherto been described. In some cases the tissue of the valves
undergoes atrophy ; and they become so thin, that it is difficult to
believe that they were capable of sustaining a column of blood. A
striking example of this came lately under my notice. A young man,
set. thirty-two, had long suffered from asthma, and becoming anasarcous
was admitted into Guy's Hospital under the care of Dr. Wilks. After
death the aortic valves were found to be most remarkably thinned ;

1 Path. Trans, xxi. p. 105.

612 A SYSTEM OF MEDICINE.

they had no more substance than the most delicate tissue-paper, and no
corpora Arantii could be felt in them. One of them was slightly fenes-
trated near its margin. They were very small, and, when left to them-
selves, fell back into the Sinuses of Valsalva. The pulmonary valves
presented the same change in a minor degree ; and the mitral valve
was likewise unusually thin. The heart was much enlarged. The
lungs were emphysematous , and it appeared to me that the thinning
of the heart's valves was due to a process of atrophy, perhaps related
pathologically to that which caused the pulmonary emphysema. I
have since found, in the records of post-mortem examinations at
Guy's Hospital, a similar case, observed by Dr. Moxon. It is that of
a man, aged fifty-six, whose lungs are stated to have been senile
and a little emphysematous, and to have contained much black matter.
The heart was small ; the right side was dilated, forming the
apex ; the pericardium was everywhere adherent ; the mitral and
aortic valves were very delicate in appearance.1 This atrophy of the
aortic valves is probably rare, and has not yet been shown to have
any clinical significance. But there would certainly appear to be
danger of the rupture of such thin structures, when strained in an
effort of coughing or in any other way.

I have still to mention another abnormal appearance in the aortic
valves, formerly supposed (by Corrigan) to render them incompetent,
but now known to interfere in no way with their functions. I refer
to the small openings which are sometimes found in the thin, crescent-
shaped borders which extend on either side of the corpora Arantii. By
some writers analogies have been found for such a fenestrated condi-
tion of the aortic valves in the normal state of the same valves in
some of the lower animals ; while others have regarded it as exhibiting
an identity of structure between the semilunar and the cuspid valves ;
the filaments which remain above the apertures being supposed to
answer to the chordae of a mitral or tricuspid segment. It has also
been doubted whether this fenestration of the aortic valves is the
result of a slow atrophic change, or whether it is simply a defect
of original development. And with reference to this point Dr.
Wilks 2 states that he has seen it in young people, and has therefore
always regarded it as congenital.

Etiology. — Before passing to the consideration of the other causes of
disease of the cardiac valves, it may be convenient to discuss the views
of certain writers, who have attributed to congenital malformation
(or to intra-uterine disease) some affections that, as it appears to mer
may arise at any period of life. These views are of considerable
antiquity. In his account of Mr. Bulstrode's case, already referred
to, John Hunter expresses a doubt whether the shrivelled appearance

1 Since this was written I have (in November 1874) met with a third instanco of
extreme thinning of the aortic valves, in another patient, who died of the eliects of juil-
mouary emphysema.

2 Pathological Anatomy, p. 93.

DISEASES OF THE VALVES OF THE HEART. 613

of the valves of the aorta was " a natural formation, or a disease."
And of another specimen, in which there were two valves only
instead of three, one of which had a kind of fnenum or cross-bar
attaching its middle to the side of the artery, — the catalogue of the
Hunterian Museum says, " this malformation was in all probability
congenital." Early in the present century, Mr. Burns described as a
" species of mal-conformation of the heart," that condition in which
the mitral valve, instead of being formed of two flaps, presents the
appearance of a septum, with an aperture in its centre, stretching
across the opening. More recently several observers have expressed
similar opinions. Dr. Conway Evans,1 in recording a case in which
the mitral valve was funnel-shaped, says this condition was "evidently
of congenital origin." Dr. Kelly has recently maintained the same
view.2 And Dr. Peacock devoted to this question a part of his first
Croonian Lecture, delivered before the Epyal College of Physicians in
1865. '

The arguments for and against the opinion that certain affections
of the valves are congenital require to be taken separately for the
different valves.

And, first, with regard to the mitral valve. Great stress has been
laid on the fact that mitral stenosis is very frequently associated with
tricuspid stenosis. It is generally said that all the valves on the
right side of the heart, whijch are so rarely subject to disease in after
life, are much more liable to intra-uterine disease and to malforma-
tion than the valves on the left side. And congenital union of the
pulmonary valves is really common, being indeed the most important
malformation of the heart, and being generally attended with other
evident malformations, such as an aperture in the septum, &c. Now,
since the relatively higher function of the right side of the heart
during foetal life is supposed to be the cause of the greater liability
to congenital disease in the pulmonary (as compared with the aortic)
valves, writers have assumed that this liability must be shared by the
tricuspid valve also. But, as a matter of fact, there is no proof that
disease of the tricuspid valve before birth is otherwise than an
exceptional occurrence, like disease of the aortic valves, or of the
mitral valve at the same period. Friedreich,8 indeed, says that in
newly-born infants minute soft granulations are not rarely found on
the auricular surface of the tricuspid valve ; but, as they do not
generally disturb the functions of the valve, he hardly regards them
as morbid, considering them rather to stand on the border between
physiological and pathological appearances. Dr. Peacock, however,
has related 4 a case in which there was a thick exudation of recent
lymph on the auricular surface of the tricuspid valves, in a cyanotic
child, who died when about seven months old. It is stated that the
cusps were thickened and adherent at their angles, so as to contract

1 Path. Trans, xvii. p. 90. * Path. Trans, xxi. p. 91

3 0]). cit., p. 216. * Path. Trans, v. p. 64.

614 A SYSTEM OF MEDICINE.

the dimensions of the orifice : but this still admitted a ball twenty-
four lines in circumference, while the mitral aperture had a circum-
ference of only eighteen lines. Friedreich has related a similar
instance. Now it is certainly possible that tricuspid stenosis may
have its origin in the inflammatory process described by these writers,
as occurring in certain infants at or soon after birth. But in that
case it might fairly be expected that the mitral valve, if affected at
all, should be so in a slighter degree. Now I believe that it is
invariably the case, that when both the valves in question are
stenosed, the mitral is much thicker and much narrower than the
tricuspid. For instance, it was so in Mr. E. Pye Smith's * case, which
Dr. Peacock cites as of congenital origin.

Another argument in favour of the view that mitral 'stenosis may
be due to malformation is based upon the fact that the patient has
sometimes been in bad health for many years, or even from birth.
Thus, in Mr. Pye Smith's case, the patient had been ailing all his
life ; and, although thirty-seven years of age, did not appear more
than fifteen or sixteen, and had never presented any signs of
puberty.2 In 1870, Dr. Kelly exhibited to the Pathological Society 8
a heart with a button-hole mitral valve, taken from a woman aged
thirty-three, who, even when a child, " could not run about well or
indulge in any severe exertion on account of great shortness of
breath and palpitation of the heart." But, so far as I can learn, such
cases are quite exceptional. Patients affected with mitral stenosis
generally state that they have had perfect health until a few months,
or at most two or three years, before they first came under medical
observation for their heart-disease. Moreover those who are practi-
cally conversant with the routine of morbid anatomy will, I think,
agree with me, that in the bodies of those who have had rheu-
matic fever some years before death, the mitral valve is very fre-
quently found presenting appearances which clearly indicate the
gradual development of stenosis. In such cases the inferior edge of
the valve is thickened, and harder than natural ; its orifice no longer
admits three fingers readily ; its chordae are beginning to cohere.
Every stage of transition may be seen between a healthy valve and
one presenting the most extreme degree of stenosis. My belief,
therefore, is that it is needless to refer this affection of the mitral
valve further back than a past attack of acute rheumatism, if the
patient has had such an attack. And even when shortness of breath
and other symptons of cardiac defect have existed from childhood, it
appears to me more likely that the stenosis is due to morbid changes
arising in the years that may have elapsed since birth, than to mal-
formation or disease occurring in the short period of intra-utexine life ;
especially since in the foetus the left side of the heart is so situated
as to be very little susceptible of morbid action.

1 Path. Trans, iii. p. 283.

3 Dr. Peacock, "Malformations of the Heart," 2nd etL, 1866, p. 139.

8 Path. Trans, xxi. p. 91.

DISEASES OF THE VALVES OF THE HEART. 615

Secondly, as concerns the aortic valves. Adhesion of two or more
of these valves sometimes occurs in very young children. Thus Dr.
Lloyd1 exhibited to the Pathological Society the heart of an infant
thirteen months old, in which there were only two aortic valves, and
these were very red, rough, hard, cartilaginous on their surface and
puckered : one of them was twice as large as the other, and had an
indistinct ridge intersecting its centre. Dr. Workman,2 again, showed
to the same Society the heart of a little girl, only four years old at
the time of death, in which the aortic orifice was much contracted,
and its valves thickened and fused together. Again, adhesion of the
aortic valves has sometimes been found in young persons, associated
with the similar change in the pulmonary valves which is believed to
be invariably of congenital origin. Thus Dr. Wilks8 has recorded
the case of a girl, ?et. eighteen, in whom the pulmonary valves were
adherent, and the aortic valves were two in number, the larger of
them having in its interior a raised line indicating the point of union
of two former valves. Dr. Ogle4 saw another instance of the same
kind, in a girl, fourteen years old, in whom " two contiguous aortic
valves had their adjoining angles torn away from their attachment to
the aorta, and subsequently united to each other at a lower level."
It is no doubt probable that in all these cases the union of the aortic
valves occurred before birth : but such cases are extremely rare, and
surely afford no ground for supposing that the adhesions which are
so commonly found at an advanced age are also congenital.

I must next insist on the fact, that the cases last referred to
have characters which distinguish them in a very important way
from those in which the union of the valves is known to be con-
genital. In the first place, partial adhesions of the aortic valves are
very commonly met with in older subjects, especially when the coats
of the aorta are also diseased. The adjacent edges of the valves are
found to have grown together for one or two lines, the rest remain-
ing free. There can be no question of any congenital defect, since I
am not aware that such partial adhesions are ever observed at an
early period of life : 6 yet it is obvious that the continuation of the
same process would lead to the complete fusion of the valves, after
which the line of union might be expected to gradually waste and
disappear. Again, when the aortic valves are adherent, the orifice is
generally irregular, and the substance of the valves greatly puckered
and often deformed by large masses of calcareous deposit. Of this
several capital illustrations are given in Dr. Peacock's published
Croonian Lectures. He supposes that in these cases the union of
the valves took place before birth. But the appearance is very dif-
ferent from that which is seen in the affection of the pulmonary
valves which (as has already been stated) is known to be congenital.

1 Path. Trans, i. p. 60. * Ibid, xviii. p. 55.

8 Ibid. x. p. 80. 4 Ibid. v. p. 70.

6 Since thin was written I have met with an instance, in which a partial adhesion of
two of the aortic valves was found in the body of a boy, a?t 16, who had been drowned.

616 A SYSTEM OF MEDICINE.

In that case the united valves form a smooth, dome-shaped body,
with a regular orifice in its centre, and three small ridges or fnena
on its upper surface, placed at equal distances from one another.

An argument in favour of the view that adhesions of the aortic
valves are congenital has been found in the fact that, when there are
only two valves, they are sometimes of equal size. It is supposed
that the union must have taken place while the valves were in
course of development In reality, however, this fact merely proves
that adhesion ooourred before they were fully grown. A case in point
recently came under my notice. A man, set. twenty-three, died in
Guy's Hospital of febrile delirium in the course of acute rheumatism.
There was no recent valvular disease : but two of the aortic valves
were adherent, and the resulting valve was scarcely larger than the
third valve, which was itself much thickened along its whole edge, and
also contracted, so that it lay flat against the aortio walL The peri-
cardial sac was universally closed by old adhesions. Now this patient
was said to have had chorea and rheumatic fever in childhood, and
afterwards to have suffered from distinct symptoms of heart-disease,
dyspncea, palpitation, &c. His illness at that time was doubtless the
cause of the morbid changes both outside his heart and in its interior.

Two points remain to be considered, which afford powerful, and to
my mind convincing, arguments against the view that adhesions of
the aortic valves are always, or even frequently, of congenital origin.
The first is the extreme frequency with which such adhesions are
found in the later periods of life. Thus, according to Dr. Peacock,1
" of forty-three cases in which the aortic valves were diseased, either
alone or in conjunction with the mitral valve, in eleven (or 25*5 p.c.)
there was malformation of the valves, which probably laid the founda-
tions of the subsequent disease." Dr. Peacock goes on to say that this
proportion is much larger than would d, priori have been expected.
I think that it shows clearly how untenable is his position. It is
scarcely conceivable that a congenital malformation, which we have
seen to be extremely rare in infants, should be so commonly found in
adults. Again, the duration of life in the cases under consideration
is altogether adverse to the opinion that the valvular disease had
existed from the time of birth. Congenital malformations may, of
course, be found in the bodies of those who have lived long, provided
these malformations were not such as to interfere with the functions
of any vital organ : and in exceptional cases, even when they did so
interfere. But, if we average a considerable number of cases, we may
surely assert with confidence that a congenital adhesion of the aortic
valves, greatly narrowing the aperture, must inevitably tend to shorten
life. Yet we find Dr. Peacock deducing from his statistical inquiries
that " in cases of aortic valvular disease assigned to malformation, the
age of all the patients averaged 42*3 years, and the extremes of ages were
eighteen and seventy-six : while the mean age of the patients in
whom aortic valvular disease originated in other ways was only

1 CrooDian Lectures.

DISEASES OF THE VALVES OF THE HEART. 617

slightly greater, or 47*4 years, and the extremes of age were twenty-
one and sixty-two."

The influence of congenital defect in the causation of diseases of
the cardiac valves is perhaps not limited to the cases which we have
hitherto been considering. According to Virchow,1 who has recently
devoted much attention to the defective development of the aorta
that is found in patients affected with chlorosis, inflammation of the
mitral or aortic valves is found with disproportionate frequency in
these cases. He thinks that the congenital narrowness of the aorta
impedes the outflow of blood from the left ventricle, and so increases
the strain to which the valves are exposed. In connection with this
subject, the late Dr. Barlow 2 must be mentioned. He believed that
in certain young subjects the trachea failed to undergo due develop-
ment. This, he thought, led to imperfect expansion of the chest,
and consequently the supply of blood to the left side of the heart
was impeded ; and not only the aorta, but likewise even the orifices
of the heart's chambers, were prevented from attaining their proper
size. Dr. Wilks has put up in the museum of Guy's Hospital 8 a
specimen illustrative of Dr. Barlow's theory. I find, however, that
in this, as in both Dr. Barlow's cases, mitral stenosis existed in a
degree quite disproportionate to that of the other changes ; and I
must confess that I am inclined to think that this was the primary
lesion, that it arose in childhood (as seems often to be the case), and
that the smallness of the trachea was but a part of a defective
development of the body generally, consequent on the imperfect state
of the circulation caused by the valvular disease.

We have now to ask, what are the causes by which diseases of the
valves of the heart are generally produced ? And the answer to this
question is, that by far the most common cause is an attack of
" rheumatic fever," or " articular rheumatism," as it is termed in Dr.
Garrod's article in the first volume of this work. Dr. Garrod has
there pointed out that as far back as 1788 Dr. Pitcaira had noticed
that persons subject to rheumatism were attacked more frequently
than others with symptoms of heart disease ; and that other writers
at the commencement of the present century mentioned the same
fact. But they were exceptions. Few things in medical literature
are more curious, than to read the works of Burns and Kreysig and
Corvisart on diseases of the heart, and to find that they had not
the slightest suspicion of the rheumatic origin of these affections.
So late as the year 1835, indeed, Bouillaud4 was able to claim for
himself the discovery that rheumatic pericarditis (a disease at that
time generally recognized), is frequently accompanied by inflamma-
tion of the lining membrane of the heart — for which disease he then
proposed the name of endocarditis.

1 "Ueber die Chlorose, und die damit zusammenhangenden Anomalien im Gefasa-
apparatus," Berlin, 1872, p. 18.

* Guy's Hospital Reports, 1st series, vol. vi. p. 235.
8 Prep. 1412M. Catalogue, vol. i p. 31.

* " Traite Clini^ue des Maladies du Coeur," Taris, torn. i. p. 275.

VOL. IV. 8 S

(518 A SYSTEM OF MEDICINE.

After this I suppose that the occurrence of valvular disease of the
heart in the course of rheumatic fever soon became universally
known ; and several writers have published numerical statements with
regard to its frequency. In these there is a fair general agreement.
Dr. Peacock l quotes Dr. Fuller as stating that in his cases of acute
rheumatism some cardiac complication was present in 49*3 per cent. ;
-while Dr. Barclay found that in his cases the proportion was 39 per
<cent. Dr. Peacock gives 42*4 per cent, as the corresponding propor-
tion in the cases which came under his care from 1846 to 1868.

It is to be observed that, in these figures, pericarditis is included as
well as endocarditis ; and also that in many cases there was old disease
of the heart from former attacks of acute rheumatism. Both Dr.
Fuller and Dr. Peacock have attempted to distinguish these cases,
and to determine the exact frequency of recent endocardial mischief ;
but I doubt whether much reliance can be placed upon their results,
which are based upon stethoscopical evidence only. Indeed, it is
questionable whether we can trust to auscultation for determining the
presence or absence of early endocarditis. I believe that at Guy's
Hospital it has been found that in fatal cases of acute rheumatism
(and still more of chorea) there has been by no means a close cor-
respondence between the observation of a murmur during life and the
detection of vegetations on the valves after death. Sometimes, when
a systolic murmur has been present, the valves have been healthy ;
and, on the other hand, when no murmur could be detected they have
been found to be diseased.

On the other hand, objections of at least equal force may be urged
against the use of pathological observations to determine the question
as to the numerical frequency of endocarditis in acute rheumatism.
As far as I know, no series of unselected cases of fatal acute rheu-
matism has as yet ever been published. But I find that at Guy's
Hospital, in a period of rather more than twenty years, there have been
thirty-two such cases, in most of which the disease was a first attack-
Now in twelve of these cases the valves were perfectly healthy ; in
twenty cases one or more of them was diseased. Six times the
mitral valve was alone affected ; three times the aortic valves alone :
in ten cases both the mitral and the aortic valves were diseased ; and
in one other case, both these and the tricuspid also. This would give
62*5 per cent., as the proportion of cases of acute rheumatism in
which acute endocarditis occurs.

Now I shall presently show that in all these cases the changes in
the valves were slight, and that they were not at all concerned in
•causing death. The fatal termination was doubtless generally due to
hyperpyrexia, wliich (as is well known) often comes on in cases that
had previously appeared to be of a mild character. Still I think it
•cannot be denied that the thirty-two fatal cases were on an average
<cases of excessive severity ; for in twenty-one of them there was

\ Clinical Society's Transactions, iL p. 222.

DISEASES OF THE VALVES OF THE HEART. 619

recent pericarditis. Probably, therefore, we cannot accept these cases
as showing that 62*5 per cent, is really the proportion of cases of acute
rheumatism in which endocarditis occurs. Indeed, if the cases could
be regarded as average ones, we should have to suppose the proportion
to be really higher still, for in many of them death occurred at a very
early stage.

After all, it may perhaps be said that the exact determination of
the frequency of endocarditis in acute rheumatism is of less conse-
quence than has been supposed : for Dr. Peacock's observations render
it probable that this may vary considerably at different periods and
among different classes of the population. For practical purposes we
may perhaps take it at from 40 to 50 per cent.

Next to acute rheumatism, chorea is the disease which most
frequently gives rise to disease of the cardiac valves. I believe that
this fact was first pointed out by Dr. Hughes in a paper in the Guy's
Hospital Reports.1 He found that out of 14 fatal cases of chorea, in
which the state of the valves of the heart is mentioned, there were
only two in which these structures were reported to be healthy. In
the last twenty years we have had at Guy's Hospital sixteen other
fatal cases of chorea, in which post-mortem examinations have been
made ; and in only two of these were all the valves perfectly healthy.
Nine times there were vegetations on the mitral valve alone ; twice
on the aortic valves alone ; three times on both the mitral and the
aortic valves. Probably, however, these figures must not be taken
as indicating the liability to the occurrence of cardiac disease in
non-fatal cases of chorea, since severe forms of the disease are at once
more likely to destroy life than mild ones, and more likely also to be
complicated with valvular inflammation.2 Thus it would not be safe
to infer (as might at first be supposed) that disease of the cardiac
valves is absolutely of more constant occurrence in chorea than in
acute rheumatism itself.

Even in protracted fatal cases of chorea, I believe that the cardiac
affection is always slight in degree ; not going beyond the presence
of a row of minute granulations on the edge of one or more of the
valves, which might easily escape notice, if not" specially looked for.
Pericarditis, again, scarcely ever occurs as a result of chorea apart
from rheumatism ; having, in fact, been present in only one of the
thirteen cases that I have collected. It is, I think, generally supposed
that acute rheumatism differs from chorea, not only in the liability to
pericarditis, but also in the much greater severity and extent of the
-endocarditis which attends it. It was, therefore, with some surprise
that I found that in each of the fourteen cases of fatal acute rheumatism,
which I have already mentioned as having presented valvular disease,
the affection consisted merely in the presence of a row of minute

1 Series ii. vol. iv. p. 360 ; and Series iii. vol. i. p. 217.

* 1 may mention, however, that in one of the fatal cases of chorea under consideration
the girl's deatli was accidental, having been due to diphtheria, which she caught from
.another patient In this instance vegetations were found in the aortic valves.

S S 2

620 A SYSTEM OF MEDICINE.

granulations, precisely like those seen in chorea. In no instance were
those larger vegetations present that are so commonly found under
other conditions, nor was there ever any ulceration.

A third disease, which may also lead to changes in the valves,
exactly like those which occur in acute rheumatism and in chorea, is
pyaemia. In 1865 I exhibited to the Pathological Society two specimens
in which there were well-marked vegetations on tlfe mitral valve, in
pyaemia after surgical operations. Similar cases have since been
recorded by other observers. In six years (from 1866 to 1871 in-
clusive) I find that the records of post-mortem examinations at Guy's
Hospital contain twelve cases of pyaemia in which one or more of the
cardiac valves has been found diseased. In two or three of these
cases, however, the affected valve has been found ulcerated. This
has sometimes been observed, when the pyaemia was evidently of
external origin. Thus in 1867 I find a case of pyaemia recorded, in
which part of the flap of the mitral valve was found ulcerated away
from its chordae. The point is of some importance, because (as I have
shown elsewhere)1 it suggests a doubt as to the interpretation of some
of the cases in which ulcerative endocarditis has been believed to
have been the cause of blood-poisoning by Dr. Kirkes and others.

Another, but an indirect, cause of endocarditis is, I believe, the
existence of chronic spinal deformity. I have recently2 recorded
several cases of this kind in which death took place from pulmonary
obstruction and dropsy. In one of them the aortic valves were found
to be retroverted and covered with vegetations. This at first seemed
to be difficult of explanation : but I subsequently found reason to
attribute it to the increased tension within the aorta that must have
resulted from the sharp bend in its descending part where it was tied
by its intercostal branches into the very acute angle formed by the
diseased vertebrae. Since then I have seen acute endocarditis affect-
ing the aortic and the mitral valves in a man who died of bronchitis
and dilatation of the bronchial tubes, consequent on anchylosis of all
the vertebrae together, and of the ribs to the vertebrae. But in this
case I did not discover any evidence that the aorta had been com-
pressed or interfered with. A somewhat analogous case to the first
one mentioned in this paragraph has, however, occurred to me, in
which the aorta was compressed by large masses of caseous glands,
and in which the aortic valves were affected with acute endocarditis.
And Dr. Goodhart lately met with a case of congenital stenosis of the
descending part of the arch of the aorta in which there was a similar
affection of the valves.

There are still some other diseases in which similar minute granu-
lations on the cardiac valves have been occasionally found in the
post-mortem theatre of Guy's. Thus in six years (1866—71) I
find their presence recorded in three cases of cancer (of the uterus,
the liver, and the gall-bladder respectively), in one case of phthisis, in

1 Path. Trans, xvii. p. 60.

1 Guy's Hospital Reports, scries iii. vol. xix. p. 199.

DISEASES OF THE VALVES OF THE HEART. 621

one case of lobular pneumonia, in one case of Bright's disease, in one
case of puerperal peritonitis, in one case of syphilitic disease of the
liver, twice in cases of dilated heart, and once when there was old
adhesion of the two surfaces of the pericardium. They were also found
in one case of cholera ; but as the disease proved fatal in 12 hours,
it must be supposed that they existed before the attack commenced.

It has been stated that in all the fatal cases of rheumatic fever
that have come under observation at Guy's Hospital within the last
few years the changes in the valves have been slight, and in fact
identical with those which are well known to occur in chorea. But I
must not omit to mention that writers have recorded instances in which
the valves have been much more severely attacked. Thus Sir Thomas
Watson l relates two cases, in which death is stated to have occurred in
a first attack of rheumatic fever, complicated with acute pleurisy, three
weeks and four weeks respectively after admission of the patients into
hospital. In neither instance was any trace of pericarditis discovered
after death. In each, one of the aortic valves was a mass of ragged
ulceration ; and the adjacent portions of the two other valves were in
a slighter degree implicated. In one of the cases the ulcerating process
had penetrated through the valve into the muscular substance beyond,
and eaten a hole completely through the septum. In the other case
an abscess as large as a hazel-nut wras found in the muscular substance
of the septum, immediately opposite the disorganized valve. Now
the occurrence of such an abscess is so rare in acute rheumatism, that
I almost think it is permissible to express a doubt whether the case
was not rather one of pyaemia, or of primary ulcerative endocarditis,
with articular pains : for such cases have often been mistaken for
cases of rheumatic fever. Sir Thomas Watson goes on to remark
that these were the only instances of the kind which he had seen.
In the other fatal cases of acute rheumatism related in his book
only slight changes in the cardiac valves were found after death.

It may be convenient here to complete all that has to be said in
reference to the general etiology of the acute destructive disease of
the valves, which has recently attracted so much notice, under the
name of Ulcerative Endocarditis — a name first given to it, I believe,
by Charcot and Vulpian in 1861. Besides its occasional origin
in pyaemia and perhaps in acute rheumatism (as just mentioned),
this affection has often been found to occur in the latter months of
pregnancy, or a few weeks after delivery. Virchow 2 says that in the
Charity at Berlin there is never a year in which several instances of
this do not occur. It is true that in the majority of these cases in-
flammation of the uterus is present, so that the endocarditis might be
supposed to be simply a manifestation of pyaemia, but occasionally
the pelvic organs are quite healthy. Very often, however, ulcerative
endocarditis can be traced to none of these conditions, and may be

i Lectures on the Principles and Practice of Physic, 4th edition, 1857, p. 315.
2 " Ueber die Chlorose .... Endocarditis Puerperalis, " Berlin, 1872, p. 20 ; see also
Trousseau, " Lectures on Clinical Medicine," N ew Sydenham Society's Trans, vol. iv. p. 459.

eSS A SYSTEM OF MEDICINE.

said to arise spontaneously, so far as our knowledge at this time
extends. The patient may have previously been a healthy subject,
and the disease may arise suddenly with shivering, so that it is often
mistaken for enteric fever or some other acute disease. But such
cases are exceptional ; much more commonly ulcerative endocarditis
attacks valves which were previously unsound, and its effects overlie
and are blended with those of chronic valvular disease.

We may now pass to consider the causation of chronic affections of
the cardiac valves; and of these a large proportion, probably the
majority, arise out of the acute affections already described as occurring
in the course of acute rheumatism and of chorea (for pyaemia, being
itself almost always fatal, can hardly be credited with a share in the
production of these more remote changes). With regard to the details
of the processes by which these results are brought about, it may be
said that at the present time we know scarcely anything. We do not
even know whether an acute affection, once developed, ever subsides
entirely, and leaves the valve perfectly healthy. I think that this
must not infrequently occur, especially after chorea, for we have seen
that the valves are very often affected in this common malady, and
yet it has in my experience comparatively seldom happened that
patients labouring under valvular disease have stated that they had
previously had chorea. Another argument to the same effect may
perhaps be found in the comparative rarity of chronic rheumatic
disease of the aortic valves in women. We have seen that the aortic
valves were found to be affected in thirteen out of twenty cases of
acute rheumatic endocarditis. Now of these cases at least seven
occurred in females. But in the years 1867-71, for 23 cases of chronic
aortic disease with history of previous acute rheumatism in males,
only 6 cases in females came under observation in the post-mortem
theatre at Guy's. It would seem to follow that in women rheumatic
inflammation of the aortic valves must often subside entirely,
without leading to chronic disease. If this be true, it is of very
great importance, for it may teach us a most valuable lesson. We
shall presently see that the aortic valves are in men liable to strain
and pressure, from which in the other sex they are free ; and that in
consequence non-rheumatic disease of the aortic valves is in men
very common, in women comparatively rare. It appears very probable
that the same freedom from strain and pressure may also enable these
valves in women to recover from rheumatic inflammation more per-
fectly than in men. And, if so, we may learn how to obviate the
ill-effects of such inflammation in both sexes, and in the case of all
the valves, by keeping the patients at rest, and making them abstain
from work and exertion of every kind, for a long period after an attack
of endocarditis.

It is at any rate certain that the granulations, which appear to be
constantly present in acute affections of the valves, have generally
but a transitory existence. Sometimes, indeed, they become calcified,
and can thus be recognized long after all acute disease has passed

DISEASES OF THE VALVES OF THE HEART. m

away. But more often they disappear, and thus in chronic rheumatic
disease the surface of the thickened and calcified valves is often found
to be perfectly free from them. When uncalcified granulations or
vegetations are found in cases of long standing, I believe that they
are always of rather recent formation, and due to the supervention of
an acute inflammation, to which (as we have seen) valves already
diseased are particularly liable.

In a considerable proportion of cases, however, chronic valvular
disease can be traced to none of the conditions that have as yet been
mentioned. And its etiology appears then to be different in the case
of different valves. Affections of the aortic valves often accompany
similar morbid changes in the walls of the base of the aorta itself,
changes often spoken of as "atheromatous," but really dependent
on a chronic inflammation of the arterial coats, or (as it is termed
by Virchow and others) an arteritis deformans. This disease occurs
especially in men (as for example, sawyers, smiths, strikers and
riveters, bricklayer's labourers, and hodmen) whose occupat ions involve
great muscular efforts, by which the arterial pressure and the strain
on the aortic coats are increased. Writers have generally stated that
persons of rather advanced age are more liable to it, but Dr. Allbutt
says that it is very common in Leeds among quite young men.1
According to Peacock, a similar affection is not infrequently observed
to occur in girls engaged as nursemaids, and in other servants, who
are subjected to straining efforts before they have attained their full
strength. It is further to be noted that, although the affection of the
valves in all these cases appears to be identical in nature with that
which occurs in the walls of the aorta, the two are by no means
invariably affected in an equal degree. Dr. Allbutt has suggested the
opinion that continuous labour, such as hammer-work, is more in-
jurious to the aorta itself, and that sudden strains, like the lifting of
weights, tell rather upon the valves. The relative frequency with
which valvular disease is thus due respectively to mechanical strain
or injury and to the effects of antecedent acute disease, probably differs
greatly among different classes of the population, and in different
localities, according to the occupations of the lower orders in them. Dr.
Allbutt tells us that in Leeds, in hospital practice, heart diseases due
to acute rheumatism are among young men fewer than those which he
has learnt to attribute to over-exertion of the body. In this statement,
however, no account is taken of the affections of different valves
separately. I believe that in hospital practice in London one fails to
obtain a history of a past attack of rheumatic fever in at least half
the cases of chronic regurgitant disease of the aortic valves that are
met with in adults, and that in almost all these cases the changes in
the valves are "associated with similar changes in the walls of the
aorta, and are the result of habitual or repeated straining efforts of
one kind or another.

1 " The Effects of Overwork and Strain on the Heart and Great Blood-vessels," st»
George's Hospital Reports, v. p. 23.

624 A SYSTEM OF MEDICINE.

It is far otherwise in the case of the mitral valve. In this structure
atheroma appears only in the form of slight cream-coloured patches,
placed near the base of the valve, and therefore incapable of impeding
its closure. Nor can any morbid change in the mitral valve be tracea
in association with the disease of the aortic valves just described as
due to arteritis deformans. Still, there are a large number of cases of
mitral stenosis in which no previous attack of acute rheumatism or
chorea seems to have occurred, and the subjects are many of them
children, in whom no definite illness could have been overlooked or for-
gotten. Such cases have been by some writers attributed to congenital
malformation, a view which I have already endeavoured to disprove.
Other observers have supposed them to be due to latent rheumatism :
that is, to manifestations of the rheumatic state, which has for some
reason failed to display itself in the characteristic articular malady.
On closer inquiry it may sometimes be elicited that such patients have
formerly suffered from " growing pains " or " rheumatic pains " of
greater or less severity, and certain observers, among whom may be
mentioned no less an authority than the late Dr. Addison, have pressed
these into service as affording evidence of the existence of a consti-
tutional state. It must be admitted that rheumatic pericarditis often
precedes any affection of the joints, and that in young people already
suffering from valvular disease of the heart without any history of
previous rheumatism, the joints sometimes become swollen and painful,
or chorea is developed. I have therefore no doubt that many of
these cases of mitral stenosis are really the results of a rheumatic
tendency. But it is still a question whether they are not too frequent
for such an explanation to be applicable to all of them in wliich no
history of previous rheumatism can be traced.

It would appear, therefore, that the mitral valve is very liable,
even in children and young subjects, to undergo those changes which
lead to stenosis, either as the result of a spontaneous chronic morbid
process, or else as the consequence of some disease (other than
rheumatism or chorea), the tendency of which to produce endo-
carditis is as yet unknown. Can this disease be scarlatina or diph-
theria ? I have read (but I do not know where) that M. Bouchut has
recently brought forward diphtheria as often leading to the formation
of granulations on the mitral valve, but in the few autopsies that I
have made these have been absent. As is well-known, scarlatina is
often followed by acute rheumatism, or an articular disease allied to
it : and this may be complicated with endocarditis, as has been shown
by Trousseau and others. Nay, in cases of chronic valvular disease it
is not very uncommon for the patient's illness to be referred back to an
attack of scarlatina. But I am nevertheless very doubtful whether
this disease can be called in to account for the cases that now need
explanation, for I fail to find any evidence that scarlatina in itself
is capable of setting up endocarditis. So far as I am aware, when a
child dies of scarlatinal dropsy, or of any one of its other sequelae,
the valves are constantly found healthy.

DISEASES OF THE VALVES OF TEE HEART. 625

Within the last few years it has been a matter of frequent dis-
cussion among pathologists whether syphilis is ever a cause of disease
of the cardiac valves. The idea is indeed no new one ; for Corvisart *
long ago suggested that vegetations of the valves were of venereal
nature. No less an authority than Virchow2 has since stated his
readiness to admit the possibility that this may sometimes be the
case : but he has given no case in proof. When Mr. Myers 8 and
other army surgeons recently showed the frequency of heart-disease
in soldiers, and attributed it to the faulty clothing and accoutrements
which they are made to wear, or to the exercises they are called
upon to perform, it was objected that soldiers are very subject
to syphilis, and that this was really the cause of the cardiac affections
to which they are liable. But to that argument a rejoinder was made
that sailors are equally apt to have venereal disease, while they are
not found to suffer in the same proportion from morbus cordis.
For my own part, I confess that I have met with no facts, either by
observation or by reading, that would lead me to believe that
syphilis has anything to do with the diseases under consideration.

The effects of sudden violence in injuring the cardiac valves still
remain to be considered. Corvisart appears to have been the first
writer who reported a case in which the valves of the heart were
clearly shown to have been injured during muscular exertion. Since
that time several instances of the kind have been placed on record :
and in 1865 Dr. Peacock 4 collected seventeen cases, four of which
had come under his own observation.

It has already been stated that in advanced valvular disease soften-
ing and laceration are very apt to occur, whether as a result of slight
muscular efforts, or independently of any such cause. But symptoms
of heart disease have then generally existed for a long time. The
peculiarity of the cases now under consideration is, that the subjects
of them are apparently in perfect health when the injury arises, and
have never had rheumatism, or been suspected of any cardiac disease.
It is indeed true that such accidents have been observed chiefly in adult
men, whose occupations had long been such as are known to carry
with them the liability to induce chronic changes in the heart and
great vessels: and some have therefore argued that the lacerated
valve might not have been in a healthy state at the time of the
injury, but might have previously undergone degeneratioa And this
supposition is very difficult to negative, since death seldom occurs in
such cases until after the lapse of a considerable interval, when of
course the state of the valves before their rupture cannot be determined.
But in this, as in so many other instances, the maxim may be applied,
" De non apparentibus et de non cxistentibus, eadem est ratio." For
practical purposes it is more important to remember that a valve
may rupture in a man who has hitherto been active and robust,
and free from the slightest symptom of cardiac disease, than

1 Op. cit. p. 194. 3 Path. Trans, xx. p. 141.

2 Arch. £ Path. Auat. xv. 1858, p. 288. 4 Croonian Lectures.

626 A SYSTEM OF MEDICINE.

to discuss whether the valve has or has not previously undergone
slight degenerative changes, which no one could have discovered
or suspected.

Perhaps the most striking example that could be quoted, in which
mechanical injury led to the' rupture of a previously healthy valve, ia
recorded by Dr. Wilks in the sixteenth volume of the Pathological
Transactions (p. 77). The patient, a youth aged nineteen, fell from a
height, and alighting on a stone struck his left side violently, so as to
lacerate a portion of the intestine, as a consequence of which perito-
nitis arose, and proved fatal on the third day. It had been observed
that he had considerable oppression at the chest, and much distress in
breathing after the accident; but unfortunately no stethoscopioal
examination was made. At the post-mortem examination it "was
found that the most posterior of the aortic valves was torn through,
from its free margin to its base, a little on one side of its attached
edge. Only a ragged portion remained attached to the aorta, while
the bulk of the valve was free to flap backwards and forwards. A
small deposit of fibrin had already commenced to form on the
ragged edges.

In this case there was no mark of bruising on the chest, nor any
sign of injury external to the heart. But I think it can hardly be
doubted, from the history of the accident, that the cause of the
laceration was the blow on the side, rather than any muscular effort
made by the youth at the moment. The case would then be strictly
parallel to those which are not unfrequently met with, in which an
accident gives rise to severe laceration of some one of the abdominal
viscera, or of the interior of the brain, without there being any bruise
on the surface, or visible track by which the vibrations had passed
to the deeper structures.

In this respect, however, Dr. Wilks' case would appear to be ex-
ceptional, if the conclusions of Dr. Peacock are to be relied on in
reference to the question at issue. The last-named observer collected
seventeen cases of rupture of a valve from injury. In three or four
of them the patient had sustained direct injuries at the same time ;
but Dr. Peacock was nevertheless of opinion that in all of them the
immediate cause of the rupture was the violent effort made at the
same moment. " In one case the patient had made a long and
rapid journey on horseback : two men were pulling or loading
heavy casks, two were running violently, one was rowing, another was
striking with a heavy sledge, a third was endeavouring to force open
a door, and others were climbing rapidly, endeavouring to leap over a
fence, and carrying heavy deals. In others, violent coughing appears
to have been the cause of the rupture."

The comparatively small number of cases which Dr. Peacock could
collect is in itself a sufficient proof that rupture of a valve in a
previously healthy subject is after all a decidedly rare occurrence;
and this conclusion is confirmed by the fact that few cases of the
kind are recorded in the Pathological Transactions, which are

DISEASES OF THE VALVES OF THE HEART. 627

generally particularly rich in examples of the more striking forms of
disease. Among the different valves, those of the aorta are the most
liable to injury, having probably been ruptured in ten out of Dr.
Peacock's seventeen cases. Laceration of the columns of the mitral
valve seems to have occurred in four instances, and of the tricuspid
in the remaining three. In the aortic valves the part torn appears to
be usually the attached margin or angle.

Effects. — Diseases of the cardiac valves produce serious effects of
various kinds, by which the patient's health is disturbed and his life
often endangered. In these are to be found the " symptoms " of the
diseases in question. But before entering upon their consideration
it will be convenient to discuss first another class of effects also
resulting from such diseases, and in the eyes of the physician no less
important, although to the patient himself they are of but little
direct concern. I refer to the altered sounds, accompanying the heart's
action, that are heard by the ear or stethoscope applied to the patient's
chest— the " auscultatory signs " of valvular lesions.

In England these altered sounds are termed indifferently "mur-
murs " or " bruits" The latter term is of course a relic of the French
influence that predominated in this country for many years after the
discovery of auscultation. But it may be worth while to note that
French writers themselves apply the word " bruit " indifferently to
the natural heart sounds, and to the murmurs heard in disease, adding
the epithet " anormal" when a murmur is to be referred Jo, or else
designating it a " bruit de souffle" from the blowing character which
generally belongs to such morbid sounds.

Numerous theories have been formed to explain the production of
cardiac murmurs; but they have attracted more attention abroad
than in this country, English writers having generally passed them
by, as of theoretical rather than of practical importance. One of
the earliest of such theories was, however, originally propounded
by Sir Dominic (then Dr.) Corrigan, in the year 1829; and, quite
recently, the labours of certain French observers have gone far
towards establishing the correctness of this view, to the exclusion
of all others.

It must be remarked that murmurs are by no means confined to
the heart, but may arise in almost any part of the circulatory system ;
and this fact has to be taken into account by any theory that would
explain their production. Laennec had ascribed the bruit de souffle
to " a special vital state — a sort of spasm or tension of an artery." l
Corrigan 2 easily showed that this opinion was untenable. " Apply/'
he says, " the stethoscope under the outermost third of the clavicle,
not allowing it to pass (? press) on the subclavian. In a strong

1 " Traite tie rauscultation mediate," seconde edition, 1826. In his first edition Laennec'
had described the bruit dc souffle as occurring when the heart was too full of blood, and
as caused by contraction of one of the heart's orifices. But afterwards, finding that
there was no organic lesion which coincided constantly with the bruit, he expressed the
opinion cited in the text.

2 Lancet, 1829, vol. ii. p. 1.

628 A SYSTEM OF MEDICINE.

healthy man, not agitated, the mere impulse of the diastole of the
vessel is felt. Now compress the artery above the clavicle, so as to
diminish the current of blood through it : a loud bruit de souffle is
heard. Make strong pressure, so as to stop the flow of blood: no
sound is heard. If the sound in this experiment arose from the
arterial tube being excited into muscular action by the stimulus of
the pressure, why does it cease when the stimulus is increased ? "
And he goes on to give the following explanation of the bruit de
souffle ; — " When an artery is pressed upon, as in the experiment
above related, the motion of the blood in the artery immediately
beyond the constricted part (looking from the heart) is no longer as
before. A small stream is now rushing from a narrow orifice into a
wider tube, and continuing its way through surrounding fluid. The
rushing of the fluid is combined with a trembling of the artery, and
the sensation to the sense of hearing is the bruit de souffle" Further
on he applies the same theory to the murmurs heard in aneurisms
and in narrowing of the auriculo-ventricular orifices of the heart, &c. ;
and he proves that the condition supposed to produce murmur may
be imitated by passing a forcible current of water through a portion of
small intestine. In this experiment, as soon as constriction was made
on any part, a very loud bruit de souffle immediately became evident
just below the narrowed part, where no sound had been previously
heard.

The writers who followed Corrigan dealt with the causation of
cardiac murmurs from an entirely different point of view. By Gendrin
(1841-2) they were placed in the same category with the morbid
sounds heard in pericardial inflammations ; and since the latter are
due to friction between the two serous surfaces, he naturally attri-
buted the former, which he termed "bruits defrottement cndocar-
diaquts" to friction between the blood and the surface over which
it passes. This, friction theory has since been generally adopted.1

But in the year 1858, Chauveau, of Lyons, published an important
memoir, in which he endeavoured to show that the friction theory was
untenable, while he revived Corrigan's views, and placed them on a
firmer physical basis.2 In the first place, he proved that roughening
the interior of an artery does not cause a bruit. Thus he exposed the
carotid artery of a horse, and tore through the internal and middle
coats, at four or five points near one another. The tube was, of course,
greatly roughened, but no bruit was produced. On the other hand,
whenever a dilatation was placed in the course of an artery, the blood
entering the dilated part gave rise to a bruit de souffle. This Chauveau
ascribed to the fact that under such circumstances a sonorous jet is
formed, such as Savart studied experimentally under the name of the
"vcinc jluidc" He even laid bare the pulmonary artery of a
horse (in which artificial respiration was kept up after pithing),

1 Sec Walslio, "A Practical Treatise on Diseases of the Heart and Great Vessels,"
1862, p. 86.
* Gazette Medicale de Paris, 1858, p. 247.

DISEASES OF THE VALVES OF THE HEART. 629

and introduced his finger into the artery through a slit in its wall.
When the vessel was narrowed by tightening a thread round its base,
he could feel the vibrations of the veine fluide which was generated,
whereas the flow of the blood had previously been scarcely perceptible.

Chauveau therefore sums up the results of his experiments in the
statement that " the bruit de souffle is produced by the vibrations of
the veine fluide, which is always formed when the blood passes into a
part of the circulating apparatus actually or relatively dilated."

Very soon after the discovery of auscultation, it was found that a
bruit de souffle could sometimes be heard even in persons in whom
the heart was perfectly healthy, especially in those who were chlo-
rotic or anaemic. Such a bruit has been generally attributed to the
thin and watery state of the blood, rendering it liable to be thrown
into vibrations while flowing through the vessels. This explanation,
however, is far from satisfactory, and has indeed been rendered
untenable by the experiments of Chauveau and others, who have
shown (in opposition to some earlier experiments of De la Harpe) that
the production of murmurs in general is altogether independent of the
nature of the fluid in which they are formed.

It would seem, however, that the theory of Chauveau, just stated,
is applicable to such anaemic murmurs. As is well known, these are
of two kinds — the arterial, and the venous, or " bruit de diable" The
former is audible chiefly at the base of the heart, along the aorta, or
the pulmonary artery. Now, Chauveau has shown that in anaemic
horses the arteries generally are one-third smaller than in healthy
animals ; the mass of blood is greatly reduced ; the heart and its
orifices become diminished in size, so as to adjust themselves to the
altered volume of the blood ; but the great arteries, being compara-
tively inelastic, retract less perfectly. The conditions for the pro-
duction of a murmur are thus satisfied. Moreover, the arterial pres-
sure during the cardiac diastole is found to be very much lower than
usual ; hence, when the artery becomes distended by the heart's con-
traction, the force with which the blood enters is far greater than in
health. In other words, the range of pressure within the arterial
system is greatly increased.

The venous anaemic murmur, or bruit de diable, receives a very
similar explanation. As Hamernyk long ago showed, it is met with
only at the root of the neck ; and the cause of this lies in the ana-
tomical fact (first pointed out by B^rard) that in this region the
lower ends of the jugular and subclavian veins on each side are
adherent to the deep cervical fascia, and therefore cannot collapse.
This venous ampulla, as it has been termed, evidently affords the
conditions necessary for the generation of a veine fluide, whenever
the blood- stream in the jugular vein above is narrowed, whether by
simple adjustment of its calibre to the diminished volume of the
blood in anaemia, or by the pressure of the stethoscope, or by both
combined. Thus, as might be expected, in some healthy subjects a
bruit de diable can be generated by nice compression of the jugular

630 A SYSTEM OF MEDICINE.

vein with the stethoscope; and, on the other hand, even in those
who are anaemic a certain amount of pressure is required to develop
the murmur, unless the morbid state is present in an extreme
degree.

Since the publication of Chauveau's essay, this subject has been
studied by several French writers, especially by Marey, Luton,1 and
Bergeon,2 who have expressed their general adhesion to his views.
And for my own part I think that they have proved that a bruit
de souffle occurring in an artery or vein at a distance from the
heart is invariably caused by the generation of a sonorous veine
fluide, and due to the passage of a narrow jet of blood into a wider
cavity or part of the vessel.

But this explanation is certainly not applicable to all cardiac
murmurs. The bruit caused by a sonorous vcine fluide is heard
only in the dilated part of the channel, and not at all (or veiy
faintly) in the narrowed part behind it. In other words, it is pro-
pagated in the direction of the stream of fluid. Now, as we shall
see presently, some cardiac murmurs obey this law; among which
are those of mitral and aortic stenosis. But in mitral and in aortic
imperfection this is not the case : the murmur is audible, not only
in the direction of the regurgitant blood-stream, but also on the
other side of the orifice (over the left ventricle in the case of the
mitral valve ; along the aorta in the case of the aortic valves). Now
Bergeon has given a complete explanation of this, and has shown
that it may be easily imitated in experiments (such as have several
times been referred to), in which water is made to traverse tubes nar-
rowed at a certain point. One has only to provide the tube at the
seat of constriction with a lip or rim projecting backwards into the
stream, and a second murmur is at once generated, which is heard
behind the obstruction. A ad de sac is formed, and the fluid which
occupies this receives the shock of the onward current, and is thrown
into sonorous vibrations. It is evident that this experiment exactly
meets the case. The incompetent valves, whether mitral or aortic,
project backwards into the blood-stream, exactly like the lip or rim
employed by Bergeon.

But I think that the very success of this attempt to enlarge the
range of conditions to which Chauveau's narrow theory would limit
the production of a cardiac bruit de sovfflc, shows how cautious we
ought to be in assuming that we are now perfectly acquainted with
all these conditions. In expressing my belief that vascidar murmurs
have always such an origin as Chauveau supposes, I am mainly in-
fluenced by the consideration that the circulation of a stream of fluid
through a tube is a very simple physical matter, the phenomena of
which have been thoroughly studied experimentally. But it is far

1 " Nouveau Diction naire de MeMecine et do Chiruigie Pratiques/' art Auscultation,
* "Des Causes et du Mfohanisme _du Bruit de Souffle," Paris, 1868, p. 103. In this

essay will be found a detailed investigation into the physical cause of cardiac and

vaaomiar bruits.

DISEASES. OF THE VALVES OF THE HEART. 631

otherwise in the case of the heart. In the left ventricle we have a
contracting chamber, with projections of various kinds from its inner
surface. During its systole, in particular, the mitral valve with its
tendons and columns must tend to project into its cavity, with a
space between it and the posterior wall of the ventricle. Under
normal conditions the chamber empties itself completely during its
systole, and this space can hardly be said to exist. No murmur is
then generated. But let the ventricle be dilated, and let its con-
traction be imperfect and incomplete — as we must necessarily suppose
it to be, if the quantity of blood poured into the aorta be not greater
than in health, and if there be no mitral regurgitation (of which,
there is certainly in many cases no evidence). Is it not very pro-
bable that under such circumstances the blood in the space behind
the mitral valve may be thrown into vibrations, and so a bruit de
souffle be generated, exactly as in the cul de sac employed in Bergeon's .
experiments ? Such a bruit would be heard at the heart's apex, and.
nowhere else. We shall hereafter see that precisely such a bruit is very
frequently heard, in various diseases, and that its interpretation is
still open to very great doubt.

Now, cardiac murmurs, instead of being soft and blowing, are
sometimes very rough and harsh. The older French auscultators laid
stress on such varieties, and gave them special names, as "bruit de rape"
" bruit de scic" " bruit d'eftiUe" devoting great pains to the determina-
tion of their precise physical causes. Little success, however, appears
to have attended their efforts : as might indeed be expected from the
erroneous views that they entertained concerning the origin of mur-
murs in general. The rough and harsh murmurs in question are very
generally accompanied with a thrill that can be felt if the hand be
placed on the surface of the body at the spot where the murmuT is
audible : and to this Laennec gave the name of frtmisscment cataire,
Now, according to Bergeon, murmurs are rough and attended with
fremissement, when they are intense, and when the tube (he is speak-
ing of simple physical experiments) is thin and elastic. It might,*
therefore, be thought that such murmurs owe their peculiar quality to,
the fact that the walls of the orifice take part in their production, and
that they are not produced by the vibrations of the fluid alone. Such
a view, however, is entirely inconsistent with Savart's experiments
already referred to. And clinical facts are equally adverse to it As
we shall presently see, no murmur is so generally harsh, and so com-
monly attended with thrill, as the so-called presystolic murmur of
mitral stenosis. But in this affection, the margin of the orifice, far
from being thin and elastic, is almost always thick and hard, and often
contains much calcareous matter. The peculiar quality of the mur*
mux in this case is evidently not due to the fact that the orifice itself
as well as the fluid, vibrates. What, then, is its cause ? There can,
I think, be hardly any doubt that it depends upon the circumstance
that the jet of blood in which the murmur is generated, entering the.
flaccid empty ventricle, impinges on its inner surface at a point which.

632 A SYSTEM OF MEDICINE.

must be very close indeed to the part of the ventricle which strikes
the chest-wall and produces the heart's impulse. The physician may
thus almost be said to receive with his finger the full shock of the
sonorous jet propelled into the left ventricle through the narrowed
mitral orifice. It would be interesting to determine whether similar
conditions are traceable in other cases in which similar murmurs occur :
for instance, in cases of aneurism. For the present it must, I think,
be concluded that the harsh rasping quality of a bruit, and the accom-
panying thrill, are not due to any peculiar state of the orifice at which
the bruit is produced, but rather to the intensity of the murmur itself,
and to the fact that the jet of blood which generates it is directed
towards the surface of the patient's body.

Another modification of murmurs is that in which they are high-
pitched and resemble the note of a musical instrument, or a whistle,
the cooing of a dove, the puling of a chicken, or the mewing of a cat.
These are generally spoken of as " musical n murmurs ; and according
to Bergeon, they may arise in either of two ways. Sometimes they arc
due to the fact that the channel into which the veine fluide passes is
not straight but bent, so that the veinc impinges on its wall on one
side. This is the case, for instance, in the jugular fossa at the base
of the skull ; where (according to this writer) a musical bruit is often
generated, which gives rise to an intolerable singing in the ears.
More frequently such a bruit is due to the presence of a thin mem-
branous flap or valve, vibrating in the stream of blood which flows
over its surface ; the musical character of some cardiac murmurs
appears generally to be due to something of this kind. But the sub-
ject is one still admitting of further elucidation. In vol. vi. of the
Pathological Transactions, Dr. Peacock has recorded a case in which
a musical murmur, exactly resembling the sound of a cuckoo-clock,
was audible at the distance of some feet from the patient : after death
no special morbid appearance was discoverable in explanation of it

But the differences in the quality of cardiac murmurs, which we
have hitherto been considering, are of trifling consequence (so far as
the interpretation of their cause is concerned) in comparison with two
other points, to which we must now turn our attention. The first of
these is their rhythm, or relation to the movements and natural sounds
of the heart ; the second their seat, or capability of being heard at
different parts of the surface of the chest.

The passage of the blood through the heart and arteries is effected
by three successive movements, each of which may, under certain
circumstances, cause a bruit. (1.) The most important of these is the
ventricular systole : and since the contraction of one or other ventricle
is invariably the cause of any murmur that coincides with it in time,
such murmurs are very fitly termed systolic (or, sometimes, ventricular-
systolic). They, of course, take the place of, or follow, the first sound :
they coincide with the closure of the auriculo- ventricular valves, or at
least occur when these ought to close. (2.) After the ventricular sys-
tole comes the elastic recoil of the aorta and pulmonary artery. This,

DISEASES OF THE VALVES OF THE HEART. 633

again, may generate a bruit, which coincides with (or replaces, or follows)
the second sound, and occurs at the moment when the sigmoid valves
should fall together. It would have been better that the name given
to such a murmur should have indicated its origin : but no convenient
title suggests itself, and since the ventricle is dilating at the time, the
bruit in question has always been termed diastolic. This is unfor-
tunate, for the ventricular diastole is only very indirectly concerned
in its production, and may indeed have nothing at all to do with it.
(3.) Moreover, there is a third movement, which likewise occurs during
the ventricular diastole, and generates a third kind of bruit. This
is the auricular systole. In health, it produces no sound; but in
disease it may give rise to a very loud murmur: the best name for
this would undoubtedly be that of auricular-systolic (proposed for
it by Dr. Gairdner) ; but in practice it is generally called presystolic,
because it more or less closely precedes the ventricular systole.

Thus it is usual to designate the rhythm of a bruit by indicating
its relation to the contraction of the ventricles; a murmur that is
synchronous with this contraction is called systolic : one that follows
it is called diastolic ; one that precedes it is called presystolic. Now,
when the heart is beating slowly, it is generally easy to distinguish
which of the cardiac sounds or murmurs is systolic, from the fact that
the pause before the first sound is very much longer than that which
follows it. But when the pulsations are more rapid, this criterion is
lost, for the increased pace is gained at the expense of the period of
rest, and the one pause may then be as short as the other. The well-
known difference in quality between the first sound and the second
may then enable the rhythm to be detected ; but this again often
fails ; and one is driven to determine the ventricular systole by noting
at what period the heart's apex strikes the chest or (which is to me
more easy) by feeling the carotid pulse with the finger while one is
listening to the heart.

A systolic sound or murmur having been thus identified, it remains
to consider whether any other bruit that may be audible is diastolic
or presystolic. And here, again, all depends on the rate of the heart's
beats. When these are infrequent, and the diastolic pause is pro-
longed, the so-called diastolic murmur, occurring at the commencement
of this pause, is easily differentiated from the presystolic murmur that
occupies its termination, and runs up to the following ventricular
systole. But it is quite another case when the heart's action is rapid,
and the pause proportionately shortened. The distinction between
a presystolic and a diastolic murmur may then, as I believe, become
quite artificial, so far as their mere rhythm is concerned. But there
still remain differences of quality and seat, which usually enable the
nature of the murmur to be determined without much difficulty.

We will now consider the three kinds of bruits in the order of their

occurrence : I. the Presystolic ; II. the Systolic ; III. the Diastolic.

And since each of these may be developed on either the right or the

left side of the heart, it will be necessary to mention two varieties of

VOL. IV. T T

634 A SYSTEM OF MEDICINE.

-each. But, as Las already been stated, disease of the left valves is
greatly more common than of the right

I. A presystolic murmur, due to the auricular systole, is never
produced unless the auriculo-ventricular orifice is narrowed. And
practically it is almost always indicative of that chronic change in
the corresponding valve that has been described under the name of
stenosis.1

a. When developed at the mitral orifice, this murmur is much louder
at the heart's apex than anywhere else. It is also remarkably local,
being sometimes audible only at a single spot, and not being traceable
round the side of the chest towards the left scapula, as is the case
with the systolic murmur of mitral regurgitation.

The quality of a presystolic, or (as it is sometimes called) " direct"
mitral murmur is in most cases peculiarly harsh, and it is often
accompanied by a thrill perceptible to the touch. It is generally
spoken of as having a "churning" or "grinding" character; and
this may enable a practised ear to distinguish it at once from other
bruits. I think I have never yet heard a direct mitral murmur
which has been soft or musical. There is, however, an important
modification of the presystolic murmur, which, I believe, I first
described in a paper on this subject in the Guy's Hospital Eeports for
1870-71. Such a murmur is often very short; and it may be so
short as to resemble a tone, and thus to be hardly distinguishable from
the natural first sound of the heart. Now, it happens that in cases of
this kind the real first sound is commonly peculiarly sharp and clear,
and so resembles the second sound ; while the second sound is itself
inaudible at the heart's apex. Thus the sounds heard at this spot may
at first appear to be normal ; while on closer examination it may be
discovered that their rhythm is "entirely different from that of the
healthy sounds; and that one of them is in fact an abbreviated
presystolic bruit. In the paper above referred to, I have described a
case in which this observation led to the confident assertion that
mitral stenosis existed in the case of a woman who had no other
sign or symptom of cardiac disease, having been admitted into a
surgical ward for gangrene of the leg. She died six weeks later; and
the mitral orifice would admit only one finger-point.

It is only within the last few years that presystolic murmurs have
been rightly interpreted. The name was invented by Gendrin.2 He
did not, however, attach any special importance or diagnostic value to
such murmurs. But in 1843, Fauvel communicated to the Archives
Gtntralcs a paper in which he showed by the narration of four cases
(three of them fatal) that a presystolic murmur was indicative of

i It is indeed possible that amass of vegetations, formed upon the surface of the valvo
during acute disense, might so obstruct the channel as to lead to the development of
such a inurmur ; but (so far as I am aware) no case of the kind has as yet been placed
on record. I have always believed hypertrophy of the auricle to play an important
part in the development of a presystolic murmur ; and this implies the existence of
chronic disease.

2 I.econs sur lcs Maladies du Cceur, Ac, 1841-2.

DISEASES OF THE VALVES OF TEE HEART. 635

mitral stenosis. Subsequent French writers, however, have thrown
very little light on this subject. For many years the Paris School
of Medicine was divided into two camps with regard to the rhythm of
the heart's impulse, which Beau would have to be synchronous with
the ventricular diastole. Agreement on minor points was therefore out
of the question ; and H^rard,1 Bouillaud,2 and Durosiez,8 may be men-
tioned as having written on the subject of mitral stenosis, and expressed
views opposed to those of Fauvel. Durosiez, in 1862, thought it suffi-
cient to make a passing reference to " ce fanieux bruit pr^systolique,
dont tout le monde a parl£, sur lequel personne ne s'entend, que Hope
lui-meme avoue n' avoir jamais entendu, que M. Bouillaud enfin neglige
et m@me nie." Eacle, again, in his " Trait£ de Diagnostic medical," pub-
lished in 1859, speaks of it as " une distinction plus subtile quer^elle."

In Great Britain the first writer who alluded to this subject was,
I believe, Dr. Gairdner of Glasgow,4 who expressed views precisely
similar to those of Fauvel, except that he preferred to term the
murmur auricular-systolic, rather than presystolic. fhriwequently
papers on the same subject were published by Br. Wflka, Dr.* Gull,
Dr. Hayden (of Dublin), Dr. Peacock, Dr. Sutton, Tk. mtapson (of
Manchester), and Dr. Hyde Salter.6

Thus in my communication to the Guy's Hospital Reports I was
able to refer tc twenty-eight cases (seven contributed by myself), in
-each of which a post-mortem examination proved the existence of
mitral stenosis, and in which this condition had been diagnosed from
a presystolic murmur heard during life. Since then the subject has
been taken up by Dr. Douglas Powell and Dr. Silver. Even now, how-
ever, there are observers who deny that the rough grinding murmur
heard in cases of mitral obstruction is really presystolic in rhythm.
In the year 1872 Dr. Barclay contributed to the Lancet0 a series
of papers in which he endeavoured to prove that the peculiarity
in the rhythm of this murmur really depends on the circumstance
that the closure of the mitral valve is delayed. Instead of this
closure occurring at the commencement of the ventricular systole, he
believes it to take place only when the systole is nearly completed ;
the first sound being of course postponed likewise. Dr. Barclay thus
regards the murmur as really regurgitant and not obstructive, although
lie does not deny its constant association with mitral stenosis. But
it appears to me that no one who has studied the relation between
the murmur and the heart's beat or the carotid pulse can admit that
1 Jr. Barclay's hypothesis is tenable. Neither beat nor pulse can be
felt while the bruit is audible ; they both follow it.

It is important here to mention that the presystolic bruit by no

1 Arch. g£ne>. do Med., ser. v., torn. ii. p. 543. 1853.

2 Traitc* cliniquc des Maladies du Cceur, 1830.

s Arch, g^ner. de Af&L, ser. v., torn. xx. p. 385.

4 Edin burgh Medical Journal, yoI. vii., part 1, p. 438. 1861.

5 In my paper in the Guy's Hospital Keports, I have gone into the literature of this
.question in much greater detail than is possible here.

8 Vol. i., pp. 283 et seq.

T T 2

. 63B A SYSTEM OF MEDICINE.

means always merges gradually into the heart's first sound, as would
appear from the accounts given of it by some writers. Much more
often it is separated from the first sound by a distinct interval, which
seems to me sometimes as long as that which separates the natural
first from the second sound. The murmur, too, is often prolonged
through a period much exceeding that of the natural auricular systole.
This has been explained in two different ways. The late Dr. Salter
supposed that the first part of the murmur is generated while blood
is flowing passively from the auricle into the ventricle. I have
argued that the auricle begins to contract earlier, and goes on contract-
ing longer than in the healthy heart, and that the whole of the bruit is
thus due to the auricular systole. This view has since been esta-
blished by the cardiography observations of Mr. Mahomed.1 I
append copies of two of his tracings, taken from the heart's apex

i so

Fig. 1. Fig. 2.

in the same patient at an interval of seven months. It will he
observed that the slight elevation which Marey proved to be due to
the auricular contraction takes place very soon after the preceding
ventricuhir systole, and is succeeded by a gradually ascending liue,
throughout the whole duration of which the auricular systole is
sustained. The figures seem to speak for themselves : and unless it
can be shown that their peculiarities are capable of some different
interpretation, it appears to me that they not only establish the point
now under consideration, but also give the coup degrdec to Dr. Barclay's
hypothesis.

It is the more necessary to insist on the fact that the presystolic
murmur is often separated from the following first sound of the heart
by a distinct interval, because I believe that this fact has had much to
do with the impression that so long prevailed as to the real rhythm
of such murmurs. The old view was that the murmur caused by
mitral obstruction should be diastolic in rhythm : and with the
single exception of Dr. Markham all writers were agreed that diastolic
apex murmurs were very rare. Evidently, therefore, those observers
mistook for systolic the murmurs which they heard : and collateral
evidence of this is further afforded by the fact that they described as
systolic the frimisscment which we know to go with the murmur.
Nor did the mistake end here. I have shown in my paper that the
real first sound of the heart at the apex was mistaken for the second
sound, which it resembles so closely in character. It might appear

1 Med. Times and Gaz

DISEASES OF THE VALVES OF THE HEART. 637

needless to discuss the errors of a bygone period. But a little
experience in clinical teaching shows that these very errors are still
committed by every student, who has not had his attention specially
drawn to them. And it appears to me that some of the most recent
German writers have not yet extricated themselves from the same pitfall.
Dr. P. Niemeyer, of Magdeburg, in an elaborate work on " Percussion
and Auscultation," published in 1870, gives as diagnostic of mitral
stenosis "a loud long systolic apex murmur and strong frtmisscment
cataire ; in rare cases, also, a short diastolic murmur.,, But Traube,
Felix von Niemeyer (of Tubingen), and Friedreich, describe the direct
mitral murmur as presystolic.

I have already remarked that presystolic murmurs are often of long
duration, and thus commence very soon after the second sound has
completed the previous cardiac movement. It must be added that
when the heart-sounds are traced downwards from the base, these
murmurs have sometimes an apparent relation to the second sound,
which is very apt to mislead the student, and which I cannot alto-
gether explain. At the base, the second sound is clear and single ;
lower down, it appears to be reduplicated ; still lower, the presystolic
murmur seems to grow out of it. In my paper in the Guy's Hospital
Keports I have discussed this subject at some length, and quoted the
statements of Hamernyk, Drasche, and Guttmann, in regard to it.
Here I must limit myself to a simple statement of the fact

An objection frequently made to the view that these long murmurs
are due to a prolonged auricular systole — and indeed to the view that
they are due in any way to mitral obstruction — is, that since the
pulmonary veins are unprovided with valves, blood would be forced
back into them during the whole duration of the auricular systole,
and the circulation through the lungs would be brought to a stand-
still. But it is forgotten that, in cases of mitral stenosis, the tension
in the pulmonary vessels is very high — much higher than under normal
conditions ; whereas the left ventricle is in the condition of an empty
flaccid sac, and thus readily receives the blood expelled by the con-
traction of the auricle. This objection, therefore, appears to have but
little weight.

b. When developed at the tricuspid orifice, and due to stenosis of
the corresponding valve, a presystolic murmur is heard, according to
Dr. Hayden,1 principally over the fifth left costal cartilage, and the
fourth intercostal space, close to the sternum. Dr. Hayden lias lately
recorded a case of this kind, in which, between the area over which
the tricuspid presystolic murmur was audible and that over which a
coexistent mitral presystolic murmur was audible, there was a space
in which neither could be distinctly heard. Both lesions, therefore,
were diagnosed ; and after death the right auriculo- ventricular orifice
would admit only the point of the middle finger ; and the left one
was smaller still. The tricuspid murmur wras even harsher in
quality than the mitral one, and began earlier in the ventricular

1 Dublin Journ. of Med. Science, May 1874.

638 A SYSTEM OF MEDICINE.

diastole. As far back as 1864, Dr. Haldane x related a similar case, in
which the tricuspid orifice was found after death to admit only the
point of the forefinger. But it must be added that a mitral presystolic
murmur was at the same time audible ; and the mitral was in fact
much the narrower of the two valves. Indeed, although tricuspid
stenosis in moderate degree is common enough when mitral stenosis
is considerable or extreme, I am not aware that it is ever clinically
met with apart from such an association.2

II. A systolic (ventricular-systolic) murmur may have various
origins. As we shall presently see, it has not always anything
to do with the valves. And when it is due to valvular disease or
imperfection, it may be formed at any one of the orifices into either
ventricle ; namely, either the mitral, the aortic, the tricuspid, or the
pulmonary. Evidently a mitral or tricuspid systolic murmur must
be due to regurgitation: an aortic or pulmonary systolic murmur
must be obstructive or direct. These four varieties of systolic
murmurs may be in part distinguished by their seat.

a. A mitral systolic murmur is loudest at or near the heart's apex ;
that is, if the left ventricle be of normal size, about the fifth costal
cartilage, and a little internal to the nipple ; if the heart be enlarged,
further downwards and outwards. It is not heard over the base of
the heart, nor near the ensiform cartilage ; or, if it can be heard there,
it is much less loud than at the heart's apex. It can very generally
be traced along the left ribs (or, to use a common expression, into
tJte axilla), and is audible at the angle of the left scapula. The
question will hereafter be discussed whether it is not invariably
heard in these positions when of sufficient intensity.

b. An aortic systolic murmur is most plainly heard in the second
right interspace, and is traceable over the ascending arch, that is,
towards the inner end of the right clavicle ; and often also along the
arteries of the neck, or even of other parts of the body.

c. A tricuspid systolic murmur is heard over the ensiform cartilage,
and sometimes to the right of it It is also (according to Gairdner and
Sutton3) heard over the surface of the right ventricle ; that is to say,
a little to the left of the sternum ; but it " is little audible above the
level of the third rib." I should myself have fixed its upper limit at
a much lower point. In some rare cases it is very loud, and may
then be heard over a wide area ; but most commonly it is a faintly

i Ed. Med. Journ., vol. x., 1864, p. 271.

* An exception mnst be made for a very remarkable case which occurred to Dr. Gaird-
ner, and in which a rounded tumour projected into the interior of the right auricle, in,
such a way that it formed a kind of ball-valve to the tricuspid orifice. In that case a
tricuspid presystolic murmur was heard several years (I think, ten years) before death
by Dr. Gairdner, who published his diagnosis in his work on Clinical Medicine. I am
not aware that he has yet placed the result of the post-mortem examination formally on
record. I saw the preparation of the heart, with the tumour, at the meeting of the
British Medical Association in 1873. One remarkable feature about the specimen was
that there was no marked hypertrophy of the right auricle. This certainly throws some
doubt on the opinion which I have expressed in a note to p. 34.

• London Hosp. Reports, iv. 1867-8, p. 288.

DISEASES OF THE VALVES OF THE JBEART. 639

audible bruit ; and I think it is then generally discoverable at one spot
only. Indeed this appears a principal reason for its presence being
often overlooked.

d. A pulmonary systolic murmur is loudest about the third left
costal cartilage, and is transmitted upwards and to the left, towards
the middle or inner end of the left clavicle.

The clinical significance of these four murmurs varies widely in
different cases. They must, therefore, be discussed separately ; and it
will be convenient to take the two basic murmurs first*

As we have seen, the pulmonary valves are scarcely liable to any
disease beyond congenital malformation. In practice, therefore, a
pulmonary systolic murmur, if due to change in the valves, almost
always indicates a congenital defect, and needs no further discussion
here. An aortic systolic murmur, on the other hand, is frequently
caused by acquired stenosis of the orifice in question. But, as has
already been stated, such stenosis is (far more constantly than is
generally supposed) accompanied by regurgitation ; and the systolic
murmur, therefore, is followed by one which is diastolic.

A systolic murmur, however, audible at the base, and traceable
along the aorta, is by no means limited to cases in which there is
actual stenosis. Formerly it was held that any roughening of the
orifice, or of its valves, or even of the lining membrane of the vessel,
would suffice to generate it. But even then it was recognized that
such a murmur was frequently heard under various conditions, when
after death no morbid change in any of these parts was discoverable.
This led to the theory that the murmur was due to an altered state of
blood ; at first, that an anaemic state only could produce it ; but after-
wards, that various changes in the composition of the blood might
generate it. I have already, in discussing the physical theory of
murmurs, mentioned the ingenious explanation given by Chauveau of
some of the more striking of these anaemic murmurs, as they have been
called. This explanation, indeed, hardly covers the whole range of the
bruits that have been regarded as haemic, in the wider sense of the
term. And it must be admitted that the precise significance of many
basic murmurs has still to be determined. It is important to note
that many undoubtedly anaemic murmurs appear to be seated rather
in the pulmonary artery than in the aorta ; and that they are some-
times of a harsh quality, such as might a priori have been supposed
to belong rather to murmurs due to some very definite organic cause.

It must be added that the so-called haemic murmurs are believed to
arise in many acute diseases, including not only fevers, but also those
affections in which endocarditis is apt to occur, as, for instance, acute
rheumatism. In this disease there is a further ground for uncertainty
as to the cause of a basic murmur, in the fact that a similar sound
may probably be caused by the presence of lymph in small quantity
outside the heart, round the bases of the great vessels.

In this connexion I must not omit to mention the fact that in
children (even when in good health) a murmur over the pulmonary

640 A SYSTEM OF MEDICINE,

valves may be generated by the pressure of the stethoscope, as is
shown by the fact that it disappears when the instrument is lightly
applied. It is said that a similar murmur has sometimes been
observed even in adults, when the chest-walls are thin and yielding.
And consolidation of the anterior edge of the left lung appears some-
times to cause pressure on the trunk of the pulmonary artery, and
consequently a systolic murmur. Yet another suggestion with regard
to these basic pulmonary murmurs has recently been made by Quincke ;
and Dr. Balfour l has adopted it. It is that they sometimes depend
upon the edge of the left lung being retracted, in consequence of
which the heart, during its systole, compresses the pulmonary artery
against the parietes of the thorax, instead of merely pushing aside this
edge of the lung. In support of this it is asserted that the murmur
disappears when the diminution of the cardiac diUness shows that
the lung has recovered its normal dimensions. Dr. Balfour even
relates a case in which the murmur ceased whenever the patient
inspired deeply and held his breath. But I must confess that I see
little probability in this explanation.

This is perhaps the most convenient place for noticing the sugges-
tion of another German writer (Naunyn), which is also quoted with
approval by Dr. Balfour ; namely, that the systolic murmur of mitral
regurgitation is sometimes heard an inch or two to the left of the
sternum, between the second and third ribs. The seat of such a mur-
mur is supposed to be in the appendix of the left auricle. I must
confess that when I read Naunyn's paper on the subject I thought
there must be some mistake : and this suspicion is not removed by
Dr. Balfour's remarks on the subject, for I find him saying that this
remarkable modification of the mitral regurgitant murmur is almost
invariably present when the insufficiency is dependent upon anaemia
and chlorosis !

Passing on to consider the clinical significance of apical systolic
murmurs, we may take first that which is audible near the ensiform
cartilage, and which is referred to the tricuspid valve ; and of this
murmur the interpretation is seldom difficult. According to uni-
versal belief, it is always due to regurgitation through the tricuspid
orifice. In some cases this is the result of primary disease of the
valve itself, which (as we shall see further on) is occasionally affected
with an acute ulcerative change. In such cases a bruit would
doubtless be heard by any physician sufficiently acute to search
for it. Most commonly, however, there is no actual change in the
valve itself; its segments are kept apart by the dilatation and distension
of the right ventricle, while at the same time its orifice is greatly
widened. The distension of the ventricle may result either from
disease of the valves on the left side of the heart, or from some
chronic affection of the lungs, such as emphysema or fibroid disease.
The cases in which I have heard the loudest tricuspid regurgitant
murmurs have been those in which there was cirrhosis of one lung.

1 Med. Times and Gaz., 1874, ii. p. 556.

DISEASES OF THE VALUES OF THE 11EART. 641

Two good examples of this are recorded in Dr. Bastian's table in
the third volume of this work (cases vi. and xiii.). I well remember
the second of these cases, which occurred in the practice of the late
Dr. Addison, when I was his clinical clerk The murmur was so loud
that it was heard over the heart's apex, as well as over the ensiform
cartilage ; and Dr. Addison, although repeatedly pressed upon the
point, would not admit that the case was other than one of primary
mitral regurgitation. Indeed, as Dr. Wilks has pointed out, cases of
cirrhosis of the lung are often so like those of primary heart disease
in their general aspect and symptoms as to be mistaken for examples
of such disease.

There might, indeed, well be the same uncertainty about the
theoretical significance of tricuspid, that we shall see to prevail in
regard to the corresponding mitral, murmurs. But in practice such
doubts have not arisen, since tricuspid systolic murmurs are not very
often heard, and they are perhaps never heard unless those conditions
of obstructed pulmonary circulation are present which most physi-
ologists regard as readily capable of inducing regurgitation through
the orifice in question. Physicians, therefore, have been more disposed
to admit the occurrence of regurgitation when murmur is absent than
to doubt its existence when murmur is present.

It is very different with those systolic murmurs which are audible
at the apex of the heart, and which (if of valvular origin at all) must
be referred to the mitral orifice. They are perhaps the commonest
of all murmurs, and their significance is the most uncertain.

There are, in the first place, certain sounds which an inexperienced
auscultator may easily mistake for endocardial murmurs, but which
really arise not in the heart, but in that little flap or tongue-like
process of the lung which commonly projects forwards over the apex
of the heart, just below the seat of its visible impulse. The con-
traction of the ventricle, altering the form of the heart, causes a
movement of air into or out 1 of this portion of the lung, and thus
produces a murmur which, though of respiratory origin, is distinctly
systolic in rhythm. The sound in question is generally soft and
blowing; but I have several times known it to be of distinctly
musical quality. Its most important peculiarity is that it is not
constant, but accompanies only those beats of the heart which occur
at a particular period of the respiratory act, this period being gene-
rally that of inspiration. Thus, when the patient breathes out, the
first sound may be quite natural ; but when he draws in his breath,
a systolic murmur may be audible, which acquires its maximum
intensity when the cardiac beat happens to coincide with the acme
of the inspiratory effort. When the patient is made to hold his

1 According to certain modern views on the theory of the respiratory murmur (of
which a full account is to be found in the Med. Chir. Review for July 1873), a sound
within the lung can bo generated only by the entrance of air into that portion of lung,
and not by its exit. We must therefore suppose that when the heart assume* a globular
form during its systole, air is sucked into the flap of lung in question.

642 A SYSTEM OF MEDICINE.

breath, the murmur in question is often, but not always, suppressed
for the time.

A little care, however, excludes this source of fallacy. If the
murmur be heard uniformly with every ventricular systole without
exception, we may conclude that it arises within the heart itself.1
And the same conclusion may also be arrived at, even when the
murmur fails to accompany certain beats, provided that its absence
depends not upon any relation to the respiratory rhythm, but upon
the circumstance that the corresponding heart-beats are feeble and
imperfect. How, then, is such a systolic apex murmur produced ?

Now, if after death some of the tendinous cords of the mitral valve
be found softened and ulcerated through by disease, — or if the edge of
the valve have become turned inwards towards the auricle, — or even
if the orifice be so thick and hard that it obviously must have re-
mained patulous : — if any one of these conditions should be presents
we may be sure that regurgitation occurred during life, and we have
good grounds for inferring that any systolic apex murmur that may
have been audible was due to regurgitation.

The conditions just mentioned are, however, comparatively seldom
met with. But it is to be observed, that, if we exclude these con-
ditions, we can never with certainty determine, when we are
examining the heart after death, whether the mitral valve was or was
not competent. We have no means of testing satisfactorily the action
of the valve. We may, indeed, tie the base of the aorta ; and having
cut open the apex of the left ventricle, may hold the heart upside
down, and pour water into the cavity to see whether it runs out.
But in such an experiment the conditions are very different from
those which obtained during life. Then, the base of the muscular
columns was moved towards the orifice by the ventricular con-
traction : while those columns at the same time underwent shorten-
ing, so as to keep the tendinous cords stretched to the proper degree.
Now, ventricular wall and fleshy columns are alike relaxed. Errors
may thus arise in either direction. When the muscular columns
are converted into non-contractile fibrous tissue, the valve may
have been very imperfect in the living body, and yet may close well
enough when tested after death. Conversely, when the ventricle is
dilated, without the the tendinous chordae being increased in length,
it may happen that the valve allows reflux to occur after death,
although it had before been efficient.

This deficiency in the proof of mitral regurgitation, when a case
has reached the dead-house, would be of but little consequence, if
the orifice or its valve were constantly found to be obviously diseased
in those cases in which a systolic apex murmur had been heard
during life. But all who have worked at the subject know that this
is not so. To quote the words of Dr. Bristowe,2 " In a large pro-

1 Evidence is, I think, wanting to show that a white patch on the serous surface o
the apex, er any like condition, can generate the murmur in question.
1 Med. Chir. Review, 1861, July, p. 215.

DISEASES OF THE VALVES OF THE HEART. 643

portion " of such cases " the mitral valve and the orifice it protects
are found to present a perfectly healthy appearance." Now Dr.
Bristowe has proposed a very ingenious solution of the difficulty.
He believes that valvular incompetence exists whenever a systolic
apex murmur is heard ; and in the cases now under consideration he
attributes this incompetence to " disproportion between the size of
the ventricular cavities and the length of the chordae tendinese and
musculi papillares." He has shown in fact that while the former are
found after death to be dilated, the latter are often small and seem to
be on the stretch. But these observations are exposed to the full
force of the objections already made to the post-mortem evidence of
mitral regurgitatioa The appearance of the mitral cords and columns
in a dilated ventricle relaxed by death can surely afford no proof that
these parts were too short to allow the valve to close, when the ventricle
itself was shortened by its own systole.

Dr. Bristowe regards it " as an axiom, that the existence of a
systolic murmur at the apex of the heart is a sure indication of
incompetence of one or other of the auriculo-ventricular valves."
And he deems it unnecessary to offer any evidence in support of this
position, beyond the fact that in all the cases recorded in his paper
the general symptoms and the condition of internal organs (lungs,
liver, spleen, &c.) were such as are found in this form of disease.
Subsequent writers, however, have dealt with this question in a dif-
ferent way. Both Dr. Austin Flint1 and Dr. Andrew2 have expressed
the opinion that the murmur by no means necessarily indicates such
regurgitation: according to the latter observer, indeed, regurgitation is
absent in 34 per cent, of the cases in which the murmur is audible.

These authorities believe that there are two criteria which may
be applied to the determination of the fact, that in a particular case
a systolic apex murmur is really due to mitral regurgitation. The
criteria are : 1, That the murmur should be audible in the left side
of the back, about the inferior angle of the scapula; 2, That the
pulmonary second sound should be intensified.

1. A good illustration of the fact that the murmur caused by
mitral regurgitation is heard in the left side of the back is afforded by
cases in which the tendinous cords are ruptured or ulcerated through.
It has been so in the cases which I have seen, and I have not met
with any recorded instance to the contrary. But in such cases the
murmur is generally loud, and the amount of regurgitation probably
large. I am not sure that when the murmur is feeble one can fairly
expect that it should always be carried backwards : for one must
remember that, though the direction of the blood-stream is towards
the vertebral column, the auricle is not itself in any close relation with
the part of the chest-wall at which one looks for the murmur. Con-
sequently, although I am prepared to admit that whenever a systolic
murmur is heard in the back, it is caused by mitral regurgitation,

1 Am. Med. Times, 1862. Quoted in Braithwaite's Retrospect, xlvii. \1S63, p. 69.

2 St Bartholomew's Hospital Ueports, 1865, i. p. 13.

644 A SYSTEM OF MEDICINE.

I cannot regard the fact that a feeble murmur is not heard in tha
position as conclusive against its being so caused.

2. Intensification of the pulmonary second sound (that is, of th
second sound heard at the second left, as compared with the secon
right costal cartilage l) is undoubtedly present in many of the mos
marked cases of mitral regurgitant disease. Its cause is evidently th
increased tension of the blood within the pulmonary system of vessel*
But this (as I shall endeavour to 'show further on) may arise fror
any cause which prevents the left side of the heart from emptyin
itself. I cannot see, therefore, how intensification of the second soun<
can be indicative of regurgitation through the mitral orifice, rathe
than of other conditions which will then be mentioned. Moreover,
believe that intensification of the pulmonary second sound require!
as a condition of its occurrence, that the right ventricle shoul
be powerful, and that the tricuspid valve should be efficient,
think I have observed that this sign is present chiefly in the earl;
stages of mitral regurgitant disease, before it has begun to tell upoi
more distant parts.

My own views with regard to the interpretation of systolic ape:
murmurs may therefore be summed up as follows :

1. If such a murmur be audible in the back, it indicates mitra
f? regurgitation.

■ 2. If such a murmur be heard only at the heart's apex, we ai

• unable at the present time to pronounce any positive opinion as to it

cause. Should the murmur be loud, we may probably conclude tha
: it is not due to mitral regurgitation : since really regurgitant murmur

I when loud, are, perhaps, always audible in the back, though for sligl

! murmurs the same statement may not be tenable.

The question still remains, How is a systolic apex-murmur pre

duced when it is not caused by mitral regurgitation ? I have alread

, (vide p. G31) suggested that it may be due simply to dilatation of th

left ventricle, as was long ago supposed by many of the earlier writei
on auscultation.

III. A "diastolic" murmur, as has been stated, accompanies th

clastic recoil of the aorta and pulmonary artery. It almost iuvariabl

i indicates regurgitation, through the space that should be closed b

one or other set of sigmoid valves, into the ventricle ; and in thl
immense majority of cases the valves affected are those of the aorta.
The quality of the diastolic murmur of aortic regurgitation varic
greatly in different cases ; it may be soft and blowing, rough, an<
attended with thrill, or even musical. It may be so loud as to b
r. audible at some little distance from the patient ; or so slight as t

require the utmost vigilance for its detection.
The seat of this murmur is somewhat variable. As a rule, it i

1 Dr. Andrew has shown that it is necessary, in instituting this comparison, 1
1 remember that the same difference may bo due to enfecblcment of the aortic secoii

sound, while the pulmonary second sound is natural ; and also that an emphysematoi
1 lung overlapping the heart on one side may modify the intensity of the sound.

DISEASES OF THE VALVES OF TUE HEART. 645

very plainly audible over the base of the heart ; its point of maximum
intensity is generally stated to be at the sternal end of the second right
costal cartilage, or in the second right interspace; and it is carried
downwards along the length of the sternum (apparently in conse-
quence of the fact that osseous substance is a good conductor of
sound), so that it may often be loudly heard near the ensiform car-
tilage. This fact has been especially insisted on by Dr. Gairdner.1
Again, this murmur is frequently plainly audible at the heart's apex,
and sometimes it is louder there than at the base. Lastly, it may be
conducted along the arteries, sometimes, to a surprising distance:
according to Dr. Gee, as far as the radial arteries.

In discussing the theory of murmurs in general, I have pointed out
the conditions upon which some of the varieties in the seat of this
bruit appear to depend (see p. 630). If the views there stated are
correct, the fact that in a particular case an aortic diastolic murmur is
transmitted upwards along the aorta may be interpreted as indicating
that the valves are so far free from serious damage that, although they
do not meet, they nevertheless project inwards into the aorta to a
greater or less extent ; while in those cases in which the murmur is
solely carried downwards it may be concluded that the valves are
more completely destroyed.

A further refinement in regard to diastolic murmurs has lately been
suggested by Dr. Balthazar Foster2 of Birmingham. He believes
that when such a murmur is heard at the apex of the heart it is due
to incompetency of the left aortic segment, so that the regurgitant
blood-stream Tails upon the mitral curtain and is carried downwards;
and, on the other hand, that a similar murmur propagated towards the
ensiform cartilage indicates defect in the right and posterior segments,
by which the blood is thrown upon the septum. He alludes to cases
corroborative of his views, to which he further attaches considerable
importance as regards prognosis. He thinks that incompetency of an
aortic segment must specially interfere with the flow of blood into the
coronary artery contained within the corresponding sinus (which flow
he, in common with many other authorities, believes to occur during
the recoil of the aorta), and so must tend to impair the nutrition of the
heart. Now the left aortic segment has no coronary artery in relation
with it. Dr. Foster therefore infers that, ca^eris paribus, life is more
likely to be prolonged when this segment is affected, or (in other word:)
when the murmur is audible at the apex. But my belief has hitherto
been that the murmur is propagated in this direction especially when
the regurgitant stream is large : and if so, one would suppose that the
prognosis must be particularly unfavourable. I think that the point
is one which needs further observations.

It has been stated that in the immense majority of cases a regur-
gitant murmur has its seat at the aortic orifice. In fact a pulmonary
regurgitant bruit is so rare as scarcely to need consideration. In

1 Clinical Medicine, ]>. 587.

» Med. Times and Gazette, 1873, ii. pp. 658, 686.

646 A SYSTEM OF MEDICINE.

1865 Dr. Wilks exhibited to the Pathological Society l a specimer
of disease of the valves in question, in which a double bruit had
been heard during life: and one or two other cases are recorded
in medical literature. In Dr. Wilks's case the question of disease oi
the pulmonary artery was considered during the patient's life, for the
pulse gave no indication of aortic regurgitation, and the bruit became
less marked towards the right, and in the course of the aorta, but wa*
equally distinct, or even somewhat more intense, towards the left,
clavicle. But the great rarity of such disease led to its rejection as
a diagnosis. Indeed, one can hardly expect in future to attain tc
greater accuracy : for (as we shall presently see) the pulse may fail
to be characteristic of aortic regurgitation even when this disease
exists: and the tendency of aortic diastolic murmurs to be trans-
mitted downwards along the sternum must always prevent a pul-
monary regurgitant murmur from being identified by its being heard
over the right ventricle. Still, acquired disease of the pulmonarj
valves is so exceedingly rare (and in congenital disease I do nol
know that marked regurgitation ever occurs), that one hardly needs
to make a reservation on account of it in attributing a diastolic
murmur to aortic regurgitation. The real necessity for reservatior
lies in the fact that aortic aneurism sometimes causes such e
murmur, probably because it receives blood during the elastic recoil ol
the aorta, as well as during the ventricular systole. It is only wher
an aneurism arises from the commencement of the arch that it*
murmur could be mistaken for one of regurgitation through the
valves: and even then the former would perhaps never be trans-
mitted to the heart's apex, as is so generally the case with the latter,
Very frequently, indeed, the two conditions are combined.

Another infinitely rare condition, in which a diastolic murmur, not
-due to regurgitation through the aortic valves, may be heard at the
base of the heart, is that in which the aorta communicates with the
pulmonary artery, either by a patent ductus arteriosus, or through ar
•aneurismal sac. Of the former affection I have recorded a remarkable
instance.2 The murmur (which was in part musical) was audible al
the second left costal cartilage, and was transmitted to the left alone
this cartilage, but not downwards along the sternum. It was not
everywhere continuous with the second sound. It had a wavj
character, quite unlike anything that I had ever heard before. Il
was clearly distinguished (during the patient's lifetime) from ar
aortic regurgitant murmur ; and it was thought not unlikely to be
due to an opening from the aorta into the pulmonary artery. A
case in which an aortic aneurism was correctly diagnosed to oper
into the pulmonary artery has been related by Dr. Wade,8 of Birming-
ham. The diastolic murmur was prolonged, and of a hissing charactei
with distinct purring tremor. It was audible over the cartilage of th<
fourth left rib, and in the neck, back, and upper part of the chest.

1 Path. Trans, xvi. p. 74.
*,* Guy's Hospital Reports, 1872-3, series iii., voL xviii. p. 23.
* Med. Ckir. Trans, vol. xliv.

DISEASES OF TBR VALVES OF THE HEART. 647

With these exceptions, a diastolic murmur (as I believe) invariably
indicates regurgitation through the aortic orifice into the left
ventricle.

It may be expected that something should be said as to the not in-
frequent coexistence of two or more of these murmurs in the same
case. I have already remarked on the rarity of systolic murmurs
indicating actual obstruction of the aortic orifice, unless a diastolic
murmur be also present, and discoverable on careful examination. It
may be added that in disease of the aortic valves the tendency is for
regurgitation to follow obstruction. In the case of the mitral valves
the opposite is observed. Commencing disease appears to produce a
regurgitant murmur : and it is only as the orifice becomes more and
more contracted that an obstructive murmur is heard. There is this
further peculiarity, that when mitral stenosis causes a marked pre-
systolic niurmur, it rarely happens that any systolic murmur is at
the same time audible. I have scarcely ever heard a systolic murmur
in association with the rough grating bruit, attended with thrill, that
is so characteristic of the more extreme degree of constriction of the
mitral valve. A more or less distinctly double murmur at the apex
is not, indeed, very uncommon : but in this case both portions of the
murmur are rather of a soft and blowing quality : and the inference
probably is that the stenosis is moderate in degree.

With regard to the coexistence of murmurs developed at different
orifices I have nothing particular to say. Their determination must
be based on the principles which regulate the diaguosis of each
murmur separately: guided, of course, by the known liability of
particular valves to undergo simultaneous or consecutive changes.

The other effects of disease of the cardiac valves — those which affect
the patient's health, and are consequently commonly called the
symptoms of such disease — are divisible into three distinct classes.

I. We may take first a class of effects, which are of great importance,
but which have only recently attracted notice, and probably do not
yet receive a due share of attention. The valves of the heart are
bathed on all sides by the circulating fluid. When they are inflamed
or ulcerated, the blood flows directly over the diseased surface.
When any portion of their substance, or of the products of inflam-
mation, becomes disintegrated, the detached fragments necessarily
pass into its stream. This is so obvious, that we may well be
surprised to find that no one had recognized it until Dr. Kirkes
pointed it out in the year 1852.1 And as he showed, the phenomena
attendant on this process are divisible into two distinct groups : —

(a.) Embolism. — In the first place, a mass of some size may be
detached, which, passing into the arterial system, sooner or later
reaches a vessel which it cannot traverse, and which it conse-
quently plugs. The result is that the circulation is entirely arrested
in the region supplied by the artery, unless indeed blood from col-
lateral arteries enters the obstructed vessel beyond the seat of the

1 Med. Chir. Trans, xxxv. p. 281.

648 . A SYSTEM OF MEDICINE.

obstruction. It might have been expected that the region in ques-
tion would become anaemic. Recent observations, however, have
shown that such is not the case. Provost and Cotard,1 and afterwards
Lefeuvre,* have studied this question experimentally. They injected
foreign bodies (especially the seeds of tobacco) upwards into the
abdominal aorta of dogs, and exposed the kidneys and spleen by
opening the abdomen, so as to make apparent the earliest effects of
obstruction of the arteries of those viscera. They found that the
regious supplied by the blocked arteries instantly became of a dark
purple colour, and in the spleen were distinctly raised above the
level of the rest of the region. This state of engorgement is believed
to be due to a paralysis of the muscular coat of the vessels. They
become unable to resist the pressure of the blood in the veins, which
consequently flows back into the capillaries and arteries, and dis-
tends them up to the point of obstruction. Haemorrhage then takes
place. After a time the effused blood and the elements of the tissue
undergo fatty degeneration : and the affected part acquires a charac-
teristic yellow colour. This always extends to the surface of the
organ, and penetrates more or less deeply towards its interior in the
form of a wedge or cone, which is generally surrounded by a red halo
of congestion. Still later, absorption takes place : and in the end
nothing is left beyond a deep fissure or puckering. It must be added
that sometimes, instead of the whole mass undergoing fatty degene-
ration and conversion into the peculiar yellow matter, a part of it
sloughs : in other cases it breaks down into pus.

The changes just described do not occur in all organs alike. They
are especially well marked in the spleen and kidneys.3 The reason
appears to be that the branches of the splenic and renal arteries
anastomose but little or (in the case of the splenic artery) not at all.
In the liver, on the other hand, a true infarctus is, perhaps, never
met with, apparently because its lobules do not derive their supply of
blood entirely from a single source. The mesenteric arteries occasionally
become the seat of embola. This occurred in one of Lefeuvre's experi-
ments with tobacco seeds. The affected part became first pale and
afterwards of a livid purple colour. Embolism of a mesenteric artery
has also sometimes been observed as a result of disease in the
human subject. The cerebral arteries are very liable to embolism;
this is believed to occur more frequently in the left middle cerebral
than in any other artery, apparently because its course in some way
favours the entrance of a detached mass. In the brain, the result of
arterial plugging is generally white softening of the corresponding
part of the brain ; but sometimes a firm yellow infarctus is pro-
duced. When embolism occurs in one of the arteries of the

1 Gaz. Mid,, 1866, p. 202.

9 £tude physiologique ct pathologique sur lcs Infarctus Visc&tiux, Th&se de Paris,
1867. A review of these observations will be found in the Med. Chir. Review for
October 1871, p. 368.

3 According to S]>erling, (Iuaug. Diss., Berlin, 1872; London Med. Record, Jan. 1873)
the kidney is more frequently the seat of embolism than the spleen, in the proportion
of 75 to 51.

DISEASES OF THE VALVES OF THE HEART. 649

extremities, the tendency is for the limb beyond the seat of
obstruction to mortify. The gangrene is not then always of the
dry variety, as was formerly taught. It may be moist, and at-
tended with the formation of bullse. This is doubtless preceded by an
hyperemia, like that which we have seen to follow plugging of an
artery in the spleen or kidneys, except that as the veins of the limbs
are provided with valves, the blood probably comes from the col-
lateral arteries of the limb. In the arteries of the extremities, and
indeed in all arteries, embola are especially apt to be arrested at
those points where the vessel is dividing, or where a large branch is
given off, so that the calibre of the channel is suddenly diminished.
Thus in the upper limb, they are most commonly found in the
axillary artery, and at the bifurcation of the brachial artery : in the
lower limb, at the points of division of the common femoral and the
popliteal arteries respectively. The left lower limb is decidedly more
subject to embolism than the right: and by VirchowHhisis attributed
to the fact that the left common iliac artery comes from the ab-
dominal aorta in a more direct line than the right. The peculiar
wedge-shaped masses in the abdominal viscera appear to have been
described independently by Hodgkin,2 Cruveilhier, and Rokitansky.
Their association with heart-disease was first noticed by the last-
named observer, and has been admitted by all modern writers on
morbid anatomy. It is, however, only within the last few years that
they have been regarded as possessing any clinical interest, or that
their formation has been supposed to be attended writh any symptoms
affecting the health of the patient. Following Kirkes, Virchow3 is
the writer to whom credit is especially due for having drawn atten-
tion to this subject : and recently several French memoirs and papers
have been written on it, in which the affection is described as a
special disease, under the title of " Ulcerative Endocarditis."

The clinical features observed in these cases are of two kinds.
In the first place, there are the direct efforts of intercepted blood-
supply to the part served by the obstructed vessel. Thus, as we have
seen, a limb may mortify as the result of embolism of its main artery.
Many of the cases of spontaneous gangrene in young subjects that
come under the care of the surgeon are of this kind ; and, with the
stethoscope, the existence of disease of the valves of the heart may often
be recognized without difficulty. It may be worth while to note
that the embolism in these cases is not always derived from the
diseased valve itself; sometimes it comes from the auricle or ven-
tricle, having been one of the little rounded ante-mortem clots which
are so apt to form in the heart's chambers behind any obstruction.4

Embolism of the cerebral arteries, again, may give rise to a great
variety of symptoms, according as one or another part of the brain

1 Gesammelte Abhandlnngcn, p. 444. * Med. Chir. Trans, xxvi.

3 Gesammelte Abhandlungcn, pp. 636—729.

4 Such an ante-mortem clot may, when a valvo is stenosed, be the direct cause of
sudden death : getting washed into the blood-current, it may completely occlude the
narrowed orifice. See a case recorded by Dr. Van der Byl, Path. Trans, ix. p. 91.

VOL. IV. Xf U

650 A SYSTEM OF MEDICINE.

is deprived of its due supply of blood. The most frequent effect is
the production of right hemiplegia, with or without aphasia. This
corresponds with the fact that the left middle cerebral artery is espe-
cially apt to become plugged. Embolism of the retinal arteries leads
to changes which can be studied with the ophthalmoscope.

It has already been stated that in the viscera, instead of the usual
yellow wedge-shaped masses or infarctus being foraged, suppuration,
or even sloughing, sometimes occurs in the regions supplied by an
artery that has become the seat of embolism. It is perhaps doubtful
whether these changes ever in themselves produce any appreciable
influence on the patient's health, or on the symptoms from which
he suffers. But they may set up a peritonitis, and this will usually
be attended with a great aggravation of his complaint, and even with
danger to his life ; and embolism of a mesenteric artery may cause
severe enteritis, which may be quite capable of clinical recognition.

(b.) Infection. — But in almost all these cases the effects of the
occurrence of embolism in particular arteries are complicated with,
and probably overpowered by, those which depend upon a general
contamination of the blood, as it passes over the surface of the
diseased valve. This was clearly pointed out by Dr. Kirkes, in his
classical paper already more than once referred to ; and of late years
many observers have worked at the subject, in the hope of ex-
plaining it more fully. So severe and rapidly fatal are some of these
cases, that Virchow has given them the designation of Endocarditis
Maligna.

A principal symptom in these cases is the presence of fever. The
temperature is raised two or three degrees, or more, above the normal
standard. Dr. Goodhart * mentions one case in which it was several
times noted at 104° ; and in a case which I recently examined it
reached 105*8°. Not rarely there are repeated attacks of shivering :
indeed, the illness is often ushered in by a sudden rigor. The pulse
is quickened; the tongue is often dry. Extreme prostration, delirium,
and somnolence, are occasionally present. According to Dr. Wilks,
articular pains are often complained of. Vomiting and diarrhoea are
common. The spleen is greatly enlarged, and is sometimes tender on
pressure. The skin has an icteroid tinge, and there may even be
jaundice, of which Lancereaux2 has recorded several examples.
Petechia may be present, or even distinct purpuric blotches.8 Ecchy-
motic spots may also be found on the surface of the pleura and peri-
cardium, and on the mucous membranes lining the larynx, stomach,
intestines, and urinary bladder. The liver after death is found to be
pale, supple, and flabby. The tissue of the spleen (which is many
times larger than natural) is soft and pulpy.

When a patient is known to be suffering from disease of the
cardiac valves, there is but little difficulty in assigning to their true

i Guy's Hosp. Keports, xv. p. 415. t Oai. M&L, 1862, p. 662.

1 Path. Trans, xxi. p. 109.

DISEASES OF THE VALVES OF TEE HEART. 651

cause the symptoms just enumerated. By carefully examining the
heart several times at short intervals, one may be able to detect such
variations in the physical signs as may demonstrate the fact that
acute changes in the valves are going on. Charcot and Vulpian x
mention one case in which the most marked signs of aortic in-
sufficiency became prominently developed within a week

But in many instances there is nothing to draw the physician's
attention to the state of the valves; and the real nature of the
case may then be easily overlooked. The valves may previously
have been quite healthy. And since palpitation, precordial pain,
and oppression of the breathing may all be absent, there may be
nothing to suggest the necessity of examining the heart The case
is thus very likely to be mistaken for one of enteric fever, or, if
there be much shivering, of idiopathic pyaemia, or even ague ; or
again, if there be marked jaundice, for one of pylephlebitis,
The relation to purulent infection has been especially insisted on
by Dr. Wilks, and he has proposed to designate the affection an
" arterial pyemia."

In the previous paragraphs it has been taken for granted that the
diseased valves are those on the left side of the heart, and that
the phenomena of embolism or of infection therefore show them-
selves in the course of the distribution of the systemic arteries.
However, when the tricuspid valve is diseased, or the pulmonary
valves, precisely similar effects show themselves; but, of course,
within the lungs. A striking case of this kind has been recorded by
Charcot and Vulpian,2 which was diagnosed during life. One flap of
the tricuspid valve was softened and perforated, and presented
numerous vegetations. The lungs contained scattered abscesses.
Other instances have been related by Dr. Kirkes and Dr. Moxon.8
Dr. Moxon's case occurred in a woman, within a month after her
delivery.

The precise nature of the process of Infection in the cases under
consideration has been much discussed of late years, and even now
it has not been fully ascertained. In almost his earliest paper on the
subject, Yirchow related some experiments that he had made of in-
jecting different substances into the jugular veins of dogs. And he
proved that while portions of caoutchouc simply produced obstruction
of branches of the pulmonary artery into which they were carried,
animal substances (pieces of muscle, fibrin, &c.) set up severe inflam-
mation of the corresponding tracts of lung tissue, leading to suppura-
tion or even to sloughing. Hence he concluded that the phenomena
of infection are not merely of mecJianical origin, but must result from
some chemical action. The same fact has since been insisted on by
Feltz4 of Strasburg, who maintains that solid elements by themselves

1 Gaz. Med. 1862, p. 888. * Gaz. MeU, 1862, p. 428. V

• Fath. Trans, xxi. p. 107.

4 Traits clinique et expe'rimentale dcs embolies capillaires. 2£nie e\L, Strasbourg,
1870.

UU 2

652 A SYSTEM OF MEDICINE.

never carry infection: this is always propagated by septic fluids.
Another writer, Panum of Kiel,1 endeavouredtto show that the imme-
diate cause of irritant effects is the decomposition, within the blood-
vessels, of the masses by which they are plugged. By Lancereaux, again,
stress was laid on the opinion that the poisoned state of the blood in
these cases is due to the alteration and transformation of the connec-
tive tissue of the valves themselves, and never to the mere disinte-
gration of fibrinous concretions.

These speculations have, however, been almost superseded by ob-
servations of a different order. As far back as 1855, Virchow2 found
that a small coagulum upon the mitral valve (in a case of erysipe-
latous perimetritis with a diphtheritic inflammation of the large
intestine) contained a number of small white miliary bodies, which
consisted almost entirely of fine closely aggregated granules, embedded
in a gelatinous substance. These granules were insoluble in potash,
acetic acid and hydrochloric acid, but were dissolved by chloroform, so
that he regarded them as probably of a fatty nature. Charcot and
Vulpian 3 afterwards insisted on the peculiar micro-chemical relations
of the detritus of diseased valves, shown in their power of resisting
strong acids and alkalies. But still more recent observations have
tended to show that the properties of these minute granules are not
due merely to their chemical constitution, and that they are in fact
living organisms. Prof. Winge, and Prof. Heiberg,4 of Christiania,
appear to have been the first writers to express this view in a decided
form : it has since been adopted by no less an authority than Virchow
himself. It is proposed by these writers to give to the affection in ques-
tion the name of Mycosis Endocardii. Winge's case, which occurred
in 1869, was that of a man, set. 44, who died with symptoms of blood-
poisoning apparently dependent on a suppurating corn. On the aortic
valves there were certain greyish masses, the size of peas or beans,
which could be easily picked off, leaving the surface slightly uneven
and ulcerated. The tricuspid valve presented similar masses. With
a microscope of moderate power these appeared to consist of a fine
network of fibrin threads. But under a higher objective these threads
were seen to be made up of rod-like or spherical bodies, arranged in
chains, and thus resembling leptothrix. There were also a number of
fine rounded or rod-shaped bodies, some of which were probably
bacteria, others fat granules. Similar bodies were found in the
cylindrical plugs in the smaller arteries of the kidney, corresponding
to infarctus. Heiberg's case was that of a girl, set. 22, who died six
or seven weeks after delivery, with symptoms of blood-poisoning.
The mitral valve was perforated by a recent ulcer, the margins of which
and the chordte were coated with vegetations. These contained
numerous minute granules, apparently simple detritus : and in addi-

1 Experimentelle Untersuchungen zur' Physiologic und Pathologic der Embolic
Ac., Berlin, 1864. ' '

> Op. cit, p. 709. « Gaz. MM., 1862, p. W5.

4 Virchow's Arch, lvi., 1872, p. 409.

DISEASES OF THE VALVES OF THE HEART. 653

tion, many rod-shaped bodies resembling bacteria, and a considerable
number of rows of granules, of uniform size, arranged in chains of
greater or less length, which Heiberg therefore regarded as leptothrix.
These, and many of the isolated bodies, resisted the action of even,
boiling caustic potass. Specimens from both these cases were for-
warded to Virchow, who confirms the accuracy of the accounts given by
the Swedish writers, and states that he has no doubt as to the para-
sitic nature of the bodies in question. He is not yet prepared,
however, to admit the propriety of using the name leptothrix for
them. Eberth,1 of Zurich, has since recorded another case of the
same kind, which differs from those previously referred to, in the fact
that there was no evident external source of blood-poisoning. He
entitles it " Diphtheritic Endocarditis." 2 It occurred in a young man,
previously healthy, who died after little more than two days' illness.
Two of the aortic valves were ulcerated through, and the disease
extended into the muscular substance of the heart, penetrating almost
to the endocardium lining the right auricle. The margins of the
affected valves were covered with soft vegetations. These consisted
mainly of a finely granular substance : and the individual granules
were shining spherical bodies of uniform size, some of which exhibited
slight movements, the majority being motionless and embedded in
a gelatinous material. Neither boiling alcohol nor boiling alkalies
affected these granules, beyond making them slightly paler. Tincture
of iodine and sulphuric acid gave them a yellow colour. It is
therefore almost certain, says Eberth, that they were really spherical,
bacteria.

So far as I am aware, no similar observations have as yet been pub-
lished in this country. But my colleague, Dr. Goodhart, informs me
that he has in three instances detected minute organisms in the fun-
gating masses attached to ulcerated valves. In each case he found,
besides innumerable spheroids/ rod- and dumb-bell-shaped bacteria,
as well as some which formed beaded strings. Most of these had
feeble oscillatory movements. Vertical sections of the deepest part
of the diseased valves showed a cell growth, to a small extent, such
as is described at page 603. On this was deposited a hyaline clot in
small rounded masses : and upon these, and in the crevices between
them, the bacteria clustered. Dr. Goodhart, however, considered that
the appearances which he observed were strongly suggestive of the
view that the bacteria were derived from the elements of disintegrating
blood-clot.

The precise scope and bearing of these observations are, as yet,
imperfectly understood ; but I think there can be little doubt thai

1 Virchow's Arch, lvii., 1873, p. 228.

* This designation has also been frequently used by Virchow. It is irai>ortant for
English readers to remember that German writers use the term diphtheritic in a sense
very different from that to which wo arc accustomed in this country, applying it to-
inflamed structures of whieh the most superficial layers, infiltrated with inflammatoij
materials, are gangrenous.

654 A SYSTEM OF MEDICINE.

they will hereafter be found to play an important part in the explana-
tion of the phenomena of blood-poisoning now under consideration.
Heiberg, indeed, expressly states that he does not attribute all cases
of ulcerative endocarditis to a Mycosis, since he has failed to find any

Earasitic organisms in specimens of this disease preserved in the
luseum of Christiania. And when bacteria are present in the tissues
of diseased valves, it is as yet quite impossible to say what relation
they bear to the processes of embolism and infection to which the
disease gives rise. This question is in fact only a part of the much
wider one which concerns the relations of these minute organisms
to pyaemia, septicaemia, and allied processes. The theory advocated by
Eberth l is that the bacteria originally enter the blood from without,
and then become aggregated together into a sticky mass, which adheres
to the surface of the cardiac valves, when it is brought to them in the
stream of the circulation. In confirmation of this opinion, he appeals
to observations showing that the ante-mortem coagula in the appen-
dices of the auricles are likewise often coated with a complete layer of
bacteria. The valves and chambers of the heart thus form a kind of
halting-place for the microphytes, which multiply, and subsequently
distribute to all the arteries of the body masses of bacteria in the form
of embola, which set up suppuration wherever they are deposited. In
the arteries of the kidneys especially, agglomerations of this nature
have been demonstrated: and also within the glomeruli and the
uriniferous tubules of the affected parts of these organs.

IT. — Another series of effects produced by diseases of the cardiac
valves consist in the modifications that they tend to induce in the circu-
lation of the blood, and in the consequent morbid changes which arise
in the several cavities of the heart, in the blood-vessels, and in distant
organs. To these effects we must now turn our attention, and as they
are both numerous and varied, it is needful that we should arrange
them in as orderly a manner as possible.

Each of the cardiac valves may be viewed as separating from one
another two of the chambers of the circulatory system, and when any
one of the valves is diseased, we may consider that (1) the primary
effect of the disease is exerted upon that chamber which lies imme-
diately behind the valve in the order of the circulation, and which was
protected by the valve when in its normal state. From the chamber
in question, again, disturbance of the circulation is, or may be, pro-
pagated in two directions : — (2) forwards, or with the blood-stream ;
and (3) backwards, or against the blood-stream. The effects of disease
of the several valves have, therefore, to be considered under these
three heads.

A. It will be found convenient that we should begin with diseases
of the aortic valves. These, as we have seen, may be of two kinds,

1 In a large number of recent cases of pyaemia Eberth has constantly found micro-
phytes, not only on the surface of the wound, but also in' the subjacent tissues, some-
times to a considerable depth.

DISEASES OF THE VALVES OF THE HEART. 655

obstructive and regurgitant ; but in the immense majority of cases,
obstruction and regurgitation coexist.

(1.) The primary effect of diseases of the aortic valves may be
said to occur in the left ventricle, which is of course the chamber
that lies behind the valves in the order of the circulation. Now in
aortic stenosis or obstruction the blood cannot be forced into the
aorta so easily nor so quickly as in health. The ventricle, therefore,
tends to be overloaded with blood, and its walls become stretched or
dilated ; at the same time it has to exert increased force to propel its
contents onwards; and it consequently becomes hypertrophied. In
aortic regurgitation the ventricle may empty itself readily enough during
its systole, but in its diastole it not only has to receive the blood
flowing onwards from the auricle, but also that which is poured back
into it from the aorta ; it therefore becomes both dilated and hyper-
trophied. The changes which occur in the left ventricle are thus the
same in the two conditions of stenosis and regurgitation respectively.
They constitute the compensation by which these several morbid
changes are more or less completely prevented from further disturbing
the circulation. But there is a distinction of some importance, which
has not, I think, been noticed by writers on this subject In aortic
stenosis, hypertrophy of the ventricle is all that is needed to restore
the balance; dilatation is directly injurious, tending to impair th<^
power of the chamber, and to render still more hypertrophy necessary.
But, in aortic regurgitation, dilatation is the main requirement, since
the ventricle has to accommodate the blood that enters it from both
sides during its diastole ; hypertrophy is needed only secondarily, and
because a dilated ventricle has to exert more force than one o£
normal size, in order to propel its contents onwards.

The dilatation and hypertrophy of the left ventricle in cases of
aortic disease may be extreme in degree. The heart then acquires a
peculiar pointed form, the right ventricle often looking like a mere
appendage. The organ often weighs between 20 and 30 ozs., and many
instances have been observed in which it has been even heavier. In
one case which I have myself examined — that of a young man, cet.
26 — the heart weighed 48 oz. I am not sure whether this is not the
largest heart on record ; the next largest being one weighing 46£ oz.,
which Dr. Bristowe exhibited at a meeting of the Pathological Society.

These changes, of course, require time for their development ; but
Dr. Peacock has adduced evidence to show that they may take place
more quickly than might have been expected. Valvular affections
themselves often arise gradually; and the compensatory processes
are induced pari passu with the disease. On the other hand, when
the valves give way or are lacerated suddenly, time may not be
allowed for the ventricle to become dilated and hypertrophied ; and
this is probably one of the main reasons why in such cases the fatal
termination is often rapid. Again, either obstruction or regurgi-
tation may of course be so extreme. as to render compensation
impossible. Lastly, when perfect compensation has existed for a

C56 A SYSTEM OF MEDICINE.

considerable time, it may begin to fail ; and then further effects arise
which will be considered hereafter. It is generally supposed that
this is due, either to the progressive increase in the valvular changes
(with which the compensatory processes are unable to keep pace),
or to the occurrence of fatty degeneration in the hypertrophied
ventricular wall.1

(2.) The onward effects of disease of the aortic valves consist in
changes in the blood current in the aorta and its branches ; in other
words, in changes in the arterial pulse. These are not the same in
aortic obstruction, as in regurgitant disease ; and the two affections
must therefore be considered separately.

In aortic stenosis the character of the pulse appears to be but little
altered, unless the obstruction to the blood current is extreme, in
which case Walshe says that " the pulse, though regular in force and
rhythm, is small, hard, rigid, and concentrated." Dr. Wilks has
mentioned to me that in certain cases he has observed the number
of pulsations of the heart, per minute, to be greatly reduced. In
illustration of this fact, I find in the notes of post-mortem examina-
tions at Guy s Hospital two cases recorded by Dr. Wilks himself.
One2 is that of a man, net. 68, in whom "two of the aortic valves were
adherent and bony; the aperture was reduced to a very narrow
chink ; the edge of one valve slightly overlapped the bony margin
of the other, and thus no doubt prevented regurgitation. The pulse
during life had been 40 per minute, very small, and sometimes hardly
perceptible." The other3 is that of a youth, eet. 19, in whom the
pulse was said to have been " small and slow. The aortic orifice would
only admit a catheter ; all the valves were adherent together, leaving
only a small rounded hole in the middle." Such cases are doubtless
exceptional ; but, as has already been stated; aortic stenosis, without
regurgitation, is decidedly a rare affection.

In regurgitant aortic disease the pulse presents characters so
remarkable that they have led to its receiving several special
designations, and that they often enable the physician to diagnose
the nature of the case without aid from any other source. A passage
has already been quoted from Vieussens (1715) * in which the peculiar
character of pulse that is now known to belong to this affection is
clearly indicated. So far as I am aware, the next writer to mention
it was Dr. Hodgkin, who, in his paper on " Eetroversion of the Aortic
Valves,,,6 published in 1829, says that in one case there was "inordi-
nately violent arterial action, which was very rapid and frequent,.

1 Dr. Allbutt has recently given another explanation of loss of compensation, which
is certainly of great interest. It was first suggested to him by Mr. Busk, who com-
pared the change in question to that which occurs in the arms of file-cut cers. These
men constantly practise rapid flexions of the elbow-joint, and the biceps enlarges
greatly. But after a few years the muscle again wastes, and falls far below the normal
value. This is so certain a consequence, that tho file-cutters receive high wages, calcu-
lated upon the average duration of an hypertrophied biceps. (" On the Effects of Over-
work and Strain upon the Heart and Great Vessels," p. 43, Macmillan and Co., 1872.)

2 Inspection 109, in the year 1859. 8 Inspection 72, in the year 1862.

* QSuvrea Francoises. J London Med. Ga*. vol iii. p. 4&ft.

DISEASES OF THE VALVES OF JTHE HEART. 657

although regular, there was a remarkable thrill in the pulse, and the
carotids were seen violently beating on both sides." But it was Sir
Dominic Corrigan,1 who in 1832 first laid stress on the peculiarity of
the pulse in this disease, a fact commemorated in the designation of
" Corrigan's pulse," which is commonly applied to it both on the Con-
tinent and in this country.

The feature on which Corrigan especially insists, as indicating
" inadequacy of the aortic valves," is the existence of visible pulsation
in the arteries of the head and superior extremities. He describes
the subclavian, carotid, temporal, brachial, and even palmar arteries
as being " suddenly thrown from their bed, and bounding up under
the skin." In the arteries of the lower extremities, even of larger
size than those which present it about the head and neck, pulsation is
not (he goes on to say) seen to any comparative degree, and generally
not at all, while the patient is sitting or standing. The pulsation of
the brachial and palmar arteries is increased in a most striking
degree by merely elevating the arm above the head : and the same
effect is produced in the lower limbs by lying down and elevating
them on an inclined plane.

In addition to these points, it may be added that, in aortic regurgi-
tation, the arteries are elongated during their pulsations much more
than in health, and can be seen in many positions to become dis-
tinctly flexuous with each beat of the heart. Consequently, one
name for the pulse in question is that of the " locomotive " pulse.

But these visible characters of the pulse of aortic regurgitant
disease are after all of little consequence in comparison with those
which can be felt. To the touch, the pulse in question "gives a sensa-
tion of peculiar largeness or fulness, immediately followed by an
eqnally peculiar collapse. Instead of the artery slowly receding
beneatli the finger, it fills as rapidly as it rose. The pulse is, therefore,
often spoken of as "jerking," " splashing," or "collapsing;" or as the
" water-hammer" pulse, from the well-known scientific toy of that
name.

Lastly, the pulse of aortic regurgitation differs from that of health
in travelling along the arteries much more slowly. Normally,
even the radial pulse follows very quickly upon the ventricular
systole ; in the disease under consideration, it may almost be syn-
chronous with the second sound of the heart.

There is little difficulty in explaining the peculiarities that have
been enumerated. We have seen that when the aortic valves allow
of regurgitation, the ventricle is greatly, often enormously, dilated
and hypertrophied. The quantity of blood injected into the aorta is,
therefore, much increased. No wonder that the pulse feels full and
large, that the arteries lengthen, and seem to bound from their seats,
beating much more plainly than in health. Then comes the elastic
recoil of the larger arteries. Under normal conditions, this is gradual.
The aortic valves are closed, and the blood moves slowly onwards

1 Ed. Med. and Surg. Journal, April 1, 188 J, p. 226.

668 A SYSTEM OF MEDICINE.

into the small arteries and capillaries, meeting considerable resistance.
But when the valves in question are diseased, and allow reflux to
take place through them, there is nothing to support the column of
blood in the aorta and its branches during their recoil ; the blood is
rapidly driven out of them, part one way and part another ; and the
pulse as suddenly collapses.

Since the invention of the sphygmograph, no description of the
peculiarities of the pulse in any morbid state can be regarded as com-
plete unless full reference is made to the results obtained with that
instrument And probably diseases of the aortic valves were among
the first in which the sphygmograph was applied. It cannot, indeed,
be said that those who have specially devoted themselves to this sub-
ject have as yet come to a complete agreement in reference to the
indications which it affords. But I believe that the existing state of
our knowledge is fairly expressed in the following account of the
matter: —

In aortic stenosis, one might expect that, in proportion as the aortic
orifice is obstructed, the exit of blood from the ventricle would be
impeded. The upstroke of the sphygmographic tracing should, there-
fore, be oblique, or sloping. According to Mahomed, this is the case.
I append (Figs. 3 and 4) copies of two tracings given by this observer
in the Medical Times and Gazette for 1872,1 which show well the
sloping upstroke and the rounded summit, indicative of the fact that
" the influence of percussion is lost ; the tidal wave alone remains."

Fio. 3. Fig. 4. Fio. 5.

Very similar to this Is another diagram (Fig. 5), which is a copy of one
given by Jaccoud.2 According to Mahomed, however, another very dif-
ferent form of pulse may accompany aortic obstruction. It is illustrated
in the following diagrams (Figs. 6, 7, 8,) which are copied from those
given by him.8 It will be observed that there is a marked separation
between the percussion and tidal waves. It ought perhaps to be men-
tioned that, in the case from which the tracing No. 8 was taken, there
was a double murmur over the aorta, but the existence of considerable
aortic obstruction was made out, not only from the characters of the
pulse, but also from the fact that a tracing obtained from the heart
showed the contractions to be very slow and gradual. It is to be borne
in mind that only extreme degrees of aortic stenosis can be expected to
affect the pulse in the ways described by Mr. Mahomed. He himself

1 Plate V., Figs. 12 and 13, p. 142.

3 Traite* de Pathologic Interne, quatrium Ed. tome i. p. 676.

8 Loc cit, PL V., Figs. 17, 18, 19.

DISEASES OF THE VALVES OF THE HEART. BSD

gives a tracing from a case in which " considerable obstruction was
produced by the adherence of two of the aortic valves ;" in this tracing
no sign of the obstruction is apparent.

In aortic regurgitation, the sphygmographic tracings of the pulse
present peculiarities which correspond in a very .striking way with
what might theoretically have been expected. The percussion-wave
is strongly marked, and the upstroke is therefore high. On the other

hand, the dicrotic wave (or " diastolic expansion ") is wanting, in con-
sequence of the aortic valves failing to support the column of blood
in the aorta during its recoil. Lastly, a high pressure is required to
bring out the characters of the pulse fully : this being the result of
the hypertrophy of the left ventricle, which is constantly present in
cases of aortic regurgitation.

The three following figures, which are copies of tracings given by
Mr. Mahomed,1 illustrate these points. It ought perhaps to be added
that Marey originally laid great stress on a little peak or point at the-

summit of the long upstroke, as indicative of aortic regurgitation ; bu
this was soon shown to be a mistake. At the present time, there seems
to be a fair agreement among different observers as to the characters
in a sphygmographic tracing which point to the disease in question.

Iu some cases of aortic regurgitation the pulse does not present its
peculiar characters in any marked degree, whether to the touch or to
the sphygmograph ; and this, although the diastolic murmur may be
loud and prolonged. This may be due either to the circumstance
that the reflux of blood is really small in amount, or to the fact that
mitral regurgitation is also present. Mr. Mahomed gives in his papers
in the Medical Times and Gazette some very valuable illustrations of the
way in which the sphygmograph may he used in cases of this kind,
both to determine the degree of valvular incompetency, and to gauge
the amount of compensatory hypertrophy of the left ventricle ; and

660 A SYSTEM OF MEDICINE.

also to decide which of two coexistent affections — mitral and aortic —
is of preponderating importance. It is in the solution of such ques-
tions as these that the great value of the instrument appears to lie, so
far as diseases of the cardiac valves are concerned. The mere detec-
tion of valvular incompetency can he effected more easily, and per-
haps as surely, by the stethoscope ; but in prognosis the sphygmograph
seems to lend great assistance.

The onward effects of diseased conditions of the aortic valves are
not necessarily confined to the arterial system. The capillaries may
be imperfectly supplied with blood, and both the nutrition and the
functions of the different organs nay in consequent* be greatly
impaired. This is perhaps especially marked in the case of the brain.
Attacks of giddiness are far from uncommon in aortic regurgitation,
and are ascribed to failure in the due supply of arterial blood to
the nervous centres. Anaemia and wasting of the whole body are
also frequent symptoms : the former being in fact so constantly present
as to be a marked feature in the physiognomy of the disease.

(3.) Backward effects of aortic disease are absent, so long as the
changes in the left ventricle above described enable the heart to do its
work efficiently, even though this result should be attained at the ex-
pense of increased labour and friction, and under augmented frequency
of beats. And since patients with aortic regurgitation very often die
suddenly while these conditions are fulfilled, backward effects are not
rarely wanting to the last. But whenever the compensatory processes
fail, so that the arteries no longer receive for transmission onwards
their full supply of blood per minute, the necessary result is that the
quantity discharged into the ventricle by the left, auricle must also be
deficient The inevitable consequence of this, again, is the develop-
ment of a fresh series of changes, which we are about to study in
detail, as the effects of primary disease of the mitral orifice. It is
often stated that in affections of the aortic valves these chauges occur
only when the mitral valve has been stretched, so as to allow of
regurgitation through it, — this being probably a common result of
the dilatation of the left ventricle. But I conceive that the state-
ment in question is an error, and that backward effects must neces-
sarily arise in the way I have indicated, even though the closure of
the mitral valve may still remain perfect.1

B. Diseases of the mitral valve, again, are of two kinds — obstruc-
tive and regurgitant : which will to some extent require to be con-
sidered separately from one another.

(1.) The primary effect of diseases of the mitral valve may be said to
be exerted upon the left auricle. In mitral stenosis the effect in

1 So far as post-mortem evidence can be brought to bear upon this question, I believe
that such evidence is favourable to the view expressed in tho text. Thus I find in my
notes one case (in which I made an autopsy in July 1873) of aortic disease with retro-
version of one of the valves. Dropsy occurred before death, and the lung9 contained
apoplectic patches. The mitral valve appeared to be auito healthy : and, after death, it
did not allow regurgitation to occur. The left auricle was dilated and hypertrophied,
ana the right auricle was still more so.

DISEASES OF THE VALVES OF THE HEART. 061

question is well marked. The cavity becomes dilated, often enor-
mously so.1 The appendix is elongated, — in one instance I find it
noted as 2f inches long by Dr. Moxon, — and acquires a peculiar
curved form ; and its aperture of communication with the auricle
is much wider than natural. The walls of the auricle also become
much hypertrophied ; they no longer collapse when the cavity is cut
open, but support themselves stiffly : the muscular substance may in
places be from -J- to \ of an inch thick. The endocardial lining is
said to be more opaque than usual.

These changes are almost constantly met with in cases of mitral
stenosis. And were the current doctrines in regard to mitral regurgi-
tation true, they would doubtless be found no less uniformly in cases
of the latter affection ; — just as dilatation and hypertrophy of the left
ventricle occur equally in aortic obstruction and in aortic incom-
petency. However, this is not so. Definitely marked hypertrophy
of the muscular wall of the left auricle is seldom present in cases
of so-called mitral regurgitant disease. It is true that the cavity in
question is often found to be dilated ; but then all the other cardiac
cavities are generally enlarged at the same time. I shall endeavour
to explain these facts further on.

(2.) The onward effects of diseases of the mitral valve are of course
seen first in the left ventricle. In mitral stenosis this chamber is
very generally found to be small, and its muscular substance is no
thicker, and may -perhaps even be thinner, than under normal con-
ditions. The aorta too is often small and thin-walled. But in some
cases of mitral stenosis and in almost all cases of " mitral regurgi-
tation" the left ventricle is large and fleshy; and not infrequently it
is as much dilated and hypertrophied as in aortic regurgitation.
Various explanations of this have been given. By Friedreich 2 it is
supposed that the augmented tension in the systemic venous system
(which we shall presently show to be one of the consequences of
mitral diseases) causes an increased resistance in the systemic arteries
likewise. But, apart from the difficulty of admitting that the effects
of obstruction thus traverse the complete circuit of the circulation,
a fatal objection to this theory is that it would require dilatation
of the left ventricle to be the rule in fatal cases of mitral stenosis,
instead of its being quite exceptional. Another view is that
when the ventricle is enlarged in mitral disease, this is not really
due to the valvular affection, but depends upon some other cause.
Thus, in rheumatic cases many other conditions generally exist (such,
for example, as diseases of other orifices, or thick pericardial adhesions)
to which the change in the ventricle may be ascribed. Indeed,

1 This condition was long ago described as " true aneurism of the left auricle " by Dr.
Thurnam (Med. Chir. Trans., scr. ii., vol. iii., 1888, p. 244), who expressly insists on
its association with contraction of the mitral orifice, and mentions that the fining mem-
brane is opaque and rough, and in some cases even ossified, and that it is lined with
.fibrinous layers very similar to those met with in arterial aneurisms.

* Op. cit., pp. 161 and 227.

662 A SYSTEM OF MEDICINE.

according to some observers, primary dilatation of the left ventricle
commonly occurs in the course of acute rheumatism, and may per-
sist after the subsidence of that disease. But, again, in very many
cases of so-called "mitral regurgitant disease" the valve is itself
healthy : and the imperfection in its working (if we are to assume
that it does close imperfectly) is itself the result of ventricular
dilatation. There is, however, one class of cases in which it cer-
tainly appears that mitral imperfection leads to enlargement .of the
left ventricle: — I refer to those cases in which rupture of the
tendinous cords of the valve occurs in persons who had not previously
exhibited any symptoms of cardiac disease.1 It may indeed be
objected that both the ventricle and the valve were possibly
affected with latent disease before the sudden rupture took place:
but of such disease there is no evidence, and to suppose its existence
is to abandon in favour of an arbitrary hypothesis the direct
interpretation of the facts observed. The explanation, indeed,
seems to be sufficiently easy. In such cases, the ventricle has greatly
increased labour ; a good deal of the blood which enters it having to
be expelled twice over from its cavity. On the other hand, in cases
of uncomplicated mitral stenosis, the work thrown upon the left
ventricle is in no way augmented, if it be not even less than under
normal conditions : and as I have already stated, I believe that in
such cases the left ventricle is always small, and its muscular
substance no thicker than natural

The arterial pulse in mitral diseases may present very varied
characters, the variations depending not merely upon the nature of
the valvular lesion, but also upon the changes secondarily induced by
it in the heart's chambers. Formerly it was supposed that in mitral
stenosis the pulse is always small ; but since the presystolic murmur
has enabled this condition to be diagnosed before severe symptoms
set in, it has been found that the pulse is often perfectly natural.
Indeed, there is no reason why it should be otherwise, so long as the
hypertrophied auricle keeps the ventricle duly supplied with blood.
In a very large proportion of cases in which a presystolic murmur
is audible, the pulse is perfectly regular, and has ample volume and
force. Accordingly, Mr. Mahomed says 2 that "in this disease the
8phygmographic tracing does not necessarily present any diagnostic
characteristics." I have already quoted this writer as having de-
monstrated that cardiography tracings, taken at the heart's apex,
often afford proof of the existence of mitral stenosis (or, at least, of
hypertrophy of the left auricle), by showing that the auricular systole
commences at an earlier period in the ventricular diastole than is

1 Thus In Dr. Dickinson's case (Path. Trans, xx. p. 150) the heart weighed 20 oz. ;
all the cavities were dilated to at least three times their natural capacity ; the auricles
and right ventricle were thinned. Tho left ventricle was hypertrophied to such an extent
as to retain, notwithstanding its dilatation, about its normal thickness. And in the
report of the post-mortem examination of a similar case that occurred in Guy's Hospital
under Dr. Habershon's care, Dr. Moxon states that "all the cavities were dilated."

• Op. cit., No. 6, p. 569.

DISEASES OF THE VALVES OF THE HEART. 663

normal. He further maintains that in some cases this premature
contraction of the auricle stimulates the ventricle to contract like-
wise ; and that in this way the tracing of the pulse at the wrist may
indicate a second ventricular systole, alternating with the main
beat, but very much less forcible. The accompanying diagram is

Fig. 12.

copied from one of Mr. Mahomed's tracings, taken from a patient of
mine who was suffering from mitral stenosis, and in whom the
double ventricular systole was made very marked by the administra-
tion of digitalis. Both contractions were felt in the pulse at the
wrist, the beats of which were alternately strong and feeble. I have
observed a similar double rhythm in several other instances of val-
vular disease ; but I am unable to say whether they were or were not
all of them cases of mitral stenosis.

In the later stages of the disease — when the peculiar murmur
can often be no longer detected — the pulse assumes very different
characters. It is now rapid, soft, small, and very irregular, both in
volume and force.

The accompanying tracings (Figs. 13, 14, 15) copied from Jaccoud,1
show the sphygmographic character of a pulse of this kind ; they
are very much what might have been expected from the impression

Fio. 18. Fio. 11

which it gives to the touch. It has long been known as the mitral
pulse ; and, in fact, it is met with, not only in the advanced stages of
mitral stenosis, but also in those cases which are c'ommonly grouped
under the heading of " regurgitant mitral diseass." Whether it is of
any diagnostic value, as indicating that the valve in question is
impaired in structure or function, is a very difficult question to
answer. I have already stated more than once that "regurgitant
mitral disease" has no constant pathological appearances, but that
it includes a variety of conditions, in some of which the valve
certainly admits of regurgitation, while in others there is doubt
whether this occurs. I must now add my belief that for the pro-
duction of the so-called " mitral pulse " the mitral valve need not be

1 Op. cit., No. 21, p. 678 ; No. 9, p. 616 ; No. 7, p. 615.

664 A SYSTEM OF MEDICINE.

either narrowed or incompetent. The same kind of pulse probably
arises whenever the ventricle does not empty itself completely during
its systole, so that the stream of blood projected into the aorta is
greatly diminished. Now it would appear that such a perversion of
the heart's action is far from being uncommon, being liable to occur

Fio. 15.

in the course of various cardiac and pulmonary diseases without pre-
senting any characters peculiar to one rather than to another of these
diseases. The condition in question was first described by Beau, who
gave to it the name of asystolie ; and most recent French writers have
adopted this designation. Dilatation of the heart appears to be the
morbid change which is most constantly present in cases of this
kind ; but very frequently valvular disease also exists. The sphyg-
mographic tracings (Figs. 13 and 14), which I have copied from
Jaccoud as illustrative of the "mitral pulse," are given by that
writer as indicating the existence of a condition of " asystolie.1'

(3.) Backward Effects. — So long as the left auricle can duly empty
itself, and receive its full supply of blood from the pulmonary veins,
the parts of the circulatory apparatus behind the auricle are in no
way affected by the existence of mitral disease, whether obstructive
or regurgitant. But, except in the earlier stages or slighter degrees
of such disease, the compensatory action of the auricle is very seldom
thus complete ; and whenever it fails, the necessary consequence is
an augmented tension in the pulmonary system of vessels and in the
chambers of the right side of the heart. It has already been stated
that the same result occurs also in diseases of the aortic valves, as
soon as compensatory changes fail to enable the left ventricle to
carry on the circulation properly.

This increase of tension in the pulmonary vessels soon leads to
changes in their walls, which become thickened, or hypertrophied.
In the main trunk of the pulmonary artery this is particularly
noticeable. The records of post-mortem examinations at Guy's
Hospital contain notes by Dr. Moxon of the case of a boy, ast. ten
years, in whom the coats of the pulmonary artery were nearly twice
as thick as those of the aorta at its thickest part ; and less striking
examples of the same kind are very commonly met with. The artery
also becomes greatly dilated.

Another result of the increased tension of blood within the pul-
monary artery is the fact that in these cases the branches of the
vessel are very apt to become atheromatous, although under normal
changes they are but little liable to such a change. Perhaps the most
striking instance of this that could be quoted is one which Dr.

DISEASES OF THE VALVES OF THE HEART. 665

Conway Evans 1 has recorded, and which occurred in a boy, who died
of dropsy, consequent on mitral stenosis, at the age of fourteen years.
It would appear that Dittrich 2 was the first to point out the fre-
quency with which atheroma of the pulmonary artery is found incases
of this kind, and that he described it as occurring especially in the
smaller branches, and as being the immediate cause of the patches of
" pulmonary apoplexy " which are so commonly met with under such
conditions. The explanation of pulmonary apoplexy, however, is
still open to doubt. The branch of artery leading to an apoplectic
patch is generally, perhaps always, plugged with fibrin; and this
lias led many modern observers to regard the affection as of
embolic origin. In the first volume of the " System of Medicine,"
at p. 201, Dr. Bristowe has discussed this question at considerable
length.

The pulmonary tissue is also liable to assume a peculiar appear-
ance, which is generally known to German pathologists under the
name of " brown induration." In the third volume of the present work,
at p. 800, Dr. Wilson Fox has given a detailed account of this affec-
tion ; but he seems to have laid hardly enough stress on the dilated
and varicose state of the pulmonary capillaries, which Buhl has
shown to be present, and which is so striking a proof of the increased
pressure upon these vessels. I have found that this dilated state of
the capillaries is recognizable without difficulty, even in uniujected
specimens.

Before leaving the subject now under consideration, I must not
omit to mention another way in wThich the left lung suffers from
cardiac disease — namely, from the dilated left auricle pressing
directly upon the bronchus. Mr. Wilkinson King 3 first pointed this
out, in the year 1838, and his preparations, which are now in the
museum of Guy's Hospital, show that the anterior surface of the tube
may in this way be rendered quite flat, and its calibre diminished by
one-half. But the most remarkable instance is one recorded by
Friedreich,4 in which narrowing of the left bronchus was diagnosed
four years before the patient's death, from the presence of a loud
humming sound accompanying both the inspiration and the ex-
piration, heard most plainly over the root of the left lung, near the
spine, but also audible over the whole left side of the chest. There
was extreme stenosis of the mitral orifice with enormous dilatation
of the left auricle. Virchow made the autopsy; and the left main
bronchus was found to be compressed, so that only a small narrow
channel was left.

The cavities of the right side of the heart also become greatly
dilated and hypertrophied under the conditions now being considered.
The muscular tissue of the right ventricle grows much harder than

* Trans, of the Path. Soc, xvii. p 90.

* Ueber den Laennec'schen Lungeu-Infarktus. Erlangen, 1850.

* Guy's Hospital Reports, Heries L, vol. iii. p. 178.
4 Op. eit., p. 30.

VOL. IV. X X

666 A SYSTEM OF MEDICINE.

natural — indeed, it is peculiarly hard, in comparison even with the
substance of an hypertrophied left ventricle. The tricuspid orifice
is stretched.

C. & D. — It is at this point that we ought to consider the effects
of primary disease of the pulmonary and the tricuspid valves re-
spectively. But such diseases are so rare (excepting malformations,
which are treated of separately) that they need scarcely interrupt us
in tracing out the backward effects of diseases of the valves of the
left side of the heart. It will suffice to state that (1) the primary
effect of disease of the pulmonary valves is to cause dilatation and
hypertrophy of the right ventricle ; and that that of disease of the
tricuspid valve (if primary chronic disease of this valve ever occurs)
would probably be to cause dilatation and hypertrophy of the right
auricle ; (2) Concerning forward effects of the diseases in question, no
definite statements could perhaps be made ; (3) Their backward effects
must be the same as those which more remotely arise from uncom-
pensated diseases of the mitral and aortic orifices, and to these our
attention may now be directed.

Taking first the vena cava superior and the veins from which it
arises, we find that they are enlarged and gorged with blood. Hence the
livid countenance, the turgid cheeks, the purple ears, cheeks, and lips,
that are so commonly seen in patients suffering from affections of the
cardiac valves. The veins of the upper limbs are also distended ; the
hands and nails acquire a livid purple colour, and the hands, and
often even the arms, become cedematous. The Hvidity may approach,
if it may not even equal, that which is seen in cases of malformation
of the heart, in the condition known as cyanosis. A further con-
sequence of the congestion of the upper limbs which exists in these
cases, is that the finger-ends often become enlarged, or (as it is
usually termed) " clubbed. " Dr. Dobell * has recently stated that the
clubbing of the fingers from heart disease differs from that which is
due to phthisis, in the circumstance that the sides and tips of the
nails are not at the same time incurved ; the reason for this difference
being, that in heart disease wasting of the adipose tissue is absent,
which wasting he believes to be the cause of incurvation.

At the root of the neck the jugular veins, besides being enlarged
and unnaturally full, present another phenomenon which requires
further consideration — they can often be seen to pulsate with each
beat of the heart. This seems to have been first noticed by
Lancisi.2 Jugular pulsation is commonly taken as a certain indi-
cation of regurgitation through the tricuspid orifice; and the
frequency of its occurrence, when the circulation through the right
side of the heart is impeded, is supposed to bear out Mr. Wilkinson
King's views of the existence of a physiological safety-valve action,
by which reflux is allowed whenever the right ventricle becomes

1 On Affections of the Heart and in its neighbourhood, 1872, p. 17.
1 De motu Cordis et ancurysinatibus. Kom. 1728, Lib. ii, Propos. 57.

DISEASES OF THE VALVES OF THE HEART. 0C7

unduly charged with blood. It has, however, been shown by Fried-
reich that the matter is by no means so simple. In the first place,
when the jugular veins are distended they often exhibit rhythmical
movements synchronous with the respiratory acts. Each expiration
causes an increased pressure upon the large venous trunks within the
thorax ; and even though the valves at the root of the neck may close
perfectly, the blood that is pouring in from the veins of the head and
upper limbs is stopped, and accumulates behind the obstruction. An
apparent pulsation may thus occur without any blood really regur-
gitating into the jugular veins from below. So, again, it is possible-
that when these veins are very full, variations in their size may occur,
synchronously with the heart's movements, from the temporary arrest of
the onward flow of blood during the closure of the tricuspid valve,
quite independently of reflux. In this case, however, compression of the
veins in the middle of the neck will at once stop the apparent jugular
pulsation.

When jugular pulsation is really due to regurgitation of blood,
it is of course necessary that the valves at the junction of the sub-
clavian and jugular veins should be incompetent. Dr. Parkes1 is
said to have taught that this is due to rupture of these valves : but
as Dr. Walshe points out, it is doubtless sufficient that the veins
should be greatly distended, so as to prevent the edges of the valves
from touching one another. According to Friedreich it is possible
for a true jugular pulsation to be produced by the pressure of the
ascending aorta, when dilating during the ventricular systole, upon a
distended vena cava superior. But this explanation appears far-
fetched, and unnecessary. Friedreich will not allow that tricuspid
regurgitation is present, unless a systolic murmur is audible. I
shall presently show, however, that almost any kind of valvular
defect may exist, without the corresponding murmur : and my belief
at present is that regurgitation through the tricuspid orifice exists
in all cases in which the jugular veins really pulsate. Indeed, I
cannot even agree with Friedreich that if pulsation disappears when
the vein is compressed higher up, the existence of regurgitation is
absolutely disproved: for this procedure may simply prevent the
wave being transmitted upwards in the empty vessel. The most
that can be said is that it renders the occurrence of reflux doubtful.

Friedreich gives sphygmographic tracings of the jugular pulse,
which appears to be dicrotic, the beat due to the ventricular systoh
being preceded by a smaller elevation accompanying the contraction

of the auricle.

It must be added that pulsation is generally more distinct in the
Tight than the left jugular vein. In exceptional cases the veins of
the face, amis, and hands have been seen to pulsate: and also the
thyroid and mammary veins.

Turning now to the vena cava inferior and its tributaries, we find
that these veins become greatly dilated as a consequence of distension

1 Walshe, op. cit, p. 138.

xx 2

668 A SYSTEM OF MEDICINE.

of the right auricle. Senac 1 mentioned a case in which the cava
itself was as thick as an arm. The hepatic veins also become much
enlarged, running as wide open channels through the substance of the
liver, and opening into the cava by orifices much larger than naturaL
These facts are of some importance, as throwing light on the epigas-
tric pulsation, which is often observed in cases of chronic disease of
the heart. It was long ago suggested by Allan Barns 2 that this is
due to regurgitation of blood along the inferior cava, and into the
vessels of the liver. And Friedreich at the present time maintains
the same view.8 English writers in general, however, describe the
dilated right ventricle as giving a shock to the neighbouring parts
which can be felt in the substernal notch: and some have even
spoken of the heart as " beating in the epigastrium," the impossibility
of which it did not need the labours of Hamemyk to point out

The probability that epigastric pulsation is often due to reflux into
the hepatic veins is increased by the fact that the liver itself is greatly
enlarged under these conditions. It is also much congested and fatty,
presenting a peculiar mottled appearance, which has gained for it the
name of the nutmeg liver. At the same time it is very liable to a
chronic inflammatory process, attended with an increase in its con-
nective tissue, approaching that which occurs in cirrhosis. The
congestion is transmitted through the liver to the portal vein and its
radicles. The spleen becomes enlarged and its tissue very hard, in
this respect contrasting with the still larger but soft spleen which is
found in association with ulcerative disease of the cardiac valves. The
veins of the omentum and mesentery are gorged with blood. The
stomach has its lining intensely reddened and coated with mucus :
haemorrhage takes place iuto its submucous tissue, and the ecchy-
mosed spots often become exposed by solution of the raucous mem-
brane over them, forming the so-called " hemorrhagic erosions." The
intestines are also greatly congested and lined with mucus: and
haemorrhoids are often developed. These changes in the digestive
organs are attended with more or less marked symptoms: partial
jaundice ; dyspepsia, nausea, sickness, even toematemesis ; constipa-
tion. The engorgement of the veins lying beneatli the peritoneum
leads to ascites, often of considerable amount.

Nor do the other veins that open into the inferior vena cava escape.
Thus the renal veins become distended ; and the kidneys are deeply
congested, a condition which easily passes into one of chronic in-
flammation, and often leads to the presence of albumen in the urine.
The return of blood from the lower limbs is impeded ; the veins are
gorged, and very often thrombosis of the femoral veins arises, which,
as has already been stated, is perhaps the remote cause of the
development of pulmonary apoplexy.

i Friedreich, p. 41. • Op. cit., p. 265.

s My colleucue, Dr. Frederick Taylor, has observed distinct pulsation of the liver in
four cases of chronic cardiac disease. When one hand was placed in the epigastrium
and the other in the right loin, the organ could be felt to expand with each beat of the
heart. Guy's Hosp. Rep. (vol. xx. 1875),

DISEASES OF THE VALVES OF THE HEART. 669

This engorgement of the veins of the lower limbs, although we mention
it last in tracing backwards the consequences of disease of the cardiac
valves, is in fact often one of the first effects of such disease to be
observed ; manifesting itself by the transudation of serum through
the avails of the most distant venous radicles, and the production of
cedeuia of the ankles and feet. The anasarca, slight at first, may in-
crease until the whole of the lower extremities, the abdominal
parietes, and even the genital organs, have become dropsical in the
highest degree. As a rule, however, the genital organs remain com-
paratively free : and in this respect cardiac dropsy differs from that
which occurs in renal disease, and the distribution of which is not in
the same way dependent upon simple mechanical conditions. On the
other hand, the icteroid tinge of the skin, which is generally present
in cases of heart disease, is wanting in other forms of dropsy.

III. A third series of effects, produced by diseases of the cardiac
valves, consist in sensations of various kinds experienced by the
patient. These are the subjective symptoms of the diseases in question.
They may present all degrees of intensity : they may even be entirely
absent.

Pain may be felt either over the heart itself, or in the left shoulder;
or it may extend down the inner side of the left arm to the elbow, or
even to the fingers. It may either be a constant aching, or have a
" shooting" or " stabbing " character. It is often distinctly paroxysmal,
especially in cases of aortic regurgitation, in which it frequently
assumes all the features of true angina pectoris. Pain in the arm
and hand is sometimes accompanied with numbness : and sometimes
(according to Dr. Dobell) these parts are deadly white while the numb-
ness lasts. In some cases the pain is limited to the little and ring
fingers, following the distribution of the ulnar nerve to these fingers :
but in other cases it affects all the fingers, and even the thumb. Some-
times the pain also passes from mid-sternum to the right shoulder
and down the right arm : but when pain occurs in these parts earlier
than in the cardiac region, Dr. Dobell thinks that the presumption is
in favour of disease of the aorta rather than of the heart.

A very important character of the reflected pains due to cardiac
disease is that they are generally aggravated by anything which
disturbs the heart's action, and especially by muscular exertion.
Not unfrequently, pain is absent so long as the patient is at rest,
but comes on at once as soon as he attempts to walk.

Another point, on which Dr. Dobell has particularly insisted, is that
the pain of heart disease is often greatly increased by distension of
the stomach with food or gas. Hence, when dyspepsia is present, it
may easily be regarded as the cause of pain really due to heart
disease ; and relieving the indigestion may prevent the return of the
pain.

Not infrequently, instead of pain, the patient speaks rather of
a fluttering sensation in the precordial region : or simply of palpi-

670 A SYSTEM OF MEDICINE.

tation. But it is to be observed that a spontaneous complaint of
palpitation is heard far more often when the patient is suffering
from due of its indirect causes, than when any of the cardiac valves
are diseased. Indeed, as a rule, the subjective symptoms of valvular
affections are subordinate to the other symptoms. And it may be said
that when a patient comes to the physician complaining of pain in
the heart, and fearing that he has heart disease, the great probability
is that that organ is perfectly healthy.

Another morbid sensation, belonging to the diseases under con-
sideration, is dyspnoea. Very often, indeed, the first thing that
suggests a suspicion that there is anything wrong with the patient
is that he is conscious of shortness of breath after mounting stairs,
or making some moderate muscular effort When he is at rest, he
may be able to breathe comfortably enough ; but this freedom from
^distress often continues only so long as he sits up. As soon as he
lies down on an ordinary bed or couch, he becomes aware of un-
pleasant feelings, which compel him to change his posture. Thus,
even in the slighter forms of cardiac valvular disease, it will gene-
rally be found that the patient lies at night with his head raised,
employing two or three pillows, whereas a man in health would
only require one. And hi the more severe degrees of such disease,
the patient is often utterly unable to lie down, or even to recline
backwards. This condition has received a special name, that of
Orthopnoea. It doubtless depends upon the circumstance that in the
recumbent posture the diaphragm is pressed upwards by the contents
of the abdomen (themselves greatly augmented in size), so that the
enlarged heart is embarrassed in its movements.1 Orthopnoea is in
many respects a serious symptom. By preventing sleep, it greatly
taxes the patient's strength, and diminishes his power of resisting the
disease. Moreover, as Dr. Dobell has pointed out, it fatigues the
lumbar muscles, and makes the back ache. It keeps the lower limbs
at right angles with the trunk, and so, leading to compression of the
veins and lymphatics in the groins, increases the oedema of the legs.
Scarcely any condition is, in fact, more pitiable than that of a patient
in this plight ; and any mechanical appliance by which it can be
remedied must certainly be an unspeakable boon. For this purpose
Dr. Dobell has contrived a " Heart Bed," of which be has given a
description and a figure in his book ; and from his account it seems
to be well worthy of trial in these distressing cases.

There are other subjective symptoms, belonging to the various
secondary effects of diseases of the cardiac valves ; but space fails me
to describe them in detail; most of them have been incidentally
referred to in other parts of this article.

Diagnosis. — Under this heading I do not propose simply to recapi-
tulate facts that have already been stated in previous paragraphs;

1 Even when the heart is healthy, the posit'on of its impulse may be higher or lower,
according as the patient sits up or lies dow n, if there be an enlargement of the liver. °

DISEASES OF THE VALVES OF THE HEART. 671

nor shall I attempt to construct any tables which might aid the student
in distinguishing diseases of the cardiac valves from other affections
with which they may be confounded. In my opinion such tables are
scarcely ever made use of in practice; indeed, I do not think that
they are applicable to really doubtful cases, in which the difficulty
of diagnosis most commonly depends upon either a deficiency of
symptoms, or their ambiguity: their being, in fact, such as might
belong indifferently to any one of several maladies; or else their
being in part such as commonly occur in one disease, in part such
as belong rather to another disease. In cases of this kind, diagnostic
skill is a matter of judgment and experience ; and all that could be
said under the present heading could do but little to further it.

There are, however, some important questions in reference to the
detection of affections of the valves of the heart which have not yet
been touched upon. In discussing each kind of murmur, I have
endeavoured to indicate all the causes to which it may be due,
and to point out how these may be distinguished from one another.
But of the absepce of murmur I have as yet said nothing. I now
propose to consider this question, and to discuss whether abnormal
sounds or bruits are constantly present in the various diseases of the
different cardiac valves.

And first, with regard to the aortic valves. It may almost be said
that in practice the diagnosis of aortic regurgitation depends wholly
upon the discovery of a diastolic murmur, audible at certain parts of
the thoracic parietes. If such a murmur is heard, the stethoscopist
regards it as certain that regurgitation exists. If no such murmur
can be detected, there is perhaps no combination of symptoms (unless
it be by the aid of the sphygmograph) that would justify the physician
in asserting that the aortic valves fail to close. It is therefore a
most important question whether a diastolic bruit can always be
detected in those persons in whom after death the valves are found
to have been incompetent. Now, on looking through the records of
post-mortem examinations at Guy's Hospital, I have found that this
condition was discovered in 40 cases during the years 1870-71. And
on referring to the clinical reports attached to these cases, it appears
that in 26 of them regurgitation was positively diagnosed during
life; and that in 11 out of the remaining 14 cases the patients
came from the surgical division of the hospital, or were less than
seven days in the wards (some having been dying at the time of
admission, or brought in dead), or had no notes taken of the
auscultatory signs which they presented. Thus the proportion of
cases of this disease that may be said to have resisted diagnosis was
very small.

It has been stated that several of the cases in which the aortic
valves were found incompetent after death during the period named
were cases of surgical disease or injury, in which one may presume
that there were no obvious symptoms of cardiac disease. This accords
well with the fact that aortic regurgitation is more frequently than

C72 A SYSTEM OF MEDICINE.

any other valvular affection discovered by the auscultator when the
patient's history and symptoms had not previously suggested any
suspicion of its existence. Dr. Walshe relates the case of a man,
about 35 years old, the very picture of robust health, who had never
had a symptom of disease connected with any organ in his body, and
who presented himself for life insurance. Almost as a matter of
form, Dr. Walshe put his stethoscope to the chest ; his attention was
at once arrested by a loud diastolic murmur. The man dropped dead
in the street within a fortnight. I lately saw a bank clerk, aged 32,
whose sole complaint was a pain in the chest about the ensiform
cartilage, with occasional pain in the back, such as might have been
due to any trifling cause. On listening to his chest I heard a well-
marked diastolic bruit.1

It might be supposed that there would often be a difficulty in dis-
tinguishing between the to-and-fro sounds of pericarditis and those
of disease at the aortic orifice. And for my own part I believe that
this difficulty would arise oftener than it does, were it not for the
very different clinical history and course and other symptoms belong-
ing severally to these two diseases. The comparatively superficial
seat of pericardial friction-sounds, their want of definite localization
at the spots where valvular murmurs are most marked, their intensi-
fication by pressure with the stethoscope, and their failing to corre-
spond accurately with the cardiac rhythm, are all valuable points of
distinction ; but as a matter of pure auscultation, I think that doubt
would sometimes be admissible; and as a matter of fact I have
occasionally experienced this difficulty, especially when (as in cases of
Bright's disease at an advanced age) the presence of either chronic
pericarditis or disease of the aortic coats would accord with the other
features of the case.

The diagnosis between a presystolic and a diastolic murmur is not
generally difficult to those who are well acquainted with the seat and
quality of these murmurs respectively. But I have sometimes found

1 A very striking instance, in which the patient discovered the murmur, has just
come under my notice in a young medical man, a friend of my own. On January 23rd,
1875, he had gone to his brother's for a day's shooting; and while at lunch, he noticed
a strange noise, which he thought came from his stomach. He forgot all about it, and
went out shooting for two hours. After dinner he heard the noise again. On the next
day, while standing in his dining-room, he became conscious of a loud sound in his
chest : and his wife, who was three or four feet off, heard it also. During four days it
remained audible at a distance. He consulted a medical friend, who discovered valvular
disease. Dr. Wilks saw him two weeks afterwards, and kindly sent him to me. His
health remained perfectly good. Ho would not have known that anything was the
matter with him, except that when he made any exertion he could feel a vibration in
his chest. A loud diastolic murmur was audible over an extensive area. There was no
excessive impulse : but the apex beat was situated below the sixth rib ; aud the heart's
dulness extended downwards and outwards for six inches. In this case I think it is clear
that, whoterer may have been the original cause of the sudden development of the
transitory murmur heard at a distauce from the patient's body, the valve had previously
been diseased. He had, however, been apparently in perfect health : able to ride, shoot,
and run as well as ever. The only sudden effort that he remembered making on the day
when he first noticed the murmur was that he had lifted his wife out of a high dog-cart :
but this he had done many times before

DISEASES OF THE VALVES OF THE HEART. 673

it* to be far from easy ; and a distinguished physician, who has himself
written much on the subject of heart disease, has informed me of
one case in which he confidently asserted the existence of a presystolic
murmur, but in which the aortic valves proved to be unsound, while
the mitral valve was healthy. The mistake most likely to happen
to the unpractised or careless auscultator is that of supposing the
murmur of aortic regurgitation, when it happens to be loud at the
apex of the heart, to be a mitral regurgitant bruit. To commit
this error is completely to misunderstand the rhythm of the heart
in the patient under examination. But I have nevertheless seen it
committed more than once. Either no pains at all were taken to
determine the period of the ventricular systole ; or the radial pulse
was employed as a guide to it. Now it has been already stated that
in aortic incompetency the radial pulse is often delayed, so as to be
almost synchronous with the recoil of the aorta ; or, in other words,
with the regurgitant bruit. Hence by feeling the wrist in cases of this
kind one may easily mistake a diastolic for a systolic murmur.

It still remains to be mentioned that an aortic regurgitant murmur
is sometimes hard to detect. I well remember that, when I was a
student, I had very great difficulty in hearing the murmur in more
than one case in which my teachers spoke confidently of its presence.
And I now find that I in my turn discover murmurs which my pupils
cannot hear, even when I tell them what to listen for. When such
a murmur is once heard, it often seems so distinct that one wonders
that one could have overlooked it. In other instances the sound is
really very slight, and it is thus drowned by any little noise, although
plainly audible at night, or when a ward is very quiet. Lately I had
a patient under my care, in whom the existence of an aortic regurgi-
tant murmur was matter of the most lively discussion. 1 was sure
that I had heard it two or three times, but on every other occasion
1 failed to detect it. After death the valves were found to be obviously
incompetent. There is of course no relation between the amount of
reflux and the loudness of the murmur.

The diagnosis of mitral disease is far from resting on so satisfactory
a footing as that of aortic obstruction and regurgitation. We may
first take the comparatively simple case of mitral stenosis. I have
already said that a presystolic murmur, when heard at the heart's
apex, is pathognomonic of this affection. But we have now to
approach the subject from the opposite point of view, and to inquire
in what proportion of cases such a murmur is audible. Some years
ago I collected for the Guy's Hospital Reports all the instances in
which mitral stenosis was found after death during a period of some
years. They amounted to forty-seven ; and in only seven (or perhaps
six) of them had a presystolic murmur been detected during life. It
is true that from them a considerable, number (fifteen or twenty) had
to be subtracted, as having proved fatal soon after admission, or as
having been cases of surgical disease or injury, or as having in some
other way failed to afford an opportunity tor diagnosis. But there

S74 A SYSTEM OF MEDICINE.

still remained at least three cases of mitral stenosis without presystolic
murmur, to one in which such a murmur was recognized.

At that time the whole question of presystolic bruits was compara-
tively a new one ; and I thought that, with further experience, the
number of undiagnosed cases of mitral stenosis would diminish. I
am bound to say that this appears not to be the case. I have not
indeed submitted to numerical analysis the observations that have
been made since my paper was written ; but my impression is that,
in the very large majority of the cases in which mitral stenosis is
found after death, there is no record of the presence of a presystolic
murmur during life. Some observers, I know, hope to reduce this
proportion of failures in diagnosis, by the more frequent detection of
a short presystolic murmur preceding the systolic murmur of mitral
regurgitation. I must confess that my own experience in this direc-
tion has not hitherto been very encouraging. In more than one
instance in which I thought I had detected such a second murmur,
the mitral orifice has been found after death of its natural size.

It remains to add that, even when a presystolic murmur has once
been detected, it may often cease for a time to be audible, or even
altogether disappear. In the later stages of the disease, when the
heart is beating quickly and irregularly, it is almost always absent.
Thus, at first there was some difficulty in verifying the correctness of
the modern view with regard to the rhythm of presystolic murmurs
by post-mortem evidence ; and in the majority of cases that have
terminated fatally soon after the diagnosis of mitral stenosis, some
accidental complication has been the cause of death. Again, when
the patient is prostrated by any depressing intercurrent disease, the
murmur may become temporarily inaudible, returning with conval-
escence. Of this Dr. Sutton has related a capital instance.1 In
other cases, no murmur can be heard as long as the patient remains
perfectly quiet ; but muscular exertion or effort soon makes it audible.
Sometimes even making the patient sit up in bed will bring out a
presystolic murmur that had a moment before been absent; some-
times it is necessary that he should walk two or three times the
length of a ward, or even go quickly upstairs. One can never safely
assert the absence of a presystolic murmur when one has examined
the patient only in a recumbent posture. It may be added, paren-
thetically, that in aortic stenosis (the chief other form of obstructive
disease at a cardiac orifice), a loud murmur may sometimes be brought
out by making the patient run upstairs, although none had previously
been audible. I state this on the authority of Dr. Wilks.2

From the remarks that have already been made with regard to the
so-called mitral regurgitant disease, it will be evident that there can
be no question here as to the frequency with which its diagnosis is
effected during life. I believe that a systolic murmur, louder at the apex

1 Lond. Hosp. Rep., vol. iv., 1867.-8. The patient was very much weakened by fre-
quent vomiting during the time wheu the murmur disappeared.

8 Dr. Wulshe taught this clinically twenty-five years ago. See his "Diseases of the
Lungs and Heart," 1851, p. 217. — Editor.

DISEASES OF THE VALVES OF THE HEART. 675

than elsewhere, and audible at the angle of the left scapula, proves the
existence of mitral regurgitation ; but it is certainly present in com-
paratively few of the cases that are commonly placed in this category.

There is, in fact, a large residue of cases of valvular disease in
which either no murmur is audible at the time of observation, or only
■a systolic murmur, confined to the apex. These cases constitute the
sandy desert of cardiac pathology — not, indeed, unexplored, but with
■a surface so precarious and shifting as to have hitherto prevented the
laying down of roads across it, much less the division of it into terri-
tories by fixed boundary lines. As we have seen, the cases in ques-
tion do not differ at all, so far as stethoscopical evidence goes, from
others in which the presence of valvular disease is altogether doubtful.
It may be true that, since advanced organic changes in the mitral
valve almost always lead to stenosis, the diagnosis of stenosis becomea
exceedingly probable in any case which can be shown to be primarily
one of organic disease of this valve. But it is precisely here that 1 he
difficulty arises; and for such cases I think that the diagnosis of
" morbus cordis " is often the most exact that can be given.

I may refer, for example, to a series of cases of fibroid disease of
the heart that I have recorded in the Pathological Transactions for
1874, vol. xxv. p. 64. In several of these cases there was a systolic
apex murmur ; and it is probable that, at least in some of them, the
mitral valve was really inefficient, since the fibroid change often
invaded one of its fleshy columns. Now, during life, there was
nothing to distinguish these cases from those of ordinary "mitral
regurgitant disease," and even in the other cases, in which no murmur
existed, valvular disease might really have existed, and been latent.
Since my cases were published, it has occurred to me that perhaps
one positive indication of the presence of fibroid disease of the heart,
rather than of any affection of the Talves, may be found in its resisting
treatment with greater obstinacy. When a considerable part of the
wall of the left ventricle has had its muscular substance replaced by
fibrous tissue, it appears reasonable to suppose that the remedies
which would be useful in a case of valvular disease should prove to
be altogether powerless.

I have still to lay stress on the importance of watching, with great
care, for the occurrence of those changes in valves already diseased
which have already been described, and the recognition of which is
so important for purposes of prognosis. The development of incom-
petency in aortic valves that had hitherto simply obstructed the
onward current, the production of stenosis in a mitral valve previ-
ously the seat of regurgitation alone, the rupture of the chordae of a
diseased mitral valve, the tearing down of a softened aortic segment,
the supervention of acute inflammation in valves long thickened,
atheromatous, or calcified, — all these might probably be discovered
much oftener than is now the case, were the physician to pay more
regard to the probability of their occurrence. Nor should the liability
to intercurrent pericarditis, and to the development of changes in the

676 A SYSTEM OF MEDICINE.

heart's muscular tissue, ever be forgotten by those who would have
their diagnosis complete for the post-mortem examination.

Prognosis. — To determine the probable duration of life in a patient
affected with valvular disease of the heart, and the chance that
existing symptoms may be relieved or removed, is generally very
difficult ; and it can hardly be discussed systematically in an article
of this kind, since it requires that all the circumstances of the case
should, one after another, be taken into consideration. But some
leading points may be briefly stated.

And in the first place, can a diseased valve ever recover its normal
structure and functions ? In reference to the acute affections of the
valves, arising in rheumatic fever or in chorea, some facts have already
been adduced which indicate that this is possible. And a further argu-
ment in favour of the same view may perhaps be found in the circum-
stance that in each of the diseases in question a systolic murmur is heard,
which in many cases disappears after recovery. If such a murmur,
when audible at the heart's apex, be regarded as proof that the mitral
valve is affected, it would seem to follow that endocarditis is curable.
Such an opinion has, in fact, been recently maintained by Dr.
Peacock, who, in an analysis1 of 146 cases of acute rheumatism that
had been under his care, found that "the proportion of cases of recent
cardiac complication (which he states to have consisted in endo-
carditis more frequently than in pericarditis) entirely cured was 41*5
per cent." But the conclusion, of course, depends for its validity upon
the question whether the determination of the cause of the murmur is
accurate. And this I am not prepared to admit unreservedly.

A valve once affected with chronic disease is no doubt almost always
damaged beyond possibility of repair. Thickened and calcified aortic
valves can never again become thin and supple.2 Nor is it probable
that a steiiosed mitral orifice can become widened. Friedreich has
indeed suggested that in young subjects this may not be impossible :
but in proof of it he can only refer, in general terms, to cases in
which there were at one time symptoms of extreme stenosis, but in
which these gradually diminished, and after death the mitral orifice
was found capable of admitting two fingers.

There is, however, no doubt that thirty years ago the most practised
auscultators of the day condemned, as the victims of organic valvular
disease that would soon destroy them, children who have since grown
up to be men and women, and who to all appearance enjoy excellent
health. It is probable that they attached too absolute an importance
to the existence of a murmur, and that they also committed the error of
supposing that the louder the murmur, the worse the disease. One can-
not insist too strongly on the fact that between these two things there is
no relation whatever. The prognosis in the cases under consideration

1 Clinical Society's Transactions, ii. p. 221.

9 The analogy of scleroderma, however, perhaps suggests that even this is no
absolutely out of the question,

DISEASES OF THE VALVES OF THE HEART. 677

must be based not upon the physical qualities of the murmur, but
upon a determination of the degree to which the disease disturbs the
circulation; or, if compensation be complete, upon the degree of
increased strain thrown upon the heart.

I have already pointed out how compensation is in many cases
effected by dilatation and hypertrophy of certain of the heart's
chambers. According to Jaksch there is another kind of compensa-
tion, consisting in conservative changes in the valves themselves, which
absolutely prevent diseases of the valves from producing their natural
consequences. When one cusp of the mitral valve is diseased, he
imagines that the other may grow broader, and its chordae may
lengthen until it meets its fellow. When one aortic valve is
puckered up, the others may gradually become deeper and wider, so
as to fill up the gap. The change last mentioned is one which I
have myself seen; but it doubtless occurs only in very young patients.

It has already been stated more than once that in valvular diseases
of the heart the development of serious symptoms is often very long
delayed. Dropsy may first show itself in a person advanced in years,
and destroy life in a few months : but the mitral disease which is
rightly regarded as the cause of the dropsy may be traceable to an
attack of rheumatic fever twenty or thirty years back : and in the
interval the patient may either have had excellent health, or may
always have suffered more or less from dyspnoea on exertion, which
has shown that the heart was defective.

It is a question discussed by almost all writers on Heart Diseases,
whether a prolonged existence, and delay in the development of
serious symptoms occur in all forms of valvular disease alike, or
belong especially to any one group of cases. Considerable interest
would indeed attach to the determination of the relative prognosis
of the various affections of different valves : and, although statistical
accuracy is not to be looked for, a general concurrence of opinion on
the subject might fairly be expected. The case is not so, however.
According to one of the most recent French writers, Jaccoud,1 stenoses
in general are more serious than regurgitations : and mitral stenosis is
more so than aortic stenosis. Again, Friedreich, the author of perhaps
the latest German monograph,2 says that " as a rule the prognosis in
obstructive forms of valvular disease is less favourable, and the dura-
tion of life shorter, in obstructive than in regurgitant affections." Now,
according to all English writers this is absolutely incorrect. Walshe
places " the chief valvular derangements in the following descending
series on the basis of their relative gravity, — that is, estimating this
gravity not only by their ultimate lethal tendency, but by the amount
of complicated miseries they inflict: — Tricuspid regurgitation: mitral
constriction and regurgitation: aortic regurgitation; pulmonary con-
striction; aortic constriction." Thus Dr. Walshe regards aortic ste-
nosis as admitting of a far better prognosis than aortic regurgitation :

1 Traite* de Pathologic Interne, tome i. p. 657.

* Krankheiten des Herzens, Handbuch der spec Path, und Ther., 2te Aufl. 1867, p. 2S2.

678 A SYSTEM OF MEDICINE.

and Dr. Peacock agrees with him, stating that in the former disease
life may be prolonged for many years, and a large amount of health
and vigour be enjoyed ; whereas in aortic incompetency it is very rare
to find life sustained for a considerable period. Dr. Peacock, indeed,
differs from Dr. Walshe and from most other English writers in be-
lieving the prospects of longevity to be actually less in persons who
labour under aortic regurgitation than in those who have mitral
disease. I confess that I am unable to reconcile these conflicting
statements. It is evident that the discrepancy is in great part due to
the uncertainty which still attaches to the interpretation both of
auscultatory phenomena and of morbid appearances. I have shown
that, according to experience at Guy's Hospital, aortic stenosis, with-
out regurgitation, is far more rare than has generally been supposed :
and certainly it would not within the last few years have been
possible to make any observations that would have allowed of a
numerical comparison between its mortality and that of regurgi-
tant disease of the same orifice. The latter disease, however, is un-
doubtedly a very fatal one. I find from the clinical records at Guy's,
that from 45 to 50 per cent, of the patients who have aortic regurgi-
tation die within the comparatively short period during which (under
ordinary circumstances) they are allowed to remain as in-patients. But
then it is to be observed that the fact of their admittance implies the
existence of severe symptoms at the time : and the observations in ques-
tion are not incompatible with the fact that the disease often exists
for a lengthened period before such symptoms show themselves. I
have already remarked that changes in the aortic valves, allowing re-
gurgitation, have often been found in persons who have presented them-
selves for life assurance, or in the dead bodies of those who have been
killed by accident. Instances of this kind appear to be fairly com-
parable with the case, on which Dr. Peacock lays so much stress, of
a woman, set. 76, who died of strangulated hernia, and in whom two
of the aortic curtains were completely blended into one, and the
orifice reduced to a mere slit, although she was not known to
have had any symptoms of disease of the heart. Unless we agree
with Dr. Peacock in supposing that disease of this kind always ori-
ginates in congenital malformation, there is no proof whatever that
in the case in question the disease had existed longer than in the
examples of unsuspected regurgitant aortic disease which are so
common. But while thus criticising some of the evidence brought
forward in proof that aortic stenosis is a less serious disease than aortic
regurgitation, I nevertheless believe that this is really the case.

Again, it is very difficult to institute a comparison between the
duration of life in mitral stenosis and mitral regurgitation respec-
tively. For, as we have seen, the cases included under the latter
designation present no one pathological lesion, but rather a variety
of more or less allied conditions. Many cases of mitral stenosis, with
marked presystolic murmur, remain under observation for some years,
and are admitted into the wards again and again, without the symp-

DISEASES OF THE FALVES OF THE HEART. 679

toms undergoing any great increase of severity, and without there
being at any time reason to apprehend an immediately fatal issue.
And on the other hand, it is well known that the systolic murmur of
mitral regurgitation may be detected by auscultation for years before
any serious symptoms show themselves.

Lastly, I doubt whether any data exist from which one could
accurately determine the relative gravity of regurgitant aortic, and of
regurgitant mitral disease. For, in addition to other points that have
already been noticed, there is between these two affections an im-
portant distinction in the fact that one of them is far more constantly
traceable to a past attack of rheumatic fever than the other. Hence,
while one can often with confidence say, in the case of mitral regurgi-
tation, that the cardiac affection began years before, when the patient
had acute rheumatism, one is commonly obliged to refer the com-
mencement of aortic disease to the date when the patient first began
to suffer from definite symptoms of heart-disease. Now it is certain
that aortic disease sometimes exists for a long time without any
symptoms at all : but whether this is the rule or the exception we
have no means of knowing.

There is, however, one particular mode of death which appears
beyond doubt to occur in regurgitant aortic disease far more frequently
than in any other affection of the cardiac valves : and it is one which
for many persons has especial terrors, — namely, that in which the fatal
termination is sudden. It is a curious circumstance that the contrary
is stated by Corrigan, in the interesting paper which is almost the first
that was written on this subject In permanent patency of the mouth
of the aorta, he says, " the fatal result is never sudden.'9 " Under proper
restrictions the patient is not only able to lead an active life for years,
but is actually benefited by doing so." All recent writers, however,
recognize the tendency to the occurrence of sudden death in the disease
in question. Thus Dr. Walshe says : l " Taken as a group, valvular
impediments cannot fairly be cited as frequent causes of sudden
death : but there is one among the number, of which the tendency to-
kill instantaneously is so strong that the fact must always be borne in
mind in estimating its prognosis, and that is aortic regurgitation. . . .
The manner of death is clearly syncopal : but the immediate
mechanism, whether mechanical or dynamic, is difficult enough of
comprehension. I have known death take place during the act of
walking, of eating, of speaking, — while the patient was emotionally
excited, and, per contra, at a moment when he was] perfectly calm."
Further on, Dr. Walshe appears to imply that the liability to sudden
death is greater when the heart itself is perfectly healthy than when
it presents dilatation and hypertrophy of the left ventricle or other
morbid changes. But in tins he differs from Dr. Peacock, who says2
that " in cases in which the neart is most remarkably enlarged, suddeiv
death is yet of common occurrence, " and who cites two instances of the?
kind, in which the hearts weighed 40 oz. and 46 oz. respectively.

1 Op. cit, p. 390. * Croon ian Lectures, p. 108.

680 A SYSTEM OF MEDICINE.

With regard to the prognosis of the diseases of the valves believed
to originate in injury, all that can be said is that in recorded cases the
duration of life lias been very variable. Dr. Peacock states that
the period of death in the different cases of injury to the aortic valves
collected by him was " twenty-one days, three months and a half,
thirteen months, two years, twenty-seven months, and three years and
a half: and two persons were still surviving after five months and
five years had elapsed " in their respective cases. " In the cases of
rupture of the mitral valve, the patients lived nine days, and twenty
months : and two still survived eighteen months, and two years, after
the occurrence of the accident."

Treatment. — The prophylaxis of acute affections of the cardiac
valves belongs to the treatment of those diseases in which such
affections are most apt to arise; and if endocarditis can really be
prevented by medicine, this is, in fact, the most important part of the
treatment of the diseases in question. But at present I do not know
that one can really say any more about it than that rest should be
strictly enforced, and that the chest should perhaps be protected from
cold by a layer of cotton- wool.

Scarcely less important is the prevention of the development of
chronic disease in valves that have once been damaged by acute
inflammation. I have already adduced facts which tend to prove that
endocarditis not rarely subsides without leaving any injurious effects
behind it ; in particular, that a large proportion of the cases of rheu-
matic inflammation of the aortic valves in women must terminate
in the restoration of the normal structure of the valves. The com-
parative immunity of the female sex from the more remote changes
which so frequently arise in the male sex can only be ascribed to the
fact that women lead less active lives than men, and are not compelled
to endure such continuous exertion, or to make such violent muscular
efforts. The plain inference is, that in either sex the way to prevent
chronic disease of the valves, after endocarditis in rheumatism or
chorea, is to keep the patient for many months — or even some years
— as perfectly as possible at rest ; to insist on abstention from violent
exercise, athletic sports and games, of all kinds ; to direct the choice
of a light, sedentary employment, and to urge the avoidance of all
emotional excitement. General hygienic conditions should at the
same time be carefully attended to. I think, too, that it may here-
after be shown that medicines are useful. I have pointed out how
the anatomical characters of chronic disease of the valves differ from
those of acute endocarditis; that the vegetations disappear, but that the
edges of the valves become thickened and fused together. Surely it is
possible that iodide of potassium, mercury, or arsenic, may be able to
arrest or prevent these changes, as much as those which belong to
certain skin diseases, or the chronic inflammations of parts accessible
to the sight or touch of the surgeon.

Similar principles must be applied in the endeavour to prevent

DISEASES OF THE VALVES OF THE HEART. 681

those forms of valvular disease which are from the first of gradual
origin. A very large proportion of the cases of aortic regurgitant
disease that occur so commonly in labouring men past middle life,
are due to the fact that these men have gone on with work involving
straining efforts, which can with safety be made only by younger indi-
viduals, whose tissues are still elastic and supple. Dr. Peacock and
Dr. Allbutt have indeed shown that such diseases of the cardiac valves
frequently occur at an earlier period of life than has generally been
supposed ; but even then they are perhaps favoured by some particular
diathetic condition, or by habitual excessive indulgence in alcoholic
drinks, which promotes degenerative changes in the tissues. It may
hereafter be possible for the physician to select certain individuals
as especially liable to suffer from the harder kinds of labour, and to
recommend for them less arduous employments. Among the higher
classes, again, chronic disease of the cardiac valves appears very
frequently to be due to men forgetting that they are advancing in
years, and to their continuing to take violent exercise long after they
have ceased to be fit for it. This is especially apt to occur in pro-
fessional men, whose habits are generally sedentary, and who, during
an occasional holiday, often run great risks. The physician should
always be on the look-out for the earliest signs of tissue-degeneration
in such persons, and should be ready to warn them of the necessity
that they should avoid too great exertions or straining efforts. It
is no longer believed that the signs in question are an early arcus
senilis, and the fact that the hair has turned prematurely grey ; and I
am myarff inclined to doubt whether tortuosity of the temporal
arteries, or an apparent rigidity of the radial arteries to the touch, is
to be much relied on, as indicative of degeneration of those vessels ;
but, taken with other points, they are probably of value ; and it
seems that the sphygmograph may here lend very valuable assistance.

Even when valvular disease is fairly established, the prophylactic
measures already referred to by no means cease to be applicable.
Probably such disease is almost always progressive ; and it is, more-
over, liable to become complicated at any period of its course by the
supervention of acute endocarditis.

But the treatment of diseases of the cardiac valves, properly so-
called, reduces itself to the treatment of their effects. To these we
must therefore refer in brief detail.

1. Very little, and perhaps nothing, is known of any effectual
treatment for the contamination of the blood with morbid materials,
which is so apt to occur in the more acute forms of valvular disease,
or for the occurrence of embolism in the larger vessels. Quinine
would seem to be indicated in the former condition, and may perhaps
be of some service ; but Lancereaux observes that its failure has often
been demonstrated in cases that had been mistaken for ague, and had
therefore been treated with this drug. The mineral acids are recom-
mended by Friedreich. I am not aware that any evidence is to be
obtained as to the upe of the sulphites or hyposulphites, as recommended

VOL. IV. Y T

682 A SYSTEM OF MEDICINE.

by Polli in septic conditions, but I should conceive that there is, at
any rate, more chance that they might be useful in the eases under
consideration than in the specific fevers against which they have
chiefly been employed. Cases in which " typhoid " symptoms occur,
with haemorrhages into the skin and mucous membranes, &c, are
probably of necessity fatal ; and it is almost useless to administer the
ammonia, ether, and musk, which are generally recommended, and
which at once suggest themselves to the mind as the drugs that can
be most appropriately given.

When there is evidence of the occurrence of embolism in any
particular artery, it is possible that the administration of ammonia, as
suggested by Dr. Richardson,1 may favour the solution of the co-
agulum — if indeed he is right in attributing success to this treatment
in cases of fibrinous deposition within the heart. The plan which he
recommends is the administration of ten-minim doses of the liquor
ammoniee in iced water, every hour, with three to five-grain doses of
the iodide of potassium every alternate hour.

2. The changes which diseases of the cardiac valves induce in the
circulation of the blood, and in the several chambers of the heart, are
capable of being modified in a very remarkable degree by various
medicines and modes of treatment; and to these we must now turn
our attention, following as far as possible the same order which was
adopted in the account of these changes given in pages 55 to 69.

In cases of aortic regurgitation, so long as the state of the ventricle
is such as perfectly to compensate for the valvular defect, medicinal
treatment is scarcely applicable. Patients admitted into an hospital
sometimes lose all their symptoms as a consequence of the rest which
they obtain, and which is so essential to them. The avoidance of all
violent or straining efforts should in fact be insisted on in this, even
more than in other forms of cardiac disease, on account of the marked
tendency to sudden death, which must always be borne in mind.

For the less severe effects of aortic regurgitant disease, the slighter
degree of malaise and discomfort oaused by it, senega is the common
remedy. It is difficult to say how this drug acts ; and as ammonia
is generally given with it, this has been supposed to be the really
efficient remedy. I have, however, repeatedly prescribed it alone, and
patients have sometimes declared that it has given them distinct
relief. I am therefore disposed to believe that it is of value, and the
more so, as the late Dr. Barlow (a physician of much experience in
such matters) used to teach that in many cases only moderate doses
could be borne. The dose usually given is half an ounoe to an ounce
Of the infusion, with or without half a drachm or a drachm of the
tincture, and perhaps the same quantity of the aromatic spirits of
ammonia, or five grains of carbonate of ammonia.

When compensation fails in aortic regurgitant disease, we have
seen that effects are developed which are identical with those that

1 Med. Press and Circular, Nov. 20, 1872.

DISEASES OF THE VALVES OF THE HEART. 683

occur iii mitral disease. They require the same treatment, which
I shall describe in the next paragraph.

In the treatment of a case of " mitral disease/' — using that term for
the moment in its widest sense, — the primary point is the due regu-
lation of the contractions of the left ventricle, for which we have in
digitalis a remedy of wonderful power. Within the last few years
a great change has taken place in our views as to the action of this
herb, and our knowledge is very much more accurate than it
formerly was. The older opinion was that it enfeebled the power of
the heart,1 and therefore that dangerous effects might in certain cases
follow its administration, from its tendency to cause fatal syncope.
It is true that Dr. Withering in the last century stated it to be most
useful in those cases of dropsy in which the pulse was feeble or inter-
mitting, declaring also that it seldom succeeded in men with a tight
and cordy pulse. But its good effects in such cases were attributed
to its diuretic action, not to its having any power of strengthening
a feeble heart

Within the last few years, however, it has been demonstrated that
the action of digitalis on the heart is in fact that of a tonic. The
proofs of this are varied. In cold-blooded animals, in which the
cardiac pulsations can be watched after exposure of the organ, digitalis
causes spasm of the left ventricle, beginning at isolated points in its
wall, and finally affecting its whole substance, so that its beats cease,
and it remains rigidly contracted and white. In conjunction with
Dr. Stevenson, I some years ago performed a number of experiments
on frogs, in which this result was uniformly observed.* In the
higher animals it is less easy to study directly the action of digitalis
on the heart, but according to Fothergill,* Handfield Jones and
Fuller have noticed similar effects as regards the state of the heart
after death in mammals.

The present doctrine with regard to digitalis, then, is that it
strengthens the heart's contractions. It is true that when very large
doses are given, the pulse may become weak, frequent, and intermit-
tent ; but this is supposed to be due to the fact that the ventricle
is in a state of spasm, and therefore that its beats are imperfect, and
throw but a small quantity of blood into the arteries.

Thus the cases of heart disease in which digitalis is most useful
are those in which the organ beats feebly and irregularly, in which a
condition of " asystolie " exists, and in which the pulse presents the
sphygmographic characters indicated at p. 63. In such cases the
action of the remedy is to diminish the frequency of the cardiac
pulsations, to make them regular, and to increase their force.

Among affections of the cardiac valves, " mitral regurgitant disease M
is that one which most commonly presents the indications for the
administration of digitalis ; and in a large proportion of cases of this

1 Pereira's Mat Med., 4th ecL, 1855, voL ii, p. 538.
3 Proc. of the Roy. Soc., 1865 ; Guy's Hosp. Hep., I860.
' " Digitalis : ito mod* of action and its use," 1S71»

YT2

884 A SYSTEM OF MEDICINE.

kind, great relief is afforded by the remedy; the symptoms may for
a time be entirely removed, and the patient restored to a state of
apparent health. On the other hand, it is often useless and perhaps
.injurious in cases of mitral stenosis ; for the left ventricle in the
earlier stages of this affection generally contracts regularly and with
due force, as is apparent from the normal character of the pulse. At
a later period in the course of mitral stenosis, digitalis is often very
useful ; but the physical characters of the disease are then less dis-
tinctive; it is often difficult or even impossible to determine its
exact nature. Again, in aortic regurgitation, when the hypertrophied
ventricle is carrying on the circulation vigorously, digitalis often
aggravates all the symptoms ; and if the patient should die suddenly,
it is liable to the charge of having caused the fatal result, a charge
which cannot be refuted, and is probably often justly made against
the drug. But Dr. Ringer has shown that the existence of aortic
disease does not contra-indicate the use of digitalis, if the symptoms
suggest its administration. When there is dilatation of the heart
(rather than hypertrophy), and the pulse is feeble, frequent, fluttering,
and (above all) irregular, it may be given with a fair expectation that
it will afford relief.

The dose of digitalis is a matter of some importance ; a drachm
of the infusion is enough to begin with, or five or ten minims of the
tincture. According to Dr. Fothergill, the injurious effects of digitalis
in aortic disease, with hypertrophy of the left ventricle, may be
avoided by employing very minute doses, which will in such cases do
as much good as is produced under ordinary circumstances by larger
quantities of the remedy.

It is doubtful whether any other remedies are capable of exerting
the same action as digitalis on the diseased human heart Dr. Steven-
son and I found that squill and two species of helleborus (H. viridis
and niger) produced the same peculiar effects in the healthy frog.
Vcratrum viride is often supposed to resemble digitalis in this respect ;
And in America it has been largely used to diminish the frequency
of the heart's beats. But in frogs its action is the very opposite of
that of digitalis ; it rather resembles aconite, paralyzing the heart,
which, when it stops, is dilated and of a deep purple colour.

The treatment for the backward effects of diseases of the valves of
the heart must of course aim at reducing the increased tension in the
pulmonary and venous systemic vessels, upon which these effects
depend. And there are two principal ways in which this can be done.
The first is the removal of a portion of the venous blood by venesec-
tion, leeches, or cupping. Now, if we take into consideration the fact
that blood is forced into the veins from the capillaries in a continuous
•stream, we shall not at first suppose that much benefit is likely to
accrue from the abstraction of a few ounces of blood from one part of
the venous system. It seems like taking a cupful of water from a
pail that is running over with the supply from a spring. We cannot
help imagining that the veins will almost instantly become again

DISEASES OF THE VALVES OF THE HEART. 685

distended. But there is abundant evidence to show that such a
supposition is erroneous. Thus the haemoptysis which accompanies
pulmonary apoplexy often relieves the patient's breathing for several
days or even weeks ; and nausea and vomiting, due to congestion of
the stomach, are frequently removed for a considerable time by an
atttack of haematemesis. It is clear that the relation, as regards
tension, of the different parts of the circulating system can be much
more steadily maintained than one would at first sight have imagined,-
Equally decided are the therapeutical proofs of the same fact The with-
drawal of a small quantity of venous blood is often attended with the
most beneficial results in cases of heart diseasa Perhaps the most
striking example that I can cite is one, recorded by Dr. Dickinson,1 of
a man who had ruptured almost all the chordae of the posterior flap of
the mitral valve. " This patient was frequently relieved temporarily
by the abstraction of blood. He was frequently cupped, always with
apparent relief of the dyspnoea and distress. Towards the close of his
sufferings, when, though there was much cardiac action, the pulse was
nearly imperceptible, and the patient was approaching a condition of
collapse, with much dyspnoea and blueness of the face, eight ounces
of blood were taken by venesection, with immediate and decided relief,
the pulse recovering itself as the blood flowed, while the distress of
the patient was much lessened. The improvement, however, was only
temporary. The patient died the following night."

The extreme gravity of the lesion in this case seems to render it
worthy of being quoted. If the removal of blood could give relief
when one-half of the mitral valve "had lost all valvular action, and
swung uselessly from its base," there is hardly any case in which one
need despair of its doing good. In the ordinary forms of valvular
disease it is often useful, and the relief afforded by it is sometimes
maintained for several days, or even weeks, so as to allow time for the
operation of other remedies. The application of leeches to the epigas-
trium relieves the sickness and nausea due to congestion of the stomach;
probably they would be still more useful if applied near the anus.

The other method of relieving the engorged pulmonary and venous
systemic circulation is by removing, not blood itself, but its watery
part alone ; in other words, by giving purgatives and diuretics. Among
the former remedies, the hydragogues are of course to be preferred ;
jalap, or even elaterium, scammony, salines, &c. As regards diuretics,
it has already been observed that one of the principal indications of
the favourable action of digitalis is its increasing the flow of urine,
sometimes to an enormous extent Whatever view may be taken of
the theory of its action, there is no doubt about the fact Other reme-
dies which are supposed to act as diuretics in the diseases under con-
sideration are squill, juniper, broom, and cream of tartar. Copaiba is
sometimes very useful. I have notes of one case of mitral disease
which had previously resisted various kinds of treatment, and in which
ascites and anasarca rapidly vanished under the administration of a

1 Path. Trans, zx. p. 151.

686 A SYSTEM OF MEDICINE.

simple copaiba mixture. I shall never forget the gratification of the
patient as the loops of string that held his trousers together soon became
unnecessary, and the buttons themselves had to be moved again and
again, in adaptation to the rapidly-decreasing girth of his belly. Dr.
Wilks has recently found the resin of copaiba no less effectual, as it
is certainly nvore pleasant

3. The third group of effects of disease of the cardiac valves
—the symptoms subjectively experienced by the patient — are fre-
quently capable of great relief by medical treatment, but too often
resist all the physician's efforts, and make the termination of a case
of this kind almost more distressing and painful than that of any
other disease.

The obvious remedies for dyspnoea, palpitation, and' the sense of
pressure and weight in the epigastrium, are the ethers and ammonia,
especially when combined with digitalis, if the nature of the disease
should be such as to indicate its employment. The application of a
large belladonna plaister to the cardiac region often gives considerable
relief to local pain and to palpitation.

Hyoscyamus is commonly given as an anodyne in these cases ; but
I have not seen it do very much good Opium is generally said to be
inadmissible, or to be used only with great caution. On the other
hand, it would appear that the subcutaneous injection of morphia
may be employed with safety, and with the most marked results. Its
use has been especially advocated by Dr. Allbutt.1 He uses the hydro-
chlorate, in doses of one-tenth to one-third of a grain. It is especially
useful, he says, in cases of mitral regurgitation, " when the head is
full of venous blood, and distress and stupor seem striving together.
An injection of morphia three or four times a week, by tranquillizing
the heart, and allowing the circulation to recover its freedom, sets free

also the organs that are oppressed Directly and immediately

the injection seems to affect the chest almost alone. The face gene-
rally becomes less turgid, and its expression calmer. The heart be-
comes tranquil and rhythmical. .... The insufferable precordial

distress ceases The quick, shallow, anxious, cardiac dyspnoea

gives way to a deeper, slower, and easier movement . . . . The pa-
tient, who hag been tossing in misery, feels the first tranquil sleep
he has enjoyed for weeks."

The attacks of angina-like pain, which form so important a part of
the symptoms in many cases of aortic regurgitation, require essentially
the treatment of neuralgias. I have more than once found the regu-
lar administration of arsenic able to prevent their recurrence. The
paroxysms themselves are often arrested by the inhalation of ten
drops of nitrite of amyl, or of a few whiffs of chloroform ; or again by
the subcutaneous injection of morphia. In one case that I saw— in
which all these were used in succession— the patient preferred the
morphia, as giving him the highest amount of relief.

1 Practitioner, iii p. 342.

ATROPHY OF THE HEART.
By W. R. Gowers, M.D.

Synonym. — Phthisis of the Heart (old writers).

Definition. — Diminution in the size and weight of the heart,
consequent on diminution in the amount of muscular tissue contained
in its walls. Of these characters the diminution in. weight is the most
important. An atrophied heart, according to the common use of the
term, is one the weight of which is less than the average weight for a
person of the same stature. It is said that, in very rare instances, a
heart, the total muscular tissue of which is lessened, and the weight
below the normal, may be larger than natural, owing to the dilatation of
its cavities. The occurrence of such instances is, by some authorities,
denied. If they occur, dilatation is their conspicuous feature, and
they come more accurately under that head. Diminished bulk
remains a character of those forms of atrophy which may most con-
veniently be considered under this designation. On the other hand,
the muscular tissue of the heart may be lessened in quantity, may
have undergone atrophy, when there is increase of other elements
in the cardiac wall. In such cases the weight of the heart is, as a
rule, not diminished, and these instances are considered under the
head of the special degenerations. Only those rare examples will
be here alluded to in which the weight of a heart so changed is less
than normal.

History. — The important functions always attributed to the heart
rendered its atrophy a more anomalous condition, in the eyes of the
earlier observers, than its enlargement. Accordingly we find that this
condition early attracted attention. Pliny states that the kings of Egypt
noted its occurrence. Riolanus alluded to it, and ascribed it to defi-
ciency of the pericardial fluid. A well-marked case was recorded by
Soumain at the beginning of the last century.1 Senac, in 1749,
described it carefully in his treatise on the heart,2 which probably

1 Relation de l'ouverture (Tune femme presque sans coror. Paris, 1728.
9 Traite de la Structure du Coeur, de son action et de sea maladiaa. Pari*, 1749, torn,
il, p. 393.

688 A SYSTEM OF MEDICINE.

remains the longest monograph yet written on cardiac anatomy and
pathology. Allan Burns, in 1809, described some very characteristic
examples.1 It is not mentioned by Corvisart, who wrote nearly at the
same time. M^rat, in 1813,2 alluded to several instances which he
had seen, and Bertin, in 1824, gave a full account of it, while by his
editor, Bouillaud,8 varieties were subsequently discriminated, whicli
have since been recognised by most writers on the subject.

Varieties. — Forms of cardiac atrophy have been distinguished
corresponding to the varieties of cardiac hypertrophy. Thus, reduction
in the weight of the heart due to mere attenuation of the walls, the
cavities remaining of normal size, was termed by Bouillaud, simple
atrophy.

Reduction in size of the heart, with diminution in the size of its
cavities, so that they still bear the normal proportion to the heart,
is the concentric atrophy of Bouillaud and Walshe,4 the simple atrophy
of Hayden.6

Attenuation of the cardiac walls and diminished weight of the
heart, with increase in the size of the cavities, is the eccentric atrophy
of Bouillaud, Forster, Walshe, and others. These cases, as just stated,
come more properly under the head of dilatation. Hayden applies the
term " eccentric atrophy "toa condition of heart, examples of which
must be very rare, in which the walls are attenuated, the whole
heart smaller, but the cavities larger than normal. As " concentric
atrophy " he classes hearts which are smaller than normal, have the
walls relatively thickened, and the cavities reduced in capacity. This
variety was described by M«5rat in 1813. It may be doubted
whether either of these two varieties has any real existence ; they
probably represent only states of contraction or relaxation in
atrophied hearts. Chomel distinguished two varieties according to
the cause of the atrophy — the congenital and accidental?

Causes. — Smallness of heart may be a congenital or an acquired
condition.

A. Congenital atrophy is usually well marked. The heart of an
adult otherwise free from disease may not exceed that of a child six
or seven years old, as in an example mentioned by Allan Burns.
The immediate causes of this condition are unknown. Hereditary
influence has not, hitherto, been traced. It is said to be more common
in women than in men. The subjects of it may be in other respects
well formed, but sometimes it has appeared to be part of a more
general arrest of development, shown by a childish aspect and
defective development of the sexual organs. Parrot7 doubts the

1 Allan Burns, Observations on Diseases of the Heart. Edinburgh, 1809, p. 110.
1 Dictionnaire des Sciences Medical es, Art. Coeur.

* Traite* clinique des Maladies du Cceur. 2ieme. edition. Foris, 1841.

4 Diseases of the Heart and Great Vessels Fourth edition. Ix>ndon, 1873, p. 276.
0 Diseases of Heart and Aorta, 1875, p. 585.

• Dictionnaire en 30 volumes.

7 Dictionnaire fincyclopedique des Sciences Medicales, 1876, art Coaur.

ATROPHY OF THE HEART. 689

congenital nature of these cases, and believes them to be due to a
simultaneous arrest of the growth o? the heart and of the sexual
organs, occurring at puberty.

B. Acquired atrophy may be the result of general or local causes.
The chief general causes are chronic wasting diseases, in which the
heart frequently undergoes diminution in size. This may occur in
cancer, phthisis, syphilis, chronic suppuration, diabetes. According to
the statistics of Quain,1 the heart is small in about half the cases
of phthisis, and the diminution in size is rather more frequent in
women than in men. Out of 17l cases, it was small in 53 per cent
of the males, in 67 per cent, of the females. There is no evidence of
any special influence exercised by these diseases on the heart. The
organ apparently wastes in common with the rest of the body, in
consequence of the defective nutrition.

The local causes are such as influence directly the nutrition
of the heart. Narromng of the coronary arteries is said to be an
occasional cause. The influence of this condition is to be more
distinctly traced in the production of local degeneration. Walshe,
however, regards the influence of pressure in causing local atrophy
as due to its effect on the blood supply.

Compression of the heart is apparently, in some cases, a cause of its
atrophy. The heart has been found small in long-continued pericardial
effusion, and the condition has been compared to the contraction of a
lung in long-continued effusion into the pleura. Pericardial adhesions
have been supposed in some cases to have caused cardiac atrophy.
The association of the two conditions was first pointed out by
Chevers.2 Hypertrophy and dilatation are more frequent conse-
quences. Kennedy3 found atrophy in only five out of ninety cases of
pericardial adhesion without valve disease. The contraction of tough
lymph, resulting from pericarditis, has in some cases been associated
with very distinct atrophy of the subjacent portion of the heart.4
Walshe corroborates this, but believes that the effect is due to pressure
upon the arteries. Compression by fatty tissue sometimes leads to
atrophy of the muscular fibres, especially when the fat is infiltrated
among them. The instances of this change in which the heart is
smaller than the normal are very rare. Wilks and Moxon mention
such a case as an example of " fatty atrophy." The heart weighed
only 5 J oz.

Local atrophy, affecting one part of the heart, is due most commonly
to the last-described condition, to local infiltration with fat. Occa-
sionally, the limited position of contracting lymph, or narrowing of
one coronary artery, may have the same effect.

Pathological Anatomy.— A heart the subject of atrophy is, as
already stated, lessened in weight The heart of an adult may weigh

1 Lumleian Lectures, 1872. Abstract in lancet, vol. i., p. 426.

* Guy's Hosp. Reports vol. vii. s Edin. Med. Journal, 1858.

4 An observation of this kind was recorded by Malpighi.

690 A SYSTEM OF MEDICINE.

only six, five, or even four ounces. Quain mentions an instance
of the heart weighing only 1 oz. 14 drs. in the case of a girl aged
fourteen, who died of phthisis.1 Its size is also lessened. The cir-
cumference at the base may be only six inches. Chomel has
recorded an instance in which the heart- of an adult did not exceed
in size a hen's egg. The thickness of the walls depends chiefly
on the condition of the heart, whether contracted or relaxed. The
degree of contraction may be estimated by the size of the cavity.
In cases of acquired atrophy almost all the adipose tissue has disap-
peared from the surface, on which the vessels stand out conspicuously.
There is often serous infiltration of the fibrous tissue from which the
fat has been removed The texture of the heart may be little changed,
or it may be pale in colour and softer than natural. On the other
hand, it may be dark, dense, and tougher than natural. The change
depends on the presence and form of degeneration, whether fatty
or fibroid, partly also on the accumulation of pigment granules within
the fibres. The microscope shows the primitive bundles to be lessened
in size. The fibres are often fattily degenerated ; their striation is
lessened, sometimes indistinguishable.2 The fibrous tissue between
the bundles may be increased in quantity. Occasionally, especially
in the old, brownish pigment may encircle the nuclei of the fibres, or
be uniformly distributed through their substance. "When it occurs,
the pigmentation is usually generally distributed through the heart,
and gives its substance a reddish- brown tint Rindfleisch3 has
described it as a special form of atrophy — " brown atrophy." Friedreich
believes that the pigment is derived from the colouring matter of the
muscle.

Associated conditions, causing the atrophy, may coexist. The
various general conditions, cancer, phthisis, &c, may be present.
Pericardial changes, effusion, lymph, plates of calcification, fatty
accumulation, may compress the heart, or there may be from some
cause obvious reduction in size of the coronary artery. The peri-
cardial fluid is, according to Bamberger, often increased in quantity
as a consequence of the cardiac atrophy.

Symptoms. — The physical signs of atrophy depend on the lessened
bulk and diminished force of the heart The extent of dulness,
especially the deep dulness, is smaller than normal. To be significant
the diminution must be independent of emphysema or any lung
condition obscuring the cardiac dulness. The impulse is weak, and
felt over a small area. The sounds may be lessened in intensity,
or they may be unchanged. The latter has been the case in
Walshe's experience. The pulse is small, the patient weakly. When
due to a local cause the symptoms of the local causative condition,

1 Lumleian Lectures, loe. cit.

* The "yellow atrophy" of Rindfleisch is fatty degeneration.

* Pathologische Gewebelehre, 1875, p. 126.

ATROFHY OF THE HEART. 691

pericardial effusion, &c, are often present. Palpitation, dyspnoea,
and dropsy, are said to occur in cases of acquired atrophy from local
malnutrition. The quantity of blood remains unchanged, and the
small heart obstructs the circulation. When due to a general state,
the heart suffers in common with the blood and the rest of the
system, so that the special failing is unnoticed.

The general conditions associated with atrophy of the heart were,
in part at least, attributed by the earlier writers to the influence of
the cardiac state. Phthisis especially was believed to be entirely due
to the small size of the heart, so often found associated with it. It is
customary now, as already stated, to regard the small size of the heart
as secondary to the general state, and to attribute to it no causative
influence.

Diagnosis. — In determining, post mortem, the existence of atrophy,
weight should be taken as the test. The error of mistaking contraction
for atrophy will thus be avoided. Burns suggested, as a means of
avoiding the same error, a comparison between the size of the heart
and of the pericardium. The size of the body should always be
taken into consideration. It is rarely that atrophy of the heart can
be diagnosed during life. It may be suspected when a weak impulse
and diminished dulness coincide with signs of cardiac failure and
with some recognised causal condition.

Prognosis. — Little can be done to remedy the condition, even when
its existence is recognised. The prognosis is therefore unfavourable,
but it is always subordinate to that of the condition to which the
atrophy is secondary.

Treatment. — The treatment is in the main that of the causal state.
In general wasting j diseases the atrophy of the heart corresponds
to its diminished use, and needs no special treatment beyond general
tonics, cod-liver oil, nux vomica, &c. When secondary to local
changes, little can be done by treatment beyond the removal as far
as possible of the fluid pressing on the heart, or the diminution, by
dietetic management, of accumulations of fat.

HYPERTROPHY OF THE HEART.

By W R. Gowers, M.D.

Synonyms. — Enlargement of the Heart, Dilatation of the Heart (old
writers) ; Active Aneurism (Corvisart) ; Uniform Enlargement of the
Heart, distinguished from dilatation (Allan Burns) ; Hypersarcosis
Cordis (Lallemaud).

Definition. — An overgrowth of the muscular tissue which forms
the walls of the heart. Besides muscular tissue the heart contains
connective tissue and adipose tissue. An increase in either of these
constituents may be, and has been, spoken of as an element in cardiac
hypertrophy. Thus " fatty hypertrophy " and " connective tissue
hypertrophy," or " false hypertrophy," of the heart have been described.
It seems more in accordance with the nomenclature applied to other
organs to consider these changes as allied to degenerations, and to
confine the term "hypertrophy" to increase in the muscular tissue of
the heart. Increased thickness of the endocardium and pericardium,
which often coexists with muscular hypotrophy, and is sometimes
regarded as part of it, is described separately in the articles " Endo-
carditis" and "Pericarditis."

History. — The earliest allusions to enlargement of the heart appear
to be those of Nicolaus Massa in 1559 L and of Vesalius. En-
largement with thickening of the walls was described in the seventeenth
century by Albertini, by our own countryman Mayow, and by Blancard.
Its origin in overwork due to obstruction in the circulation was clearly
pointed out by Mayow, who in 1674 described the dependence of
hypertrophy of the right ventricle on mitral constriction.2

Vieussens3 in 1715 alluded to the origin of hypertrophy of the
left ventricle in the overwork caused by constriction of the aortic

1 Nicolaus Massa, Anatomise Liber Introductorius. Venice, 1559, p. 56.

s " Inasmuch as the blood, on account of the obstruction, could not pass freely into the
left ventricle, it necessarily happened that the vessels of the lungs, and also the right
ventricle, were distended with blood ; as a consequence the heart, jwrticularly the right
ventricle, would have to contract more violently, in order that it might as far as
possible propel the blood through the lungs on to the left ventricle. This again explains
why the walls of the right ventricle were so strong and dense, since this chamber, t>eing
submitted to more violent action, would be enlarged beyond the rest" Mayow,
Tractatus medico-physici, Oxonii, 1674. DeMotu Musculari, cap. vii. The translation
is that of Cockle, On Insufficiency of the Aortic Valves. London, 1861.

1 Traite du Cceur, 1715.

HYPERTROPHY OF THE HEART. 693

orifice, and the effect of obstruction in causing enlargement was sys-
tematically described by Senac in his treatise published in 1749.1

Enlargement from overgrowth without dilatation was mentioned by
Morgagni2 in 1779, by Burserius in 1798,3 and later by Corvisart in
1806, and distinguished by Allan Burns in 1809, who recorded an
example of a heart " weighing several pounds, in which the cavities
were not more capacious than natural." Corvisart gave a clear
description of the various forms of hypertrophy with dilatation, and
recognised the frequency with which the left ventricle is affected.
Although he mentioned the occurrence of hypertrophy without dila-
tation, he did not include it in his account of the forms of enlarge-
ment,4 but described all enlargements of the heart as " aneurisms,"
classifying them as " active " or " passive/' according as there was or
was not hypertrophy. Bertin, in a memoir read before the Academie
des Sciences in 1811,6 pointed out the special character of hyper-
trophy and its isolated occurrence. It was also carefully distinguished
by Kreysig in 1816.6 But in France the nomenclature of Corvisart
continued in use by M£rat, Cloquet,7 and Cruveilhier until, and indeed
long after, the publication of Bertin's treatise on diseases of the heart8
in 1824 gave currency to his distinction of the "concentric," "simple,"
and " eccentric " forms of hypertrophy. Bertin also demonstrated by
microscopical examination that the increase of the heart's substance in
hypertiophy depends on an overgrowth of muscular tissue, and also
endeavoured to show, by a chemical examination of the tissue of the
two ventricles, that the quantity of fat in the hypertrophied muscle
was less than in the normal portion.0 He also ably vindicated hyper-
trophy from some of its supposed consequences.

Avenbrugger in 1763 first employed percussion as a means of
ascertaining and estimating enlargement of the heart. The example
was followed by Corvisart, who translated Avenbrugger's work. Bertin
advocated auscultation as a means of distinguishing the " concentric "
and " eccentric " forms. The alterations in the heart-sounds in hyper-
trophy were, however, first accurately stated by Laennec.10

1 Traits de la Structure du Cceur, de son action ct de ses maladies, par M. Senac
Paris, 1749. Tom. ii., p. 408.

' *' Ventriculus dexter corveam quidem secundum naturam, sed crassissimas parietes
habebat." De sedibus et Causis morborum. Epist. xvii., art. 22. See also Epist.
xxix., art. 20.

3 The Institutions of the Practice of Medicine, by J. Baptist Burserius, of Kamfeld,
1798. Translated by Cullen Brown. Vol. v. p. 312. Edinburgh, 1803.

4 This accounts for Laenuec's assertion that the occurrence of hypertrophy without
dilatation escaped the notice of Corvisart. Bertin pointed out that the condition is
described by Corvisart in a case of aneurism of the aorta. " The left ventricle, without
being so dilated, had much stronger and thicker parietes than usual." On Diseases of
the Heart, Hebb's Translation, p. 283.

8 Mem. de l'Acade'mie Royale des Sciences, 1811.

• Die Krankheiten des Herzens, Theil ii., Abt. i., p. 460.

7 Diet, des Sciences M6dicales, art. Cceur. 1813.

8 Traits des Maladies du Coeur et des Gros Vaisseaux, by R. J. Bertin. Itedige' par
Bouillaud. Paris, 1824. • Loc. cit., p. 300.

10 A Treatise on Diseases of the Chest, Forbes* Trans. 1821, p. 372.

694 A SYSTEM OF MEDICINE.

Varieties.— The hypertrophy may be general, when each portion of
the heart is affected, or local, when only part of the heart is changed.
When the result of the change is a simple increase in the thickness of
the wall, without any change in the size of the cavity, the hyper-
trophy is called " simple ; " when there is dilatation of the cavity as
well as hypertrophy of the walls, the hypertrophy has been termed
"eccentric." " Hypertrophy with dilatation," or "dilated hypertrophy"
are other names which have been applied to this condition. If, on
the other hand, the cavity is lessened in size, the hypertrophy has
been termed " concentric" The existence of this form is doubtful ; it
is probable that the supposed permanent reduction in the size of the
cavity is merely the result of a strong contraction. " Mixed n hyper-
trophy was the designation given by Bertin to the condition in which
one part of a ventricle is thinned and another thickened.

Causes and Pathology. — A. Predisposing Causes. — Strictly speak-
ing, hypertrophy of the heart cannot be said to have any morbid pre-
disposing causes. It is a healthy reaction against a morbid influence,
and the conditions which permit its occurrence are those of health.
Every divergence from a state of health, which does not immediately
excite hypertrophy of the heart, tends to hinder its occurrence. The
only general or distant morbid states which are concerned in its pro-
duction are the antecedents of its exciting causes, and these cannot,
strictly, be regarded as " predisposing." Hereditary taint, sex, and age
influence the occurrence of the exciting causes of hypertrophy, and
render the condition twice as frequent in males as in females ( Walshe),
and frequent in proportion to age, because men are by occupation and
exposure liable to the causes of hypertrophy more than women, and
hypertrophy is frequently the result of degenerative changes, the
tendency to which increases with age.

Four conditions of health may be considered as especially predis-
posing to hypertrophy.

(1) General nutritive energy of the system. This influence is shown
in the tendency of the normal tissue elements to increase, under certain
local stimuli ; its defect by their tendency to waste, to degenerate, and
give place, under the local nutritive stimulus, to tissue elements of
lower vital capacity. This influence is greater in the young than in
the old. Its effect in determining the occurrence or the degree of
hypertrophy is masked by the greater frequency and greater force of
the causes of hypertrophy in later life. It is seen, however, in
the rarity with which considerable hypertrophy is developed in
old age.

(2) Nutritive quality of blood. The influence of this condition is
obvious, and is seen in the distinct increase in hypertrophy which often
follows the administration of haematinics, as iron, and a good supply
of food.

(3) The supply to the cardiac walls of a due quantity of blood.
The force of the circulation within the cardiac walls is proportioned

HYPERTROPHY OF THE HEART. 695

to the distension of the aorta.1 Hence, whatever interferes with the
quantity of blood entering the aorta lessens, ccetcris 'paribus, the capa-
city of the heart for overgrowth ; whatever increases the quantity of
blood sent into the aorta, and increases the tension of the blood in it,
increases the blood-supply to the heart, increases its capacity for
overgrowth. This is no doubt one of the conditions which determines
the great hypertrophy so common in aortic regurgitation. The dis-
tension of the aorta at the end of the ventricular systole, when the
coronary arteries are being filled, is, in that disease, extreme.2

(4) The greater (within limits) the proportional amount of rest of
the heart, the more perfect is its nutrition. The period available for
nutrition is greater when the contractions are infrequent than when
they are frequent. The systole is nearly of the same duration at
different frequencies; increased frequency in contraction is at the
expense of the diastole. Hence infrequent contraction favours the
development of hypertrophy when its exciting cause exists. The
actual influence of this condition is obscured by the increase in the
exciting cause, overwork, which frequency of action involves.

B. Exciting Causes. — As far as is at present known muscular hyper-
trophy has but one immediate cause — increase of work. The opera-
tion of this cause, the " physiological stimulus/1 as it has been termed,
may be traced in almost every instance in which hypertrophy is
found. Each apparent exception becomes conformable to the rule
when the conditions under which the hypertrophy began are accu-
rately known. The over-action of the heart is the cause of its over-
growth. Such over-action may be primary, or it may be secondary to
an increased resistance to its action. Primary over-action commonly
takes the form of increased frequency of contraction. Secondary
over-action is in the form of increased force of contraction. But the
distinction is not absolute, as will appear immediately.

Other causes have been assumed to account for hypertrophy in cases
in which the influence of increased work could not be clearly traced.
An irritative influence of the blood on the heart, leading directly to
its overgrowth, has been assumed in order to account for some cases of
hypertrophy. But there are at present no facts to support the idea that
any blood state, any nutritive influence other than the physiological
stimulus, ever leads to overgrowth of muscular tissue.8

I. Simple Over-action, of the Heart, the conditions of the circula-

1 This was very clearly taught by Corvisart. " The heart . . • will have to drive
forward, through the narrow artery, too great a column of blood . . . which will neces-
sarily react upon the agent which impels it . . . Finally, the coronary arteries as well
as the capillaries of the heart, remaining in a permanent state of fulness, will supply more
nourishing matter to the fleshy . substance of this organ ; whence arise, without doubt,
the increase, at least in part, of its vital energy . . . the greater consistence of the
parietes, and the more vigorous action of the organ." — Loc. cit., p. 60.

3 Milner Fothergill (Diseases of the Heart, p. 65) maintains that the blood-supply
to the heart walls is deficient in aortic regurgitation, because the tension in the aorta
so soon falls. But, from the short course of the coronary arteries, their distension
must be rapid, and related, in degree, to the degree of the tension of the aortic blood,
rather than to the duration of the tension.

3 The conditions of overgrowth in different tissues no doubt vary widely. In some,

696 A SYSTEM OF MEDICINE.

ticm and heart entailing no increased resistance, i.e. no primary increase
of work — is always the consequence of deranged innervation. Its
nervous mechanism is at present ill-understood. It is extremely
doubtful whether a simple increase in the force, without change in
the frequency, of the heart's action, ever results from this intiuence.
Increased frequency is the common result. The more frequent
contractions are often appaieutly more forcible. Such over-
action of the heart is well seen iu simple nervous palpitation, and
most strikingly in exophthalmic goitre. Continuous emotional ex-
citement is a powerful cause of it. It is produced also by the
influence of many agents, such as alcohol, tea, and coffee. It is pro-
duced also by general muscular effort. Effort acts, it must be remem-
bered, in another way, by causing increased resistance to the movement
of the blood.1

Such increased frequency of contraction tends to cause hyper-
trophy only in so far as it increases the total work of the heart. It
does this, however, in more than one way. (1) Part of the work of
the heart consists in the movement of its own mass. No doubt this
is but a small fraction of its total labour, but it is a definite
quantity, and increases directly as the frequency of contraction. (2)
Although simple increase in the frequency of contraction of the heart
does not necessarily increase that part of the heart's work which
consists in the propulsion of the blood, it does practically effect such
an increase. If a heart contracts at twice the normal frequeucy, and
the blood enters the heart at the normal rate, only, say, one-half of
the normal quantity of blood will at each diastole enter, and at each
systole be discharged. The work of the heart in propelling the blood
would thus remain the same. Piactically, however, increased fre-
quency of contraction tends to quicken the whole circulation, so
that under the circumstances assumed, more than half the normal
quantity of blood would at each contraction enter and leave the heart.

hyperplasia of the proper tissue-elements is induced by any local irritant. This has
suggested a generalisation which asserts a common basis for hypertrophy and inflamma-
tion. The conclusion, true of some tissues, is quite inapplicable to muscular fibres. ( VuU
Moxon, Med. Times and Gazette, Nov. 26, 1870.) But the theory has obtained in Ger-
many wide currency and application, so that a recent writer (Zielonko,Virchow's Archiv,
1872) gives, as an example of hypertrophy of the heart, the enlargement which resulted
from the insertion of a seton in its substance, although microscopical examination
showed
Gre<

sometimes

dence which he has adduced is chiefly clinical, and possesses little weight in comparison
with the almost uniform significance of pathological facts.

1 Los mouvemen8 violents dounent souvent plus de masse au cceur de meme que lea
maladies : nous reduirons ces mouvemens aux exercises fntiguants, a l'agitation qui suit
les exces du vin, et u- celle qui causent les passions (Senac, loc. cit, torn, ii., p. 400).
Corvisart recorded his conviction that the passions were the most powerful cause
of organic diseases of che heart, and instanced the influence of the French revolution
in causing the malady (loc. cit., pp. 822 and 328). Statistics furnished by Fair, and
given by Quain in his Lumleian Lectures, show that the deaths of males at all ages
from heart disease have increased fifty per cent, on the increase in population, and that
this increase affects adult life almost exclusively (Lancet, 1872, vol l. p. 392).

HYPERTROPHY OF THE HEART. 697

Hence the tension of the arterial blood becomes increased, and the
pulse fuller and less compressible. Reflex relaxation of the peripheral
arterioles, the natural effect of increased tension, relieves, but often
incompletely, this increased tension. Thus the intra- ventricular pres-
sure and the work of the heart are increased. (3) The heart, acting
thus with excessive frequency, may act also with excess of force. The
increased force may be felt under such circumstances. The heart
"thumps" against the ribs. In the pulse the increased force often
is unnoticed on account of the smaller quantity of blood which
leaves the left ventricle at each contraction. It should be remembered
that many circumstances which increase the frequency, also, at the
same time, increase the force of the heart's action. Muscular effort
is one of these.

This then is the mechanism by which increased frequency of con-
traction may cause hypertrophy. Its total influence is not, however,
great. Increase in frequency of contraction is rarely of long duration
imder circumstances of due nutritive energy, and it is not often that
hypertrophy can be ascribed with probability to simple primary over-
action of the heart.

II. Increased Resistance to the Action of the Heart is unquestionably
the chief cause of its hypertrophy. Such resistance may be in the
form of (1) traction from without, or of (2) pressure within the con-
tracting organ.

(I) As a matter of fact pericardial adhesions are frequently asso-
ciated with caidiac hypertrophy;1 and, according to Wilks,2 with
hypertrophy of the right ventricle much more frequently than of the
left. It is easily conceivable that such adhesions may oppose the
diminution in size, and change of shape, which the heart undergoes
during its contraction. But for such adhesions to hinder a contracting
heart, the external surface of the pericardium must be connected with
more than usual firmness to the adjacent structures. It is not certain,
moreover, that resistance to contraction applied from without has the
same effect as resistance applied within the heart, and the conditions
are so complex that it is impossible to trace the direct influence of
the adhesions in causing the hypertrophy. Dilatation is invariably,
under such circumstances, associated with the hypertrophy of the
heart. It would seem to be a more direct result of the pericardial
adhesion than the hypertrophy, both as the simple effect of the external
traction, and as the result of the weakening of the wall of the heart
by the sub-pericardial changes. But dilatation tends in itself, as will
be shown immediately, to produce hypertrophy, and the hypertrophy
in an adherent heart, without other cause of hypertrophy, is commonly
not more than the dilatation might account for. The effect of peri-
cardial adhesions is considered at greater length, in the article on
Dilatation of the Heart. Their direct influence in causing hypertrophy
must be regarded as possible, but unproved.

1 As Morgagni, Beau, Hope, and others have especially noticed.

2 Guy's Uosp. Rejwrts, vol. xvL, p. 202.

VOL. IV. Z Z

698 A SYSTEM OF MEDICINE.

(2) Increased blood-pressure within the heart during its systole is
the common cause of its muscular over-growth. This is the element
which underlies most of the conditions capable of giving rise to
hypertrophy. This increased pressure may be due to one of two
causes ; (a) the mass of blood to be moved may be abnormally large ;
(b) there may be an abnormal obstruction to the movement of the
blood. The effect of each condition is to augment the resistance to
be overcome by the contracting fibres — to increase the work of the
heart.

(a) The mass of blood to be moved may be abnormally large. This
condition exists in all forms of over-distension of the heart. Dilata-
tion cannot exist without an increase in the work of the heart.
Hence hypertrophy is its almost invariable concomitant — invariable
when the nutritive conditions are such as to render growth of muscular
fibre possible.

The mechanism of over-distension is considered fully in the article
x>n Dilatation of the Heart. It may be direct or indirect. It is direct
when a cavity is over-filled by the contraction of an over-distended
chamber behind it. Thus in mitral regurgitation the left ventricle is
over-filled by the contraction of the over-distended left auricle, and be-
comes dilated and hypertropliied; or the over-distension may be indirect,
the result of a supply of blood to the chamber from a double source —
the regurgitation of blood into the chamber and its supply in the
normal course of the circulation. Thus the left ventricle becomes
over-distended, dilated, and often enormously hypertropliied in aortic
regurgitation ; and the left auricle becomes dilated and hypertropliied
in mitral regurgitation. So, too, in dilatation from the weakening of
the wall consequent on pericarditis, hypertrophy commonly ensues.
No doubt in these conditions of dilatation the whole of the blood is
not always expelled from the ventricle at each systole, but the intra-
cardiac pressure during the systole is still increased, and with it the
work of the heart.

Plethora has been supposed to cause cardiac hypertrophy. Nie-
meyer points out that the transient plethora induced by a hearty meal
with much fluid may, if habitually repeated, have such an influence.
The action of the kidneys commonly prevents any permanent dis-
tension of the vessels from tliis cause.

(b) There may be an obstruction to the movement of the blood
superadded to that which exists in health. This obstruction may be
situated within or without the heart. Within the heart, it may be at
the orifice by which the blood leaves the chamber affected. Thus an
obstruction at an auriculo-ventricular orifice will cause hypertrophy of
the corresponding auricle ; obstruction at the orifice of the pulmonary
artery will cause hypertrophy of the right ventricle ; obstruction at the
aortic orifice will cause hypertrophy of the left ventricle. In all these
cases dilatation may be conjoined with the hypertrophy, and increase
its amount.

The obstruction may be outside the heart. It may be in the larger

HYPERTROPHY OF THE HEART. 699

arteries, the aorta and pulmonary artery. Their calibre may be
reduced by pressure upon them (as by an aneurism of another vessel),
or by constriction due to changes in their walls.1 The hypertrophy
which occasionally occurs in long-continued displacement of the
heart, whether from pleural effusions or deformities of the thorax,
consequent on curvatures of the spine, &c, is probably due
chiefly to the increased obstruction in the great vessels from their
displacement and altered course.2

Aortic aneurism has been regarded as a cause of hypertrophy
of the left ventricle since the days of Corvisart. The association of
the two has frequently been noted, and has been referred by
Niemeyer to the law in physics according to which the resistance
encountered by a liquid moving through a tube is increased if the
tube be suddenly expanded, just as if it be contracted. But it is a
matter of considerable doubt whether hypertrophy does occur as a
simple consequence of aortic aneurism. Senac long ago expressed a
doubt upon the subject.3 Stokes affirmed that "we have no
reason to believe that the existence of aneurism in any portion of the
aorta throws additional labour on the heart, and hence we commonly
find a small heart co-existing with *a vast aneurism."* Walshe
also regarded the hypertrophy as an occasional consequence, and not
invariable even when the sac of the aneurism was situated near the
sigmoid valves. The observations of Axel Key,5 indeed, suggest the
question wrhether hypertrophy of the heart is not more common when
the aneurism is far from, than when near the heart. He has recorded
eighteen cases of aneurism near the heart, in not one of which was
there hypertrophy of the left ventricle. In most of the cases, indeed,
the muscle was more or less thinned, with or without slight dilatation,
especially of the lower part of the cavity. Considerable dilatation
seemed related to disease of the aortic valves, not to the aneurism.
In several cases the cavity of the ventricle was positively diminished
in capacity, although the walls were thinned. In some instances the
muscle of the conus arteriosus was thick, while the rest was thin.
The atrophy of the muscular tissue was most marked in some cases in
which the aneurism lay near the heart. He suggests as an explana-
tion of this singular atrophy of the left ventricle, the pressure of the
aneurism on the pulmonary artery, lessening the amount of blood
reaching the left ventricle, and the withdrawal from the circulation
of the blood contained in the sac of a large aneurism.

1 Hypertrophy of the loft ventricle Las been produced artificially by Zielonko, in the
guinea-pig by tying a ligature round the aorta, and thus reducing its calibre. Virchow's
Archiv, Bd. 62, Heft I. p. 22.

* See Hilton Fagge, Path. Trans., vol. x?ii.

3 " It is certain Jhat the dilatation of these vessels (aorta and pulmonary^artery) have
not always the consequence (of causing enlargement of the heart).'1 lie goes on to
describe a case in which the aorta was dilated to the size of a head, from the arch to the
diaphragm, in which the volume of the heart was normal. Senac, Traite*, &c, 1749,
torn, ii., p. 407.

4 Diseases of the Heart and Aorta, p. 579.

* Nord. Med. Ark. 1869, I. 4, Nr. 22, and Schmidt's Jahrbuch, vol. 150, p. 21.

z z 2

700 A SYSTEM OF MEDICINE.

Degenerative changes in the arteries cause a considerable increase
in the total work of the heart, and are effective causes of hypertrophy.
The increased resistance which they produce is due to the loss of
elasticity in the vessels, their more tortuous course, and the increased
friction from roughening of their inner surface. In health the elastic
vessels yield before the blood which is thrown into them. When
elasticity is lost the vessels approximate to rigid tubes, and the resis-
tance they present is consequently increased. By the increased
tortuosity of the vessels, due to the loss of elasticity, their absolute
length becomes greater, and the friction of the blood against the wall
of the vessel is also increased. These degenerative changes are
usually found, in greater or less degree, after middle life, and are
probably the cause of the increase in the thickness of the left
ventricle, -which has been said by Bizot1 to occur during the later
period of life. Degenerative changes may be a consequence as well
as a cause of cardiac hypertrophy, the result of the increased strain
to which the vessels are exposed. This fact, which will be considered
presently, must not be forgotten in estimating the significance of the
association.

The obstruction may be situated in the minute arterioles and
capillaries. In certain diseases of the lungs obstruction from this
cause may be traced. In emphysema many vessels are destroyed, and
those which remain are elongated and narrowed by the over-distension
of the air-cells. The obstruction to the passage of the blood through
the lungs is thus very much increased, and hypertrophy and dilatation
of the right ventricle result, and may be carried to a high degree.
Hypertrophy of the heart is not infrequent in phthisis ; Quain
states that in 171 cases it was present in 25 per cent, of the males,
7 per cent, of the females. The conditions of lung to which it is
related have not yet been ascertained, but in cirrhosis of the lung it is
especially frequent ; the compression and destruction of the minute
vessels by the contracting tissue produce the obstruction. Compres-
sion of the lung tissue by pleural effusion is said to have a similar
effect. In all these conditions, if long continued, hypertrophy of
the right ventricle may occur.

Long-continued muscular effort entails cardiac hypertrophy. As
Clifford Allbutt and Myers have shown, the influence of this cause
cau often be distinctly traced, especially (Milner Fothergili says)
among those who work with the arms. Animals frequently afford
instances of the remarkable effect which this cause is capable of pro-
ducing. The most celebrated instance is that of the Irish greyhound
" Master Magrath," the heart of which bore three times its normal
proportion to the body-weight, and no cause for the enlargement
but extreme and long-continued exertion could be discovered.2 The
increased work in which the hypertrophy arises is probably in
part the result of the increased frequency and force with which, in

1 Memoirs de la Sociite Medicale d'Observ. de Paris, 1836.
1 Haughton, British Medical Journal, Jan. 20, 1S72.

HYPERTROPHY OF THE HEART. 701

consequence of the respiratory needs, the heart acts. But it is in
part the result of the compression of the capillaries of the muscles
by the contracting fibres, and also the result of the compression of
the arterial trunks by the rigid muscles. The total resistance to the
action of the heart is thereby considerably increased. This resistance
is not a matter of conjecture. Increase in arterial pressure during
general muscular contraction has been demonstrated experimentally
by Traube.

During pregnancy the addition of the placental to the systemic
circulation involves a considerable addition to the work of the heart.
Larcher1 found, on examination of the hearts of 100 women who died
in child-birth, that the wall of the left ventricle was invariably
thickened. The average thickness was 015 m. (about § inch). His
observations have been confirmed by the clinical investigations of
Duroziez, who found that the greater the number of pregnancies the
more permanent is the enlargement. He asserts that the enlargement
continues through the whole of the lactation period. Friedreich,
however, expresses some doubt on the subject.2

The remarkable hypertrophy of the heart which is met with in
Bright's disease must be considered among those which result from
obstruction to the flow through the minuter vessels. It occurs in all
forms of chronic kidney disease, most frequently in the contracted
kidney, least frequently in the lardaceous form. According to Grainger
Stewart, it is invariable in the last stage of the acute inflammatoiy
affection, in which, the disease having assumed a chronic form,
the kidney undergoes reduction in bulk.

The hypertrophy which occurs in this condition is confined to the
left ventricle, and is often uncomplicated by dilatation. It is frequently
considerable in amount. Among such hearts the best examples of
simple hypertrophy are met with. After death the heart often
remains firmly contracted, and the characters of a concentric hyper-
trophy are simulated. Dilatation may co-exist with the hypertrophy
in consequence of coincident degeneration.

The association of this hypertrophy of the heart with kidney
disease was first pointed out by Bright in 1827s as so remarkable
that some causal connection between the two must exist, and he
afterwards, in 1836,4 expressed his opinion " either that the altered
quality of the blood affords irregular and unwonted stimulus to the
organ immediately, or that it so affects the minute and capillary
circulation as to render greater action necessary to send the blood
through the distant subdivisions of the vascular system." The latter
theory is that which has obtained general acceptance, with certain
modifications to be alluded to more fully. Modern investigation,
while it has extended our knowledge of the conditions under which

1 Archives Gen. de Med., Mars 1850, and note by Larcher appended to a paper by
Meniere, Ibid, torn, xvi 1828, p. 521.
* Herzkrankheiten, p. 288. s Med. Reports, p. 23.

4 Guy's Hosp. Reports, vol. i. p 397.

702 A SYSTEM OF MEDICINE.

the hypertrophy arises, has scarcely carried us further in our
explanation.

The most important addition to our knowledge is certainly the fact
that increased tension of the arterial blood commonly occurs in those
cases of Bright's disease in which hypertrophy of the heart is so
often found. The hardness of the pulse in such cases had long been
remarked, but its significance was not generally recognised until the
sphygmograph, by supplying a measure of its degree, drew attention to
its importance as supplying independent evidence of an obstruction to
the movement of the blood through the smaller vessels.

Traube,1 who first called attention to the significance of the in-
creased arterial tension, assumed, in effect, that the increased resistance
within the kidney was the cause of the obstruction. The theory has
been largely accepted in Germany, but its manifest inadequacy has pre-
vented it from meeting even partial acceptance in this country. It is
said2 that Traube himself before his death ceased to hold it in its
original form.

In the smaller arteries a remarkable change of structure was
pointed out by George Johnson in 1850 as hypertrophy of the
muscular coat.3 First discovered in the kidney, the change was soon
found to be general throughout the system. The occurrence of such
increased thickness of the walls of the arteries is now generally
admitted, and the view that the thickening is due to hypertrophy of
the muscular coat has received very wide confirmation. Muscular
over-action being the only kuown cause of muscular hypertrophy,
Johnson at first ascribed the vascular change to the same cause as the
hypertrophy of the heart — the resistance to the movement of the
blood through the capillaries. It was assumed that the arteries
by their contraction aided the circulation of the blood, and over-
acted to overcome the increased resistance. But with the fall of the
theory of arterial propulsion, this explanation became untenable. The
function of the muscular coat of the vessels being, as far as is known,
the adjustment of the calibre of the vessel, permanent spasmodic
contraction became the only explanation of the hypertrophy, and has
been for many years ably maintained by Johnson. That such
spasm exists is, on Johnson's facts, highly probable, and may, the
writer believes, be actually seen in the arteries of the retina in most
cases of Bright's disease in which a high arterial tension exists. The
effect of such spasm must be an increased resistance to the movement
of the blood in the arteries, an augmentation of its tension. Instead
of aiding, it thus directly opposes the action of the heart. That it is
the sole cause of the increased resistance may be doubted. Even if it

1 Zusammcnhang zwischen Herz u. Nierenkrankheitcn, Berlin, 1856.

8 By Milner Fothergill, Diseases of the Heart, p. 2S(>. The inadequate character
of Traube's theory led Bamberger into a denial of Traube's facts, relative to the
increased obstruction to the movement of the blood, and consequently increased arterial
pressure. But these facts may now be considered to be established, and the details,
of ^the controversy between Traube and Bamberger have ceased to be instructive.
Chir. Trans., vol. xxxiii., 1850, p. 107.

HYPERTROPHY OF THE HEART 703

were the only cause, the difficulty is not lessened, for we arc almost
as ignorant of its origin as we are of the nature of any obstruction
due to the changed composition of the blood. The natural effect
of increased arterial tension, increased endocardial pressure, is im-
mediate relaxation of the minute arteries, and freer circulation. The
spasm of the vessels under these circumstances is therefore a pheno-
menon very difficult to explain, ^udwig asserts on experimental
grounds that it is due to the action of the retained urinary salts on
the vaso-motor centre.

The existence of the hypertrophy of the muscular coat of the
arteries has, however, been denied by iGull and Sutton,1 who ascribe
the thickening to a "fibrosis," and attribute the resistance to the
movement of the blood to the obstruction in the vessels due to
the inelasticity of this tissue. They do not regard the fibrosis as
the consequence of the renal disease, but as a primary general change, of
which the affection of the kidney is only one local instance. This theory
of the primary general character of Bright's disease accords very well
with the phenomena of some cases, but as an explanation of all cases
of contracting kidneys it is open to some objections apart from the
weight which must be attached to Johnson's observations. In
many cases of contracting kidney there is certainly fibroid over-growth
to be found widely distributed, but the degree of change in the kidney
is incomparably greater than that in other organs, so as to suggest
strongly the idea of a primary affection of the kidney. Another
fact to be taken into consideration is that, whatever be the cause
of the hypertrophy of the heart in the contracted kidney, a similar
hypertrophy results as a remote consequence of kidney disease un-
questionably local in its origin. In later stages of an acute nephritis,
hypertrophy of the heart is even more frequent than in the primary
contracting kidney, and is associated with the same increased arterial
tension.

The conclusion then seems to be that hypertrophy of the heart
occurs in kidney diseases as a result of increased arterial blood-
pressure, the result of some obstruction to the movement of the
blood in the minute vessels ; that such obstruction is in many cases
the indirect consequence of the kidney disease ; that it is accom-
panied in most cases with a morbid state of the smaller arteries, to
which it is in part to be ascribed.

Lastly, in some cases, the obstruction causing the hypertrophy of
one ventricle may be situated, not in the vessels, large or small, but
beyond them, in the other side of the heart. Thus in mitral ob-
struction, the right ventricle is very constantly hypertrophied ; in
obstruction in the pulmonary system and right side of the heart, the
left ventricle may become hypertrophied. The obstruction may even
be on the same side of the heart, and act through both systems of
vessels, the pulmonary and the systemic. Thus mitral regurgitation

1 MecL-Chir. Trans vol. lv. 1872.

704

A SYSTEM OF MEDICINE.

may, as Friedreich has remarked, cause not only congestion of the
lungs, distension of the right side of the heart, over-611ing of the
systemic venous system, but increase on the tension of the arterial
blood, and thus cause an increase in the work of the left ventricle, and
an increase in its hypertrophy. It is not easy to understand the me-
chanism by which this arterial distension is effected, but as a clinical
fact it is unquestionable, and occurs especially in cases of mitral
regurgitation, in which the left ventricle is greatly dilated and hyper-
trophied. It is perhaps to be ascribed to the effect of the secondary
dilatation of the right side of the heart in augmenting the mechanical
obstruction. A tracing from a pulse in such a condition is shown
in Fig. 1, p. 714.

It may be convenient to group the causes of hypertrophy which
have been described, first, according to their position (Table I.),
secondly, according to their effect (Table II.).

TABLE I.

EXCITING CAUSES OP CARDIAC HYPERTROPHY.

Over-action

f Nervous palpitation, effect of

, primary ( alcohol, tea, coffee, Ac,

I muscular effort (in part).

Exocardial Pericardial adhesions.

Over-action,
secondary
to increas-
ed resist-
ance . .

, Increase in mass of blood to be moved

k Endocar-
dial .

{Dilatation of heart, primary
or secondary to regurgita-

tion, Ac.

' W!Sdl*Ulyhe^ ^^ !mi } Contraction °f orifice*.

Incroa.se in ob-
struction to
movement of x
blood, situ
at*:d . .

Outside tho (
heart.

Arteries
' large,

Arterial

system

generally.

Constriction of aorta, or pul-
. monary artery, aneurism (?),
\ displacement

(Degenerative changes, loss of
elasticity, atheroma, Ac.

Emphysema, \ Pulmonary,
cirrhosis, ^ acting on

Arterioles

and
capillaries.

pleural ef- ( right ven-
tricle.

fusions . )
( Muscular ef- \

fort (in pt) I General, ae-

Sreunancv, S ting on left
right's [ ventricle,
disease. . I

Within heart, acting circuit-
ously, through circulation. Valvular disease, &c.

TABLE IT.

CAUSES OF nYPERTROrnY.

Affecting-
All parts of Heart —

Over-action from nervous and toxic influences.
Dilatation of cavities.
Displacement of* heart.

HYPERTROPHY OF THE HEART. 705

Left Ventricle —

Mitral regurgitation.

Constriction an<l regurgitation at aortic orifice.
Constriction or compression of aorta.
Aneurism of aorta (?).
Degeneration of arterial system.
» Renal disease.

Pregnancy.
Muscular efforts.

Valvular disease of right side of heart, and all causes of dilata-
tion of right ventricle.

Left Auricle—

Mitral constriction and incompetence.

Right Ventricle —

Constriction or regurgitation at pulmonary orifice.
Constriction of or pressure on pulmonary artery.
Degeneration of pulmonary arteries.
Lung diseases, obstructing, compressing, and destroying vessels.

Chronic bronchitis.

Emphysema.

Cirrhosis.

Pleural effusion.
Affections of mitral orifice.

Right Auricle — Regargitation and constriction at tricuspid orifice.

By what mechanism the increased work leads to muscular over-
growth we have little knowledge. The theory has been put forward
that the effect depends on reflex dilatation of the coronary arteries.
Increased blood -pressure within the heart is known to inhibit, by the
depressor nerve, the vaso-motor system, causing dilatation of the minute
arteries, and freer circulation. The coronary arteries are believed to par-
ticipate in this effect, and the readier circulation through them has
been thought to be the cause of the hypertrophy. That such an action
occurs is most probable, and it is probable that thus the nourishment
necessary for overgrowth is supplied. But that it is not the sole cause
is almost certain, from the fact that if the wrork of a muscle remains
the same, a larger supply of blood to it has no power to increase
the muscular tissue. We are driven to assume a direct influence of
the increased contraction on the growth of the fibre. The average
force exerted habitually by a muscle is far below its possible maximum
at any moment. It would seem as if this average force, and the bulk
of the muscle, were proportioned, that an increase in the habitual force
leads, in clue nutritive conditions, to muscular over-growth. Whether
this over-growth is the result of the direct mechanical stimulus to the
contracting fibre, or whether it is the result of a reflex influence exerted
through the nervous system, and excited by the increased pressure on
the endocardium or by the increased tension on the contracting fibres,
we do not know.

One condition is, however, essential for the development of hyper-
trophy— time. A certain period is necessary for growth of old, or
for the development of new tissue. Dilatation may occur quickly ;
hypertrophy can only take place slowly. Hence the rapidity with
vhich an increased resistance is developed largely influences the

706 A SYSTEM OF MEDICINE.

resulting condition of heart. Obstruction is usually slowly developed,
regurgitation may occur rapidly, and this is one reason why the
former entails so much simpler an hypertrophy than the latter. So,
too, in the obstruction which is developed in the most gradual
manner, that of Bright's disease, uncomplicated hypertrophy is
commoner than in any other morbid state. The related conditions
of origin of hypertrophy and dilatation are considered more fully in
the article on Dilatation.

A few cases of hypertrophy have been recorded in which no me-
chanical cause for the hypertrophy could be discovered. Their pro-
portion to the cases of hypertrophy in which a mechanical influence
can be traced is very small, so small that it is probable that some
such cause may have existed and have escaped observation. Some
of the cases were recorded before the relation of hypertrophy of the
heart to kidney disease was well known, and the existence of the
latter may easily have been overlooked. In Bristowe's case of
" hypertrophy without sufficient cause/' recorded in the Path. Trans.,
vol. v., p. 82, the heart, which weighed twenty-seven ounces, was
uniformly enlarged and hypertrophied without local disease, but
the kidneys were reduced in size, and granular, and presented atrophy
of the Malpighian bodies. In other cases the increased bulk of the
organ is due to an increase in the fibrous, as well as in the muscular
tissue. Such was the case in a heart weighing forty ounces, preserved
in St. George's Hospital Museum, and supposed to be an example of
true hypertrophy, until Quain examined it, and discovered its real
nature.

Pathological Anatomy. — Hypertrophy may occur in each division
of the heart, but varies in different parts, both in the frequency of its
occurrence and in the degree commonly attained. The comparative
affection of the different parts of the heart depends partly on the
frequency and degree with which the causes of hypertrophy affect the
different portions, and partly on the amount of muscular tissue each
part possesses, and by which it is enabled to resist rather than yield
to the internal pressure, which is the cause of the hypertrophy. The
left ventricle is that affected most frequently, and in the greatest
degree. Next in frequency and degree comes the right ventricle : then
the left auricle ; lastly, the right auricle. It is rare for the hypertrophy
to be general, and to affect all parts of the heart. More commonly it
is partial, affecting one part only. The increase in the weight of the
heart is the invariable characteristic of hypertrophy. Since the healthy
heart consists almost exclusively of muscular tissue, over-growth of
that tissue cannot occur at the expense of any other constituent,
and must result in an absolute increase in the weight of the heart,
proportioned to the hypertrophy.

There is also in most cases an increase in the size of the heart. If the
cavities of the heart are unaltered, the increase in its size is proportioned
to tho hypertrophy. This is the case in the so-called "simple" hyper-

HYPERTROPHY OF THE HEART. 707

trophy. The cavities rarely, however, remain unchanged. They are
believed by some authorities to be occasionally diminished in size. The
heart then may be of normal size, or may be very slightly enlarged.
The increased thickness of the walls is at the expense of the cavity,
which may become reduced to very small dimensions, it is said
incapable of containing a walnut. This constitutes the concentric
hypertrophy of Bertin. Lastly, the cavity is, in the majority of cases,
dilated, and the dilatation adds greatly to the size of the heart. This
constitutes the eccentric variety of Bertin.

Concentric hypertrophy of the heart has, in most recorded examples,
been local, and confined to the left ventricle. Its existence has,
however, been the subject of much discussion. It wras thought to be
common until Cruveilhier, in 1833,1 pointed out how perfectly its charac-
ters were simulated by hearts the subjects of simple hypertrophy and
post-mortem contraction. When the heart is at the time of death in
systole, the final contraction is fixed by the rigor mortis, the thickened
walls are, by their contraction, further increased in thickness, and so
remain, and the cavity is reduced to very small dimensions. The resem-
blance of such a heart to "concentric hypertrophy " is admitted by all
authorities. Cruveilhier maintained that all cases of the supposed
change are thus explicable, that the cavity of such a ventricle can
always be opened out with the fingers, and in this he has been followed
by Budd 2 and many later pathologists, who urge further that the
contraction of the cavities supposed to occur is incompatible with
the absence of symptoms of impeded circulation of the blood.
Other authorities believe that concentric hypertrophy does rarely
occur. Skoda, Eokitansky, Bamberger, Forster, Walshe are all of
this opinion. They assert that hearts are occasionally met with, the
cavities of which are so small that the hypothesis of mere contraction
is untenable, and is not verified by the effect of post-mortem decom-
position, which should relax completely the contraction of rigor
mortis. Dechambre and Forget maintained that such hearts could
not be expanded, as simply contracted hearts can be.

The balance of recent pathological evidence is certainly opposed
to the occurrence of concentric hypertrophy. It is to be noticed
that the careful pathological observation of recent years has brought
to light few supposed examples of this change. One specimen only
has been brought before the Pathological Society.3 There is in
the museum of University College a specimen (No. 2,140) which has
been described as itself establishing the existence of the change
But on close examination its characters are far from satisfactory
evidence — it is obviously merely an example of the permanent con-
traction of a heart the subject of simple hypertrophy.4 The known

i Diet, de Med. et de Chir. Prat., art. Hypertrophic.

2 Med. -Chir. Trans., 1838.

3 By AVickham Leg£. Trans. Tath. Soc. vol. xxv., p. 105. The specimen presented
contraction of the mitral orifice. Details of the measurement and weight of the heart
are not given.

4 The specimen in question has been appealed to as so decisive, and illustrates so well

708 A SYSTEM OF MEDICINE.

mechanism of hypertrophy renders the origin of this form of over-
growth scarcely conceivable. If hypertrophy is the result of increased
work, increased intra-ventriciilar pressure, the volume of the blood
within the ventricle can scarcely have been lessened ; but without such
lessening, reduction in the size of the cavity cannot have occurred.
Thus the increased thickness of the wall and lessened size of the
cavity are, on etiological grounds, almost incompatible. Moreover,
post-mortem decomposition relaxes hearts, firmly contracted, in a
very imperfect manner.

Concentric hypertrophy of the right ventricle has been described
as an occasional consequence of some congenital malformations of
the heart

Eccentric Hypertrophy. — The thickening of the wall in eccentric
hypertrophy is not always conspicuous. The cavity is dilated, and the
superficial area of the wall increased, and the increase in tissue may be
only enough, or even not enough, to maintain the normal thickness of
the wall. Thus the wall of the left ventricle may be so hypertrophied
as to lead to a considerable increase in the weight of the heart, and
yet may be only of the average thickness. In estimating the presence
and amouit of hypertrophy, therefore, the size of the cavity must
always be taken into consideration. In one of the heaviest hearts
recorded, a heart much dilated, the thickness of the wall of the left
ventricle was not more than is common in less dilated hearts of
only half the weight.

The increase in the size and weight of the heart is often very
considerable. In estimating »them it should be remembered that the
normal average weight varies according to the sex? age, size of the
individual. These are considered elsewhere (art. " Size and Weight
of the Heart") A heart which exceeds 9 oz. in a man or 8 oz. in

the characters which have led to the establishment of this variety, that it is worth
detailed description. In the circular glassjar in which it had been preserved for many
years it certainly had striking proportions. The walls appeared of great thickness, and the
cavity " scarcely capable of containing a hazel nnt. " When removed from the jar it appeared
considerably smaller. Its weight, with the root of the aorta, is 11} oz., but it has been
kept for many years in spirit. The external length of the ventricle is 4 inches. The
heart has been divided transversely midway between the base and apex of the left
ventricle. The diameters of the section are antero-posterior 2£ inches, lateral 3 inches.
It is evidently a firmly contracted heart, for the cavity of the right ventricle is a mere
curved line. The cavity of the left ventricle is, on close examination, stellate ; from the
centre thrco linear branches radiate, and can be opened up. Between them lie the
enlarged papillary muscles. On measurement with a wire, the circumference of this
stellate cavity, following its branches but excluding the loose papillary muscles, is 4$
inches. But the most conclusive evidence is afforded by the thickness of the walls
measured at the extremities of the radii of the cavity. On the left side the wall measures
| of an inch, in front and behind just J inch in thickness. After every allowance has
been made for the effect of the spirit, it seems clear that the thickness of the wall is only
a little above the normal. The increased weight is proof that the extent of the wall
cannot have been below the normal. It is clear also, from the state of the right ventricle,
that the heart is firmly contracted, and also that the circumference of the inner surface of
the left ventricle — the test of the actual reduction in size of the cavity —is little, if any,
less than the normal. It seems, therefore, to be merely an example of firm contraction
iu a heart the subject of moderate simple hypertrophy. The history of the specimen is
not known. *

HYPERTROPHY OF THE HEART. 709

a woman, probably possesses an excess of some constituent, in most
cases of muscular tissue. A common weight for hypertrophied hearts
is 12-16 oz. Hearts are occasionally seen of much greater weight,
especially when dilatation extends the area, and hypertrophy the
thickness of the cardiac walls. Under these circumstances the
enormous " bovine " hearts are met with. Walshe has met with one
weighing 40 oz. ; Lancisi mentions one which weighed, emptied of
blood, two pounds and a half; Croker King one of 44i oz. ; Austin
Flint one of 46 oz., while hearts weighing 46J oz. have been shown
by Bristowe and by David at the Pathological Society. The
enormous weight of five pounds., mentioned by Lieutaud, must be
regarded as doubtf uL How much more then the '• quinze livres " of
Marchetis ! l

The shape of the heart is altered according to the part affected. If
one ventricle is more affected than the other, that which is the more
hypertrophied forms a larger share of the apex than in health, and
the chief enlargement of the heart is on the side of the affected
ventricle. Thus in simple hypertrophy of the left ventricle, the
extremity of that ventricle extends beyond the other, so as alone to
constitute the apex, while increased width results from the lateral
enlargement. The resulting shape resembles an obtuse-angled triangle
when the heart is relaxed, an elongated ovoid when partially contracted.
In hypertrophy of the right ventricle the extremity of that ventricle
extends to the apex of the heart, but does not usually pass beyond
the other. Hence the apex is much rounder than in health, and
may be indistinguishable. When dilatation is joined to the hyper-
trophy, the width of the heart is much increased, and the transverse
may exceed the vertical diameter. This is especially the case when
the right ventricle is affected, when the heart may assume an almost
spherical shape. Hypertrophy of the auricles is never sufficient to
alter the shape of the heart; the efiect of their dilatation is considered
elsewhere.

The increase in the thickness of the wall is in direct pro-
portion to the amount of hypertrophy, but in inverse proportion to
the amount of dilatation. The hypertrophy is usually so much in
excess of the dilatation as to cause an absolute increase in the
thickness of the wall. This is commonly greater in the outer wall
than in the septum. In the ventricles the trabecule and papillary
muscles usually participate in the hypertrophy, and, it is said, to a
greater extent in the right than in the left ventricle. Sometimes they
are thinned, when the heart is dilated.

In health the thickness of the ventricular wall varies considerably

1 Quoted by Senac, loc. cit., torn, ii., p. 408. BelHngham is said, by several writers,
to have met with a heart weighing 80 oz. The only ground for the assertion seems to be
that BelHngham states that he had seen a heart pieserved in the museum of St. George's
Hospital which was said to weigh five pound?. This seems to refer to the large heart
alluded to by several writers and mentioned above (p. 706) as lately examined by
Quain and found to weigh 40 oz.

710 A SYSTEM OF MEDICINE.

in different parts. The average thickness of the wall of the left
ventricle is about half an inch in men, rather less in women. The
measurement should be always exclusive of the papillary muscles, and
the place at which the measurement is made should always be
specified. The increase is usually greater towards the base than towards
the apex. Hope pointed out that the greatest thickening is a little
above the middle of ventricle, at the place where the columnae carneae
are inserted. Thence it decreases suddenly towards the aortic orifice,
gradually towards the apex of the heart. Occasionally the reverse
obtains, especially in aortic regurgitation (Walshe), and the wall is
thicker towards the apex than towards the base.

When the wall of the left ventricle measures three-fifths of an inch
in thickness it may be considered hypertrophied. An increase in the
average thickness to three-quarters of an inch, or an inch, is not
uncommon. An inch and a quarter is occasionally reached, and
it is said, an inch and a half, or even two inches. The larger
dimensions were probably in cases in which there was little dilatation,
and the heart was contracted. In the large heart described by
Bristowe, the weight of which was forty-six and a half ounces, the
wall of the left ventricle was only |ths of an inch in thickness
at the base; the length of the cavity of the ventricle being six
inches.

The right ventricle yields readily to internal pressure, and presents
a marked increase in the thickness of the wall much less frequently
than the left ; simple hypertrophy is very rare. The average normal
thickness of the wall is two-and-a-half lines in men, two lines in
women. When hypertrophied it is often a third, or half an inch in
thickness, and even in rare instances three-quarters of an inch, an
inch, and even, it is said, an inch and a quarter (Bertin, 88th case,
"eleven to sixteen lines.") The numerous columme camera are
•commonly much thickened. The cavity is usually enlarged, but may
be lessened in rare cases; probably, however, only in cases of mal-
formation. When the ventricle is thus hypertrophied, and the left
ventricle is dilated, the two may, as Morgagni and Bertin remarked,
seem to have become transposed.

The left auricle is not unfrequently hypertrophied. The average
. normal thickness of its wall is one line and a half; where hypertrophied
it may reach two to three lines. The right auricle is rarely hyper-
trophied, and always in least degree. The average thickness of its
walls is one line; when hypertrophied it may attain one-and-a-half or
two lines. The auricles have never been found to present contraction
of their cavity.

In pure hypertrophy the part changed is of firm consistence, firmer
than the normal heart, so that the walls do not collapse when cut
across. It presents little deviation from the normal colour, it is some-
times a little darker. Such unmixed hypertrophy is rare. More
commonly the tissue has undergone degeneration, and is paler and
softer than normal, sometimes generally, sometimes partially. Koki-

HYPERTROPHY OF THE HEART. 711

tansky points out that in the hypertrophy of the ventricles the
changed wall of the right ventricle is always tougher than that of
the left.

The hypertrophied wall of the heart usually contains more fibrous
tissue than the healthy wall. The tissue lies between the primitive
bundles, separating them, and here and there forms more extensive
tracts. This change, when more considerable, is considered as " fibroid
degeneration/' It is more abundant in the wall of the right ventricle
than in that of the left, and doubtless is the cause of its greater
consistence.

The nature of the change in the muscular fibre in hypertrophy has
been the subject of much discussion. Does the increase in the size
of the heart depend on an increase in the size, or in the number of
fibres ? The evidencei in some degree conflicting, is on the whole
strongly in favour of the view that the increased thickness of the wTall
is due solely to increase in the number of the fibres constituting it,
i.e. to the formation of new fibres. The chief evidence of an increase
in the size of the fibres is obtained from the measurements of Hepp,1
still quoted as authoritative, and who asserted, and gave measure-
ments to show, that the average thickness of the fibres in hypertrophy
is about four times the thickness of the fibres in health. This con-
clusion, however, by itself suggests a fallacy, since the average
thickness of the wall in hypertrophy is less than double the average
normal thickness. Vogel and Henle, Rindfleisch and Walshe con-
clude that there is no increase in the size of the fibres, while Eobin
thinks that there is a slight increase, although not enough to
account for the increased size of the heart. Wilks and Moxon are
convinced that the chief share in the increase in size is due to
increase in number. Considerable weight must be attached to the
careful observation of Zielonko,2 who finds that the average of a
large number of measurements of the fibres of hypertrophied hearts
is a little less than the average of the normal fibre. His observa-
tions also corroborate the fact (long before stated by Forster) that
the normal fibres are smaller in early than in later life, i.nd are
increased in size by good general nutrition. The writer has 1'cund
on direct enumeration of the fibres in a transverse section of the
wall that their number is in the main proportioned to its thickness.
The conclusion appears justified that there is no increased size
of the fibres in hypertrophy, that the over-growth of the heart is
entirely dependent on the development of new and less perfectly
nourished tissue elements, liindfieisch suggests that they may arise
by fissuring of the pre-existiug fibres. He has observed that the
square cells, of which the muscular fibres of the heart have been
shown to consist, contain several nuclei, instead of a single nucleus,
as in health.8

1 Zcitschrift fur rat Med. 1S54, p. 257.

3 Virchow's Archiv, 1W. (J2, Heic I. p. 29.

* Patkologiste Gewcbekhre, Viertc Aufl. 187?, p. K3.

712 A 8YSTJSM OF MEDICINE.

Symptoms. — Cardiac hypertrophy gives rise to certain distinctive
physical signs, and may be accompanied by certain definite symptoms.
These signs and symptoms depend on the increased size of the heart,
and on the increased force with which it acts. They vary according
to the part of the heart which is affected, and according to the amount
of dilatation which is associated with the hypertrophy. It will be
convenient to consider separately the symptoms of the change in each
division of the heart, beginning with the left ventricle. In it the
change is carried to the greatest degree, and gives rise to the signs
and symptoms commonly understood as those of hypertrophy of the
heart.

Whenever hypertrophy is considerable, the heart, unless fixed by
adhesions, lies, in consequence of its greater weight, lower in the thorax
than in health. The weight of the base is said to increase the natural
obliquity of the organ, so that it may assume a nearly transverse
position.

Left Ventricle. — Physical Signs. — The increased bulk of the heart
may cause precordial bulging, noticeable chiefly in the area between
the. nipple and the left edge of the sternum. The intercostal spaces
are widened, and the surface of the chest is more prominent than is
the corresponding part on the opposite side. This bulging is most
marked in hypertrophy occurring in early life.

The area of dulness is increased. The superficial dulness is usually-
more extensive, the deep dulness invariably larger, and the increase
is chiefly to the left. The left edge of the deep dulness, instead of
passing from the middle of the third left cartilage to the apex, extends
from the inner extremity of the third rib to the nipple, or even to the
anterior axillary line, one, two, or even three inches outside the
nipple. It may also, although less commonly, extend upwards to
the second interspace. Its shape is thus usually more oval than in
health.1 Resistance on percussion is greater than in health. In
extreme enlargement the resonance in the left back is defective, and
Walshe has even known the dulness to be so marked, and respira-
tion so weakened by pressure upon the lung, that pleural effusion was
simulated. The apex-beat, marking approximately the limit of the
heart, is moved outwards and downwards, with its enlargement, into
or outside the vertical nipple line, and into the sixth or seventh
interspace, into the latter probably only in dilated hypertrophy
(Walshe).

The increased force of action manifests itself by increased impulse.2

1 The deep cardiac dulness is, except in the presence of extreme emphysema, an
accurate and convenient measure ot the enlargement of the heart By many authorities
it has been strangely undervalued. Niemeyer's assertion that percussion often fails to
reveal hypertrophy of the left ventricle is comprehensible only in consequence of the
guide employed being the superficial dulness, wnich depends much more on the state of
the lung than on the state 01 the h«*art. For a very full and clear account of the rela*
tions and significance of the diminished resonance caused by the heart in its various con-
ditions, see Balfour, Clin. Iject, on Diseases of the Heart, 1876, Lect. 1 .

« According to old writers, Fernel, &c, the impulse of a hypertrophicd heart had beer
twn to fracture the ribs ! All the instances, however, seem to have occurred m con-

HYPERTROPHY OF THE HEART. 713

The area of impulse is increased ; it may be felt in the fourth, fifth, and
sixth interspaces. A larger portion of heart comes in contact with the
chest wall, and the increased force aids also in producing a more exten-
sive impulse. In pure hypertrophy a maximum apex-beat is still per-
ceptible, bearing a normal proportion to the rest of the impulse. But
the impulse is not only more forcible, it presents a special change ; it
is slower, more deliberate, as well as more forcible, and hence has been
for long termed " heaving." In dilated hypertrophy the impulse is more
abrupt than in simple hypertrophy, in which the slow heave is carried
to its greatest degree. The extension of the impulse is often visible, and
the whole left front of the chest may be raised by it. It was spoken of as
" jarring " by old writers, and still is occasionally so described But a
"jar" implies vibration, and although a vibratory character is often
felt in the impulse of a hypertrophied heart, it is due to co-existing
valvular disease, not to the over-action of the heart itself. Occasionally
a double impulse can be felt with each beat of the heart. Barely it is
a double systolic impulse (Walshe), the origin of which is obscure.
More commonly the second and slighter impulse corresponds with
the commencement of diastole, at the end of the " sinking back/' as
Hope expressed it, who first pointed out the phenomenon. He explained
it as due to the sudden filling of the ventricles with blood. Hayden,
who adopts a similar explanation, has pointed out the coincidence
of this second impulse with the second sound. Walshe remarks
that the movement is rather a succussion than an impulse against
the chest walls. This character, and the obvious coincidence with
the second sound, have, in several cases, suggested to the writer the
probability that the impulse is really due to the shock commu-
nicated to the whole heart by the closure of the aortic valves, a closure
rendered more forcible by the greater distension of the aorta. It is in
accordance with this explanation that, as Hope and Walshe both point
out, this second impulse may occur in simple hypertrophy, but is most
marked in dilated hypertrophy (in which the distension of the aorta is
greatest), and that it is absent in simple dilatation.

The sounds of the heart are altered. The first sound is rendered
less loud, but longer, the change being especially marked over the
ventricle. The sound may be normal at the base and ensiform car-
tilage (Walshe). Sometimes the muffling of the sound amounts almost
to extinction. The second sound is usually loud. When dilatation is
added to the hypertrophy the first sound becomes louder and clearer.
The post-systolic silence is shortened, as Laennec noted, in consequence
of the lengthening of the first sound. Laennec thought that this
lengthening may amount to a faint murmur, apart from valve disease
or hsemic state, and Walshe corroborates the opinion. During attacks
of palpitation the first sound may be much more distinct than when
the heart is acting uniformly.

vents or monasteries. Csesalpinus and others assert that two ribs of St Philip de Neri
were torn from their cartilages bv the palpitation of his heart. Senac wisely doubted the
occurrence of such fractures, unless the ribs had Icon previously weakened by disease.
VOL. IV. 3 a.

714 A SYSTEM OF MEDICINE.

Reduplication of tlie first sound is occasionally met with iu hyper-
trophy : rarely according to Walshe ; almost invariably in eccentric
hypertrophy, according to Hayden. It is certainly frequent in some
forms of hypertrophy, especially in that due to Bright's disease
(Sibson). Irregularity in force is not common, in frequency very rare,
except in association with dilatation and degenerative changes.

Symptoms, proper. — A great number of morbid phenomena have
been ascribed to the influence of cardiac hypertrophy. The list, how-
ever, has been shortened according as the symptoms of the causes of
hypertrophy and of the other associated consequences of those causes,
are distinguished from the symptoms directly due to the hypertrophy
itself.1 Almost all the consequences of dilatation of the heart were
formerly ascribed to the conjoined hypertrophy. The credit belongs
to Bouillaud of having first vindicated hypertrophy from its supposed
influence in causing dropsy and other consequences of cardiac failure.

Subjective symptoms of cardiac hypertrophy may be absent, wlien
the hypertrophy is moderate, with little or no dilatation, and is ade-
quate to overcome the obstruction which has produced it In such cases,
however, the varying force of the heart's action, the varying amount
of the obstruction, and the common conjunction of relative weak-
ness with absolute strength, lead to sensible evidence of derangement

_ — Tracing from pulse in grant hypertrophy and dilatation of left »«.™,c „, a
case of rnitral regurgitant disease, with general venous diotanaion and ultimate increase
. m arterial tension. Artery large and incompressible. Tracinc taken at very hieh
pressure, which did not modify its character. n

Consciousness of the increased force with which the heart acts is a
more or less frequent symptom in all except the slightest forms of
hypertrophy. Under excitement the conscious beating may amount
to " palpitation." Slight irregularity may increase the discomfort, but
much irregularity or considerable palpitation is rare, except in dilata-
tion, and to that the symptom is to be ascribed. Pain, as Walshe
points out, is extremely rare in simple hypertrophy, and anginal
attacks are almost confined to cases in which the dilatation is con-
siderable. The force with which the left ventricle contracts has an
immediate effect on the arterial pulsations. The carotids throb

' Sumc, in speaking of this subject, aaya :— " ltien n'est plus ordinaire que lea Wtum
des ot.s,rvateura dans L. recherche des cuscs ; tout ce qo'lfi (movent du. lea cadavrea
lit 'toll ii Tm <1<™«=™ tiiaiadie, ou a telle qui a attire leur attention." l*c

HYPERTROPHY OP THE HEART. 71ft

visibly. The pulse is large, full, hard, sustained. When dilatation is
conjoined with the hypertrophy, the pulse is still full, but is softer and
more compressible and. less sustained. The sphygmogram shows these
characters in a sudden and high rise, and, where the hypertrophy is
simple, there is a high and often sustained tidal wave. Where there,
is coexisting dilatation, the tidal wave may not be sustained in conse-
quence of the imperfect emptying of the ventricle (Fig. 1.) Aortic
obstruction may, however, modify considerably these characters, render-
ing the pulse smaller, while it remains hard, sustained, and incom-
pressible. If considerable, it also renders the contraction slow, and the
percussion stroke may be lost in a slowly rising tidal wave, as in the
accompanying tracing : —

Fia. 2. —Tracing from infrequent and slow pulse of aortic obstruction, with coexisting
mitral disease, and hypertrophy of the left ventricle. The slowness or the contraction
had been increased by the administration of digitalis. Taken at a high pressure ;
pulse small but almost incompressible.*

The force with which the blood is driven into the smaller vessels
may modify the function of certain tissues and orgaus. The face is
often flushed. Tinnitus aurium, flashes of light, and muscre volitantes
may be complained of. Headache and mental dulness are sometimes
observed, but as a rule the intellect is unaffected. The general nutri-
tion also suffers little. Organic functions are little interfered with.
Increased arterial pressure might be supposed, as AValshe remarks, to
modify considerably the urinary secretion, increasing the quantity of
water. The urine presents, however, no distinctive change. Swelling
of the bronchial mucous membrane, and increased secretion are con-
nected by Niemeyer with the active distension of the bronchial
arteries. Shortness of breath on exertion is common, and is by Walshe
connected directly with the hypertrophy. True cardiac dyspnoea is
rare ; and any considerable shortness of breath is probably to be
ascribed to the cause of the hypertrophy, »r to concurrent dila-
tation. The pressure exerted on the lungs by an enlarged heart may
cause some interference with their function and increase the dyspnoea.

Consetptences of Hypertrophy. — A long train of evils which are met
with in more or less frequent association with hypertrophy, were
formerly regarded as its consequences. Many of them are in no way
related to its occurrence, but are the result of the dilatation, or
remotely of the cause of the hypertrophy. Such are ccdenia, capil-
lary engorgement, venous congestions, passive hcemorrhages. These
were enumerated by Hope as consequences of hypertrophy. Bertin

1 These two tta;ii!gs vre.-e taken for me by Mr. H. S. 0. Sankey.

716 A SYSTEM OF MEDICINE.

long before taught clearly that they cannot be regarded as such, since
they are absent when hypertrophy exists in its most simple form, and
occur in proportion as the hypertrophy is complicated by other con-
ditions, such as valvular disease, dilatation of the ventricle, &c,
themselves capable, without hypertrophy, of causing the symptoms.

Not only does hypertrophy not produce these effects, but its
tendency is to prevent their occurrence. Its power of arresting the
mechanical effects of its causes is very great, and proportioned to its
degree. Disease of the aortic orifice, for instance, as long as the
hypertrophy is great and unweakened by degeneration, produces no
backward effect. So in mitral obstruction, hypertrophy of the left
auricle may for a long time save the lungs from passive congestion.
So, too, hypertrophy of the right ventricle may prevent any over-
distension of the venous system from obstruction to the circulation
through the lungs or the left side of the heart.

The only morbid effects of hypertrophy which can accurately be
thus regarded, are those which result from the greater force with
which the blood is driven into the arterial system. These conse-
quences are seen best when there is no impediment to the escape of
blood from the ventricle, and especially when the cause of the hyper-
trophy is occasional or is situated in front of the arterial system.
The tendency is for the due proportion between the contents of the
arteries and the veins to be disturbed, for the arteries to become
over-filled, the veins and the pulmonary system under- hlled with blood.
It has been said that the whole circulation is accelerated, but this
Can only be the case when the action of the heart is for the time
being more than enough to overcome the resistance which has
evoked it.

It has been supposed that the increased supply of arterial blood
may lead to the overgrowth of organs, but the conjecture is unsup-
ported by observation.

A more direct effect upon the vessels may often be traced. When
the obstruction is situated beyond the arteries, their walls are exposed
to a greatly increased pressure. The same effect occurs when the
obstruction is at the aortic orifice, and the action of the heart is
from any cause (as dynamic excitement, or the cessation of another
cause) in excess of the obstruction. Both the large and small arteries
suffer under these circumstances. The increased pressure on the
aorta may cause its dilatation, although, as Senac observed, the enlarge-
ment from this cause is not often considerable. A more frequent
consequence of the pressure to which the arteries are exposed is seen
in the degeneration of the vessels.1 Modern observation has established
the frequent association of so-called endarteritis deformans (atheroma)
with increased strain. The change is seen in the aorta, in the
pulmonary artery, and in the smaller vessels, especially in those in
which the relative pressure is the greatest, as in those at the base of
the brain.

1 Pointed out by Kirkes in 1857, Med. Times and Gaz., No. 370, 371.

HYPERTROPHY OF THE HEART. 717

But degeneration is not the only effect of the increased strain upon
the vessels ; they not unfrequently give way, and haemorrhage results.
Haemorrhage into the brain is, on account of its frequency, magnitude
and importance, that form to which attention has been chiefly directed.
The frequent association of apoplexy and enlargement of the heart led
Corvisart first to assume a causal relationship between the two.1 In
this he has been followed by most subsequent writers — Bertin, Hope,
Bouillaud, Audral, Burrows, and others. But the conclusions of the
earlier observers require some abatement in the light of modern
knowledge of the frequency with which apoplectic attacks result, by
another mechanism, from cardiac disease. Embolism may give rise to
symptoms not unlike those of cerebral haemorrhage, and embolism is
almost constantly associated with hypertrophy of the heart But even
when these cases are eliminated from the discussion, the pathological
evidence of the association of apoplexy and hypertrophy of the heart
is still unimpeachable. In sixty-five cases of apoplexy collected by
Quain2 the heart was enlarged in two-thirds, and in one-half there
was no valve disease. The significance of the latter fact is that in these
cases the cause of the hypertrophy was probably situated away from
the heart, in or beyond the arterial system, which would thus have to
bear the whole force of the over-acting heart. But this is the condition
in which arterial disease is produced ; the small vessels degenerate,
and, becoming weaker, are less able to bear the increased pressure to
which they are exposed. This is the case, notoriously, in Bright's
disease, especially in the contracted kidney, with which cerebral
haemorrhage and cardiac hypertrophy are so constantly associated.
In primary degenerative changes in the smaller vessels the same result
io seen — a like obstruction may cause hypertrophy, and a like weak-
ness yield before the increased pressure. The same sequence is
sometimes seen when the cause of the obstruction is situated beyond
the arteries and capillaries, and acts, it may be, through both systems
of the circulation. Mitral disease may lead to extreme blood tension
in the arterial system, as the sphygmographic tracing on page 714
shows. Cerebral haemorrhage sometimes occurs in such cases, even
in the young, from the rupture of an overstrained artery.

All authorities are agreed as to the causal relationship between
hypertrophy of the heart and the rupture of diseased vessels. But to
this some, as Watson, Eulenberg, Rokitansky, would limit the con-
nection. It must be considered still doubtful whether an over-acting
heart can rupture a healthy artery. It is true the large arteries of the

1 " Where apoplexy takes place in a person in whom there is an excess of muscular
substance and strength in the heart, it is easy to conceive that the resistance of the
vessels of the brain is not in unison with the extraordinary impetus which the heart
impresses on the blood ; it necessarily follows that the smaller vessels of the brain become
more permeable to this fluid, or that they give way and cause effusion and apoplexy."
Corvisart, 1. c, p. 164. It, however, would seem to have been first suggested by the
death of Malpighi, who died from cerebral haemorrhage, and whose heart was found
greatly hypertrophied, " the parieteaof the left ventricle were two fingers in thickness."
(Boglivi.) * Lumleian Lectures, loo. cit.

718 A SYSTEM OF MEDICINE.

brain are often found healthy in cases of cerebral hemorrhage, but
this affords only slight evidence of the condition of the smaller vessels
of the cerebral substance. These are frequently diseased when the
vessels at the base of the brain appear healthy.

Statistics on this point corroborate, but do not extend, the conclusion
from isolated observations. Quain found that diseased vessels are
more common in cases of cerebral haemorrhage when the heart is
healthy than when it is hypertrophied. They are present in two-
thirds of the former, and only in about half of the latter. The inference
suggested is that, since extensive disease of vessels shown by the impli-
cation of the larger trunks is less common, in cerebral haemorrhage,
when the heart is hypertrophied than when it is healthy, an over-
acting heart needs less diminution in the strength of the vessels, in
order to effect their rupture, than a healthy heart.

The occasional, though rare, occurrence of cerebral haemorrhage
in the young does not help to decide the question. Disease of the
cerebral vessels is now known to be not uncommon in early life, and
some of the cases occur in the subjects of heart disease, in whom there
exists circuitous increase of arterial tension, just described. Moreover
in such subjects cerebral aneurisms, perhaps from imperfect embolism,
are frequent, and in many cases it has certainly been by the rupture
of such an aneurism that cerebral haemorrhage has occurred.

Concentric Hypertrophy of the Left Ventricle. — The symptoms are
as uncertain as the existence of the malady. Theoretically, the signs
of simple hypertrophy might be expected, and with them some
dyspnoea in consequence of the impediment which must be presented
to the passage of blood through a heart so much lessened in
capacity.

Right Ventricle. — Considerable increase in the size of the right
ventricle causes prominence of the lower part of the sternum, epigastric
fulness, and often bulging of the lower left cartilages adjacent
to the sternum. The superficial cardiac dulness is little changed,
but the deep dulness extends further to the right than normal, the
right edge being one or two fingers' breadth to the right of the
sternum. This dulness is partly dependent on the enlargement of
the ventricle, partly on over-distension of the auricle, which always
accompanies the change in the ventricle. Pulsation may be felt at
the epigastrium. The apex- beat is in its normal situation, or moved
a little to the left, extended as far as, but not beyond, the nipple line. It
is frequently changed, being obscured and diffused when the right
ventricle lies in front of it. A distinct impulse may be felt over the
right ventricle, i.e., over the lower part of the sternum,1 and
in the adjacent left interspaces. In health a distinct impulse is very
rarely to be felt in this situation. In hypertrophy the impulse may
have considerable strength, but it is generally quick, rarely of the
slow, heaving character which hypertrophy of the left ventricle

This was pointed out by Burggrave in 1754 (Act. Acad. Nat. Cur. vol. x. p. 140.)

HYPERTROPHY OF THE HEART. 719

produces. It may sometimes be felt as far as the base. Little altera-
tion in the sounds of the heart is caused by hypertrophy of the right
ventricle. The pulmonary second sound is usually intensified by the
increased tension within the pulmonary artery. Sometimes the second
sound is reduplicated. Jugular pulsation has been associated with
hypertrophy of the right ventricle by Lancisi, Laennec, Hope, and
others. It is doubtless due to actual regurgitation through the
tricuspid orifice, and coexisting dilatation of the ventricle is necessary
for its production.

Few symptoms proper can be associated with the condition. The
pulse is natural. The venous system shows no sign of engorgement.
It is remarkable how completely hypertrophy of the right ventrick
will prevent the development of dropsy, and other signs of venour
stagnation, by an obstacle in front of it. The lungs or left side of
the heart usually present evidence of the condition causing the
hypertrophy, emphysema, disease of the mitral orifice, &c. Dyspnoet,
is common, as Walshe points out, but is more frequently the
result of the cause of the hypertrophy, than of the hypertrophy
itself.

Consequences of Hypertrophy of the Right Ventricle, — The immediate
effect of over-action in the right ventricle is to over-distend that part
of the pulmonary vascular system which lies between the ventricle
and the obstruction which has caused the hypertrophy — the pulmonary
arterial system, when obstruction is in the tissues of the lung, the pul-
monary veins also, when the obstruction is on the left side of the heart
Atheroma of the pulmonary artery frequently exists in conjunction with
this condition, and has been regarded as causal, but in few cases have the
two been observed except in conjunction with some other recognised
cause of such hypertrophy, and it seems more reasonable to conclude
that the degeneration is the result of the increased strain to which
the pulmonary artery is exposed. Where the degeneration is con-
siderable and of old standing, as in cases in which the artery is found
calcified, it may be the only discoverable cause of a moderate
hypertrophy of the ventricle.

Pulmonary congestions, cedema, and especially pulmonary apoplexy,
have, since the days of Bertin, been commonly ascribed to hypertrophy
of the right ventricle. Where the obstruction causing the hypertrophy
is situated on the left side of the heart, the increase in the strength
of the right ventricle will add considerably to the strain upon the
distended pulmonary vessels, and may constitute the efficient cause
of their rupture. Modern pathological research, however, has shown
that diseases of the right side of the heart frequently cause pulmonary
apoplexy in another way, by leading to pulmonary embolism. We are
only beginning to learn how large a proportion of pulmonary apoplexies
is due to this cause/ When such embolism occurs, hypertrophy
of the right ventricle will increase very much the strain on the
collateral circulation, and, in consequence, will augment the amount
of haemorrhage.

720 A SYSTEM OF MEDICINE.

Auricles. — Hypertrophy of tht Left Auricle is usually attended with
evidence of its enlargement, i.e. dulness, commonly relative only, in
the inner part of the second left interspace. Less frequently a distinct
impulse is to be recognised in this situation, preceding in time the
ventricular impulse and due to the auricular systole. Evidence of
mitral disease is commonly present, a systolic or presystolic murmur.
Dilatation of the auricle invariably coexists. No symptoms are
known to be associated with the hypertrophy. Its tendency is to pre-
vent the mitral mischief from influencing the pulmonary circulation.

Hypertrophy of the Right Auricle is very rare, and is always associated
with dilatation. Its signs are dulness to the right of the sternum in
the third and fourth interspaces, and, in very rare cases, an impulse,
presystolic in rhythm, in this situation. It is often attended with
marked jugular pulsation, and with the evidence of disease of the
right ventricle or of the tricuspid orifice.

Diagnosis. — The diagnosis of hypertrophy depends on the recognition
of increased force of impulse, and especially, in the case of the left
ventricle, by the deliberate heaving character which indicates the
contraction of a large mass of muscle. In the case of right ventri-
cular and of auricular hypertrophy, the increased force is indicated
by impulse, where in health none is present. Evidence of enlarge-
ment of the heart, by percussion dulness, or by movement of the apex-
beat, or by extension of the impulse, is usually also obvious. In
left ventricular hypertrophy the character of the pulse assists the
diagnosis. Where doubt remains, the presence of a morbid state,
capable of causing the hypertrophy, may afford evidence of its pro-
bable existence.

In judging of the existence and degree of hypertrophy the condition
of the lungs must always be taken into consideration. Considerable
emphysema may conceal all the signs of a hypertrophy of high
degree. The impulse may be imperceptible, the dulness masked, and
the heart-sounds weakened. The existence of hypertrophy must then
be inferred from the condition of the arterial system.

There are certain conditions from which hypertrophy has most
frequently to be distinguished.

Undue Exposure of the Heart in very flat- or narrow-chested persons,
with small lungs, may simulate hypertrophy. The heart comes into
more extensive contact with the anterior wall of the chest than in
health. Its impulse is felt over a larger area, and may appear to have
undue force. A maximum apex-beat is still preserved. The super-
ficial dulness is more extensive than in health. The distinction from
hypertrophy rests on the absence of a heaving character in the
impulse, on the normal or nearly normal position of the apex-beat
(it is never outside, though it may be in the nipple-line), on the natural
extent of the deep dulness, on the unchanged pulse, on the absence of
any causal condition, and on the recognition of the short antero-
posterior or transverse diameter of the chest. The difficulty of

HYPERTROPHY OF THE HEART. 721

diagnosis in such cases is sometimes increased by the presence of an
exocardial murmur, produced by the undue friction of the heart against
the bony chest wall, and, by the circumstance, that patients with very
flat chests are often weakly and anaemic, and suffer from shortness of
breath and extreme consciousness of any dynamical heart-disturbance.

Dynamical Disturbance of the Heart may be mistaken for hyper-
trophy. Under excitement the heart may beat with apparently
increased force, and be brought into abnormal contact with the wall of
the chest, so that there is an increase in the area as well as in the
force of the impulse. Sometimes the increase in force is more apparent
than real, and the pulse is small and weak. Frequently, however, the
rapidly-acting heart distends the arteries, and the pulse becomes hard
and full. There is an entire absence of the deliberate heave of
hypertrophy, and of evidence of permanent change in the form of
the heart ; there is no bulging, no increased dulness. Rest in the
recumbent posture soon reduces the impulse to the normal It must
not be forgotten that an hypertrophied heart readily palpitates under
excitement, and any irregularity in the excited action is ground for
suspicion.

Displacement of the Heart may lead to an apparent extension (really
a movement) of the impulse and dulness in a given direction. Dis-
placement to the left, moving the apex outside the nipple line, may
simulate hypertrophy of the left ventricle; and displacement down-
wards, rendering the impulse of the right ventricle perceptible at the
epigastrium, may resemble dilated hypertrophy of the right ventricle.
But under these circumstances there is no alteration of the character
of the impulse as there is in hypertrophy; the opposite boundary
of the heart may be found to have undergone a corresponding change
of position, and a cause of the displacement will be discoverable.

Dilatation of the Heart resembles hypertrophy in causing increase
in size, shown by extension of dulness and increased area of impulse.
The impulse is, however, diffuse and weak ; the proportional intensity
of the apex -beat is lost, the pulse is soft, and the action of the heart
often irregular. The distinction between the two conditions can
rarely be absolute, since they are usually, in varying degree, conjoined.

Pericardial Effusion may cause bulging and an increase in the area
of dulness. The impulse, however, is less, instead of more forcible ;
and the apex is raised, instead of being moved outwards or down-
wards. The dulness extends upwards in the pyramidal form, and its
left boundary is beyond, instead of corresponding to, the left limit of
the impulse. Apart from auscultatory signs, the acuteness of the
symptoms in pericarditis, sudden pain, dyspnoea, fever, will usually
prevent an error in diagnosis. In auricular hypertrophy, the exten-
sion of dulness above the normal limits of the cardiac dulness is
usually slight. If sufficient to simulate pericardial effusion, a pre-
systolic impulse will, in most cases, be detected.

Aneurism has been confounded with hypertrophy, but the
conditions under whioh such a mistake could arise must be very

722 A SYSTEM OF MEDICINE. *

rare. The double centre of pulsation usuolly affords a sufficient
distinction.

Local diagnosis of the part of the heart affected with hypertrophy
has been alluded to in describing the symptoms produced by the
change in the several chambers of the heart. The chief difficulty
arises in some cases of ventricular hypertrophy. In hypertrophy of
the right ventricle, slight hypertrophy of the left ventricle may be
concealed or simulated by the strong impulse of the anterior right
ventricle and the displacement outwards of the apex-beat consequent on
the enlargement of the right side. The diagnosis of the state of
the left ventricle must then depend on the character of the apex-beat
— on the presence or absence of a distinct heaving impulse. On the
other hand, considerable hypertrophy of the left ventricle may cause
an impulse over the position of the right ventricle. In such a case the
impulse of the left ventricle possesses great force, and the diagnosis
must be based on the relative proportion of the impulse over the two
ventricles.

In all cases a comparison of the extent of causal lesion, with its
mechanical effects, will often suggest an accurate opinion as to the
existence and degree of hypertrophy when the part affected is not
accessible to physical examination. For instance, congestion of the
lungs is the necessary mechanical effect of mitral constriction. The
absence of such congestion, when considerable mitral constriction
exists, is valid ground for suspecting compensatory hypertrophy of
the left auricle. So too we sometimes find that such compensation
has not occurred — that the lungs are constantly overloaded with
blood, but that the general venous system has not suffered ; the
jugular veins are uudistended; there is no anasarca or albumen in the
urine. In such a case we may be sure that there is hypertrophy of
the right ventricle.

Prognosis. — The difficulty of extricating hypertrophy from the
various conditions with which it is associated has led authorities
to entertain very different opinions regarding its influence on the
life and well-being of the patient. The gravest consequences of
hypertrophy (as formerly described) are now known to be those of
its attendant conditions ; the "conservative" character of hypertrophy,
as a healthy reaction against a morbid influence, is generally recognised,
and its prognosis is admitted to be,"as a rule, favourable ; any un-
favourable element being due rather to coexisting dilatation, or
to other effects of the cause of the hypertrophy, than to that condition
itself.

It is rarely that evil results can be traced directly to the overgrowth
of the heart. The unpleasant sensations attending the action of a
hypertrophied heart suggest many possible evils which experience
rarely justifies. It may produce hemorrhage, especially into the
brain, when vessels are rotten, but probably d( es uot rupture healthy
vessels ; it may render inflammations more severe, but never initiates

HYPERTROPHY OF THE HEART. 723

them. Most observers will share Walshe's profound doubt whether in
its most extreme forms, hypertrophy can ever per se lead to death.

Does hypertrophy ever diminish or disappear ? It is probable that
hypertrophy lasts as long as its cause exists. Many facts on record
support the opinion that, if the cause of simple hypertrophy cease to
act, the heart gradually resumes its normal size. Atrophy may occur
in an hypertrophied as readily as in a normal heart. Whether a heart
the subject of dilated hypertrophy ever regains its normal volume is
doubtful. The occurrence of the so-called concentric atrophy, in
which the size of the cavities lessens, and also the disappearance of
the dilatation of atony, support the idea that a moderately-dilated
heart may regain its normal size.

The prognosis in hypertrophy must, therefore, largely depend on
the extent to which its cause is removable. For practical purposes
the work of the heart in these cases may be divided into three cate-
gories : — (1) that which is required to carry on the healthy circulation,
the body being at rest ; (2) superadded work, temporary and variable,
such as is involved in muscular exertion, emotional excitement,
local inflammation, pregnancy, &c. ; (3) some permanent abnormal
resistance to the movement of the blood, increasing the pressure
ivithin the cavity affected. The second of these is alone amenable
to treatment. The chance of removing or curing hypertrophy
depends on the extent to which causes of this cla3s constitute the
work of the heart. Where hypertrophy is developed when the
work of the second class is as slight as possible, where no avoidable
exertion is made, and where no occasional causes of obstruction exist,
the chance of removing or lessening hypertrophy is small. In the rare
cases in which the whole increase over the normal work of the heart
depends on causes of the second class, the prognosis is the most
favourable. Such cases are sometimes met with among athletes, as in
an instance Walshe records.

The probable permanence of the hypertrophy on the one hand, the
likelihood that it may give place to dilatation on the other hand,,
must influence the prognosis in any individual case. This probability
must be estimated by the degree to which the causes of dilatation are„
or are likely to be, in operation. Impaired general health, or the
presence of degenerative tendencies, local or general, render the prog-
nosis less favourable.

Where the cause of hypertrophy is permanent, the influence of the
hypertrophy varies, and with it the prognosis. In certain condition*
the increased force with which the heart acts may lead, directly or-
indirectly, to evil consequences, and in such cases the presence and!
degree of the hypertrophy may entail, per se, a corresponding increase
in the gravity of the prognosis. In all forms of valvular disease in
which the hypertrophy depends on direct obstruction to the escape
of blood from the cavity, the hypertrophy is purely beneficial in
its effect ; it secures a due supply of blood to the parts beyond the
obstruction ; it saves the vessels and organs behind from suffering from.

724 A SYSTEM OF MEDICINE.

the impediment. It is only when hypertrophy is due, in part, to a
variable cause beyond the obstruction, that it may be occasionally in
sufficient excess to produce prejudicial arterial distension.

In cases of regurgitation, in which the heart has to exert undue
force in the propulsion of an undue quantity of blood, the hypertrophy
is less simply beneficial in its influence. The muscular force with
which the ventricle contracts tends to increase the amount of blood
regurgitated, and so increase its own repletion. This is the case
directly in aortic regurgitation, indirectly in mitral regurgitation. The
degeneration of the arteries is hastened by the strain to which they
are exposed by the action of the hypertrophied ventricle in aortic
regurgitation; while in mitral regurgitation, although the stronger
action of the ventricle may drive a larger quantity of blood into the
aorta, it also increases the amount regurgitated through the incompetent
valves. But it must be remembered that in these cases the hyper-
trophy is a substitute for dilatation, and may be accepted as the less
of the two evils ; or it counteracts the influence of dilatation which
coexists.

When the obstruction causing the hypertrophy is situated in the
vascular system, pulmonary, or systemic, whether the consequence of
degeneration, Bright's disease, &c, the hypertrophy is also less simply
beneficial, since the increased strain to which the vessels are subjected
increases their liability to degeneration and to rupture.

In Bright's disease this danger reaches its height, since degeneration
of the strained vessels is very apt to occur and renders their rupture
easy. In senile changes cardiac and vascular degeneration often
correspond, and the hypertrophy which at first is evoked by the
change in the vessels yields to dilatation, by which the blood-tension
is lessened. But this retro-compensation is not without new risks.

In all cases, however, it is still true that the prognosis of the hyper-
trophy is subordinate to that of the lesion causing it, and also to that
of co-existing dilatation. Once established as the result of a perma-
nent cause, it usually increases, and bears a simple proportion to its
cause. It is extensively employed in prognosis, but is used rather as
an indication of the extent and gravity of the lesion causing it than
as affording in itself much information. As far as it goes, its presence
renders the prognosis of the causal lesion better. Compensatory in its
action, it wards oft' evil and promotes health.

Treatment. — Current opinion as to the treatment of hypertrophy
has undergone great changes, in accordance with the altered ideas
of its relation to the common consequences of organic heart disease.
When most of these were considered to be the direct effects of the
over-acting heart, every effort was made to diminish its over-action and
to lessen its over-growth. Low diet and frequent bleedings are the
measures which Albertiui and Valsalva handed down to a long series
of their successors ; and the effects of their doctrine is even now to be
traced, although perhaps rather in the pages of text-books than in

HYPERTROPHY OF THE HEART. 725

practice. Even after the purely consecutive nature of hypertrophy
was clearly recognised by Bertin, the same treatment was advocated.

The judicious management of hypertrophy depends on the recog-
nition of the fact that it is sometimes purely beneficial, usually wel-
come as a substitute for its too frequent associate, dilatation, and rarely
directly prejudicial. No universal rule for the treatment of hyper-
trophy can therefore be laid down, since the proper course may be
sometimes to foster its occurrence, sometimes to lessen its excess, or,
failing that, to prevent its increase.

Hypertrophy of the heart being the result of two factors, nutritive
activity and increased work, its increase may be to some extent pre-
vented, and its amount diminished, by lessening each factor in its pro-
duction. The nutritive activity of the heart can be lessened only by
diminishing that of the general system by low diet, bleeding, &c.
But to attempt this while the causes of hypertrophy continue, is to sub-
stitute dilatation for hypertrophy. The system has been advocated, how-
ever, in conjunction with causal treatment, from the time of Bertin. It
may be questioned whether the causes of established hypertrophy
can ever be sufficiently reduced to permit the safe employment of
" antiphlogistic " measures. Moreover they can rarely be necessary.
We see in the voluntary muscles that reduction of work is in-
variably followed by reduction in size of muscle. Every analogy
suggests that cardiac hypertrophy will rapidly subside when the con-
dition which excited it has lessened or has ceased. It is not often
that this result can be proved to occur in the case of the heart, but
instances are not infrequent in which it seems to take place. The
reduction of the causes of hypertrophy, i.e. the work of the heart,
to a minimum, constitutes, then, the main object in the treatment
of hypertrophy. This work is partly of a constant, partly of an
occasional nature. The normal work of the circulation must be
carried on ; the permanent organic cause of the hypertrophy can rarely
be lessened ; but the occasional addition to the heart's work involved
in violent muscular exercise, increased frequency of contraction from
alcohol or emotion, increased obstruction from remediable states of
blood or local inflammations, may all be to a large extent removed.
Eest of body and mind is therefore the first and most essential ele-
ment in treatment. All exercise which quickens the pulse must be
absolutely forbidden.1 Emotional tranquillity must be as far as
possible secured. The utmost temperance in food and alcohol
should be enforced. A fair amount of nitrogenous food, and a very
little light wine with it, constitute the best diet If food is well
taken without alcohol, the latter may often with advantage be prohi-
bited. The digestive organs should be carefully attended to. Nothing
disturbs the action of the heart so readily as a distended stomach.
Food must be moderate in amount, and every cause of transient
plethora avoided. The secretions must be carefully regulated, and

1 "On doit reearder le repos comme un remede*. pre'servatif 5 mais ce repos n'exclut pas
nn exercice modere, lorsque les grands accidents sont calmes." — Senac, 1. c, p. 419.

72G A SYSTEM OF MEDICINE.

impaired action of the kidneys or the skin must be supplemented by
mild purgation or diuresis. Local inflammations, bronchitis, &c,
must be carefully guarded against, and when they occur, removed as
speedily as possible.

Too often, however, the amount of obstruction which can by these
means be removed bears but a small proportion to the total against
which the heart has to contend. Can this permanent obstruction be
further reduced ? To some extent the work of the heart can always
be lessened by reduction in the total quantity of the blood. This
formed an important element in the old system of treatment, and it
was partly with this object that frequent and repeated bleedings were
recommended. Their condemnation in the present day is superfluous.
It may be doubted whether occasional leeching, which still finds
advocates, is justified by its ultimate results, although its immediate
effect is to give relief to the heart. Restriction of fluids has been
suggested. It is at any rate a harmless measure ; but the rapidity
with which urinary secretion regulates the volume and density of the
blood renders it doubtful whether more than a very transient effect is
produced.

It will be gathered from these statements that the conditions under
which an attempt at the removal of hypertrophy is indicated are very
rare. Whenever the hypertrophy can act immediately on the causal
resistance, its influence is always, on the whole, and sometimes entirely
beneficial. Only when the over-action of the heart is primary, or is
due to a cause which has ceased to operate, is it to be attacked
directly. In the rare instances in which violent exercise has called
out persistent hypertrophy, or some obstruction has been removed,
the condition may call for immediate treatment to reduce its effect.
Where the obstruction is situated far from the heart, and degenerated
vessels are interposed which have to bear the full force of au over-
acting ventricle, as in Bright's disease, the question also sometimes
arises of the chances of evil from vascular rupture, on the one hand,
and from a weakened heart on the other. The certain, slow, but sure
evil of a weakened heart will generally counterbalance the possible
•catastrophe, and any attempt to lessen the cardiac strength will be
avoided.

The use of drugs in hypertrophy is a subject on which various
opinions have been held.1 Most observers agree with Walshe,
that the reduction of the bulk of the heart is beyond the direct power
of any drug. The cliief rdle of medicine lies in regulating the cardiac
-contractions and in freeing the circulation from removable causes of
-embarrassment. Frequent action involves a great increase in the work
of the heart. Force is needed, it has been stated already, to move the
heart, apart from the movement of the blood. The minimum fre-
quency consistent with the due supply of blood to the system gives

1 Their possible use seems not to have occurred to the French school of physicians at
the begiuuiiig of this century, although the chief cardiac medicine, digitalis, had long
before been employed in this country.

HYPERTROPHY OF THE HEART. 727

the heart its best conditions of action. Moreover, very frequent action
may fill the arteries to repletion, and so increase their distension as
greatly to augment the intra-cardiac pressure. Lastly, frequent action
lessens the total rest of the heart, and favours degeneration. No remedy
has been discovered which lessens the undue frequency of the action
of the heart so effectually a3 digitalis. But digitalis strengthens the
cardiac action, and hence its use in hypertrophy has been dis-
countenanced by most modern writers, and by some strongly condemned.

The experience of clinical observers is not, however, in complete
accord with theoretical conclusion. By many the value of digitalis in
hypertrophy is strongly asserted. One explanation for this may lie
in the fact that hypertrophy is so rarely simple. Almost invariably,
dilatation is conjoined with it. In dilatation, digitalis is of extreme
value, and its use in hypertrophy is to a great extent proportioned
to the existence and amount of dilatation. Moreover all irregular
action of the heart involves waste of force, involves useless work.
Too frequent contraction does the same. Each may generally be
controlled by digitalis. Even where there is no irregularity and little
dilatation, the cardiac action may be below the actual needs of the
system ; the compensation is insufficient, and the additional strength
of contraction imparted by digitalis is purely useful. The dose of
digitalis needed in these circumstances is smaller than that required
in dilatation. Five minims of the tincture, or a drachm of the infusion,
three times a day, will usually effect all that is required. A larger
dose, is, as Milner Fothergill states, much more frequently deleterious
than in dilatation, in which large doses are borne, not only with
impunity, but with advantage. In pure hypertrophy, digitalis is
rarely necessary. Veratrum viride has been used, especially in
America, to reduce the strength of the heart, when in hypertrophy
its force appears beyond the present need of the system. Doses of
five minims of the tincture may be given three times a day. Both
the force and frequency of the heart's action are reduced. Inunction
of Ung. Veratria} has also been employed for the same purpose.

Where hypertrophy is not pure but is great, and acts directly on
the vascular system, or tends to increase its cause (as in aortic regurgi-
tation), it may be necessary, by similar measures, to reduce the force
of the heart to a minimum necessary for the work of the circu-
lation. Digitalis has been employed in small doses and recommended
strongly by B. Foster, but most authorities discountenance its use
under these circumstances, and Ringer1 points out that the same
eiul may be attained. by small' doses of aconite. A combination
of a« onite and veratrum is recommended by H. C. Wood.2

The consciousness of the cardiac contractions, which constitutes so
troublesome a symptom of hypertrophy, is only in pait due to the
force witli which the heart acts. It is much more frequently the result

1 llanlbook of Theiap uti<s, fifth elition, p. 427.
* l'hil 'delphia Med. Tines, 1874, N>v. 14 and 21.

728 A SYSTEM OF MEDICINE.

of irregular or too sudden contractions, and related to coincident dilata-
tion rather than to hypertrophy. It is commonly controlled by rest
and digitalis.

For the relief of cardiac pain, direct sedatives may be needed.
Opium, or morphia, is very effectual. Aconite is strongly praised
by Walshe. Belladonna, Indian hemp, hydrocyanic acid are also
useful in some cases. The Virginian prune bark, which contains
hydrocyanic acid, is sometimes useful, but its tonic properties render
it more suitable for dilatation. Cold locally applied to the cardiac
region is strongly recommended by Niemeyer.

The treatment d hypertrophy of the right ventricle must be conducted
on the same general principles as that of the left. It is almost always
united with dilatation, and is never excessive. Hence it needs as far
as possible to be strengthened, both absolutely by tonics, digitalis,
&c, and relatively by diminishing its work, by lessening as far as
possible the obstruction to the movement of blood through the lungs,
and by the avoidance of over-exertion, &c. Hypertrophy of the auricles
rarely calls for special treatment. Never simple, the conjoined dila-
tation always predominates.

The more detailed treatment of dilated hypertrophy is described
in the next article, on Dilatation of the Heart.

DILATATION OF THE HEART.
By W. E. Gowers, M.D.

Synonym.— Enlargement of the Heart (old writers) ; Aneurism of
the Heart (Baillou ; Lancisi) ; Passive Aneurism, or Passive Dilatation
(Corvisart) ; Herzerweiterung (Freysig) ; Cardiectasis (Jaccoud).

Definition. — Increase in the size of one or more of the cavities of
the heart. Such increase in size may or may not be attended with
obvious thickening or thinning of the cardiac walls.

History. — Dilatation of the heart received much attention from the
earlier pathologists, being rightly regarded as the chief cause of its
enlargement. In the middle of the sixteenth century, Vesalius gave
an account of a heart, the left ventricle of which contained two pounds
of blood, and Baillou1 mentioned one that equalled in size a man's
head. Harvey2 also in 1628 alluded to this condition. Dilatation
of the auricles was described by Willis. Dilatation of the right
ventricle and left auricle, as the result of mitral constriction, was
described by Mayow in 1674. Vieussens,3 in 1715, described a
case, observed in 1695, of extreme dilatation of left ventricle, the
consequence of aortic regurgitation. Peyer, Lancisi, and all suc-
cessive writers alluded to, or related instances of the condition.
The first systematic account of its mechanism and causes was given
by Senac4 in 1749, who distinguished dilatation with and with-
out thickening of the walls. Morgagni,6 in 1779, described very
clearly its origin, and effect on the circulation. Several cases were
related by Ferriar,6 in 1792, and the general causes and symptoms of
dilatation were described by Allan Burns, in 1809. In France, after
the writings of Lancisi had given the word currency, Baillou's term
" aneurism," had been used to designate enlargements of the heart, as

1 Epidemics et Ephemerides, 1574. Yvaren's Trans., Paris, 1858, p. 289.

9 De motu cordis et sanguinis.

» Traits du Cceur.

4 Traite* de la Structure du Cceur, &c, torn, ii

8 De Sed. et Caus. Morb., Epist. xxvii.

6 Medical Histories and Reflections, by John Ferriar, M.D., vol. i., 1792, p. 144.

VOL. IV. 3 B

730 A SYSTEM OF MEDICINE.

well as of the great vessels. Corvisart, in his description of dilatation
in his work, published in 1806, designated the two varieties described
by Senac, " active " and " passive " aneurism, with a subprotest against
the application of the term to conditions with such different tendencies.
He described accurately, as far as the description went, the different
symptoms and tendencies of the two conditions, and pointed out the
association of dropsy, or the " serous diathesis," with dilatation, rather
than hypertrophy. A further account of dilatation of the left auricle
as a mechanical consequence of mitral constriction was given by
Abernethy in 1806.1 Dilatation consequent on carditis, and associated
with adherent pericardium, was described, as the result of articular
rheumatism, by Sir W. Dundas in 1808.2 Its varieties were recognised
a little later by Kreysig. Bertin, in 1811, distinguished the conditions
and processes of dilatation and hypertrophy (in the sense in which
the words are now used), and Laennec's work on Auscultation, pub-
lished in 1819, gave the terms authoritative use. In Bertin's systematic
treatise, edited by Bouillaud in 1824, the chief varieties were dis-
tinguished which have since been generally recognised.

The detection, by percussion, of enlargement of the heart, of which
dilatation is the chief cause, is due to Avenbrugger (1763) ; that of
the altered impulse by palpation, to Corvisart (1806) ; that of the
auscultatory signs, to Laennec (1820).

Varieties. — From the condition of the cardiac walls, their in-
crease or diminution in thickness, certain varieties have long been
distinguished.

(1). Dilatation with Hypertrophy (active aneurism of Corvisart), in
which the walls are increased in thickness, as well as the cavities
in size.

(2). Dilatation ivith Attenuation (passive aneurism of Corvisart), in
which the cavities are increased in size, while the walls are reduced
in thickness. To these Bertin proposed to add that of simple dilatation,
in which the dilated walls preserve their normal thickness, and mixed
dilatatio7i} in which the walls are in one place increased, in another
diminished, in thickness. These varieties have been adopted by most
subsequent writers. The name, " simple dilatation," cannot, however,
be considered an accurate designation of the condition which it denotes,
dilatation without hypertrophy of tissue. If a heart be dilated only,
its walls, extended in area, are necessarily lessened in thickness. For
the normal thickness of the walls to be preserved when the cavity is
dilated, overgrowth of tissue must occur. Thus the condition of
" simple dilatation " necessarily produces dilatation with attenuation,
while the state to which the term is applied is really dilatation with
moderate hypertrophy: this was shown clearly by Stokes. Forget
applied to the condition the term hypertrophie dilatoire. Many writers
have suggested, and Wilks and Moxon maintain, that pure dilatation

1 Mevl.-Chir. Trans., vol. i., p. 27.
1 lbR, p. 37.

DILATATION OF THE HEART. 731

never oscurs, that hypertrophy is the invariable accompaniment, as the
increased weight testifies, and that recorded examples of hearts dilated
and not increased in weight have been examples only of relaxation.
They prefer the simple distinction into dilatation with thickening, and
dilatation with thinning.

Other varieties which have been distinguished are those of general
dilatation, in which all four cavities of the heart suffer, and partial
dilatation, in which the change is confined to one or some of them.
It has also been proposed by Hayden1 to designate those cases in
which an obvious active cause of dilatation can be distinguished,
consecutive, and those in which no such causes exists, primary.
Lastly, dilatations have been classified as temporary or permanent.
Bertin suggested that the latter only should be included under the
term, the temporary forms being rather examples of distension than
of dilatation.

Causes. — The maintenance of the normal size of the heart ultimately
depends on the existence of a due proportion between its elastic and
contractile force, and the blood-pressure to which it is exposed in
passive resistance and active contraction. A disproportion between
these two forces is the ultimate cause of its dilatation ; such dispro-
portion may result from a change in the amount of either factor, an
increase in the blood-pressure, a decrease in the cardiac strength.
Often the two conditions are conjoined : a weakened heart yields before
an increased pressure, and thus becomes over-distended ; and, the con-
ditions being permanent, becomes permanently dilated. To these two
causes must, probably, be added the effect of traction from without,
which acts by lessening the effect of the contractile force of the heart,
and so corresponds in its action with the weakening of the wall.

Thus diminished strength of the walls of the heart constitutes a pre-
disposition to dilatation, and the causes of that weakening may be
considered as the predisposing causes of dilatation ; the increased en-
docardial pressure being regarded as the exciting cause of the dilata-
tion. But, as is the case with many predisposing causes of disease,
the weakness of the wall of the heart may be the only morbid
antecedent Moreover, the action of these two causes of dilatation
is not simply predisposing and exciting. It will be convenient, however,
to consider the mechanism of their action after they have been described
in brief detail. The antecedents of the predisposing and exciting
causes may be spoken of as the remote causes of dilatation.

It must be remembered also, that increased endocardial pressure is
the immediate cause, not only of dilatation, by its mechanical effect,
but of hypertrophy, by the vital reaction which it induces. Its effect
in producing dilatation is influenced in part by the existence of the
predisposition (weakness of the cardiac wall), in part by the condi-
tions under which it acts, and which may be regarded as determining
causes. Commonly, however, the double tendency of the increased

1 Diseases of Heart and Aorta : Dublin, 1875, p. 558.

3 B 2

732 A SYSTEM OF MEDICINE.

pressure results in the double effect, and hypertrophy and dilatation
are conjoined. We have thus four classes of causes to consider, the
remote, predisposing, exciting, and determining causes.

(A.) Remote Causes. — The general conditions of hereditary influence,
age, sex, occupation, previous illness, &c, enter largely into the causation
of dilatation of the heart, as the antecedents of the conditions on which
it immediately depends. They can only be fully understood when the
immediate causes are known. Hereditary taint has a powerful in-
fluence in disposing to special degenerations and to certain diseases,
such as acute rheumatism, on which the immediate causes largely
depend. Age has a similar influence. Degenerative changes are
concerned in the production of both causes of dilatation, and hence
the disease increases in frequency with advancing years. Sex in-
fluences the occurrence of dilatation by determining exposure to one
of the commonest causes of increased endocardial pressure, muscular
exertion. Degenerative changes in the vascular system are largely
due to the same influence, and are causes of dilatation. Hence the
disease is more frequent in men than in women. Occupation has a
similar influence; all those occupations which involve considerable
effort tend to cause dilatation of the heart

(B.) Predisposing Causes. — Conditions of weakness of the cardiac
walls may consist in acute or chronic changes in the muscular fibres,
or in destruction of those fibres and their replacement by tissue
elements which yield more readily to the pressure of the blood.
Morbid states of the muscular fibres are, (1.) Atony, in which the
relaxation of the fibres at rest is more absolute, their contraction
less complete. (2.) The granular degeneration of acute disease.
(3.) Fatty degeneration, resulting ultimately in the actual destruc-
tion of fibres. (4.) Fatty overgrowth, in which the muscular fibres
undergo secondary atrophy. (5.) Fibroid degeneration, the sequel to
an acute inflammatory change or the result of a chronic perversion
of nutrition. (6.) Special degenerations and growths. (7.) Weak-
ening of the fibres due to the state of dilatation. Beau pointed
out that the fibres common to the two ventricles may be so
weakened by dilatation of one, as to lessen considerably the con-
tractile force of the other ventricle, and so to aid its dilatation. (8.)
Lastly, it has been stated by Niemeyer1 that the muscular fibres
may so lose their contractile power as to permit dilatation when*
no structural change in the cardiac wall, or in the fibres themselves,
can be detected by the microscope. Seitz2 has lately advocated
the same view. In all the recorded examples, however, over-exertiou
has been the exciting cause of the dilatation, and the cases appear
to have been characterised rather by insufficient power to react
against the augmented pressure, than by any primary degeneration.

The conditions by which these pathological processes are produced

1 Textbook of Practical Medicine, American Trans., vol. ii p. 320.
* Zur Lehre von der Ueberanstrengung des Herzens. Deutscnes Archiv fur klin. Med.
1873, xi, xii.

DILATA TION OF THE HE A RT. 733

constitute the predisposing causes of dilatation. The most important
of these conditions are: (1.) Anaemia and chlorosis, in which the
general mal-nutrition results in atony, and, it may be, granular dege-
neration of muscular fibre throughout the body. (2.) Acute febrile
diseases, especially rheumatism, erysipelas, pyaemia, typhus, typhoid
fever, &c, having a similar effect. (3.) Inflammation, primary or
secondary to endo- or peri-carditis, the inflammation in the latter case
invading the adjacent layer of the heart. (4) Obesity, with local
overgrowth of fatty tissue. (5.) Chronic degenerative changes in the
system, as yet ill-defined, but often due to chronic alcoholism, and
causing fatty and fibroid degeneration of various organs, including the
heart (6.) Derangements of the blood-supply to the walls of the heart
Chronic and intermitting passive congestions cause, as Sir William
Jenner points out,1 degeneration of the heart, toughening its walls and
lessening its contractile power. Diminished blood-supply is a common
cause of fatty and granular degeneration. It may be due to imperfect
distension of the coronary arteries in consequence of the defective
distension of the aorta, or it may result from narrowing of those
vessels by the contraction of lymph outside the heart, or by degenera-
tion, atheromatous and calcareous, of their walls. (7.) Defective nerve-
power probably in some cases leads to inefficient contraction and
dilatation of the heart. Dr. Dobell believes that sexual excesses are
powerful causes of cardiac weakness.

Traction from vrithout, the result of pericardial adhesions, is some-
times a cause of dilatation of the heart The two conditions are
constantly found associated, but in the majority of cases there exists
also endocardial mischief sufficient to account for the dilatation.
Hence, Morgagni and many subsequent writers doubted whether the
state of the walls was not always the consequence of the coexisting
valvular disease. But cases are not infrequent in which dilatation
exists, and no morbid condition can be found to explain its occurrence
except an adherent pericardium. Beau,2 arguing from a small number of
such cases, inferred that dilatation was the invariable result of pericardial
adhesion. The same view was very strongly maintained by Hope.8
Wider observation showed, however, that adhesions were frequent
enough with no morbid state of the heart's walls. Laennec, Bouillaud,4
Barlow, Stokes, and others maintained, therefore, that pericardial adhe-
sions have no direct effect in causing dilatation. The same view has
been still more recently maintained by Hayden.6 Gairdner,6 however,
emphasized the fact that in a minority of cases no other cause can be
discovered for the changes in the walls of the heart At the same time
he showed that, in other cases, the adhesions not only do not tend to
cause dilatation, but they do not prevent the reduction in size which

1 On Congestion of the Heart, Med.-Chir. Trans., vol. xliii.

2 Arch. Gen. de M6d., ser. ii.,tome x., 1837, p. 426.
8 Diseases of the Heart, p. 192.

* Traits' Clinique, &c., 1835, p. 454.

0 Diseases of the Heart and Aorta, p. 863.

• JSdin. Med. Journal, February 1851.

734 A SYSTEM OF MEDICINE.

accompanies chronic wasting diseases. The most extensive statistical
evidence on the question is that furnished by Kennedy,1 of Dublin,
who collected ninety cases of adherent pericardium without valve
disease, and found that the heart remained healthy till death in thirty*
four, and was enlarged in fifty-one. But some of his cases were from
museums, into which hearts of the normal size would be little likely
to find their way, and it is probable, therefore, that his proportion of
healthy hearts is too small. Dr. Hayden has collected twenty-three
cases of adherent pericardium, without valve disease, and found that
in seven there was enlargement without any other discoverable cause.2
Putting together these facts, and those recorded by other authorities,
it seems fair to conclude that adherent pericardium causes enlarge-
ment of the heart in one-third of the cases.

The difference in the effect of the adhesion is not to be explained
by difference in its extent The most marked hypertrophy and dila-
tation was due, in one of Gairdner's cases, to a firm adhesion of
very limited extent, near the apex of the left ventricle. In other
cases in which no influence was exerted, the adhesion was universal.
Dr. Wilks 8 has pointed out that, when general adhesion is associated
with dilatation, the effect is more marked on the right ventricle than
on the left. This is no doubt due to the thinness of the muscular wall
of the right ventricle. In estimating the effect of pericardial adhesions
it must be remembered how frequently they are associated with
another cause of dilatation, the damage to the subjacent portion of
the cardiac wall by the extension to it of the pericardial inflammation.
For the settlement of the question of #their influence more facts are
needed which shall embrace not only the state of the heart's walls,
and the fact of adhesions, but the extent, firmness, and probable dura-
tion of the latter, the extent to which the pericardium is connected
with parts around, and the extent to which the muscular fibres of the
heart have suffered from the inflammation.

Dr. Gairdner 4 has maintained that when the expansion of the lungs
is interfered with by their atrophy, the inspiratory efforts to distend
them, which he regards as the great cause of emphysema, may lead to
over-distension of the heart. He believes that it is by this mechanism
that emphysema is associated with dilatation of the heart, and appeals
in support of the theory, to the fact that the dilatation is not confiiied to
the right side but affects in slighter degree and a little later in time the
left side also. This view depends for its probability on the inspiratory
theory of emphysema. If, with Sir William Jenner and most modern
authorities, emphysema is believed to arise chiefly, not from primary
atrophy of the lung, but from its over-distension during expiratory
efforts, this explanation of the origin of dilatation of the heart falls to
the ground. No dilating influence by traction can result from

1 Edin. Med. Journal.

1 Loc. cit., table on p. 862.

3 Guy's Hosp. Rep., vol. xvi., p. 202.

4 British and Foreign Medico-Cnirurg. Rev,, July 1853, p, 212.

DILATATION OF THE HEART. 735

violent expiratory efforts, and when emphysema is once established
the inspiratory effort which can be made is far less than in health. If
the dilatation of the right ventricle in these cases is referred, as is
generally taught, to obstruction to the flow through the lungs, the
simultaneous affection of the left side can be explained in another way.

(C.) Exciting Causes. — Increase in the endocardial blood-pressure
has been mentioned as the chief exciting cause of dilatation of the
heart. Such increased pressure opposes the contraction of the heart,
and leads, by a mechanism to be presently described, to its dilatation.
It depends on increased resistance to the movement of the blood, the
result of au increase in its mass, or an obstruction in the orifices or
vessels through which it flows. This increased pressure leads to two
results, directly to dilatation, indirectly to hypertrophy. The causes
of the increased pressure, which are more fully considered in the
article on hypertrophy, are as follow : —

(1.) Increase in the mass of blood to be moved, consequent on over-
distension of the heart. Thus, regurgitation through an orifice causes
dilatation of the chamber behind. Thus, too, the dilatation tends to
its own increase, a process which is only arrested by the occurrence
of hypertrophy.

(2.) Resistance to the movement of the blood in consequence of
narrowing of the orifice by which it leaves the affected chamber. The
influence of this condition in causing dilatation is not great. The
obstruction is gradually developed, and unless associated with weak-
ness of the cardiac walls, the latter become hypertrophied to overcome
the increased resistance. In aortic obstruction, for instance, dilatation
is rare.

(3.) Resistance to the movement of the blood through the vascular
system is a powerful cause of dilatation, and is most effective when
suddenly developed or intermitting, and especially when the condition
in which it arises is such as to impair the nutrition of the walls of the
heart. Disease of the large vessels, aorta and pulmonary artery, rarely
causes dilatation. Obstruction of the smaller vessels is a more effective
cause, and especially those forms of obstruction which affect the
pulmonary circulation alone, or in conjunction with the systemic
vessels.

Long-continued and severe muscular efforts are, as Ferriar * pointed
out, a powerful cause of dilatation and hypertrophy. The resulting
condition of heart depends largely on the existence of the conditions
which favour the occurrence of one or the other state. The effect of
effort is to obstruct the circulation through both the general and
pulmonary system. Its influence on the left ventricle has been des-
cribed in relation to hypertrophy. Clifford Allbutt has especially
pointed out the direct effect on the right ventricle and the influence
of undue smallness of lungs on its occurrence. The obstruction to
the pulmonary circulation by the pressure of the air on the inner
surface of the air cells obstructs the escape of blood from the right

1 Med. Hist, and Ref., vol. i. 1792.

736 A SYSTEM OF MEDICINE.

side of the heart. The compression of the heart itself interferes with
the entrance of blood from the veins, tends to their over-distension,
and when the pressure is removed, to the over-distension of the right
auricle and ventricle. Thus the intermitting obstruction causes inter-
mitting over-distension of the right side of the heart, and that inter-
mitting congestion of the walls of the heart which leads to the
degeneration of its substance and renders dilatation permanent.

It is by a similar mechanism, according to the views generally
accepted, and fully stated by Sir William Jenner in the third volume
of this work, that emphysema of the lungs causes dilatation of the
heart. Intermittent distension results, as just described, from the
violent expiratory efforts with closed glottis, which constitute the
efficient cause of emphysema ; and as the latter condition is developed,
degeneration, elongation, and destruction of capillaries render the
obstruction permanent, which before was occasional. The right side
of the heart undergoes dilatation, sometimes to an extreme degree.
Hypertrophy is usually also produced. The congestion of the cardiac
wall disposes the left ventricle to yield before the increased pressure
of the aortic blood, which is an ultimate effect of the venous disten-
sion acting through the capillary system.

Other forms of pulmonary change have a slighter tendency to cause
dilatation of the heart than emphysema. An exception must, however,
be made for cirrhosis of the lung, which produces, in a large number
of cases, hypertrophy and dilatation of the right side. Such a change
was present in one-third of the cases of cirrhosis collected by Bastian.1
Mechanism. — The consideration of the mechanism by which dilata-
tion is effected is necessarily, in the main, theoretical. It has, perhaps
on this account, received little attention, and has even been sometimes
dismissed as useless. But any clear conception of the way in which
a morbid state is reLited to its causes, if correct, must afford a clearer
view of its pathological significance, and of the way in which by
treatment it may best be met.

The dilatation of the heart is produced, in every case, by its
over-distension with blood. Just as the various causes of hyper-
trophy involve, as the efficient cause, overwork, so the various
causes of dilatation involve over-distension. The immediate cause of
this over-distension is, in each case, the existence at the end of the
diastole of an endocardial pressure disproportioned to the resisting
power of the wall of the heart, and before which the wall yields. The
act of dilatation thus occurs during the diastole of the heart. This
circumstance lessens the simplicity of the relative action of the
exciting and predisposing causes of dilatation, since, as will be imme-
diately explained, each may act by producing a similar effect.

Three sources of over-distension may thus be recognised. (1.)
The mass of blood entering in the normal course of the circulation
may be abnormally large ; simple over-distension. (2.) Blood may enter
the cavity from an abnormal source (regurgitation), and being added

1 Art. Cirrhosis of Lung, vol. iii.

DILATATION OF THE HEART. 737

■

to that entering it in the normal course of the circulation, increases
the mass of blood and so the distension of the chamber ; over-distension
from regurgitation. (3.) The whole of the blood previously in the
chamber may not be expelled from it during contraction, the residual
blood being added to that entering from behind increases the disteusion
of the chamber ; over -distension from imperfect contraction, or residual
over-distension.

(1.) Simple over-distension is the result of over-distension of the
source from which the blood enters the affected chamber. It is well
seen in the effect of mitral regurgitation on the left ventricle. The
over-distended auricle drives an abnormal quantity of blood into
the ventricle, into which probably an increased quantity has already
passed in consequence of the heightened tension of the blood within
the auricle. It is probable that a large quantity of blood enters the
ventricle during diastole, enough to equalise, or almost to equalise, the
pressure within the ventricle and within the auricle,1 before the auri-
cular contraction effects the actual distension or over-distension of the
ventricle. The pressure to which the inner surface of the ventricle is
exposed at the end of the auricular systole is very great, for in accord-
ance with the well-known law of hydrostatics it is multiplied directly as
the area of the inner surface of the ventricle exceeds that of the auriculo-
ventricular orifice. Simple over-distension may occur, especially in the
auricles, in conditions of acute weakening of the cardiac walls. The
lessened tone of the muscular fibres allows them to yield unduly before
the pressure of the incoming blood, and as the current is continuous, they
thus become directly over-distended. Similarly the flaccid ventricles
may yield unduly before the current which enters during diastole,
and the systole of the auricles may over-distend the ventricles. This
mechanism has been described by Beau 2 as dilatation sans asystolie.
But the conditions are those under which contraction is imperfect, and
the small pulse renders it probable, in many cases, that such imperfec-
tion occurs. Eesidual over-distension will then increase the dilatation.

(2.) Over-distension from regurgitation is one of the most efficient
causes of dilatation. The cavity is filled with blood from a double
source. That which enters in the normal course of the circulation
is added to that which has regurgitated into the cavity, and over-distenr
sion results. In aortic regurgitation, for instance, it is the addition
of the contents of the auricle to the blood regurgitating into the
ventricle from the aorta, which actually distends the chamber and
dilates it until, ultimately, the dilating process is met by compensating

1 That this is the case is highly probable, from a phenomenon sometimes to be observed
in cases of mitral constriction. When diastolic and presystolic murmurs are both
present, the former due to the slow passage of blood through the orifico in consequence of
the tension of the blood within the auricle, the latter due to the contraction of the
auricle, there may be, during an occasional prolonged diastole, an interval of silence
between the two in u mm vs. When the diastolic murmur is loud, this silence can only
be explained by a cessation, or almost cessation, of the flow of blood, which means,
of course, an equalisation of the pressure in the two cavities.

* Beau, Traite* d* Auscultation. Paris, 1856.

738 A SYSTEM OF MEDICINE.

hypertrophy. In permanent potency of the semilunar valves the
intra-ventricular pressure at the end of the auricular systole must be
very great, since the pressure of the aortic blood will be added to that
produced by the contraction of the auricle.

(3.) Over-distension from imperfect contraction ; residual over-dis-
tension.— Whenever, from any cause, systole is incomplete, blood must
remain in the chambers and render the entrance of the normal
quantity of blood an over-distending agent Incompleteness of con-
traction is theoretically possible from two causes, diminished con-
tractile force, and increased resistance to contraction. It is probable
that each of these does actually prevent complete contraction, since
each is found to be an efficient cause of dilatation.

(a) The various conditions which weaken the cardiac walls, already
considered, must tend to render the heart incapable of overcoming all
the resistance that is opposed to it, whether that be normal or increased.
Hence the contraction is imperfect and the residual blood is the ultimate
cause of over-distension. To this condition Beau gave the name of
asystolie. This weakening of the wall not only leads to over disten-
sion, it also renders the effect of the over-distending force greater in
degree and in duration, for the weak wall yields more to the increased
pressure, and the yielding of the degenerated wall is permanent.
Among the conditions weakening the heart must also be reckoned the
state of dilatation. The dilated heart has increased work, for it has to
move an increased mass of blood, to overcome a greater pressure. To
this it is even less competent than a healthy heart. Hence the dilata-
tion itself renders the contraction additionally incomplete, and is thus
perpetuated and increased. The influence of dilatation is of course
here considered apart from that of the hypertrophy commonly conjoined
with it, and to some extent counteracting its effect.

It is by interfering with contraction that pericardial adhesions must
be considered to exert whatever influence they possess in causing
dilatation of the heart. Connections of the pericardium with parte
around, consequent on the extension of inflammation to its outer
surface, may cause the adhesions to the heart to oppose consi-
derably the reduction in size during systole, and thus to render the
contractions incomplete.1 Moreover, a similar effect may be produced
by the interference with the approximation of different parts of the
surface during contraction, wThich must occur if a thick inelastic mem-
brane covers the heart. Such an influence will interfere chiefly with
the contraction of the thin-walled right ventricle, and this may be que
reason why it suffers most. The effect will be to cause a residual over-
distension, just as does the simple weakening of the cardiac wall with
which the adhesions are so often associated.

(b) Increased resistance from some obstruction to the circulation is

1 Thus in Gairdner's case, already mentioned, in which marked hypertrophy and dila-
tation of the left ventricle were associated with, as the only discoverable cause, a local
adhesion near the apex, a corresponding adhesion connected the other side of the
pericardium with the left lung.

DILATATION OF THE HEART. 739>

another cause of incomplete contraction. Such increased resistance
may interfere with the contraction of a healthy heart, but probably
rarely does this unless great and suddenly developed. The reserve of
power usually prevents imperfect contraction, and compensating hyper-
trophy gradually renders the heart efficient But when suddenly
developed, or when the nutrition of the heart is interfered with, the
chamber dilates. This dilatation was formerly, and is still by some,
ascribed to the direct effect of the increased pressure on the contracting
fibres.1 It was compared by Senac to the effect of an extending force
in elongating a cord.2 Niemeyer 8 pointed out that such an explana-
tion is entirely inapplicable to the conditions of the phenomenon.
Increase in the capacity of a contracting chamber from increased pres-
sure within it during contraction, is inconceivable. Such increased
capacity can only be explained by an increased quantity of blood
entering it under a pressure sufficient to overcome the resistance of
its walls. The influence of increased resistance to contraction may
be to weaken the muscular fibres, to lessen the elasticity of the
walls, and to render over- distension easier, but more than this it
cannot directly effect

(D.) Determining Cames. — The exciting causes of dilatation and
hypertrophy are thus to some extent the same; the occurrence of
the result is influenced not only by the predisposition already de-
scribed, but also by certain determining conditions.

(1.) The rapidity of the development of the increased blood-pressure,
i.e., the rapidity with which the valvular disease, or the systemic or
pulmonary obstruction is produced. Time is necessary for the pro-
duction of that hypertrophy which alone can prevent dilatation, and
a suddenly -developed obstruction invariably leads to dilatation.

(2.) The small amount of muscular tissue normally existing in the
wall of the affected chamber of the heart. This is naturally pro-
portioned to the work of each segment of the heart, i.e., to the blood-
pressure, to be by it passively resisted and actively overcome. The extra
pressure induced by the abnormal obstruction or regurgitation bears
no necessary proportion to the normal blood-pressure, and before
absolute equal increments of pressure, the smaller the normal amount
of muscular tissue, the more readily does dilatation occur, because
the systole is the more readily rendered imperfect, and residual
over-distension produced.

Each cavity of the heart affords an illustration of these influences,

1 Lately by Chirone in IjO Sperimentale, Angust 1874.

2 " La contraction qui resserro les vcntricnles est peut-etre l'instrument qui augment
les dimensions, que le sang soit en trop grande quant ite dans ces reservoirs ; qu'il trouve
quel quo barriere que l'empeche d'en sortir avec la liberte qu'U a ordinairement, Taction
des fibres sera plus forte : or cet execs de force doit nlcessairement les al longer : un
raccourcissement force produit le meme effet qu'une action qui tire et qui tend ur.e
corde, scs elements doiveut n£cessairement s'ecarter, et meme se separer, s'lls sont tires
avec trop de violence." — Senac, Traite, Ac, 1749, torn, ii., p. 897.

3 Loc. cit., vol. ii. p. 816.

UO A SYSTEM OF MEDICINE.

and although our knowledge is still very imperfect, we can understand
something of the origin of the condition found in each instance, and
it is worth while to recapitulate briefly the way in which the different
results are brought about.

In aortic obstruction the left ventricle is commonly hypertrophied,
less commonly dilated. The left ventricle, containing the greatest
amount of muscular tissue, possesses a large reserve of force, and can
overact so as to overcome a moderate increase in resistance, and so
prevent residual over-distension and dilatation. The development of
obstruction is usually slow, and thus there is time for hypertrophy to
occur. In aortic regurgitation there is always dilatation, and usually
much, often very much, hypertrophy. The regurgitant blood causes
the ventricle to be overfilled, and the patent aortic orifice transmits to
the interior of the ventricle, during its passive state, the intra-aortic
pressure. The regurgitation is usually slowly developed, and the
muscular tissue of the ventricle considerable, and hence hypertrophy
occurs. This is favoured by the abundant blood supply to the heart,
consequent on the great distension of the aorta.

In mitral disease, obstructive and regurgitant, the left auricle
undergoes dilatation and hypertrophy, the former predominating in
regurgitation, from the direct over-distension and frequently rapid
development of the pathological state. Hypertrophy of the auricle is
usually more frequent in obstruction, from the slowness with which
the lesion is developed. Dilatation is always, however, conjoined,
from the ease with which the contraction of the weak auricle is
rendered imperfect by obstruction. In mitral regurgitation, the left
ventricle is hypertrophied and dilated, and the dilatation is usually
considerable, in consequence of the direct over-distension of the
chamber, and perhaps also of the imperfect distension of the coronary-
arteries and consequent damaged cardiac nutrition.

The right ventricle, in disease of the left side, usually undergoes
dilatation, from its small amount of muscular tissue, but often is
also hypertrophied, in consequence of the slowness with which the
obstruction in the left side tells back upon the right. The hyper-
trophy is usually less and the dilatation as much marked, when the
obstruction is situated in the pulmonary system, in consequence of
the directness with which such obstruction affects the ventricle, the
rapidity with which it is frequently developed and increased, and
the damage to the cardiac nutrition, which results from the extreme
and sudden passive congestion to which the heart is, in these cases,
very often liable.

In obstructions to the systemic circulation, hypertrophy is the
common change in the left ventricle, and often, especially in Bright's
disease, is wholly unattended with dilatation. The extreme slowness
with which the obstruction is developed is, no doubt, a chief factor
in determining the occurrence of hypertrophy rather than dilatation.
Occasionally, however, dilatation occurs instead of hypertrophy.
Such cases are perhaps instances of simultaneous cardiac and vascular

DILATATION OF THE HEART. 741

degeneration, in which the increased blood tension is the result of the
latter, and the damaged heart is incapable of resisting the abnormal
pressure.

The sequence of the conditions of hypertrophy and dilatation varies
under different circumstances. It is certainly not uniform, as has
been maintained by some writers. When an increased resistance or a
cause of over-distension is suddenly developed, dilatation results at
once, and hypertrophy slowly, when time allows overgrowth to occur.
This is frequently seen in aortic and mitral regurgitation. The order
is the same when the initial state is one of defective power in the
walls of the heart ; dilatation precedes and is the cause of hypertrophy
— as in that which results from carditis. On the other hand, dilatation
may be secondary. Degeneration occurs in the hypertrophied tissue
more readily than in the healthy heart Nutritive influences fail from
impaired health or advancing years.1 Again, the coronary vessels
suffer from undue strain, degenerate, and lessen the blood supply.
This, as pointed out by Mauriac, is a frequent occurrence in aortic
regurgitation. Under all these conditions the degeneration weakens
the cardiac wall, and dilatation occurs at a later period than the
hypertrophy.

Pathological Anatomy. — Dilatation may affect all the chambers
of the heart or only some of them. It has been a subject of rather
unprofitable discussion whether general or partial dilatation is the
more common. It is rare for one chamber to suffer considerably alone.
When the cause of the dilatation is disease of an orifice, the chambers
behind the orifice are usually alone affected. An exception is mitral
regurgitation, in which the cavity in front of the orifice is dilated also.
The chamber immediately behind the diseased orifice commonly suffers
more than the others. In mitral constriction, for instance, the left
auricle is most dilated. In all diseases of the left side of the heart,
the right side may ultimately become dilated. Hence the most widely
distributed change occurs when the obstruction is in front of the left
ventricle, and affects each part of the heart successively. In aortic
regurgitation, for instance, enormous hearts are met with, in which
every cavity is dilated. Occasionally a similar result follows ob-
struction in the aortic system.

The dilatation, as already stated, is rarely simple. Hypertrophy is
usually present, and varies in amount according to the conditions
described in the last article. From the variations in the amount of
dilatation and associated hypertrophy very different effects on the
form and size of the heart are produced.

The amount of dilatation is estimated by comparison with the
normal capacity, by measurement of the external size of the heart,
the thickness of the walls, and the length and mid- circumference of
the cavity. In estimating it, regard must be had to the age of the

1 Niemeyer pointed out how frequently from this cause the hypertrophy which result*
from senile vascular degeneration gives place to dilatation.

742 A SYSTEM OF MEDICINE.

patient, and to the state of the body. The capacity of the heart
naturally increases with age. In decomposition the relaxation of the
heart is extreme, the cavities present their maximum capacity, the
walls their minimum thickness. The existence of decomposition,
which in some cases is very rapid, must therefore induce caution in
inferring actual dilatation from a flaccid and apparently dilated state
of the heart

A heart, the subject of general or partial dilatation, is increased
in size and altered in shape. The increase in size may be considerable ;
the circumference being two, three, or four times the normal.
Occasionally the left ventricle is so large as to be " capable of con-
taining another heart" — a favourite comparison since the time of
Malpighi. The left auricle may be dilated, in disease of the mitral
-orifice, to very large dimensions. In a case recorded by Cruveilhier,
it had four times its normal dimensions. The greatest dilatation,
■however, occurs on the right side. Both ventricle and auricle may be
very large. The right auricle, as Burserius * remarked, may undergo
greater dilatation than any other part of the heart. Stokes2 mentions
a case in which the auricle was so capacious as to contain a pound
of blood.

The shape is altered according to the part of the heart affected. In
general dilatation the heart is increased in width, so that it has a
more globular shape. This depends especially on the dilatation of
the right chambers, and is marked when these alone are affected.
♦Considerable dilatation of the auricles may alter considerably the
normal shape' of the heart. Thus in the case mentioned by Stokes,
the dilated right auricle " formed a vast purple tumour, which con-
cealed the whole of the anterior portion of the right lung."

In pure dilatation the weight of the heart is normal. Instances of
this are, however, to say the least, very rare. As a rule the weight of
the dilated heart is greater than normal, in consequence of the almost
invariable coexistence of hypertrophy.

The walls of the heart the subject of simple, or nearly simple,
•dilatation are flaccid, and collapse when cut across. They are thinner
than normal in proportion to the amount of dilatation, and to its
freedom from accompanying hypertrophy. In most cases the attenua-
tion, however considerable, is the result of the extension of the wall.
In rare cases the wall may actually be atrophied. In the ventricles
the thinning is most marked towards the apex. The wall of the left
ventricle may be reduced to one-sixth of an inch at the middle and
one-twenty-fifth of an inch at the apex. The walls of the auricles
may, in extreme dilatation, be reduced to an almost membranous con-
dition. Very frequently, coexisting hypertrophy prevents noticeable
diminution in the thickness of the walls, even when the dilatation
is very great. The thickness of the wall may even be above the

1 The institutes of the Practice of Medicine, 1798. Cullen Brown's Tians., rol. v.,
p. 312.

* Diseases of Heart and Aorta, p. 275.

DILATATION OF THIS HEART. 743

normal, notwithstanding the dilatation, especially when the latter is
moderate in degree.

The muscular tissue is sometimes normal in appearance, sometimes
pale or mottled. Under the microscope it usually presents evidence
of degeneration, especially when the dilatation is comparatively pure.
The muscular fibres present indistinct striation, or granular or actual
fatty degeneration. The connective tissue between the fibres is often
increased, and may also present granular degeneration. The endocar-
dium may be thicker or thinner than normal ; it is often irregularly
thickened and opaque, especially in the auricles. The pericardium is
stretched in proportion to the dilatation, and is also often unduly opaque.

The orifices participate in the dilatation of the cavities of the heart.
The auriculo-ventricular orifices undergo the greatest extension,
especially when the cavities on each side of them are dilated. The
ultimate result is that the valves become incompetent to close the
orifice, in consequence of the disproportion between their area and
that of the enlarged orifice. This effect is increased by the removal
of the bases of the papillary muscles to a greater distance from the
orifice, in consequence of the extension of the wall. For a time the
incompetence may be averted. The segments of the valves may
undergo some amount of dilatation so as to close the enlarged orifice,
and the papillary muscles may undergo at their apices transformation
into fibrous tissue, which, being incapable of contraction during the
systole, effects a practical elongation of the muscle, and so helps to
counteract the effect of the removal of their points of attachment.
Ultimately, however, the dilatation of the orifice exceeds the influence
of these compensations, and incompetence of the valves results. This
is the case especially in the right side of the heart, in which the
dilatation of the two cavities is usually simultaneous and consider-
able, and is the common cause of tricuspid incompetence.1

In dilatation of the auricles, the large venous trunks opening into
them, unprotected by valves, commonly participate in the dilatation, and
may be greatly enlarged, so that their openings into the auricle may be
hard to determine. The auricular appendices are also much dilated.

Certain associated conditions are commonly met with in cases
of dilatation. Some of these are causal, such as valvular disease,
pericardial adhesions, emphysema of the lungs, kidney disease.
Others are sequential, such as passive congestion of organs, and its
consequences in alteration in their texture.

Consequences. — From the incompetence of the valves due to the
dilatation of the orifices, regurgitation of blood with all its consequences,
results. Before, however, sequential regurgitation is developed, the same
consequences, although in less degree, may result from the diminished
power of propelling the blood. The resistance of a larger quantity
of blood has to be overcome, and the power of moving it is absolutely

1 This was first insisted on by Forget, Gazette Medicale de Paris, 1844, p. 657. Th«
dilatation of the orifice was pointed out by Corvisart, loc. cit. p. 164.

744 A SYSTEM OF MEDICINE.

diminished by the dilatation. Hence, unless compensatory hypertrophy
assist, less blood leaves the dilated chambers at each systole. The
amount of residual blood may be so large that the quantity which
can enter in the normal course of the circulation is less than in health.
Hence, as Morgagni pointed out,1 the dilatation acts as an obstruction
to the onward movement of the blood, the vessels behind (venous system)
become overfilled, the vessels in front (arterial system) underfilled.

The effect of dilatation of a cavity may thus come to be the same
as that of obstruction at the orifices of the heart by which the
blood should enter the chamber. If the chamber affected be a
ventricle, the first effect is the over-distension of the corresponding
auricle, and its consequent dilatation and perhaps hypertrophy. The
veins by which the blood enters the auricles are over-distended, and
when valvular incompetence is added, the pulmonary and larger
systemic veins may be enormously dilated. I have known the right
internal jugular to be so large, in dilatation of the right side of the
heart, as to be mistaken for an aneurismal dilatation of the common
carotid artery. Pulsation may be communicated to the veins as a
result of the valvular incompetence (see article on Diseases of the
Valves). The venous congestion affects alike the general tissues,
causing various dropsies into the cellular tissue and serous cavities, and
the organs, especially the lungs, brain, liver, portal system, and kidneys.
Lastly, the other side of the heart may be overloaded and dilated, and
ultimately even the side of the heart first affected, by the trans-
mission of the influence through both systems of circulation. The
last effect, which occurs only when the primary disease is at the
mitral orifice, is perhaps due to the secondary dilatation of the right
side. The effect of this venous congestion is to overload the venous
radicles of the organs with blood, and cause their permanent dilata-
tion. The proper tissue-elements of the organs undergo atrophy, or
it may be granular, or fatty degeneration, partly in consequence of the
pressure upon them of the distended veins, partly from the imperfect
supply of arterial blood. Lastly, the connective tissue of the organs
overgrows, and their consistence is thereby increased. The effect
of these changes is somewhat modified by the characters of the organ
affected.

The heart itself may suffer from the mechanical congestion of its
walls, the consequences of which have been already pointed out The
mechanical congestion, however, it is believed, affects the heart later
and less than the other organs, in consequence of the obliquity of
the opening of the cardiac veins which produces a valve-like effect.

1 Morgagni, speaking of a case of aortic regurgitation, says : — "Some portion of (the
blood) returned into the left ventricle of the heart when the ventricle ought to receive
the blood that was coming in from the lungs, it would necessarily happen that the
returning portion, as well as the portion which had not been extruded just before, must
occupy some part of that space which, from the design of nature, was entirely due to
the blood that was coming in from the lungs, which circumstance finally could not but
overload the lungs and heart." De Sedibus et Causis Morborum, 1779, letter 23, art.
12. As translated by Cockle, loc. cit.

DILATATION OF THE HEART. 74*

The lungs are overloaded with blood, and serosity exudes from
their walls into the air-cells and minute bronchi, and probably blood
corpuscles migrate into the parenchyma. Ultimately the capillaries
become varicose,1 the blood-pigment collects in the cellular elements of
the lung, giving it a brown colour, and the connective tissue is
increased in quantity,2 augmenting considerably the consistence and
to a slighter extent the size of the lung, and producing ultimately the
condition of " brown indication."

The brain undergoes slighter changes, no doubt in consequence
of the effect of gravitation in opposing the movement of the blood.
Its venules are enlarged and the distension of the surface veins may
be very great. The pressure of the distended vessels in the interior
may lead to their rupture into the perivascular sheaths, or to atrophy
of the adjacent brain substance. The consistence of the brain is
often lessened. Induration does not result. Corvisart maintained
that rupture of large vessels and cerebral haemorrhage might result
from venous congestion, but his opinion has not received much
confirmation.

The liver is congested, in a very high degree, from the directness
with which the hepatic vein suffers from increased distension of
the inferior vena cava. The organ becomes uniformly enlarged,
first and mainly from the distension of the radicles of the hepatic
vein, and afterwards by fatty degeneration of the liveT tissue, or by
fibroid overgrowth around the vessels and between the lobules, by
which the organ may become indurated. On section, the distended
venules are very conspicuous, and their enlargement is such that the
hepatic tissue is compressed between them, and the appearance is
produced of lobules lying between the distended venules, and thus
a portal congestion is simulated. The liver tissue is frequently pale
from fatty or fibroid degeneration, and, contrasting with the dark
vessels, the so-called "nutmeg liver" is produced. Ultimately the
liver may undergo reduction in size from atrophy of the proper
elements and contraction of the fibrous tissue (Murchison).8

The flow through the liver capillaries is necessarily impeded, and
thus the obstruction is transmitted to the portal system. The spleen
is enlarged, and, like the liver, may be the seat of fibroid overgrowth,
causing its induration. The peritoneal and intestinal vessels are
distended, and fluid may be effused into the peritoneal cavity. The
fibroid overgrowth in the liver may ultimately lead to compression
of the portal venules, and consequent portal congestion, out of pro-
portion to the congestion which results simply from the cardiac
state.

The kidneys suffer similar congestion, and present the appearance
which was produced artificially by ligature of the hepatic vein, by

1 Buhl, quoted by Wilson Fox, vol. iil, art. Brown Induration of the Lung, p.
801.
8 Rokitansky, "Wilson Fox, loc. cit.
3 Clinical Lectures on Diseases of the Ltrer, 1*68, p. 120.

VOL. IV. 3 C

746 A SYSTEM OF MEDICINE.

Eobinson.1 They are enlarged, smooth, and dark in colour from the
venous distension. The cortical and pyramidal portions preserve their
relative proportions. At first their consistence may be lessened,
and the capsule separate readily ; after a time fibroid overgrowth
occurs and the kidneys become indurated. Ultimately this tissue
may contract, the organs becoming smaller and harder, their surface
slightly granular, and the capsule unduly adherent.

The veins of the body generally are also over-distended. Serum
escapes from them into the connective tissue and accumulates in the
more depending parts. Usually the condition comes on gradually,
and the oedema commences in the legs. It is first noticed in the
evening and disappears during the night, when the legs are raised ;
but it continues increasing, until, although lessened, it is not removed
by the horizontal posture. If the patient be in bed it may be first
noticed in the lower part of the back. It may increase until the dis-
tension of the legs is extreme, and the skin, if not relieved, may
slough. Lastly, coagulation may occur in the distended veins, but this
accident is not common. The amount of congestion varies from time to
time in dependence upon accidental causes of increased obstruction, due
sometimes to variable cardiac strength, more frequently to variations
in the cause of the dilatation in the lungs, &c. Again, the manifes-
tations of venous congestion are not uniform in different cases. An
accidental cause, a local inflammation, may determine a large effusion
of serum in some special position, as the pleural or peritoneal cavity.
Some accidental obstruction may lead to local oedema. A special
predisposition to disease in some one organ, as the liver or the kidney,
may cause that organ to suffer in undue degree and give a special
character to the symptoms. Moreover a vicarious action is often
observable between the vessels of the organs and of the limbs and
cellular tissue. The extreme affections of organs, the very large
livers, the extreme albuminuria, are often seen where the general
oedema is slight; whereas when the anasarca is extreme there may
be even to the last only a trace of albumen in the urine, and the
enlargement of the liver may be trifling. Fibroid overgrowth in
organs may hinder the distension of their vessels, and so throw an
additional strain upon those of the general system.

The over-distension of the venous system, on which so many of the
symptoms depend, can only be in part ascribed to the dilatation of
the heart. It is in large part due to the cause of the dilatation.
Dilatation of the right ventricle permits the obstruction in the lungs,
which exists in emphysema, to tell back upon the venous system. But
it also adds to the obstruction. When due to no increased resistance,
but to muscular degeneration, it will give rise to similar symptoms.
So in the latter case, degeneration of the cardiac wall, the weakness
in its contractile power which permits dilatation, is itself, as Kiemeyer
pointed out, a cause of the impaired circulation. The resulting

1 Me,\ Chir. Trans., 1843, p. 51

DILATATION OF THE HEART. 747

dilatation, by its mechanical influence, intensifies what may be called
the potential obstruction which results.

Symptoms. — The existence of dilatation is declared by certain
symptoms and physical signs. Some difficulty in their determination
has arisen from the circumstance that pure dilatation is so rarely met
with ; dilatation is usually accompanied by hypertrophy. But pure
hypertrophy is not uncommon, and by comparison of these cases with
those in which dilatation co-exists, and especially with those in which
dilatation predominates, the symptoms of the latter condition have
been ascertained. They are most marked and characteristic in general
dilatation.

The Physical Signs depend on the increased size and lessened strength
of the heart. The area of dulness, both deep and superficial, is
increased. The deep dulness may extend from the anterior axillary
line, to two fingers' breadth to the right of the sternum, even in rare
cases as far as the right nipple ; upwards it may reach to the first
rib, and downwards to the seventh rib. It inclines to squareness of
outline, in consequence of the lateral increase in the size of the heart.
The greater the dilatation, the greater is the lateral increase in the
dulness. The impulse is perceptible over an abnormally large area.
It may be felt from the epigastrium to the axilla. It is also diffused.
A maximum apex-beat may or may not be perceptible. It is always
less distinct than in health. When it cannot be felt it may sometimes be
seen (Walshe). The impulse is weak and sudden in proportion to the
amount of dilatation and to its purity, i.e. its freedom from associated
hypertrophy. It may be somewhat undulatory in character, in conse-
quence of different parts of the heart striking the chest wall succes-
sively, not simultaneously. Successive beats may be unequal in
strength, and may also strike the chest-wall at different points.
Bulging of the chest-wall is slight in dilatation, and is said to bs
always absent when there is no hypertrophy ; now and then in a
large dilated and slightly hypertrophled heart it is very distinct. Dis-
placement of organs occurs in the hypertrophied form, the lungs are
pushed out of the way, the liver may be displaced downwards, so
that its rounded upper surface is visible beneath the ribs.

The sounds of the heart are weakened, the first sound is shortened
and its tone raised. As Flint,1 puts it, the valvular element in the
sound predominates. When there is co-existing hypertrophy, the
first sound may be clear and ringing, but the sound becomes weaker
in proportion to the amount of dilatation. The shortening may cause
the first sound to resemble in its characters the second sound, so that,
as Stokes2 pointed out, it may not be easy to distinguish between
them. Laennec taught that clearness of the first sound is a sign
of dilatation. Stokes and Gairdner3 showed that this clearness

1 On Diseases of the Heart, second edition, p. 86.

8 Op. cit, p. 260.

3 Edinburgh Medical Journal, July 1856, p. 56.

3 c 2

748 A SYSTEM OF MEDICINE.

exists only when hypertrophy is combined with the dilatation.
Beduplication has been noticed in some cases, and may be due to the
asynchronous contraction of the two ventricles.

In dilatation of the ventricle, especially of the left ventricle, a
systolic apex murmur is frequently heard. In a large number of
cases it depends on incompetence of the auriculo-ventricular valves,
primary (in the case of the mitral valve), or due to the extension of
the orifice in the dilatation of the heart In many cases, however,
no incompetence can be discovered after death although a systolic
apex murmur was heard during life. But the post-mortem tests for
incompetence of the mitral valve are not very satisfactory. Slight
inefficiency may remain undetected, and on the other hand, slight
regurgitation cannot be accepted as conclusive evidence of functional
incompetence. In each case the action of the papillary muscles during
life may vitiate the post-mortem conclusion. Hence some authorities
believe that such a murmur, when heard in dilatation of the ventricle,
is always due to auriculo-ventricular regurgitation. Others, among
whom are Stokes 1 and Walshe, believe that a murmur is occasionally
to be heard in cases in which the post-mortem evidence of valvular
competence is so conclusive that regurgitation is a very improbable
explanation. They consider that the contraction of the ventricle
alone may throw the blood into audible vibrations. The conditions
are certainly such as to render the result conceivable. It is probable
that the systole of a dilated ventricle is never complete. A consider-
able amount of blood remains in its cavity. The spaces between the
various projections into the cavity,— the trabecular, papillary muscles,
the cuspid valves, — are larger than in health, and remain unobliterated
at the end of the ventricular contraction, and the eddies into which
the blood is thrown must be considerable. Moreover, the irregularity
of the blood current is no doubt sometimes increased by irregu-
larity in the contraction of the ventricles. By these means it seems
probable that a murmur may be produced within the ventricle, the
consequence and the sign of dilatation only.

The pulse is weak in proportion to the amount and purity of the
dilatation. It is sometimes of moderate size, sometimes small; its
size is largely influenced by the condition of heart to which the
dilatation is secondary. It is often quick, and is unduly quickened
by exertion. Sometimes it is infrequent, either because the heart's
action is infrequent, or because the irregularity in force is so great
that every systole does not influence the pulse. Thus the effect of
intermission is produced. Actual intermissions may also occur.

Dilatation of the left ventricle alone, is attended by the changes in
the impulse which have been already described as among the most
conspicuous signs of general dilatation. The impulse is diffused, and
both impulse and dulness are extended to the left. The first sound
is weak ; the pulse presents the characters just described. Sooner

1 Diseases of the Heart and Aorta, p. 261,

DILATATION OF THE HEART. 749

or later the mitral orifice is stretched to incompetence of the valves ;
then general dilatation, with all its symptoms, quickly follows.

Dilatation of the left auricle may lessen the resonance at the innef
end of the second left interspace, and a feeble presystolic impulse mftjr
be perceptible there. Pressure on the left bronchus may interfere with
the expansion of the left lung (Barlow).

Dilatation of the right ventricle causes pulsation to be transmitted
to the epigastrium, and extension of dulness to the right of the
sternum in the fifth and sixth interspaces ; the apex of the heart is
in the normal position. Jugular fulness is common, and pulsatioti
consequent on tricuspid incompetence is not rare, and, as tricuspid
incompetence is rarely due to any other cause, it affords additional
evidence of the existence of dilatation of the right ventricle. The
pulse may, as Lancisi pointed out, be little changed.

Dilatation of the right auricle causes dulness to the right of the
sternum, where pulsation may sometimes be detected, generally pre-^
systolic, rarely systolic in consequence of the tricuspid insufficiency
fas in a case of Dr. Stokes,1 in which an aortic aneurism was simulated).
Jugular pulsation, systolic in rhythm, occurs, and may be in rare cases
diastolic also.

Symptoms. — Dilatation of the heart affects, secondarily, almost
every organ in the body, and its symptoms, direct and indirect, are
veTy numerous. They vary widely, however, in distribution and
degree, in different cases.

Cardiac discomfort is frequently present ; it varies from mere
uneasiness to acute pain, constant or paroxysmal (pseud -angina).
Palpitation is very common. The sudden contraction of the enlarged
heart is perceived unduly by the patient, especially when irregularity
in force or rhythm is superadded. The heart is easily excited to
frequent contraction by slight causes — muscular exertion, emotional
excitement, or mechanical disturbance, as by a distended stomach.

The general strength is always lessened. The patient complains of
lassitude and languor, and faints easily.

All parts of the general system present evidence of passive conges-
tion. The venous stasis is seen in the distended superficial veins and
the cyanotic tint. Subcutaneous oedema is often present and may be
considerable. Its occurrence is influenced, not only by the cardiac
obstruction, but by the state of the blood. In anaemic persons the
normal blood-pressure may suffice to cause slight oedema of the feet,
and a similar state of blood assists very much the effect of the increased
venous pressure in cardiac dilatation. The local dropsies, effusions
into the pleural, pericardial, or peritoneal cavities are attended by
their special symptoms. Their occurrence may alter the character,
and add much to the gravity of the symptoms present in a given
case.

Special symptoms result also from the congestion of organs. The

1 Diseases of the Heart and Aorta, p. 275.

750 A SYSTEM OF MEDICINE.

congestion of the lungs is indicated by cough, dyspnoea, cyanosis.
Cough is often a very troublesome symptom. It may be paroxysmal
and independent of any bronchial secretion, or a small amount of
mucus may excite an excessive cough. Secretion is often, however,
abundant enough from the congested vessels, and the sputa may be
abundant, watery, or mucous, often stained with blood. The congested
bronchi are liable to inflammation, by which all the symptoms are
increased.

Dyspncea is a very constant symptom, due chiefly to the imperfect
pulmonary circulation and deficient aeration of the blood. At first it
is slight, and is felt only when exertion increases the need for oxygen ;
especially on ascending a hill or stairs. Later on it may be constant,
and be increased when the body is recumbent (probably because
the descent of the diaphragm is impeded by the weight of the
abdominal viscera). Respiration may be quickened to thirty or
forty acts per minute, and is panting in character, with noisy expi-
ration. It varies in intensity, sometimes in correspondence with
cardiac failure, sometimes without apparent cause. The patient, never
free from a sense of want of breath, may from time to time start up
in an agony of dyspnoea, undo the clothes upon his chest, and grasp
convulsively at any object within his reach. Often even the re-
clining posture with the head backwards cannot be borne, and the
sufferer can only rest or sleep sitting up with his forehead supported.
Sometimes a rhythmical character may be observed in the dyspnoea,
analogous to, though not identical with, the Cheyne-Stokes breathing.
Brief attacks of panting dyspnoea commence suddenly, and gradually
subside to comparative, perhaps dozing, calm, with which they
alternate. These spasmodic forms of dyspncea may be singularly out
of proportion to the interference with the aeration of the blood, as
estimated by the amount of cyanosis.

The congestion of the brain causes frequent headaches. Vertigo
is common. The patient sleeps and dreams much. He dozes during
the day, and at night is disturbed by restless starts. Corvisart
pointed out that the passive congestion sometimes causes a " sub-
apoplectic "' state during the last hours of life. Delirium is not
uncommon, and may be violent ; a state of approaching chronic
mania sometimes results.

The congestion of the liver is indicated by an icteric tint of skin,
by pain and weight in the right back, right shoulder, or hepatic
region, and by abdominal discomfoit due to the increased size of the
organ. Frequently the enlargement can be both seen and felt. Pul-
sation may be felt in it, either communicated to it directly by the
heart, or, it is said, transmitted through the venous system. The
liver is veiy constantly depressed as well as enlarged. More urgent
symptoms result from the transmitted obstruction in the portal system.
The functions of the stomach and intestine are interfered with by
the mechanical congestion of their walls. Vomiting is a common,
and often a most troublesome, symptom. It is probably due to the

DILATATION OF THE HEART. 751

mechanical congestion of, and direct pressure upon, the stomach.
Possibly, in some cases, it may, as Walshe suggests, be the reflex
result of an irritation of the pneumogastric nerve. It sometimes
results from a catarrhal condition, which is easily excited in the con-
gested organ. The distended vessels may give way, and hsemate-
mesis result. Piles are common. The haemorrhage from them may
relieve the congestion and prevent other symptoms. In other cases,
from the mechanically congested vessels, serum escapes into the in-
testinal canal, or the peritoneal cavity, causing diarrhoea or ascites.
In the former the stools are copious and watery, and give little pain.
Such diarrhoea may constitute the earliest symptom of cardiac mischief.
All these symptoms of portal congestion may, in the later stages, be
intensified by an increase in the obstruction due to secondary changes
in the liver itself.

The mechanical congestion of the kidneys produces changes in
the urine, which becomes scanty, dense, high-coloured, often loaded
with lithates, and may contain albumen. The quantity of albumen
varies, and does not always correspond, as might be expected, with
the amount of venous congestion. Roberts 1 suggests that it depends
on the pressure to which the arteries are exposed in the congested
state, and he points out that it is often greater, the stronger the
force with which the heart acts. Tube-casts are frequently present
in the urine, 'and are generally hyaline or slightly granular, and of
medium size.

The ultimate effect of general dilatation is to act through the venous
and capillary system on the arteries and the left ventricle, increasing
the tension of the pulse and the effect on the left side of the heart.
The variation in the amount of obstruction at different times pro-
duces great alterations in the organic symptoms. As Stokes pointed
out, attacks of dyspnoea due to cold, &c, may be accompanied with
a rapid increase in the size of the liver, which will descend in a
short time far into the abdomen, partly from the enlargement, partly
from displacement, and on the subsidence of the attack will return
to its ordinary volume. The albumen in the urine may undergo a
similar modification, although in less simple dependence on the venous
stasis*

Diagnosis. — The essential sign of dilatation, by which its existence
and degree may best be ascertained, is the diffusion of the cardiac
impulse, its comparative uniformity over the whole area in which it
can be felt In proportion to the purity of the dilatation the first
sound is toneless, high pitched, and short and weak ; the pulse is small
and feeble, and the lungs and general system suffer from the secondary
consequences of the cardiac failure.

Obscuration of impulse may simulate diffusion, and thus lead to a
mistaken diagnosis of dilatation. A thin layer of over-distended
lung may intervene between the heart and the chest-wall, and so

1 On Urinary and Renal Diseases, third edition, p.. 356.

752 A SYSTEM OF MEDICINE.

render the apex -beat indistinct and apparently diffused. The in-
creased resonance over the cardiac area will indicate the cause of the
indistinctness. Dilatation may also be simulated, as Niemeyer pointed
out, when the apex strikes against a rib, and the impulse is felt
equally in the interspace above and below the point of contact. This
is most frequent in narrow-chested persons, whose ribs are near to-
gether. A mistake may be avoided by noticing this conformation of
thorax, and by observing that the apex- beat is nearly in the normal
situation, and that the apparent diffusion is vertical only ; there is no
lateral extension of the impulse.

From hypertrophy the diagnosis can rarely be one of absolute
distinction. Some hypertrophy usually coexists with dilatation, and
often confers on the diffused impulse increased force, and sometimes
the pathognomonic " deliberate," heaving character. In proportion to
the predominance of the dilatation, the impulse is weak and sudden,
the precordial region is not bulged, the cardiac dulness is increased
laterally rather than vertically, the impulse is extended laterally
rather than lowered, and the pulse is weak rather than strong.

Froni pericardial effusion dilatation is principally to be distinguished
by the direction ol the increase in dulnes.? which occurs in each
condition — in dilatation laterally, in pericardial effusion upwards.
The pyramidal apex of the latter, when distinct, is not simulated by
the dulness of the dilated heart. The impulse of the heart and the
dulness are conterminous, to the left at all events, in dilatation ;
while the dulness of pericardial effusion may extend beyond the
impulse. The apex-beat is not raised in dilatation, and the sounds of
the heart .are as loud over the precordial region as at the top of the
sternum, where in effusion they are most distinct (Walshe). Lastly,
there is no frictiou-sound, and far less displacement of organs or
precordial bulging, than in pericardial effusion. But precordial bulging
and obliteration of intercostal spaces may be present in dilated
hypertrophy, and in extreme dilatation the sounds may be much
weakened. In a case recorded by Evans the right ventricle was
actually tapped under the idea that it was a pericardial effusion.1

From fatty degeneration dilatation may be distinguished by the
evidence of enlargement of the heart, by the diffusion of its impulse,
and by the proportion between its diffusion and its weakness. In
fatty degeneration, when it exists alone, there is no enlargement of
the heart, and the change in the impulse is a simple weakeniug
without diffusion. Often the two conditions are conjoined.

Prognosis. — The prognosis in dilatation of the heart is always
grave. Unless compensated for by hypertrophy, its direct effect is to
interfere with the function of the heart, and to lead to those serious
results to which death is often due. Hence the gravity of the prognosis
is proportioned (1) to the purity and extent of the dilatation ;
(2) to the existence of a tendency to degeneration rather than to

1 Clin. Soc. Trans., 1874 -5.

DIJLATATION OF THE HEART. 753

growth, and of states of general malnutrition, defective food-supply,
&c, which interfere with the occurrence of hypertrophy ; (3) to the
extent to which the dilatation is due to causes beyond control, to
the amount of irremovable work which the heart has to perform.

Most the state, once established, be regarded as permanent?
The relative amount of dilatation may certainly be lessened by the
development of hypertrophy. There is some reason to believe that
apart from the development of hypertrophy a dilated heart may lessen
in size. It was long ago asserted by Beau and Larcher that dilatation
is sometimes temporary when due to a temporary cause, and it has
been said that a similar diminution may occur when, by absolute rest,
the work of a recently dilated heart is reduced to a minimum.
Individual cases have conveyed this idea very strongly to careful and
unbiased observers. Milner Fothergill has lately brought forward
strong evidence to show that such reduction in size may occur. He
has shown that diminution in the cardiac dulness may correspond with
the disappearance of the symptoms of dilatation, and afford evidence
that the condition is itself diminished. The same conclusion is indicated
by the completeness with which the acute dilatation of adynamic
diseases, such as fever, may pass away.

Treatment. — The object of treatment in dilatation of the heart
must be to restore as far as possible the disturbed balance between
the cardiac work and the cardiac strength. The increased blood
pressure, to which the dilatation may be primarily due, must be
reduced to the minimum compatible with the work of the circulation.
Accidental causes of obstruction must be removed. Bronchitis must
be got rid of as soon as possible. Especially, exertion must be
avoided. Best, mental, moral and physical, is of the greatest importance.
Muscular exertion involves a large increase in the work of the heart,
and its cessation will often suffice to restore the disturbed balance.
In extreme dilatation, confinement to bed or the couch for a time is a
wise measure, and will not seldom remove most of the troublesome
subjective symptoms, and even some grave objective signs of dilatation.
Where this cannot be secured, or is unnecessary by reason of the
moderate degree of the dilatation, the rigid avoidance of all needless
and severe exertion should be enforced.

The blood-pressure may also be lessened by the reduction of the
total volume of the blood. This may be accomplished in more than
one way. The most ready method is by the abstraction of blood by
venesection or cupping. The relief which it affords is often immediate
and striking. The ultimate effect, however, is that the volume of the
blood is soon reproduced, while the Jieart is permanently weakened.
Hence it must only be employed when the need for immediate
relief is paramount, and renders the danger of the ultimate damage
a secondary consideration, — that is to say, when the patient is in
imminent danger of death. It is especially useful when the right
heart and venous system are overloaded. The quantity of blood

754 A SYSTEM OF MEDICINE.

taken need not be large. In less urgent cases the same end may be
obtained by other means, by purgation and diuresis. The former must
not be severe, or the subsequent depression is not easily rallied from.
Diuresis is often of great service in these cases, even where there is
no dropsy.1 The amount of fluid taken as drink should be small.

The power of the heart should be increased so that it may resist
the blood-pressure, and may contract completely, so as to expel the
whole of its contents. To this end the general nutrition must be,
as far as possible, improved. A dry bracing air is useful, and gentle
exercise should be taken which does not increase materially the work
of the heart ; food must be nutritious and easily digested. Iron is of
great service, and seems to aid directly the production of the needful
hypertrophy.2

Excited action of the heart must be calmed by avoiding the causes
of excitement, and by sedative medicines. Moral emotion must, as
far as possible, be avoided, and the sources of gastric disturbance
guarded against or relieved. A distended stomach easily excites
an attack of palpitation.

Of drugs having a direct action on the heart, none is so useful as
digitalis, which increases the tone of the heart, lessens the frequency
and increases the force of the contraction. There has been much
discussion as to the action of digitalis, and the condition of heart
in which it is of most service, but there is at present a consensus
of opinion that its action is tonic and that in dilatation its most
marked beneficial effect is produced.8 The heart's action is reduced
in frequency and increased in force ; irregularity in force and rhythm
is lessened or removed. The sphygmographic tracing shows this
effect The grave consequences of dilatation are lessened, venous
congestion, dyspnoea, and oedema, general or local, are all diminished.4

Concerning its modus operandi, there is still some difference of
opinion. The lessened frequency of contraction probably lessens the
work of the heart by diminishing that part which consists in moving
its own mass, and at the same time the longer periods of rest probably
conduce to the perfectness of the cardiac nutrition. Frequency of

1 " In morbis pectoris, s< mper ducendum esse ad vias urina?." Baglivi, quoted by
Ferriar.

a Chalybeate waters were recommended by Senac in commencing dilatation (Tnute,
1769, t. ii., p. 330), and his recommendation was endorsed by Ferriar (Med. Hist, and
Ref., voL i., 1792, On Dilatation of the Heart, p. 168).

3 Withering pointed out that digitalis "seldom succeeds in men of great natural
strength," but does much good "if tnc pulse be feeble or intermitting, the countenance
pale, the lips livid, the skin cold." An Account of the Foxglove, &c. Birmingham,
1785.

4 " I do not intend to say how this medicine (digitalis) acts, but I can, from observa-
tion, declare, that it has a very powerful effect in obviating the urgency of the symptoms
n dilatation of the heart" (Allan Burns, 1809, loc. cit., p. 57). Ferriar had previously
largely used digitalis in dilatation. The verbal accord between these writers and those
of the present day is more complete than is that of their meauing. Dilatation of the
heart was to the former synonymous with its enlargement and over-action, and they
valued digitalis for (and believed that it did good by) its supposed power of lessening
such over-action, when it was really strengthening the* heart's defective power.

DILATATION OF THE HEART. 755

action is at the expense of rest, for the length of the systole remains
nearly the same at various degrees of frequency of contraction, in-
creased frequency being obtained at the expense of the diastole.
It has been calculated that the time of rest to the heart which is
contracting 144 times per minute, is increased by one-third if the
pulse is reduced to 72.1 Moreover, the smaller cardiac vessels,
arteries, and veins, as well as capillaries, must be emptied of blood
during the cardiac systole.2 A certain time must elapse on each
diastole before the capillaries can be filled with blood and transuda-
tion of nutritive fluid through their walls can take place. This period
will be nearly the same in every diastole, and hence the total period
of rest available for cardiac nutrition will on this account also be
greater the less frequent the contraction.3

Digitalis appears to act also by increasing the completeness of the
contraction of the heart. Under its influence the heart of an animal
becomes firmer at the end of systole. Such contraction ensures the
expulsion of the whole of the blood contained in the chamber. Eveiy
approximation to this is, in dilatation, a direct gain. It not only
assists directly the circulation, but it arrests a process whicli is pro-
bably the main mechanism of the origin and increase of dilatation,
viz., the over-distension of the chamber in consequence of the addition
of residual blood to that which enters it from the ordinary source.
Increased firmness of contraction will not only lessen the tendency
to further dilatation, but will improve the condition of the cardiac
walls,4 and increase the tendency to compensatory hypertrophy.

Digitalis acts also by steadying the heart, diminishing its irregularity.
Dr. Kinger5 suggests that its main effect in dilatation of the left
ventricle accompanying mitral regurgitation is thus produced. By
preventing irregular contraction it arrests that part of the regurgita-
tion which depends on the irregular action of the papillary muscles,
and so relieves the over-distension of the auricle, and indirectly of
the ventricle.

Five to fifteen drops of the tincture of digitalis may be given with
advantage three times a-day. Most observers have found the tincture
convenient and reliable, but the infusion is believed by Ringer to
be a surer preparation, in doses of one or two drachms. Much larger

i Milner Fothergill, Diseases of the Heart, p. 4.

2 Harvey observed that the substance of the heart becomes pale during its
contraction.

3 Assuming, for instance, that the period required for the vascular distension of the
heart, and not available for nutrition, to be uniform at different frequencies of contrac-
tion, and to amount at each contraction to one-tenth of a second, the total period then
available for nutrition would be increased about three per cent, from this cause only,
by a reduction in the frequency of the pulse from 100 to 80. But it is probable that
the time needed for the vascular distension of the heart is shorter the greater the disten-
sion of the aorta, and hence that it is shorter the less frequent the contraction, and the
actual increase in the period available for nutrition will be rather greater than is represented
by the above estimate.

4 Partly, no doubt, by rendering perfect the expulsion of the blood from the cardiac
veins, as Dr. H. C. Wood points out (PhiL Med. Times, 1874, Nov. 14, 21).

8 Handbook of Therapeutics, 5th ed. p. 421.

766 A SYSTEM OF MEDICINE.

doses have been given, but these should be employed with caution.
Ringer recommends strongly that the minimum effectual dose should
be employed in the first instance, since an increase after a time is
often necessary.

The Virginian prune has been long employed as a cardiac tonic in
America, and was introduced into this country by Clifford Allbutt,1 who
has found it very useful in cardiac dilatation. I have found its power
as a tonic, although marked, inferior to digitalis ; but it is of much
value for the relief of continuous cardiac discomfort, and may
with advantage be given for a time, while digitalis is omitted.
Twenty or thirty minims of the tincture may be given three times
a-day. Nux vomica and strychnia are also useful in improving the
cardiac tone. Arsenic has been recommended for the same purpose.

Treatment of Special Symptoms. — Cardiac discomfort, in various
forms, whether as pain or palpitation, is the source of much distress.
The tranquillising influence of digitalis on the heart relieves much of
the pain. Aconite is of use in the same way, and is of most service
when " extreme irritability of contraction coincides with great weak-
ness of beat " (Walshe). Half a minim or a minim may be given ; its
effects being watched. Drawing a few deep breaths will often arrest
an attack of palpitation (Brown-S^quard). Belladonna may be given
internally in doses l^v. to TTlxv. three times a-day, and is often of much
service. Belladonna plasters have been condemned by some autho-
rities as useless, but they certainly give relief to the cardiac discom-
fort. Patients constantly ask for their repetition. The tincture of
the Virginian prune sometimes gives very marked relief to continuous
pain, and will sometimes stop for a time slight pseud-anginal seizures.
Opium has the same power over cardiac as over other pains. Hypo-
dermic injections of morphia give quick relief, but their use has been
discountenanced in grave heart diseases, on account of the fear of too
profound a sedative influence on the heart. But Clifford Allbutt and
Ringer have employed them extensively, and assert that T\jth or Jth
of a grain may be injected with perfect safety, even in grave dilata-
tion. The relief to the patient is certainly in many cases most
striking. A very small quantity will sometimes procure sleep, in
cases of cardiac insomnia, when sedatives given by the mouth fail
altogether. Tolerance of sedatives by the mouth in these cases
does not always imply a corresponding tolerance of the hypodermic
injection, and the first injection should therefore always be very
small.

For paroxysmal pains, antispasmodics may also be given. Nitrite
of Amyl in inhalation, so useful in true angina, also gives relief to the
pseud-anginal seizures, and to the sense of suffocation, which is some
times troublesome. If necessary, it may be employed diluted with
spirit. A few drops of chloroform, or what is more convenient, half
a teaspoonful of chloric ether, inhaled with steam, is also useful.

Attacks of increased cardiac failure need general stimulants and

\ Medical Times ami Gazette, Feb. 16 an«l March 2, 186/.

DILATATION OF THE HEART 757

antispasmodics. Alcohol, given with hot water, is one of the most
rapidly diffusible stimulants. Sal-volatile and ether, with tincture of
lavender, are the most convenient and most effective drugs. Stimula-
tion of the ends of the pneumogastric nerve in the stomach seems to
have some influence in exciting the heart's action, and effervescing
drinks and carminatives are useful in that way.

In syncopal seizures the head should be placed low, and the
remedies just enumerated should be employed. Active respiratory
movement should be restored as quickly as possible. It is thus,
and by arousing consciousness and will, that cold affusions and
stimulating applications to the nostrils are of service.

The lung complications of dilatation of the heart, bronchitis, oedema,
congestion, need the most stimulating special treatment for each
variety. Stimulating expectorants, as ammonia, are necessary for the
bronchitis ; and congestion is best relieved by the cardiac tonics and
stimulants already described, and by mild counter-irritation.

Cough is often an exceedingly troublesome symptom in these cases,
it may be paroxysmal or constant, and out of all proportion to the
expectoration. Morphia is generally necessary to control it; one-
twelfth of a grain may be given by the mouth, and with it a few
minims of the tincture of belladonna.

Dyspnoea is among the most obstinate, as well as the most dis-
tressing, symptoms of dilatation. Its chief treatment is that of the
cardiac failure, and the same diffusible stimulants are needed. The
paroxysmal form is relieved most effectually by more direct sedatives :
opium, Indian hemp, belladonna, lobelia inflata. Dry-cupping, and a
few leeches to the precordial region, are recommended by Walshe
when there is palpitation as well as dyspnoea. Posture is important ;
the head should be well raised, and Walshe recommends an attitude
leaning forward, with the forehead supported by a sling. When the
dyspnoea is dependent on pulmonary oedema, relief is often only to be
obtained in the sitting posture.1

Headache is not often a troublesome symptom except in dependence
on the cough. It is best relieved by posture, and by bathing the
forehead with hot water. Sleeplessness is often a distressing
symptom. Rest is disturbed by sudden starts, or the patient wakes
up in a sudden fright with a sense of great distress. Such symptoms
may usually be removed by the administration of the third dose of
digitalis at bedtime in combination with bromide of potassium.
Indian hemp (gr. £ of the extract or TI^x. of the tincture), will also,
though less uniformly, give relief. Actual insomnia may be relieved
by chloral, chloral and bromide, and morphia by the mouth or skin,
employed with caution.

The congestion of the liver may be lessened to a marked extent by

i A rccliuing-chair, with a cross rest on which the forehead can be supported, has
been for some years in use at University College Hospital, and a M heart-bed " for the
same purpose is described and recommended by Dobell.

768 A SYSTEM OF MEDICINE.

mercurials. Every relief given to the portal congestion no doubt
lessens immediately the pressure upon the hepatic lobules.

Vomiting is sometimes a very troublesome symptom. Effervescing
ammonia, with bismuth and hydrocyanic acid or morphia, is the most
useful. The amount of ammonia need not be large ; gr. x. of the
carbonate with gr. xi. of citric acid is sufficient. Ice should be sucked,
and food given in small quantities. Counter-irritation to the epigas-
trium is sometimes useful. Any portal congestion must be relieved,
the bowels being kept open. Diarrhoea sometimes demands treatment,
and should be moderated rather than restrained. If constipation is
present, moderate doses of hydrogogue purgatives are most useful, as
Pullna or Hunyadi Janos water, colocynth, or podophyllin. Flatulence
is often very troublesome, and adds much to the cardiac and general
distress. Hot fomentations externally and carminatives internally
give most relief; sal-volatile, peppermint, chloric ether, spirit of
horse-radish, are all useful. The relief which is afforded to the suf-
ferers from dilatation of the heart by the removal or diminution of
their gastric troubles is often very great. Dobell has lately drawn
attention specially to this subject.1

The scanty urine consequent on the kidney congestion may call for
treatment. Mild diuretics, with digitalis for its double action, often
suffice to relieve the kidneys. Often, however, this long-continued
congestion induces tissue changes in them, and dry-cupping to the
loins, or stronger diuretic treatment — broom, juniper, &c. — may be
necessary. Stokes2 remarks that diuretics often succeed after a
mercurial, where they have previously failed.

Dropsy is almost invariably a troublesome symptom in the later
periods of a case. It is dependent partly on the blood-state, favouring
osmosis, partly on the mechanical congestion, increasing the pressure
of the blood in the small vessels, and increasing it to the greatest
extent in the most depending parts, where gravitation aids the cardiac
failure. It can only be effectually combated by treating each of these
causes, first by strengthening the heart, and secondly by improving
the blood-state. Hsematinic and cardiac tonics are needful for
this. But it may be lessened by other measures. No remedy can
promote, directly, the absorption of the effused fluid from the cellular
tissue back into the blood-vessels, but reduction in the volume of the
blood exercises a marked influence. The abstraction of blood will be
necessary only when acute pulmonary oedema threatens life, and then
cupping on the chest is preferable to venesection. Often purgation
is sufficient, and hydrogogue cathartics, bitartrate of potash, elaterium,
jalap, are the most effectual. Where there is evidence of enlargement
of the liver, a dose of a mercurial is stated by Hayden to increase the

i On Affections of the Heart, 1872. The value of carminatives has long been known.
Albrecht relates that Sylvius removed all symptoms in a case of cardiac dilatation bv
their use. According to Tliny, the Egyptians lwlicved the juice of horse-radish to be the
onlv cure for atrophy of the heart.

** Loc. cit., p. 263.

DILATATION OF TEE HEART. 759

effect of the purge upon the dropsy. Diuresis occupies a position
hardly second to purgation for the removal of dropsy ; copaiba, iodide of
potassium, nitrate of potash, juniper, broom, nitric ether, and especially
digitalis, may be given. The dose of digitalis for the removal of
dropsy by its diuretic action needs to be larger than when its tonic
action alone is needed ; 3ij. or 3iv. of the infusion, or \x. or xx. of the
tincture, may be given twice a day. Dry-cupping over the kidneys
sometimes, it is said, increases the effect of the diuretic.

In severe cases all these means, successful at first, may ultimately
fail to remove the dropsy, and it becomes necessary to relieve the
distended limbs, or sloughing will occur. It is necessary to anticipate
this and to scarify or puncture the skin, and allow the limb to drain.
Scarification is the more effectual, but is said to be attended with
greater risk of erysipelas. Erysipelas will rarely occur when the
precaution is taken to wrap up the limbs in flannel, wrung out of
warm water, immediately after the scarification, renewing it every
two hours during the first two days. A harelip pin is a convenient
instrument for the punctures.

Jaccoud l recommends, as a substitute for punctures, friction each
day with croton oil : in a day or two the characteristic eruption is
produced, and from it the serum escapes abundantly. The frequency
with which a slight inflammation is the starting-point of a slough
makes it difficult to believe that the risk of gangrene is lessened by
this method.

In all cases of dropsy, as little fluid as possible should be taken.
When the kidneys are underacting from congestion, its effect is, as
Milner Fothergill2 has insisted, only to throw an increased strain
upon the heart.

1 Pathologic interne, 4th ed. vol. i. p. 621.

■ The Progress of Heart Disease, Lancet, vol. i., 1875.

760 A SYSTEM OF MEDICINE.

FATTY DISEASES OF THE HEART.

By W. R Gowers, M/D.

Fatty degeneration of the heart consists in the substitution of fat
for its muscular substance. This result may be reached by two
processes of different pathological and clinical relations. The one
process effects simply the molecular substitution of fat for the proper
substance of the muscular fibres. The other consists in the overgrowth
of the normal fatty tissue of the heart among the muscular fibres, so as
to compress, and ultimately to destroy and replace them. The former
process needs the microscope for its demonstration ; the latter is ob-
trusively conspicuous to the naked eye. The one is an indication of
diminished vitality, and may be its initial stage, a necrosis ; the other
is at first a growth. Some varieties of the two processes present common
pathological features, and their effect on the function of the organ is
the same ; but their diverse conditions of origin and anatomical char-
acters need separate description. In pursuing this course the example
is followed which was set by Dr. Quain Mn a memoir on the subject,
which has served as a model for most subsequent writers. The
hypertrophic form of " fatty infiltration " will first be described, and
then the " necrobiotic " process of fatty degeneration.

Fatty Overgrowth.

Synonyms. — Fatty Infiltration (Rokitansky) ; Fatty growth, Fatty
Hypertrophy (Quain) ; Adipose Cardiaque, Surcharge Graisseuse,
OWsitd du Coeur (French writers).

Definition. — An abnormal development of adipose tissue on and
in the substance of the heart. Fatty tissue is always present on the
surface of the heart, and varies in amount according to the age, and the
nutritive conditions and tendencies of the individual. In abnormal
development this fat may become so excessive that mechanical
interference with the function of the organ is the result. It is a

1 On Fatty Diseases of the Heart, Med. Chir. Trans., vol. xxxiii.

FATTY DISEASES OF THE HEART. 761

local " instance of the extension into the domain of disease of the
physiological process of growing fat" *

History. — Some of the symptoms of obesity, which are in part
cardiac, were among the earliest medical observations. Hippocrates
noticed the tendency of fat persons to earlier death than others, and
both he and Celsus observed the dyspncea which is associated with
obesity. Harvey described an excess of fat around the heart of Old
Parr. Since that time almost every writer on diseases of the heart
has alluded to or described a similar condition. Kerkering,2 in 1717,
noted its occurrence at so early an age as two years. Senac 8 in 1749
described carefully the normal variations in the quantity of fat
according to time of life, &c. Morgagni 4 recorded examples of hearts
so loaded wTith fat that no muscular tissue could be seen. Portal 6
noted the concurrence of fatty overgrowth in the heart with a similar
condition in the voluntary muscles. The state wras fully described by
Corvisart, who suspected that it might be a cause of sudden death.
Morgagni thought that the muscular fibres of the heart suffered in
this condition of fatty growth. The microscope, long after, showed
that this is actually the case. It was inferred, however, from the
apparent substitution of the fatty for the muscular tissue, and from
the evidence of cardiac weakness. Hearts subject to this mixed
change were described, and the disease ably discussed, by Duncan
(1810), Cheyne (1818), Townsend (1832), and E. W. Smith (1838).«

Causes. — Excess of adipose tissue on the heart is usually
associated with excess of adipose tissue elsewhere, and is due to the
same causes. Quain found that in almost every case of fatty growth
about the heart there was general obesity. The converse holds
good to a less extent. King Chambers 7 records that of thirty-six
corpulent persons a considerable excess of fat at the base of the heart
was found in twelve On the other hand, in 165 bodies not remarkable
for fat, there was excess of fat about the heart of four only.

Hereditary predisposition exercises a marked influence on the
occurrence of obesity, and no doubt also on the occurrence of
fatty infiltration of the heart. In two-thirds of the cases of general
obesity it is found that hereditary or collateral obesity exists. Sex
also influences its occurrence. If the statistics of Quain 8 be
combined with the cases of fatty growth contained in the valuable
tables of Hayden,9 we have thirty-five cases of this condition of
which twenty-five were men and ten women. The condition is

1 Hayden, Diseases of Heart and Aorta, p. 596.

* Opera Omnia Anat, 1717, p. 134. » Traite\ &c., vol. i. p. 187.
4 De Sed. et Caus. Morb. Ep. iii. Obs. 20 ; xxvii. 2 ; xxx. 18.

6 M6m. de FAead. des Sciences, 1784. • See Fatty Degeneration— Hiatory.

7 On Corpulence, I860, p. 92. 8 Loc. cit.

• Diseases of the Heart and Aorta, p. 648, et sea. These tables are compiled from
the Transactions of the Pathological Societies of Loudon and Dublin, and from Dr.
Hayden 's own case-books.

VOL. IV. 3 D

762 A SYSTEM OF MEDICINE.

therefore more than twice as common in the male as in the female
sex. Age also exercises a distinct influeuce. At birth, as Senac
pointed out, the heart is free from fat, and the amount increases as
years go on. After six years fat is always present between the
auricles and the ventricles. Fatty infiltration follows the same law and
commonly occurs after middle life.1 The combined cases of Quain and
liayden illustrate this very clearly. Under 20 there was but one case,
between 20 and 30, three cases ; between 30 and 40, none ; between
40 and 50, four; between 50 and 60, eleven; between 60 and 70,
nine; and over 70, seven cases. Sedentary habits increase the
tendency to this condition. Food is an effective agent if the
disposition to grow fat exists. Starchy, saccharine, and fatty foods
are the chief fat-forming elements. Their effect is the supply to
the system of a quantity oi carbon in excess of the respiratory needs,
and this carbon is stored up as fat. But if the oxygen supplied be
in considerable deficiency, nitrogenous food may yield fat by its
imperfect oxidatioa Alcoholism also exercises a remarkable influence.
Malt liquor seems to be more effective in causing fatty growth than
spirits, but any form of alcoholism conduces to it; the blood in
chronic alcoholism has been found to contain far more fat than in
health. Sudden changes in the conditions of the system seem some-
times to determine the overgrowth of fat, general and local An
acute illness, and confinement to bed owing to an accident, are among
the causes which Chambers mentions as having set the obese
tendency in operation which litis continued after the cause ceased
to act

Pathological Anatomy. — The fat normally present on the heart
exists chiefly in the auriculo-ventricular and inter-ventricular sulci,
extending thence on to the ventricles, especially on to the surface of
the right ventricle. When excessive it may conceal from view almost
the whole of the muscular tissue of the heart. It may remain
confined to the surface, but when considerable it usually invades the
substance of the heart, passing in between the muscular fibres. On
section the muscular substance appears narrowed, its junction
with the surface fat being much nearer to the inner surface of
the wall than in health. Streaks of fat may extend into the
muscular tissue. Sometimes the latter is reduced to a thin endo-
cardial layer, and even, as Laennec pointed out, the papillary muscles
may appear to arise from a mass of fat. The muscular fibres are
not really destroyed so completely as they appear to be : under the
microscope they may still be seen in considerable number among
the fatty tissue by which they are separated and displaced, and often
pressed upon. Fatty degeneration of the fibres does, however, occur
in a very large majority of the cases. Of the twenty cases contained
in Hayden's table, in two only were the muscular fibres stated to be
healthv.

1 The cast.* wliicli is described by Kerkering stands almost alone.

FATTY DISEASES OF THE HEART. 763

The fat does not, however, always form such extensive and
continuous layers. A follicular variety of fatty overgrowth was
described by Laennec, and has since been generally recognised. In
it the fatty tissue occurs in minute areas, which can be seen as specks
in the substance of the heart, especially beneath the endocardium. In
all conditions of fatty growth the fat is contained in oval and round
cells, having an average diameter of -j^th inch, and very similar
to those which contain fat elsewhere. In cases of fatty overgrowth
upon the heart there is usually also an excess of fat outside the
pericardium.

Symptoms. — A considerable increase in the amount of fat upon the
surface of the heart may be unattended by morbid signs. This was
remarked by Corvisart and Laennec, and their observations have
since been abundantly confirmed. Where the fat has invaded the
substance of the heart, is infiltrated in the muscular tissue, the effect
is a simple weakening of the heart, identical with that presently
to be described as the result of the fatty degeneration, which is so
frequently combined with the fatty growth. The impulse and sounds
of the heart are weakened. The apparent weakening is greater than
that wThich actually exists, because the subcutaneous and mediastinal
fat obscures the impulse and dulls the sound. From the same cause
the slight increase in the size of the heart which commonly exists is
rarely to be detected. The actual diminution in the strength of the
heart is often considerable. The pulse is weak, but may be perfectly
regular even to the last. Dyspnoea is frequent, and syncope, and
even rupture of the heart, may occur. The tendency to sudden
death is very marked. Out of thirty-four cases in which the character
of the death was noted it was sudden in twenty-four. Of these a third
died from rupture of the heart, and another third from syncope. In
every case of rupture, and in most of those in which syncope occurred,
there was fatty degeneration of the remaining muscular fibres.

Diagnosis. — The diagnosis of fatty overgrowth in this condition
depends on the recognition of the association of cardiac weakness and
general obesity. The signs and symptoms are those of fatty degene-
ration. With such signs, if general overgrowth of fat is present,
we are justified in suspecting the existence of fatty overgrowth and
infiltration of the heart.

Treatment. — The treatment is essentially that for the general
obesity of which the local overgrowth is but a part. The main object
is to lessen the supply of the fat-forming hydrocarbons, and to
increase their consumption in the system. The amount of food
taken, if excessive, should be restricted ; and fat, starch, and sugar
should be, as far as possible, excluded from the diet. As much
exercise should be taken as is practicable without putting undue
strain upon the weakened heart. It. is doubtful whether drugs

3 D 2

764 A SYSTEM OF MEDICINE.

possess auy power of lessening the local accumulation of fat Alkalies
are believed by Chambers to diminish general obesity : whatever
l>eneficial influence they exercise on general obesity they will also
exert on the local state.

In other respects the treatment of fatty overgrowth is the same aa
that of fatty degeneration of the heart presently to be described.

Fatty Degeneration.

Synonyms. — Ramollissement (Corvisart, Laennec), Softening of the
Heart; Carditis (Bouillaud) ; Greasy Degeneration (Hope); Fatty
Metamorphosis (Rokitansky) ; Atropine Graisseuse (Parrot) ; Steatose
Parenchymateuse (Blachez).

Definition. — A change in the muscular fibres of the heart, by
which the transverse striae are at first obscured, and afterwards dis-
appear, being replaced by granules and globules of fat. This granular
and fatty degeneration of the heart, as far as we at present understand
it, has nothing in its nature of specific character, but is simply the
expression of defective nutrition of the proper substance of the fibre.
Hence, as might be expected, the conditions with which it is associated,
and to which, directly or indirectly, it is due, are widely differeut in
their nature and mode of action. So diverse are they that it is
evident that the condition of the heart is rather a common conse-
quence, than a special disease. It has, however, its own symptoms
and its own consequences, and so needs special description.

History. — Fatty degeneration was a late discovery in cardiac patho-
logy. Morbid appearances, such as are now kuowu to result from fatty
degeneration, were mentioned by Robert Fhull1 iu the beginning of
the seventeenth century, and by Lancisi a hundred years later, but
received little attention. Overgrowth of the surface fat, and its in-
vasion of the muscular tissue, were indeed described by Morgagui
and many other writers, as has been already stated, and there can
be little doubt that, in some of the instances recorded, true fatty
degeneration of the remainiug fibres was present. Such a change in
voluntary muscles was discovered by Hatler and Vicq d'Azyr; and
some French pathologists at the beginning of the present century
suspected that a similar process might be the cause of some morbid
appearances in hearts which did not present the ordinary characters
of fatty growth. Corvisart,2 who was perfectly familiar with the
latter, had heard of this opinion, and considered the explanation
plausible, although he had not himself seen the change referred to.
In 1816, Andrew Duncan3 described a heart which was probably an

1 Senac ([notes from Fludd an account of a heart so soft and brittle that the fingers
could be placed in its substance. It is said that the man from whom it was taken had
played at cards two days before his death. (Senac, Traite*, &c, vol. ii. pp. 382, 389.)

* Diseases of the Heart, Hebbs* Translation, p. 168.

9 Edinburgh Medical and Surgical journal, 1816.

FATTY DISEASES OF THE HEAHT. 765

example of the mixed change, fatty growth and degeneration, and a
similar case was recorded by Che) ne x in 1818. The naked eye
characters of the simple degeneration were first accurately distin-
guished by Laennec2 in 1819, who described the change in a limited
area in very exact terms, recognised its identity with the degeneration
described by Haller and Vicq d'Azyr, and gave to it the definite name
of "fatty degeneration of the heart."8 Bertin,4 quoting Laennec's
description, believed he had noticed the change in question, but
admitted that he had confounded it with chronic softening, " of which,"
. he said, " it is perhaps only a variety." General softening of the
heart was described by Bertin as the effect of carditis.6 It was
thus described also by Bouillaud.6 The combination of fatty over-
growth with softening and degeneration of the remaining fibres was
especially noted by Adams7 in 1827, Elliotson 8 in 1830, Townsend*
in 1832, and Latham in 1839. Simple fatty degeneration was
described and distinguished from fatty growth by Hope 10 in 1839, and
by Williams u in 1843, who compared it to the formation of adipocere.
Fresh interest was given to the subject in 1844 by the publication
of Rokitansky's observation of the microscopical characters of the
degenerated fibres.12 In 1845 Peacock u published similar observations,
made apparently in 1843, independently of Eokitanksy's discovery.
In 1847 a very clear description of the process in its wider associa-
tions was given by Paget,14 and of its chemical pathology by Virchow.15
In 1849 a series of cases illustrating the facts previously ascertained,
were published by Ormerod18 and by Kennedy,17 and in 1850
Quain18 contributed the very full account of the whole subject of
fatty diseases of the heart, which has been already mentioned.

Varieties. — According to the appearance of the fibres, whether
they contain granules or globules of fat, the two stages have been
distinguished of granular and fatty degeneration, and it has
been held that these two varieties are sometimes distinct forms of
degeneration. There are, however, reasons for regarding them as stages
of the same process, and both forms will be considered here. For con-

I Dublin Hosp. liep., vol. ii. 1818, p. 216.

* On Diseases ot the Chest, Forbes' Translation, 1821, p. 229.

3 It is difficult to believe ihat Laennec did not recognise the identity of "softening
and fatty degeneration, for he descrilied the two < otiditions in identical terms.

4 Traite des Maladies du Cceur, 1824, p. 431.

8 Bertin noted (p. 400) as symptoms of "softening " many which are now ascribed to
fatty degeneration, such as weakened or inappreciable impulse, d illness of sound, and
extreme frequency or slowness of the pulse.

4 Traite Clinique des Maladies du Cceur, Ed. Quinzieme, tome i. p. 615.

7 Dubliu Hosp. Rep. vol. vi. 398. 8 Lumleiau Lectures, p. 32.

» Dublin Journal of Medicine, 1832, p. 165. ,0 Diseases of the Heart, p. 348.

II Principles of Medicine, 1843, p. 304

» Handbuch der Path. Anat Bd. ii. 1844, p. 463.

18 Monthly Journal of Medical Scieuces, Jan. 1845, p. 20.

14 London Med. Gazette, 1847 licet, vi.).

18 Virchow's Archiv, Bd. i. p. 152. 14 London Med. Gazette, 1849.

17 Dublin Med. Press, vol. xxL :8 Med.-Chir. Trans, vol. xxxiii.

766 A SYSTEM OF MEDICINE.

venience' sake the single term " molecular degeneration " may be used
to denote them. " Primary " aud " secondary " degenerations were dis-
tinguished by Quain, the former occurring without, the latter
dependent on, preceding inflammation. Ponfick * would divide the
degeneration into two forms, according as the muscular tissue of the
heart was or was not in a preceding abnormal condition, and would ■
further divide the cases in which the muscular tissue presents no
other change than the degeneration, into " toxcemic," " senile," and
" anaemic " varieties, according to their supposed causes.

Etiology. — (a) Predisposing Causes. — Hereditary Influence. —
A few facts are on record which suggest that fatty degeneration of
the heart may own an inherited cause, and thus be transmitted. The
cause may be a tendency to early decay of the muscular fibres,
due to their defective vitality, or it may be a predisposition to
one or other of the exciting causes of fatty degeneration, to be
immediately described, especially to fatty overgrowth or arterial
disease.

Sex has a marked influence. This is established by all the
statistics which have been collected. The disease is at least twice as
frequent in men as in women. Quain found the proportion 4 to 1 ,
Ormerod about 3 to 1, Hay den more than 2 to 1. Ponfick
states that the fatty degeneration which results from general ansemi.i
is an exception to the rule, and is more common in women than
in men.

Age. — Fatty degeneration of the heart may occur at any age. It has
been found in the foetus, and has been met with at every period of life
from infancy to old age. But it is much more common in the
second than in the first half of life. It is itself a degeneration, and
it owns, as its frequent exciting causes, other degenerations, and is thus
most frequent during the degenerative period. About three- quarters
of the cases occur after forty years of age.

Habits of Life have probably less influence in causing fatty degene-
ration, than on the occurrence of fatty growth. The condition is more
common among the lower classes than among the upper — the reverse
of the proportion that obtains in cases of fatty growth. Sedentary
habits predispose to imperfect nutrition of the muscular fibres, and
some occupations act also by rendering the individuals liable to the
exciting causes.

Depressing Emotions are believed by Quain to predispose, in some
cases, to fatty degeneration. Moral emotion or long-continued
physical pain is said to have such an influence.

Nutritive Influences. — The tendency to the formation of fat, which
has so marked an influence on fatty growth, has apparently much less
effect in causing fatty degeneration. Quain found that the disease
occurred with almost equal frequency in fat and in thin persons.

1 Berlin Kliiiischc Wocheiischrift", 1873, Nos. 1 aud 2.

FATTY DISEASES OF THE HEART. 767

(b) Exciting Causes. — The exciting causes of fatty degeneration of
the heart comprehend all those conditions which can interfere directly
with the nutrition of its fibres. They are very diverse in character,
but fall naturally into the two groups — general and local. They may
act in conjunction with, or apart from, the predisposing causes.

I. General Conditions causing molecular degeneration of the heart are
numerous, and various in their character. The tendency to degene-
ration may (1) be primary, or (2) it may be secondary to other morbid
states, of which the most important are certain causes of general
impairment of nutrition, certain states of poisoned blood, and
certain poisons introduced from without.

(1). Fatty degeneration of the heart may own as its only cause the
tendency to general degeneration which is natural to old age and
which may occur at a much earlier date. This constitutional
tendency is undoubtedly one of its chief causes. The degeneration is
rarely confined to the heart ; it is in most cases more widely spread
and is seen in the inelastic skin, the rigid vessels, the white hair, the
arcus senilis. But the tendency of such degeneration to unequal
distribution is well known and may be manifested by disproportionate
degeneration of the heart, especially when the conditions of life
are such as to put an undue strain upon the organ. This degenerative
tendency may or may not be associated with overgrowth of fatty tissue,
and thus two types of degeneration are met with, the pathological ten-
dencies of which Paget long ago pointed out.

(2). Fatty degeneration may be the result of some general condition
of imperfect nutrition.

Anamia both quantitative and qualitative may cause it. The
influence of repeated losses of blood in causing this degeneration
has long been observed as a clinical fact,1 and it has been recently
studied experimentally by Perl.2 It can be readily produced in dogs
by repeated bleedings, but much more readily by occasional large
bleedings than by more frequent smaller bleedings. It was especially
marked when the loss of blood amounted to three per cent, of the
weight of the body. The papillary muscles of both ventricles are
said to suffer first, then the walls of the left ventricle, and lastly the
walls of the right ventricle. Stokes pointed out that depressing treat-
ment may act in a similar manner. In idiopathic anaemia fatty
degeneration of the heart also occurs. Biermer 3 has remarked that
fatty degeneration of the blood-vessels often coexists. In pregnancy,
intense anaemia sometimes occurs, and in such cases fatty degenera-
tion of the heart has been found.4

Wasting Diseases were noticed first by Ormerod, to have as one of
their consequences fatty degeneration of the heart. Those in which it is
most frequently met with are phthisis, cancer, and chronic suppura-

1 Ormerod, loc. cit. p. 832.

* Virchow's Archiv, fix. 1. Similar ex|>erimonts ha«l also been made by Tschudncwsky.
Botkin's Archiv, Bd. ii. 1866—7. t

3 ttericht iiber der 42en Versammlung deut. Natnrforscher u. Aerztc. Dresden, 18o8.

4 Gusscrow, Archiv fur Gyiwkologie, 1871, ii. 2, p. 218.

768 A SYSTEM OF MEDICINE.

tion. In each condition the amount of degeneration may be consi-
derable. In cancer it has seemed to the writer to be sometimes
associated in degree with the degree of the fatty degeneration in the
new growth. In Addison's disease it has also been met with.1

Toxcemic Influences constitute another group of causes. Fatty
degeneration may result from many acute and some chronic blood
changes. These include the various acute febrile conditions, specific
and non-specific, and certain chronic diseases which alter the constitu-
tion of the blood.

In acute febrile diseases, molecular degeneration of the heart has
been noticed by a large number of observers. Its naked-eye charac-
ters were distinguished by Laennec, and its conditions of origin and
consequences were carefully studied by Louis and Stokes. Laennec
pointed out that it occurred especially in those cases in which marks
of " putridity " were present. By most writers the change has been
regarded as inflammatory, as due to " myo-carditis." It is certain
that actual inflammation, as by extension from the pericar-
dium, causes a similar degeneration. But in most of these cases, as
Louis and Stokes pointed out, other evidence of inflammation is
wanting ; there is no purulent infiltration, no effusion of lymph on the
pericardium ; and Stokes pointed out that local inflammations are rare
in the conditions in which this change occurs.

Moreover, identical changes may occur from other influences with
equal rapidity, in which there is no suspicion of inflammation, but
proof of a profound alteration in the state of the blood — as for ex-
ample in phosphorus poisoning. Simple elevation of the tempera-
ture of the body has been shown capable of producing a similar
defeneration.2

Many acute diseases are attended with this molecular degeneration.
In acute rheumatism the condition is usually associated with un-
doubted inflammation outside or inside the heart, and is confined to
the adjacent fibres, and other evidence of inflammation is to be found
where the change is most intense. But in other cases in which the
blood-change is profound, a simple degeneration may extend through
the whole thickness of the wall and be apparently related to the
pyrexia or to the degree of the blood-change, as in other febrile
diseases, rather than to the special form of the toxaemia.

The other diseases in which the change occurs are the various
febrile affections, and especially those in which any pyogenic influence
is at work. It is common, for instance, in erysipelas, puerperal
fever, and small-pox. In the last it has been found to be very
frequent.3 It occurs also in yellow-lever,4 and malarial fevers.5 In

1 E. Wagner, Die fette Metamorphose des Herzfleisches. Leipsig, 1865.

* Iwasehkewitsch, Journal fur Militararzte, 1870, and Virchow'sJahresb, 1870, i. 179.
"Wickham Legg, Path. Trans, vol. xxiv. 1873, p. 226.

* P. Sick quoted in Cuustatt's Jahresbericht, 1866, ii. 39. Deauos and Huchard.
Senae noted the frequency of syncopal death in this disease. Traite, Ac. 1749, ii. 551.

4ffeat. Smith, quoted in London Aled. Record, 1874, p. 517.
« PonHck, loc. cit. ; VaJlin, J/Uuion MeU 1874, No. 2?.

FATTY DISEASES OF TEE HEART. 769

typhus and typhoid fevers,1 it is also common, although other forms
of degeneration are also found in the heart as well as in the voluntary
muscles in these diseases. In typhus Stokes found that it marked
some epidemics much more than others, and that it generally com-
menced about the sixth day. In typhoid, Wagner2 found extensive
fatty degeneration in nine cases out of fifty-nine. In diphtheria
the change is also common. G. Homolle found it in six out of
fourteen cases which he examined, and Parrot found it in almost as
large a proportion.8

In measles aLso Parrot found it present in about one-fourth of fifty-
four fatal cases. In one case it was extreme. Extreme degenera-
tion of the heart has also been met with in acute atrophy of the liver.

Chronic alterations in the blood may cause fatty degeneration of
the heart. It occurs in gout, as Charcot has pointed out.4 At first
it is slight, but as the disease progresses it may become very consider-
able and become a cause of sudden death. In the altered state of
blood, which results from chronic renal diseases, it also occurs. It
has also been found in purpura, scurvy, and the hemorrhagic diathesis f
in the latter perhaps as a result of the loss of blood. It has also been
seen in trichinosis.

Certain poisons possess a remarkable power of inducing fatty
degeneration of the heart in common with that of other parts.
Foremost among these must be placed phosphorus, which has a
very rapid action on the heart, liver, kidneys, and other organs,
causing marked fatty degeneration in a tew days. In a case recorded
by Habershon, on the fifth day after a dose of five grains of
phosphorus all the organs were the seat of fatty degeneration. The
heart becomes yellowish or reddish-grey, soft, and friable, the fibres
being filled with fat drops. According to Schraube 6 the affection
of the heart is almost invariable hi phosphorus poisouing. Arsenious
acid, lead, and antimony 7 are said to cause a similar molecular degenera-
tion. In poisoning by sulphuric and other acids it has also been
found; and it occurs in greater degree the more readily the acid can
get into the blood.8

Alcohol is, if not the most powerful, at any rate the most frequent
toxic cause of fatty degeneration. In chronic alcoholism the blood
is loaded with fat. The habitual use of ether and chloroform is said
to have a similar effect.

II. Local Causes. — All local causes of atrophy of the heart (q.v.)

1 Stokes, Diseases of the Heart, p. 366 ; Murchison, On Fever, pp. 256, 631.
1 Loc. fit.

3 Diet. Encyclopedique des Sciences M&l., vi»l. xviii, 1876, ait. Cajur. It has also been
observed in diphtheria by Bengelsdorf (Berl. Klin. Wochensvhrift, 1871), and Bouchut
(Gaz. des K6p. 1872, p. 117).

4 Maladies des Vieillards et Maladies Chroniques. Paris, 1868.

• Warner, loc. cit. • Schmidt's Jalirb. 1867, 209.

7 Salkowsky, Virchow's Archiv, xxxiv. 1 and 2.

8 Munk and Leyden, Berlin Klin. Wochen&chrift, 1865, Nos. 49 and 50.

770 A SYSTEM OF MEDICINE.

may also cause the fatty degeneration of its fibres. This is, indeed,
partly the mechanism by which the atrophy is produced.

External yrcssurc may have this effect. Compression by fluid
rarely causes molecular degeneration, but pressure by the contraction
of lymph, limited in area, or by the pressure of calcified plates, may
produce it. It is possible that the effect is in many cases produced,
not by the direct pressure on the muscular fibres, but, as Walshe
suggests, by the compression of the arteries and consequent defective
supply of blood, a powerful cause of fatty degeneration.

Interstitial pressure on the muscular fibres may certainly, however,
be an immediate cause of this fatty degeneration. It is seen in fibroid
and fatty overgrowth. It is well seen in the effects of syphilitic and
other growths in the heart. In each condition the fibres are com-
pressed directly by the new tissue which is developed* between them. In
fatty overgrowth tbey may be little changed, but they frequently suffer,
presenting narrowing and indistinctness of striation, sometimes simple
atrophy, sometimes very distinct fatty degeneration. This latter occurs
especially when any predisposing cause of fatty degeneration coin-
cides in operation, such as congestion of the heart in fibroid over-
growth, sedentary habits, degenerative tendencies, or alcoholism in
fatty overgrowths.

Local Anosmia from vascular obstruction is a frequent cause of
extreme fatty degeneration. The obstruction is usually gradual, and
due to atheromatous changes in the walls of the coronary arteries,
calcification, &c. ; sometimes it is sudden from thrombosis, or less
frequently embolism. The left coronary artery is said to be affected
more frequently than the right. The degeneration is limited to that
part of the heart to which the diseased vessel is distributed. This
connection was noticed by Quain, and his observations have since
been abundantly confirmed. He found diseased coronary vessels
present in thirteen out of thirty-three cases, and pointed out that the
effect depends on the absence of anastomoses with other vessels, by
which a collateral circulation could be established, the " terminal
character " of the arteries, as it would now be termed, first demon-
strated by Swan.1

Congestion of the walls of the heart is, as Jenner2 pointed
out, a cause of fatty degeneration of the muscular fibres. The
degeneration is rarely simple, more or less fibroid growth is
usually conjoined. The chief cause of such congestion is dilatation
of the right side of the heart and obstruction, consequent on the
distension of the auricle to the escape of the blood from the coronary
sinus. Hence fatty degeneration of the heart is frequent in emphy-
sema, long-continued pleural effusion, and diseases of the left side of
the heart, which overload the right chambers.

Inflammation of the substance of the heart, "carditis," is also
attended with molecular degeneration of the fibres. The effect is

1 Med. Gazette, xlii. 751. * Med.-Chir. Trans, vol. xliii.

FATTY DISEASES OF THE HEART. 771

clearly seen in cases of pericarditis in which the inflammation invades
the subjacent layer of muscular tissue. The depth to which the
change extends varies according to the degree and duration of the
inflammation. Sometimes only a sixteenth, sometimes a quarter, or
more, of the whole thickness of the heart is thus damaged. Wagner
found fatty degeneration of muscular fibres present in seventeen
out of thirty-five cases of severe pericarditis which he examined.
In other forms of carditis the muscular fibres suffer in the same
way. In the rare cases of suppurative carditis the degeneration
proceeds to the complete destruction of the fibres. It has been already
stated that inflammation has been regarded as the mechanism by
which the heart suffers in the acute febrile diseases, and that these
cases cannot justly be regarded as inflammatory.

Defective vitality of the muscular fibres of the heart has already
been described as part of a general proneness to degeneration ; it may
also occur as a local condition. This influence is seen in the prone-
ness of the fibres of certain individuals to undergo such degeneration,,
apart from any other exciting cause. It is seen also in the
tendency of hypertrophied hearts to undergo this change. Other
hypertrophied muscles have been said, after a certain period of use,
to fail and undergo degeneration.1 Fatty degeneration occurs with
undue readiness in the newly-formed fibres, and in the majority of
cases hypertrophied hearts present degeneration of some of the fibres.
This is the case especially in conditions of valvular disease which-
entail venous congestion of the walls of the heart, but it is also found
in other conditions of hypertrophy. In that which occurs in Bright's-
disease, for instance, E. Wagner found fatty degeneration in one-third
of the cases (twelve out of thirty-five).

Pathological Anatomy. — In considering the pathological anatomy
of fatty degeneration it will be convenient to reverse the usual order
and to describe first the microscopical changes in the fibres, and after-
wards the alterations in the naked-eye characters which result from
the minute changes.

The first indication of the degeneration is the appearance of minute
black granules within the substance of the fibres. At first they
may co-exist with the normal transverse striatum and seem to lie
in rows between the primitive fibrillar As they increase they appear
to replace the transverse striae, which diminish in distinctness and
finally cease to be recognisable. Often from the first no regularity
can be observed in the disposition of the granules ; they are scattered
uniformly through the primitive bundle.

As the degeneration progresses the granules increase in size, and
become translucent in the centre, being, in fact, globules of fat.
These become larger, but rarely, as Quain observed, exceed the
size of a blood- corpuscle. A linear arrangement of these fat

1 The hypertrophied biceps of the file-cutter is said by Clifford Allbutt, on the-
autliority of Busk, to waste after a certain time.

772 A SYSTEM OF MEDICINE.

globules is frequently to be observed : some are scattered through-
out the substance of the fibre, while others are arranged in rows.
Ultimately they may occupy the whole area of the fibre : some-
times they are aggregated in one part of it, and the remaining space
is clear, free from granules or stria*. The globules constantly appear
to accumulate outside the primitive bundles; whether by the
coalescence of granules formed there, or by migration from within
the fibres, is not clear. The appearance is too constant to be accounted
for by the accidental escape of globules when the section is being
made. The muscular fibres are ultimately left clear ; empty fibre
sheaths appear to remain in their place. The existence of a sarco-
lemma to the muscular fibres of the heart has been denied : if absent,
the appearance of the empty sarcolemma is simulated by the unchanged
fibrous tissue between and separating the primitive bundles.

The affection of different fibres is rarely uniform. Some may con-
tain many fatty globules, and others only minute granules, while
others are still healthy. Similar degrees of affection may be ob-
served in the course of the same fibre : one part may be healthy,
in another part the granular stage may be present, and in another
there are only globules of fat.

The globules and larger molecules of fat are soluble in ether
and resist acetic acid. It is necessary to rupture the fibre in
order to apply this lest. There is some doubt whether the finer
molecules at the earliest stage of the degeneration are all soluble in
ether. It has been affirmed by some writers, but lately denied by
Eindfleisch,1 who maintains that at the commencement of a true fatty
degeneration die granules are insoluble in ether. The point will be
alluded to in its bearing on the pathology of the process. To the
last the molecules and globules of fat maintain their appearance.
They never blend into uniform masses such as occupy the cells in
fatty overgrowth.

The effect of this molecular degeneration is fo modify considerably
the naked-eye characters of the affected part. It is changed ii.
colour. The granules and globules reflect light strongly, and lende;
the tint paler. It becomes grey, ashy-grey or greyish-yellow. Laennei
aptly compared the colour often seen to that of a faded leaf. In tlu
degeneration which occurs in acute diseases, the substance of tht
heart may be dark in colour, from the rapid staining of the tissues
consequent on the decomposition of the blood-corpuscles, and the
escape and transudation of their colouring matter.

At the same time the consistence is changed. The affected part
is soft and flabby. The fibres become brittle and break up easily
into short pieces, so that a scraping from a cut section shows much
shorter fragments of fibres under the microscope, than does that from
a healthy heart. The effect of this brittleness of the fibres is to
render the tissue friable and easily broken under the finger, and some*
times the change is so great that the tissue softens and breaks dowt

1 Path. Gewebelelire, 1875, p. 16.

FATTY DISEASES OF THE HEART. 773

in a limited portion, or the substance may be torn by a violent
contraction of the heart. This diminished consistence may be the
most conspicuous feature, and hence the change was described a3
" pale softening."

The part so changed may have a greasy aspect and feel, and
may actually grease paper which is applied to it. The increase
in the quantity of fat contained in the tissue is, however, smaller
than might be expected. Hermann Weber indeed affirmed that
there was no increase ; and it has been established by other investi-
gators that in slight fatty degeneration only the same amount of fat
is to be obtained from a heart fattily degenerated as from a healthy
heart. But it has been shown that in more considerable fatty degene-
ration, the amount of fat is increased from two or three per ceut, to
four or five per cent, over the quantity contained in a healthy heart.1

The distribution of the change varies. In the form which is second-
ary to acute diseases, the degeneration is often distributed uniformly
through the whole heart. But frequently, as Louis and Stokes pointed
uut, the left ventricle is affected much more than the right. When
secondary to pericarditis only the superficial layer is affected, adjacent
to the inflamed pericardium. Occasionally, in fever, according to
Stokes, the change may affect only the superficial layer. When
arising from a chronic process it may be confined to the inner layer
beneatli the endocardium, or mav be greater in that than in the
superficial layer.2 More commonly it is widely distributed through
the heart, generally in the form of minute foci of degeneration, pale
spots, lines, crescents, in apparent isolatiou, or connected, and forming,
as has been said, a plexus of degenerated areas throughout its sub-
stance. The resulting mottling appears on section or may be visible
through the endocardium. This fofm is often presented by the
degeneration which succeeds haemorrhage. Lastly, a limited area
of the heart's wall, generally near the apex, may be affected in-
tensely and uniformly ; the affected region is sometimes sharply
limited. It was this variety which first attracted the attention of
Laennec. This form commonly results from vascular disease. Not
rarely a diseased vessel may be traced passing directly into the area,
as in cases which have been described by Quain and others.

When degeneration affects part of the heart the frequency varies
with which different portions suffer. The ventricles are affected
much more frequently than the auricles. Indeed, Ormerod doubted
whether the auricles are ever affected : they are certainly occasionally
the seat of this degeneration, and their wall may be affected in a
limited area through its entire thickness. Quain found that in about
half the cases both ventricles are affected, and that where one ventricle
only is affected the left is diseased twice as frequently as the right.

The size of a heart the seat of fatty degerieration may seem to be

1 Bottcher, Virchow's Archiv, xii. ; Krylow, ibid. 1868, xliv. 4. Stevenson, quoted in
Wilks' and Moxou's Pathological Anatomy, p. 119.
* Ormerod, loc. cit. p. 832, case vii.

774 A SYSTEM OF MEDICINE.

Increased, but this is due to the diminished firmness of the organ, in
consequence of which it does not maintain its shape when placed on
a table. In pure fatty degeneration the size of the heart is normal
or only increased slightly by the occurrence of secondary dilatation,
and not rarely it is diminished. A wall partially degenerated may
be bulged out so as to cause a local dilatation of the cavity. Fatty
-degeneration, however, may and often does occur in hearts pre-
viously enlarged. Hypertrophied tissue, as already stated, uudergoes
degeneration more readily than healthy fibres.

Associated changes may be found in other organs, especially those
which are causes of this condition or are other results of a common
cause/ Those most frequently met with are degenerated vessels, and
fatty degeneration in other organs. Ormerod thought the fatty degene-
ration in other organs was more commonly associated with fatty
degeneration of the right than of the left ventricle.

It has been already stated that hearts, the subject of fatty growth,
frequently present fatty degeneration of the remaining fibres.

In all seats of fatty degeneration calcareous salts are apt to be
deposited, but this seems to occur less frequently in the substance of
the heart than in some other seats of degeneration. Most cases of
4t ossification of the heart " are cases of calcareous deposits in subperi-
•cardial inflammatory tissue. (See "Adherent Pericardium.") The
papillary muscles are occasional seats of calcification of degenerated
tissue. In rare cases calcareous deposits are found in the substance
of the heart. In a case mentioned by Renauldin1 the substance of
the left ventricle of a man, aged 33, was infiltrated with grains of
calcareous matter, larger towards the cavity of the ventricle. Some
of them were as large as the tip of the finger. Two remarkable forms
of calcification have been described by Coats : 2 in one the fibres were
dotted with spherules of calcareous matter like globules of oil ; in
the other the process had resulted in a " petrifaction " of the fibres
without change of form.

The blood has been said to contain fat in some cases of fatty-
degeneration. R W. Smith stated that he had seen globules of fat
visible to the naked eye in the blood after death, and Stokes noted
the same thing. Some doubt attaches to these observations from
the difficulty of avoiding the escape of fat from the divided tissues
into the blood. Dumenil and Pouchet, 3 however, state that they
found a considerable quantity of fat in the blood of a person, the
subject of chronic alcoholism, who, on subsequent death, was found
to have fatty degeneration of the heart aud liver. Magnus Huss also
.affirmed that he had seen fat in the blood of drunkards.

Pathology. — The significance of this molecular degeneration is
clear ; it is a sign of lessened vitality, sometimes of actual death. But

1 Journal de MeM., Jan. 1816. Quoted by Laeunec, ]». 231.

2 Glasgow Med. Journal, August 1872.

3 Gazette Hebd. de Med. ct Chir. 1862, p. 32.

FATTY DISEASES OF THE HEART. 775

the nature of the process has been the subject of much discussion,
and is still, to a considerable extent, obscure.

It seems probable that the first 3tep in fatty degeneration is a mole-
cular change in the muscular fibre, by which the fat which exists
within it in an invisible form, combined with the protein constituent,
is separated and precipitated in visible granules and globules.
Invisible fat, to be detected by chemical analysis only, exists in the
blood, the heart, and, in fact, all the animal tissues,1 and is believed
to be combined with the nitrogenous material, because it is found
that the different nitrogenous substances have their own special forms
of fat ; that the fat of fibrin, for instance, is different from the fat of
serum.* In the healthy heart the fat thus combined amounts to about two
or three per cent. In moderate fatty degeneration, even when granules
and some globules of fat are visible under the microscope, chemical
analysis shows that there is no increase in the total quantity of fat8
It would thus appear that the first step of the degeneration is a
separation and precipitation of the combined fat. It is probable also
that the granules, which constitute the first stage of degeneration, are
not all of a fatty character ; that some of them are of protein nature.
Virchow suggested that the protein material may ultimately be
changed to a soluble extractive and pass away, leaving the preci-
pitated fat.

But in more advanced fatty degeneration the quantity of fat is
greater than this explanation will account for. Fibres are seen to be
filled with globules of fat, and analysis shows that the amount of fat
in the tissue is actually considerably increased, often to double
the normal quantity. What is the source of this additional quantity
of fat ? It must be either formed in the fibre or introduced from
without. The former is the simpler explanation ; by it the fat is
supposed to arise by a chemical change, an imperfect oxidation, of the
nitrogenous constituent of the fibre. This is the explanation which
harmonises well with the visible characters of the change, since the
transverse striation disappears as the fat is formed. Rindfleisch4
points out that the stage of " cloudy swelling " of cells, in which
they are filled with minute granules soluble in acetic acid, if
it does not resolve, passes into one in . which the granules resist
.acetic acid and dissolve in ether. This view was suggested by
Fick 6 and Rokitansky,6 and has been adopted by Virchow, Paget,
■Quain, and others. It is certaiu that fat may be formed from nitro-
genous material. The vegetable world affords many instances of this.
Butyric acid, a fatty acid, may be formed by the decomposition of
fibrin (Wurtz). Chemistry supplies other examples of the same
class. If the fat, in molecular degeneration, is not formed by a change
in the protein matter, it must be introduced from without. But the

1 Virchow, in his Archiv fur Path. Anat. i. 1847, p. 156.

2 Lehmann, Physiological Chemistry ; Virchow, loo. cit

8 Hermaun Weber, Ormerod. " * Pathologische Gewebelehre, p. 16.

* Muller's Arch. J842, p. 19. • Path. Aiiat.

776 A SYSTEM OF MEDICINE, .

increase in the fat is sometimes fouud in situations in which it
cannot have been introduced from without. Prolonged maceration
in dilute nitric acid, for instance, will produce such a degeneration
in healthy muscular fibres ; a similar change is often seen in
preparations preserved in dilute alcohol. Doubtless this is chiefly due
to the separation of the combined fat, and it has accordingly been
found that there may be no increase in the total quantity of the fat
contained in the fibre before and after the occurrence of the degenera-
tion. In some cases, however, a considerable increase in the amount
of fat has been found ; that is to say, there has been a considerable
formation of fat. Hand field Jones1 found the increase of fat to
amount to nearly fifty per cent., and as any accession of fat from
without is impossible it can have arisen only by the decomposition of
the protein material. The formation of adipocere is another illustra-
tion of the same process, but this substance seems somewhat variable
iu its character and mode of formation. Ormerod, indeed, main-
tained that its composition always agrees with the composition
of the fat of the animal, and that its fatty element is due to a
change in, and infiltration of, the normal fat into the muscular and
other tissue. But he found that one specimen consisted of at least
half pure fat, and Quain found that adipocere from the muscle of a
horse was almost entirely soluble in ether.

Other evidence, although less conclusive, of the origin of the
fat from the protein matter; is drawn from the occurrence of
extreme fatty degeneration in parts to which the blood cannot
gain access. It is seen, for instance, in "infarctions." The area
from which the blood-supply is cut off by embolism is the seat
of intense fatty defeneration. It is seen also in the experiments
(performed first by Wagner) in which portions of animal tissue have
been inclosed in the peritoneal and other cavities of living animals,
and have become changed to masses of fat. But these experiments
are deprived of some of their significanca by the fact that the inclosure
of the fragments in an impermeable coiting prevents any increase in
the fat beyond that present in the healthy tissue (Burdach). In-
organic substances permeable to the animal fluids become charg *d
with fat in just the same way as the organic tissue. These facte,
indeed, negative all the significance of these experiments as proof of
the transformation of protein substance. They do not, however, ex-
clude the possibility that some of the fat may have arisen in this way,
since an impermeable coating will prevent the access of oxygen,
without which the oxidation of the protein material, imperfect though
it be, cannot occur.

The fatty degeneration found in phosphorus poisoning, in poisoning
by acids, and intense anamiia, has been regarded as further evidence
of the formation of fat by im perfect oxidation of nitrogenous material,
since it is believed that all these conditions act by a common
mechauism, the diminished supply of oxygen to the tissues consequent

1 British and Foreign Medico-Chirurgical Review, July 1853, p. 59.

FATTY DISEASES OF THE HEART. Ill

011 the diminished number of blood- corpuscles. The diminished
oxidation is also indicated by the fall in the temperature of the body.

These facts prove that in fatty degeneration some of the excess of
fat present in the fibres may be, and probably is, due to a chemical
change in the protein constituent of the fibre. They do not, however,
exclude the entrance of some of the fat into the fibre from without. It
has been argued, indeed, by Eobin1 and Ormerod,2 and the view is sup-
ported by Walshe, that all the fat seen in the fibres in fatty degenera-
tion enters them from without, that it is essentially an infiltration of
the fibres with fat, derived directly from the blood, and replacing the
protein constituent of the fibres, which has been removed by a process
of atrophy. There are two ways in which such infiltration of fat is
conceivable. Minute fatty globules may enter the fibre from the
blood, passing through its wall as fat, just as the fatty molecules of
the portal blood pass into the liver cells adjacent to the portal canals.8
Or the fat may enter the fibre in invisible combination with the
liquid protein material which must, in the normal course of nutrition,
always permeate the fibres. Within the fibre this fat may be separated
and precipitated by a process similar to that concerned in the
separation and precipitation of the fat contained originally in the
muscular tissue, the nitrogenous material passing out as " extractive."
The constant repetition of such a process may fill the fibre with fat
globules. There is some reason, as just stated, to believe that most of
the fat which is found after a time in pieces of tissue inclosed in the
peritoneal cavity of another animal passes in from without. If this
is so with regard to substances separated from all structural con-
tinuity with the living tissues, it may be the same with the fat which
is found in such excess in areas in which, in consequence of arrest of
blood-supply, necrosis has occurred. The permeation of these areas
with fat-containing plasma, from the adjacent healthy region, must
constantly go on. The analogy of calcification, which often succeeds
fatty degeneration, affords some support to this theory. Normally,
the blood, heart, and other organs contain a small proportion of
calcareous salts, probably combined with the protein substance. No
transformation of the other elements can produce the lime salts which
are found in the calcified tissue. They must enter the tissue from
without, with the blood plasma, from which they are separated and
deposited, while the nitrogenous element passes away. This pro-
cess, continuing during a long time, ultimately effects a complete
infiltration of the tissue with calcareous matter.

A consideration of all the facts of fatty degeneration make it
probable, then, that, as Handfield Jones suggested, each process may
be concerned in the production of the excess of fat which is found in
advanced fatty degeneration ; that the fatty material at first seen in

1 Chimie Anatomiquc.

s Brit. Med. Journal, 1864, ii., p. 152 ; St Earth. Hosp. Rep., vol. iv. 1868, p. 30.
5 Fatty " degeneration " (infiltration) of the liver was produced artificially by Magendie
and Gluge injecting fat into the portal vein.

VOL. IV.' 3 E

778 A SYSTEM OF MEDICINE.

the fibre is merely separated and precipitated in visible form, and
that the subsequent excess arises in part by a transformation of the
protein material, and in part by the entrance of fat from without.

Consequences. — The effect of fatty degeneration on the function
of the heart is to lessen its propulsive power, and thus to lead to
imperfect filling of the arterial system, and consequent visceral
anaemia. This effect is much more marked than is the correlative
venous distension, which is so prominent an effect of dilatation of the
heart. The relative defective supply to the arterial system is recog-
nisable in the symptoms which it causes during life, rather than by
any pathological consequences wliich can be observed after death.
These symptoms are described further on.

The fatty degeneration of the fibres may not only affect the
function of the heart, it may lead to changes in its condition which
have their own results. The weakened walls may yield unduly before
the pressure of the blood, and the heart may become dilated. Such
dilatation is rarely very great. Its mechanism and conditions have
been already considered (Art. " Dilatation"). But the weakness
which fatty degeneration produces may have a much graver
result. The brittleness of the fibres may lead to their rupture, and
when the degeneration extends through the whole thickness of the
wall of the heart, the whole wall may give way. This accident,
" rapture of the heart," is of such gravity and importance as to need
detailed consideration, and it is therefore described at the end of this
article.

Symptoms. — The physical signs and the symptoms which attend
fatty degeneration of the heart are usually indistinct and never
distinctive. All are common to other morbid states. They depend on
the diminished power of the heart, wliich modifies the signs of its
action, and affects the function of other organs.

As the size of the heart in simple fatty degeneration is little
changed, the area of dulness presents no alteration. The slight
dilatation, which is the consequence of the fatty degeneration, rarely
leads to the signs of enlargement of the heart. In a considerable
number of cases the dulness is increased, but this increase depends
rather on pre-existing hypertrophy or dilatation, or else it is due to
concurrent fatty growth.

Diminished force of impulse is the most important physical sign
of cardiac degeneration. The area of impulse, like the area of dulness,
is only increased by coexisting conditions. As long as the im-
pulse is perceptible, the apex-l>eat may, in m<5st cases, still be felt
When dilatation has occurred in consequence of the weakening of
the cardiac wall, the impulse may be diffused and peculiar in
character, resembling, as Stokes remarked, rather the slight, general
impulse of an aneurism than the normal impulse of the heart.
When the patient is thin, and the lungs are small, so that the

FATTY DISEASES OF THE HEART. 779

impulse of the heart can be well felt, a partial change in impulse may
be observed to correspond to a partial degeneration. Stokes, for
instance, observed that in fever, when the left ventricle was much
more degenerated than the right, while an apex impulse might be loBt,
an impulse in the lower sternal region, due to the right ventricle,
might be still perceptible.

The sounds of the heart are weakened in correspondence with the
weakness of the impulse. The first sound, to which the contraction
of the heart directly contributes, is that which presents the greatest
change. It is usually toneless, shorter, and relatively high-pitched,
and may become almost or even quite inaudible at the apex,
only the second sound remaining. The first silence is longer than
normal in consequence of the shortening of the first sound. The
second sound is also weakened in consequence of the deficient
distension, and therefore deficient recoil, of the aorta and pulmonary
artery. When the first sound is shortened and raised in pitch it may
resemble the second. The sounds of the foetal heart are then
very closely simulated, especially if the heart acts rapidly. When
the degeneration is local, the sounds may be modified locally,
just as the impulse. In the acute degeneration of fever, Stokes
observed that the first sound might be lost over the left ventricle
when it was still audible over the right, in cases in which the
post-mortem examination showed the left ventricle to be the more
affected. Walshe has observed a similar alteration of intensity in
chronic disease under similar circumstances. According to Stokes, if,
after ceasing to be heard for a time, the first sound reappeared, it was
heard first over the right ventricle and afterwards over the left. In
one case both sounds were inaudible for thirty-six hours before death.

Stokes believed that a systolic basic murmur might exist during
the early stage of the degeneration. Other observers have noted
the occurrence of an apex murmur due to regurgitation, and have
ascribed it to fatty degeneration of the papillary muscles.

The rhythm of the heart's action varies much. It may be regular
throughout, but is often irregular, chiefly, Walshe thinks, when dilata-
tion coexists ; sometimes it is frequent, even to an extreme. It may
be slower than natural, and the diminution in frequency may proceed
to a degree met with in no other affection. This wa3 first pointed
out by Adams. It may fall to forty, thirty, or twenty beats per
minute. In rare cases it has sunk as low as eight or ten beats per
minute for hours before death.1 The pulse is weak and small, in
proportion to the cardiac failure. Its rhythm, as a rule, corresponds
with that of the heart; rarely it is less frequent than the heart's
contractions, in consequence of the weaker beats of the heart failing
to send a wave along the vessels sufficient to be felt.

Tain is not a common symptom, but now and then is complained
of, and is sometimes very troublesome. It may be confined to

1 Ormorod thought that iu frequency was associated rather with fatty infiltration than
-with fatty degeneration. Lond. Med. Gaz. 1319, p. 917.

° E 2

780 A SYSTEM OF MEDICINE.

the cardiac region, may be referred to the sternum, or may extend
down the arm. It may be paroxysmal, and simulate angina pectoris
in its characters. Occasionally true anginal seizures occur, but no
direct relation is known between their occurrence and the fattv
degeneration of the heart.

Syncopal attacks, as might be expected from the nature of the
disease, are not rare ; they are usually produced by some effort. They
vary in intensity, sometimes amounting only to a sense of faintness,
sometimes to loss of consciousness. They may be accompanied by
a sense of great distress, as if death were impending. Death does
not unfrequently occur in such an attack. Often in this condition
cerebral symptoms are associated with those of cardiac failure. Con-
vulsions may occur. Vertiginous sensations are not unfrequent.
Walshe mentions a case in which loss of memory for recent events
preceded each attack of syncope. Or the loss of consciousness,
commencing as apparent syncope, may continue, and deepen, slowly
or rapidly, to coma, with stertorous breathing. These "pseudo-
apoplectic " seizures, as they have been termed, are usually brief, and
leave no paralysis. They have, however, a great tendency to recur.
They were referred by Adams and R W. Smith to congestion of the
brain, but Stokes pointed out that their association is with a deficient
supply of arterial blood, and that they are probably due to cerebral
anaemia, the immediate cause of the syncopal seizures. In confirma-
tion Stokes mentioned a case in which they could be averted at their
onset by hanging down the head so that it nearly touched the floor.
When death has occurred in these attacks, the brain has appeared
free from organic disease. It is needless to remark that apoplexy
from actual organic changes in the brain may occur in subjects of
fatty degeneration of the heart. Other occasional symptoms on the
part of the nervous system are numbness and formication, such as
have been attributed to anaemia of the spinal cord.

Dyspnoea is a common symptom. It may be slight, felt only on
exertion, especially on ascending an incline or on making some other
effort. Or the dyspnoea may be severe, constant, amounting to a con-
tinuous sense of suffocation. Considerable dyspnoea is said to be
present in one half of the cases of pronounced fatty degeneration.
Occasionally it has a special form. Sometimes frequent sighing is
observed, as Stokes pointed out. Sometimes the dyspnoeal breathing
possesses a peculiar rhythm of striking character, which has attracted
much attention since it was first described by Cheyne.1 It was very
carefully studied by Stokes,51 and by him especially associated with
fatty degeneration of the heart, although further observation has shown
that it is by no means confined to that affection.

This form, which has been termed the " Cheyne-Stokes dyspnoea/'
or " ascending and descending respiration," is characterised by recur-
ring series of respiratory acts, first increasing and then decreasing in

1 Dubl. Hosp. Rer„ 1818, p. 216.

2 Dubl. Journal of Med. Science and Diseases of the Heart, August, 184t>, p. 324.

FATTY DISEASES OF THE HEART. 781

intensity. In the intervals breathing seems to have almost or entirely
ceased; then slight respiratory movements are noticeable, which
gradually become deeper and deeper, until an acme of very deep and
laboured breathing is reached, after which the respirations gradually
become shallower until they subside into the same apparent apnoea,
which is again broken by the gradual onset of another series. In the
classical case recorded by Cheyne, the cycle included about thirty
respirations and lasted a minute. In most of the other cases recorded
it has occupied a shorter time. Hayden has found the pulse unchanged
during the paroxysms.

As just stated, this form of dyspncea is by no means confined to
fatty degeneration of the heart. It has been seen in other forms of
heart disease, especially in valvular disease with dilatation * and in
atheroma of the aorta.2 It has been met with even more frequently
and at all ages in affections of the nervous system, in cerebral hsernor-
rhage,8 in tumours of the brain, uraemia, and tubercular meningitis.4
It has frequently been seen in cases in which affections of the heart
and brain coexist. It has been produced artificially in animals by
Filehne 5 by the injection of morphia and subsequent inhalation of
ether and chloroform. It has also been observed in a case of fatty
degeneration of the heart, during the narcosis which followed a fatal
injection of morphia, and also in chloral narcosis. Its probable
explanation lies in a lowered sensibility of the respiratory centre
in the medulla oblongata, as was suggested first by Walslie,6 and
after him by Laycock and Traube.

A form of dyspncea which has in several instances been described
as that of Cheyne, is that in which the dyspncea subsides slowly into
dozing apnoea, to be broken after a few seconds by a sudden rouse to
conscious, or half-conscious, dyspncea, which, after a few seconds,
slowly subsides. This occurs rather in dilatation than in fatty
degeneration of the heart. It seems readily explicable on the theory
of diminished sensitiveness of the respiratory centre wThich requires a
voluntary or half voluntary reinforcement. The latter is only excited by
a stronger degree of the physiological stimulus ("anoxa?mia ") than the
former; the blood, when well aerated by the dyspnceal respirations, ceases
to excite it ; sleep gradually withdraws the reinforcement, and the
respiratory centre ceases to act; the apnoeal venosity of blood increasing,
at last awakes the higher mechanism to renewed action. But the true
Cheyne-Stokes breathing differs from this in the very gradual in-
crease in the breathing, from shallow to deep, as the dyspncea comes on.7

1 Seaton Reid, Dub. Hosp. Gaz. 1860.
3 Hayden, loc. cit. p. 682.

3 Laycock, M. Fothergill, &c. The writer has also seen it in one case of cerebral
hemorrhage, and has been informed of two other cases in which it was marked.
* Traube, Roth.

5 Berlin. Klinische-Wochenschr., 1874, No. 13, 14, 32, 35.

6 Diseases of the Heart and Aorta. Third Ed. 1862, p. 345.

7 Several theories have been framed to explain the details of the phenomena. Traube
accounted for the slow accession of the dyspnoea by supposing that the venosity of the

782 A SYSTEM OF MEDICINE.

In some cases there may be from first to last no embarrassment of
the breathing. Walshe has pointed out that this freedom from
dyspnoea may accompany even the syncopal and apoplectic seizures.
Cough is sometimes present without bronchitic or other cause.

The other symptoms referable to the general system are in the main
those of defective blood supply. The skin is pale, the muscular power
deficient, the surface and extremities cold; the mind is weak, often
depressed. The digestive organs suffer ; anorexia is common. Symp-
toms of over-distension of the venous system are rare. Slight oedema
may occur, but marked dropsy probably never occurs as a consequence
of the fatty degeneration. It sometimes results from coexisting dila-
tation, especially when primary. It is only under such a condition
that the urine contains albumen. In simple fatty degeneration of
the heart the urine presents no deviation from the normal Co-
existing degeneration of other organs often modifies the general
characters of the symptoms of fatty degeneration.

Course and Terminations.— The course of molecular degeneration
of the heart varies according to the circumstances under which it
arises, and especially as it occurs gradually as a slow degeneration,
senile or premature, or acutely in consequence of blood-poisoning.

In senile degeneration the symptoms are gradual in onset, and may
be marked, or may be very obscure. The duration of the affection
may be long, sometimes twelve to fifteen years. In these cases
other causes often increase the effect of age, and may be to some

blood first excites the terminal branches of the vagus in the lungs, which, it is known, can
liberate only slight reflex respiratory movements, too slight to prevent accumulating
venosity and general stimulation of the afferent nerves, producing the intenser dyspnoea.
The gradual onset of the returning respiration is not, however, difficult to explain, for it
is the natural form in which the physiological stimulus manifests its returning action after
it has been withdrawn by the abundant aeration of the blood in the dyspnceal breathing.
A state of apncea may easily be produced in health by a series of very deep respirations.
The highly oxygenated blood no longer stimulates the respiratory centre ; no bcsoin de
re&pircr is felt, and, except by a voluntary elfort, no respiratory movement is made,
until, after a few seconds, the slowly increasing state of blood causes respiratory move-
ments, slight at first, afterwards deeper, until the normal respiration is reached. To
explain the degree and duration of ihe dyspnoea, as well as its gradations, Filehne
assumed that vaso-motor spasm causes continued stimulation of the respiratory centre,
until that spasm is slowly relaxed by a degree of aeration of the blood which ceases to
stimulate tne respiration, and thus the. slow relaxation of the spasm causes a slow
diminution, and finally cessation, of the respiratory movement. He found that by
Bimple alternate compression and relaxation of the arteries in a guinea-pig (right
innominate and left subclavian) he could produce perfect C'heyne-Stokes respiration. In
further confirmation of his theory he states that he has arrested the characteristic
breathing by inhalation of nitrite of amyl.

It is not difficult to understand the origin of this form of respiration in cerebral
diseases, in which the lowered sensitiveness of the respiratory centre is likely, and
the withdrawal of higher influence may leave its tendency to rhythmical action live to
modify a series of iU actions. Its connection with cardiac diseases is less easy to under-
stand. Little's theory of unequal action of the ventricles is certainly unsupported.
Hayden suggests that the etiological condition is atheroma of the aorta interfering with
the supply of arterial blood to the peripheral vessels. This explains the occurrence of
dyspnoea better than its rhythmical cessation. Long-continued over-stimulation of the
respiratory centre may possibly lead to its diminished sensitiveness.

FATTY DISEASES OF TEE HEART. 783

extent removable, and the extension of the degeneration may
be arrested for a considerable time. Sooner or later the cardiac
failure comes; late, if the conditions of a tranquil unemotional
existence can be secured ; soon, if the sufferer has still to face the
storms of life, physical and moral In an acute illness, preceding
degeneration of the heart prejudices very much the patient's state.
The pulse becomes weak and irregular, often, as Kennedy showed,
extremely frequent ; and, if the acute disease be at all severe, syncopal
failure occurs. Under other conditions the end may come as slow
failure, or sudden stoppage from loss of power, or from rupture. The
latter occurs in a considerable proportion of the cases in which the
disease is well marked. When the coronary vessels are diseased
and the heart degenerated, the sudden complete obstruction of a large
branch will stop the damaged heart.1 The more acute degeneration
commonly occurs in the course of some pyrexial affection. It is
characterised by more or less sudden failure of the heart's action, out
of proportion to the other evidences of intensification of the general
disease. The condition usually corresponds with a high temperature,
and often occurs before the primary disease has begun to subside.
When the patient recovers, and the pyrexial stage is over, the action
of the heart may become very infrequent or may remain unduly
frequent.

The form of degeneration which succeeds a haemorrhage is marked
by more gradual sinking, the patient Jbecomes weaker and weaker, and
dies asthenic at the end of a few days or a week or two from the loss
of blood.

Diagnosis. — It will be gathered from the preceding remarks that
the diagnosis of fatty heart is never easy and is often difficult or
impossible. The opinion of Latham that the existence of the disease
does not admit of positive recognition, only of probable conjecture,
is that of most later authorities. Many of the symptoms which
are the most uniformly connected with fatty degeneration of the heart,
are also due to so many other conditions, that they have not, even
conjointly, much significance. The diagnosis, as far as it can be made,
depeuds on the following points : —

(1). On the Simple Loss of Power. — A very similar loss of power
may be due to dilatation, but dilatation diffuses the impulse and en-
larges the heart ; neither effect belongs to degeneration, unless dilatation
is associated with it, and then the muscular degeneration can rarely
be detected. Such simple loss of power may, however, occur in either
a normal or a hypertrophied heart. In each it has the same signifi-
cance, but in the latter the weakness is commonly relative only. It
needs in all cases to be carefully distinguished from concealment of
impulse in consequence of over -distension of the lung. A mistake
may be avoided by attention to the other signs of emphysema, and
especially to diminution or obliteration of the superficial cardiac

1 Payiic, Brit. Med. Journal, Feb. 5th, 1870.

784 A SYSTEM OF MEDICINE.

dulness, which always occurs when a distended lung pushes the heart
away from the chest wall. Weakness of the first sound of the heart
is also most valuable, in the absence of emphysema, as concurrent
evidence of the diminished force of its contraction. Other symptoms
of fatty degeneration are of less significance, except perhaps slowness
of pulse, which is, however, rare ; the special forms of dyspnoea
are also too rare, and they are also too equivocal, to be of much value.
Some weight has been attached to the syncopal seizures wrhich occur
in this disease, and especially to the mixture of syncopal and cerebral
symptoms. Mental depression has also received attention as adding
weight to other symptoms. Tailor of the surface has a similar
significance.

(2). On the Presence of Similar Degeneration elsewhere. — Senile
degeneration is in some persons local, much more commonly it is
general, and its wider manifestation may give significance to cardiac
symptoms, which alone would be of little import. Of these degene-
rations the most important are those of the vascular system, of which
the heart is part. The smaller vessels are accessible to direct ex-
amination, and their degeneration is manifested by hardness and
tortuosity. Perhaps of next significance is the change in the cornea
known as " arcus senilis," and which, since it was shown by Canton
to depend on fatty degeneration, has attracted much attention as con-
venient indication of a diathetic tendency to such a change. That it
has such significance in some cases is unquestionable,1 and it has been
thus accepted by Quain, Barlow, Paget, and others. But its value
may easily be over-rated. Like every other local degeneration, it may
be part of a similar widely-spread change or it may be an isolated
phenomenon. The latter is the case perhaps, more frequently than
the former, and has led many observers to deny that any weight
can be attached to it as evidence of fatty degeneration of the heart.
Haskins2 has recorded twelve cases with no affection of the
heart. A wider observation has shown that the truth lies between
the two extremes, and that the arcus senilis, as already stated, may
give weight to other characters but alone is of little significance.
Other evidences of degeneration are of still less value ; but greyness
of hair is probably a stronger evidence of degenerative tendencies
than is its loss.

(3). The existence of a recognised cause of fatty degeneration is
also of considerable value as an aid to diagnosis. Of the various
causes, chronic alcoholism is that which is most frequently associated
with the degeneration ; and most frequently assists the diagnosis.

Prognosis. — Molecular degeneration of the heart is always serious,
but its gravity varies much under different circumstances. The con-
dition to which danger is especially related is the persistence of the
cause of the degeneration. As long as the cause lasts, the degeneration

1 Luithlen, VirchcVs Archiv, 1871, p. 91. A

* Ann. Jour. Med. Sciences, January, 1853.

FATTY DISEASES OF THE HEART 785

continues and increases. Life depends on the maintenance of the
functional power of the walls of the heart., and progressive degeneration
must sooner or later produce death. If the cause of the degeneration
ceases to act, the disease ceases to progress, and if moderate in degree,
may, it is probable, even be recovered from. When a certain point of
damage has been reached, the condition seems to preclude more than
partial restoration of structure.

The forms of degeneration which occur in acute diseases are those
in which the immediate danger is greatest, but at the same time the
.. ultimate prognosis is usually favourable. It is immediately grave,
because the heart is often unable to resist the prostrating influence of the
general disease. It is ultimately good, because the causal disease soon
ceases, and often before the change in the heart has reached an irre-
parable degree. After the acute illness is over, the patient may die
from the subsequent slow failure of the heart, but frequently he
recovers, sometimes completely, sometimes with some permanent
damage to the substance of the heart.

In chronic degeneration the immediate prognosis is less grave, but
the ultimate prognosis is worse than in the acute cases. Those are
the most hopeful in which there exists a removable cause of degenera-
tion, such as the consumption of alcohol. Where the malady has
arisen as a senile degeneration, or as a widely-spread idiopathic change,
and the conditions of life are unalterable for good, the prognosis is
very unfavourable. It is worse also the earlier in life the patient is
attacked, since, as Quain pointed out, early age often entails an in-
ability to obtain that rest which alone can ward off the consequences
of the disease.

The fatty degeneration of the heart which coexists with a like
degeneration in the vessels has been regarded as being not without
advantages : adapted, in senile atrophy, to the lessened mass of blood,1
and diminishing, by the lessened strength of contraction, the strain to
which rotten vessels are exposed.2

Treatment. — Advanced fatty degeneration of the heart is generally
an irremediable condition. Something may be done to ward off ite
effects, but little to restore the heart to its normal state. In slight
degeneration, improvement, even perhaps recovery, may take place.
The great end to be aimed at is the removal of the cause. In the
acute degeneration of pyrexia there is, as stated, every reason
to believe that a state of granular degeneration may be recovered
from, when the cause has ceased to act. A chief object in treatment
must therefore be to maintain the strength of the patient, to keep
his heart going by judicious stimulation until the disease is over.
General tonics will then aid recovery. Strychnia has been thought
by many to be of great use.

In the chronic forms of degeneration there is frequently little room

1 Crisp, Treatise on the Blood-vessels, 1851, p. 363.

2 Sir W. Jenner, Address to the British Med. Association, 1869.

78C A SYSTEM OF MEDICINE.

for therapeutics. The cliange is too often due to conditions beyond
the influence of any means at our disposal. All removable causes, how-
ever, such as chronic alcoholism and gout, must be carefully searched
for, and their influence, if possible, removed or neutralised. A
fair amount of nitrogenous food is necessary. Eestriction of fat is
of more doubtful benefit. Tonics are useful— iron, quinine, or strych-
nine. Digitalis has been recommended to strengthen the fibres which
are weakened but not destroyed. Walshe says it is most useful where
the pulse is frequent and dilatation coexists. If the degeneration can
be arrested, hypertrophy of the remaining fibres may occur, and help to
restore the functional power of the heart.

In every form of degeneration care must be taken not to overtax
the heart. Its weakened texture is easily damaged still further, and
approximate health depends on the avoidance of exertion, &c. Effort
with closed glottis must be especially avoided, such as pulling on
boots, lifting weights, straining at stool; the latter has in several
instances been the immediate cause of cessation of the heart's
action. All causes of syncope must also be carefully avoided. In
acute illness, the horizontal posture must be carefully maintained
as long as the cardiac failure continues, and it must be left off with
caution. The general health must be carefully attended to. A life
in the open air is strongly praised for such cases by Stokes. The
digestive organs must be put right, and the heart preserved from
every cause of embarrassment to its action.

Stimulants are needful for the cardiac failure, and a diffusible
stimulant may be kept at hand for the syncopal attacks. Coffee
has been strongly praised by Desnos and Huchard in the degeneration
of small-pox.

Hayden has found the nitrite of amyl of service in the paroxysms
of rhythmical dyspncea. It is equally useful in the attacks of suffo-
cative oppression or anginal pain.

Pain may be relieved by sedatives such as have been recommended
for the pain in dilatation of the heart. But equal caution is needful
respecting the use of opiates, especially by hypodermic injection. I
have known half a grain of morphia, injected hypodermically,
followed by death, of which there was no premonition. Ormerod
relates a case in which the same quantity was taken by the mouth,
and death occurred during the ensuing sleep. Chloroform should not
be inhaled ; ether should be employed instead. In a large majority of
cases of death while under the influence of cliloroform, fatty degene-
ration of the heart has been found.

Rupture of the Heart.

This accident occurs in a considerable proportion of the cases of
fatty degeneration, both simple and associated with overgrowth of fat.
Conversely, fatty degeneration is by far the most common cause of rup-
ture. Spontaneous rupture never occurs in a Wealthy heart, and the

FATTY DISEASES OF THE HEART. 787

number of cases due to any other cause, as abscess, or aneurism, or deep
endocardial ulceration, is very small. Out of one hundred cases of rup-
ture collected by Quain,1 in seventy-seven fatty degeneration was
detected by the microscope, and of the remaining cases, in all but two
either softening was noticed, or the state of the heart was not men-
tioned. It is thus probable that in at least nine-tenths of the cases of
rupture fatty degeneration is the condition of the cardiac wall to
which the accident is due.

The degeneration which permits rupture is raTely uniform throughout
the whole of the cardiac walls. Uniform degeneration causes uniform
weakening ; the force of contraction is lessened, and there is no spot
specially incompetent to bear the lessened strain. It is when the
degeneration, as is so commonly the case, is unequal, and especially
when the degeneration in a limited area reaches a high degree, that
rupture takes place. The contraction of the more healthy portions of
the cardiac wall puts upon the more rotten portion a strain which the
former can bear, but which the latter is quite unable to. bear. This
unequal change is the form which is associated, as its immediate cause,
with local and degenerative, rather than with general or inflammatory
causes. It rarely, for instance, results from the damage to the cardiac
wall, from endo- and peri-carditis, or from pyrexia ; whereas it is com-
mon in the degeneration secondary to unequal fatty growth and
infiltration, and still more frequent in that which results from vascular
obstruction, chronic or acute. It is not uncommon to find a degene-
rated or thrombosed branch of the coronary artery going straight into a
patch of intense fatty degeneration in which the rupture has occurred.2
The sudden occlusion of a vessel by embolism may cause a similar
patch of softening.

There is another way in which rupture has sometimes been produced
by the association of diseased vessels and fatty change. The degene-
rated vessels may give way ; the resulting extravasation readily tears
its way in the softened tissue, and may reach the surface, being assisted,
no doubt, by the contractions of the heart. The systole of the heart
empties its vessels of blood, and when a haemorrhage has occurred
into the substance of the wall, the contraction must compress the effused
blood, and force it in the direction of least resistance. It is not un-
common to find more than one extravasation in the wall of the
heart.3 Such haemorrhages are said to be sometimes the result of
embolism.

The chief other causes of rupture, aneurism of the heart, cysts in
its walls, &c, are considered elsewhere.

The influence of the degenerative conditions is seen in the effect
of age on the occurrence of rupture of the heart. The accident
occurs chiefly in the old. Of the cases collected by Quain,
two-thirds were over GO. The mean of forty-eight cases has been

1 Lumleian Lectures, Lancet, 1872.

2 Quain, Path. Trans, iv. 80. Simon, Bcrl. Klin. AVochenschrift, 1872, No. 45.

3 Colin, Gaz. des Hopituux, 1867, p. 104.

788 A SYSTEM OF MEDICINE.

found to . be 68 years.1 Most collections of cases have shown the
accident to be more frequent in the male sex, but Quain's statistics
give an equal number of cases in each sex. Occasionally, hereditary
predisposition has appeared to influence the occurrence, and even the
seat of rupture, perhaps by similarity of vascular distribution. A
classical instance is the death of George II. and his relation, the
Princess of Brunswick, of rupture of the right ventricle.

In primary rupture of the heart the immediate cause of the tear
is probably a contraction of undue strength, the strain upon the
fibres being greater than the degenerated texture can resist. Thus the
accident has commonly occurred during conditions of excited action
of the heart, during unusual effort, such as running to catch a train,
lifting a weight, cough, straining at stool,2 or during emotional excite-
ment. Of twenty-four cases collected by Barth, in five death occurred
during the act of defsecation. Sometimes no undue exertion can be
traced, the symptoms come on suddenly while the patient is at rest,
even during sleep.8

All parts of the muscular substance of the heart are liable to
rupture. It has occurred in the walls of each ventricle, of each
auricle, in the septum between the ventricles, and in the papillary
muscles. It is however far more frequent in the left ventricle than
elsewhere. All statistics agree in showing that the left ventricle is
the seat of rupture in three-quarters of the cases, and that it is at
least twice as frequent in the anterior as in the posterior wall. The
usual seat is near and parallel to the septum, and not far from the
apex. About twelve per cent, of the cases occurred in the right
ventricle, about six per cent, in the right auricle ; while only two
or three per cent, have occurred in the wall of the left auricle and
in the septum.

The size of the rupture varies from a point scarcely recognisable to
an inch in length. It may be larger on the inner surface than on the
outer surface. Sometimes it is larger outside, and the inner opening
may be small, and concealed among the columnar carnere. When the
latter is the case, Blaud thought that the rupture had occurred from
without inwards. The course of the rent is often oblique, so that
inner and outer openings do not correspond. It is usually parallel
to the muscular fibres, less frequently across them. The rupture is
usually single ; sometimes there are several partial ruptures, and one
.complete. A coagulum usually lies between the lips of the rent, and
the cavity of the pericardium is usually filled with clot.

A morbid state of the heart, to which the rupture may be ascribed,
is always present. In the rare cases in which fatty degeneration or

1 In tin- few cases on record of rapture of the heart at earlier ages, most were due to
other causes than fatty dogciu ration. In rupture of the left ventricle, for instance, in a
woman aged 49, described by Gregorie (Virchow, Jahresb. 1870), the cause was the per-
foration of a circular ulcer, probably, since the woman was the subject of constitutional
syphilis, due to a softened gumma,

* Arch. G^n. de Med. 1871.

3 Quain, Path. Trans, i. 62.

778 A SYSTEM OF MEDICINE.

The fatty degeneration of the fibres may not only affect the
function of the heart, it may lead to changes in its condition which
have their own results. The weakened walls may yield unduly before
the pressure of the blood, and the heart may become dilated. Such
dilatation is rarely very great. Its mechanism and conditions have
been already considered (Art-. "Dilatation"). But the weakness
which fatty degeneration produces may have a much graver
result. The brittleness of the fibres may lead to their rupture, and
when the degeneration extends through the whole thickness of the
wall of the heart, the whole wall may give way. This accident,
" rnpture of the heart," is of such gravity and importance as to need
detailed consideration, and it is therefore described at the end of this
article.

Symptoms. — The physical signs and the symptoms which attend
fatty degeneration of the heart are usually indistinct and never
distinctive. All are common to other morbid states. They depend on
the diminished power of the heart, which modifies the signs of its
action, and affects the function of other organs.

As the size of the heart in simple fatty degeneration is little
changed, the area of dulness presents no alteration. The slight
dilatation, wliich is the consequence of the fatty degeneration, rarely
leads to the sigus of enlargement of the heart. In a considerable
number of cases the dulness is increased, but this increase depends
rather on pre-existing hypertrophy or dilatation, or else it is due to
concurrent fatty growth.

Diminished force of impulse is the most important physical sign
of cardiac degeneration. The area of impulse, like the area of dulness,
is only increased by coexisting conditions. As long as the im-
pulse is perceptible, the apex-beat may, in mdst cases, still be felt
When dilatation has occurred in consequence of the weakening of
the cardiac wall, the impulse may be diffused and peculiar in
character, resembling, as Stokes remarked, rather the slight, general
impulse of an aneurism than the normal impulse of the heart.
When the patient is thin, and the lungs are small, so that the

FATTY DISEASES OF THE HEART. 779

The sounds of the heart are weakened in correspondence with the
weakness of the impulse. The first sound, to which the contraction
of the heart directly contributes, is that which presents the greatest
change. It is usually toneless, shorter, and relatively high-pitched,
and may become almost or even quite inaudible at the apex,
only the second sound remaining. The first silence is longer tJian
normal in consequence of the shortening of the first sound. The
second sound is also weakened in consequence of the deficient
distension, and therefore deficient recoil, of the aorta and pulmonary
artery. When the first sound is shortened and raised in pitch it may
resemble the second. The sounds of the foetal heart are then
very closely simulated, especially if the heart acts rapidly. When
the degeneration is local, the sounds may be modified locally,
just as the impulse. In the acute degeneration of fever, Stokes
observed that the first sound might be lost over the left ventricle
when it was still audible over the right, in cases in which the
post-mortem examination showed the left ventricle to be the more
affected. Walshe has observed a similar alteration of intensity in
chronic disease under similar circumstances. According to Stokes, if,
after ceasing to be heard for a time, the first sound reappeared, it was
heard first over the right ventricle and afterwards over the left. In
one case both sounds were inaudible for thirty-six hours before death.

Pain is not a common symptom, but now and then is complained
of, and is sometimes very troublesome. It may be confined to

1 Onnerod thought that iufretjucncy was associated rather with fatty infiltration than
•with fatty degeneration. Lond. Med. Gaz. 1849, p. 917.

° E 2

792 A SYSTEM OF MEDICINE.

Etiology. — The causes of fibroid degeneration are still little known.
It is certainly more frequent in men than in women, and chiefly occurs
during or after middle life. The right side of the heart is said to
be affected occasionally in foetal life. It is not commonly associated
with fibroid degeneration of other organs, and it seems not specially
related to the habits or conditions of life of the individual.* Walshe
believes, however, that it is sometimes due to chronic alcoholism. Its
occurrence is chiefly influenced by local causes. Long-continued
intermitting congestion of the heart causes, as Jenner1 showed,
toughening and induration of the organ, with increase in the inter-
stitial tissue. The frequent existence of fibroid overgrowth in
hypertrophy of the heart is probably due to the congestion which
results from the cause of the hypertrophy. Local inflammation may
result in fibroid change, as in the superficial layers of the heart after
pericarditis. Where the fibrosis is limited in area, it has also been
ascribed to an extension to the wall of adjacent endo- or peri-carditis, but
Hilton Fagge has suggested that the traces of inflammation which are
found may be secondary to the fibroid change, and cannot be taken
as proof of such an origin. Injuries, blows on the precordial region,
have been assigned, in some cases, as the cause of the symptoms.
Lastly, there is clear evidence that syphilis is capable of causing
local indurations of the heart ; most probably by the transformation
into fibrous tissue, of gummatous growths.

Pathological Anatomy. — The slighter diffused form of fibrosis may
affect the whole heart, or only one chamber. The intenser form is usually
limited to a portion of one chamber. Occasionally a high degree of
fibroid growth may extend around the heart, and has been described
as a true " stenosis of the heart.2 " In the fibroid change secondary to
pericarditis the outer layers of the heart are most affected, and
sometimes one-half of the thickness of the wall may be transformed
into fibrous tissue.

The local forms of fibrosis affect the papillary muscles more fre-
quently than any other parts. These may be entirely transformed
into fibrous tissue of tendinous aspect. More rarely the wall of the
heart is the seat of circumscribed changes, especially the neighbour-
hood of the apex. They are also found in the septum, and in the
posterior wall at the base. In the right ventricle the degeneration is
usually near the base. The local forms are commonly most marked
towards the inner surface of the wall. If the whole thickness of
the wall is affected, it is rendered thinner, even apart from aneu-
rismal bulging. The endocardium over the degeneration is ofteu
thickened.

The diffuse fibrosis renders the wall of the whole heart tougher, more
resistant to the fingers and knife. Sometimes, when the new tissue
is soft, and the muscular fibres are degenerated, the consistence may

1 Med. Chir. Trans, xliii.

2 Dittrich, loc. cit.

FIBROID DlaEASE OF THE HEART. 793

not be increased, may even be diminished. The change may alter
veiy little the naked-eye appearances, or the enlarged intermuscular
septa may be visible in the cut section. The localised change usually
presents a glistening fibrous appearance, grey or white, sometimes of a
greenish or bluish tint. The section may have a spongy appearance.
(Hilton Fagge.) Where less advanced, whitish bands and tracts of
fibrous tissues may be seen in the muscular substance. In some
cases several separate areas are affected. Occasionally calcareous
deposits have been found in the changed tissue.

Under the microscope the localised forms present well-developed
fibrous tissue with nuclei. In more recent cases a fusiform cell-
growth has been found, developing into fibres. It is said to begin
around the blood-vessels, in the intermuscular septa, with an infiltra-
tion of nuclei and leucocyte-like cells. Sometimes, it is said, the
new substance appears very obscurely fibrillated or amorphous, and
may undergo fatty degeneration. Pelvet has sefen much elastic tissue
in some specimens. Through the fibrous tissue the muscular fibres
may be seen passing, lessened in number, sometimes narrowed by
pressure, or the seat of fatty degeneration. It is rare for them to
disappear entirely. Occasionally the degeneration is in excess of
the development of fibrous tissue, and the affected area softens.

Consequences. — The effect of fibrosis on the form and size of the
heart varies. Hypertrophy and dilatation usually co-exist with the
diffuse change, and sometimes the overgrowth of the muscular and
fibrous tissues, advancing pari passu, may enlarge the heart to vast
dimensions, as in the specimen preserved in St. George's Hospital
and described by Quain.1 The increase in the fibrous tissue which
results from congestion is commonly greater in the right ventricle
than the left Localised fibrosis also often occurs in hypertrophied
hearts, although it may be found in hearts which are normal in size.
The cavity may present little change, or it may be generally dilated.
More commonly the wall of the affected spot is bulged out into an
aneurism. (See Aneurism of the Heart.)

Symptoms. — The necessary effect of fibrosis of the heart will be,
as Corvisart clearly taught, to lessen its contractile power. The
diffused form, therefore, promotes dilatation or lessens the effects of
the hypertrophy which it accompanies. The symptoms of the
localised form, in marked cases, have commonly been those of cardiac
weakness. Dyspnoea and dropsy have been the chief troubles, and
in their general character the symptoms resemble those of dilatation
of the heart. The impulse is weakened.2 The first sound is weak
and toneless, and it has been noticed to be much weaker over the

1 Lumleian Lectures, loc. cit.

* Laennec taught that induration increases the firmness of the heart's contraction ;
but this was probably a hasty conclusion from th j firmnes.3 of hypertrophied and strongly-
contracted hearts.

VOL. IV. 'A F

194 A SYSTEM OF MEDICINE.

left than over the right ventricle, when the former was most affected.
A systolic murmur has been present in many cases, due, in some, to
regurgitation from fibrosis of papillary muscles. The pulse is weak,
and has been, in some cases, very infrequent ; only thirty beats per
minute have been noted. Cardiac pain is present in a considerable
number of the cases. In many instances, however, the symptoms have
been entirely latent. These differences depend no doubt partly on
the extent and position of the fibrosis, affecting the action of
the rest of the muscular tissue more in some cases than in others.
Death in many instances has been sudden, apart from the rupture,
or even the existence of an aneurism.

Diagnosis. — Fibroid degeneration of the heart is at present hardly
more than a pathological curiosity, for it is doubtful whether it has
ever been recognised during life. Its detection, apart from the signs
of aneurism of the heart, must depend on the symptoms of cardiac
dilatation without its physical signs.

Treatment. — The treatment needed is that for cardiac weakness —
for the dilatation which it resembles in its effects. Rest, the avoid-
ance of all strain on the circulation, and the administration of digitalis,
to strengthen the remaining fibres, are the chief measures. If there
is any suspicion of syphilis, iodide of potassium should be given,
although it is doubtful whether the stage of induration can be
modified by that drug.

INDEX.

3 F 2

INDEX.

Abdomen, tympanitic distension of the, a
cause of displacement of the heart, 15,
27, 180 1 collapse of the, also affects the
position of the heart, 127.

Abscess of the heart, 530 ; a cause of aneu-
rism of the heart, 155 ; of rupture of
the heart, 787.

Abscesses, multiple, in the lungs, from
embolism, 951.

Aconite, value of, in the treatment of
hypertrophy of the heart, 727, 728 ; of
dilated heart, 756.

Adherent pericardium, article on, 438 ;
including, — pathological anatomy, 438;
physical signs, 442.

Adventitious products in the heart, article
on, 165.

Age, predisposing to aneurism of the heart,
162 ; to angina pectoris, 548 ; to dila-
tation of the heart, 782 ; to fatty over-
growth of the heart, 761 ; to fattv de-
generation of the heart, 766 ; to fibroid
disease of the heart, 792 ; to hyper-
trophy of the heart, 694 ; to rheumatic
pericarditis, 187 ; to renal pericarditis,
408; to tubercular pericarditis, 168;
to rupture of the heart, 787.

Age, influence of, on the position of the
heart, 89 ; on the weight of the heart,
6 ; on the area of pericardial didness,
331.

Albuminuria, see Bright'* disease.

Alcoholic excess, habitual, a cause of dila-
tation of the heart, 733 ; «f fatty heart,
762, 769; of fibroid disease of the
heart, 792 ; of valvular disease of the
heart, 681 : predisposes to the occur-
rence of delirium in rheumatism, 273,
285.

Ammonia, value of, in the treatment of
angina pectoris, 586 ; of dilated heart,
757 ; of chronic valvular disease of the
heart, 682, 686.

Amyl, nitrite of, value of, in the treatment
of angina pectoris, 573, 589, 686 ; of
dilated heart, 756 ; of fatty heart, 786 ;
occasional alarming effects of, 592 ;
mode of administration, 5P3.

Anemia, predisposes to dilatatiou of the

heart, 733; to fatty degeneration of the
heart, 767.

Anaemic measures, so-called, mode of pro-
duction, 629, 639.

Anasarca, see Dropsy.

Aneurism of the aorta, a cause of displace-
ment of the heart, 129, 148 ; of angina
pectoris, 544; of hydrops pericardii,
532 ; of hypertrophy of the heart, 699;
of pericarditis, 425.

Aneurism of the heart, 729 ; acute, 530 ;
false consecutive, 161, 154.

Aneurism, lateral or partial, of the heart,
article on, 149; including, — aneurism
of the left ventricle, 150 ; of the left
auricle, 162 ; of the valves, 163.

Aneurism of the cardiac valves, 168 ; mode
of origin of, 458, 606 ; of the mitral
valve, 163 ; of the aortic valve, 164.

Angina pectoris, article on, 535 ; including,
— symptom*, 535 ; diagnosis, 642 ;
etiology, 548 ; pathology, 569 ; pro*
gnosis, 583 ; treatment, 586.

Angina pectoris, relation of, to the neural-
gias, 577, 582.

Angina sine dolore, 566.

Aorta, aneurism of the, see Aneurism.

Aorta, arch of the, anatomical relations of,
in front, 80 ; at sides, 90 ; at back, 99,
1 06, 1 22 ; variations in the position of,
18, 111 ; position of the, affected by
respiration, 73, 81 ; by shape of chest,
86.

Aorta, the ascending, variation in the posi-
tion of, 37 ; in the length of, 22.

Aorta, the, descending, relations of, in the
chest, 107.

Aorta, root of the, connections of, in the
chest, 84, 116, 123; variations in the
position of, 37, 39.

Aortic aperture, the, size of, in health, 5 ;
extreme enlargement of, 8.

Aortic murmurs, diagnosis of, from pericar-
dial friction, 346, 672 ; systolic anatmie
murmur occurs in rheumatic endocar-
ditis, 491, 496.

Aortic obstruction, characters of murmur,
638 ; rarely uncomplicated by regurgi-
tation, 611 ; effects of, on the heart,

79S

INDEX.

740 ; a cause of hypertrophy, 655 ;
prognosis of, 677.

Aortic regurgitation, a consequence of rheu-
matic endocarditis, 494; early characters
of murmur, 496, 498 ; signs of estab-
lished disease, 500, 644 ; late appearance
of, 504 ; effects of, on the heart, 740 ;
a cause of dilatation of the heart, 655 ;
of angina pectoris, 566 ; diagnosis of,
671, 673 ; prognosis of, 677, 679 ; treat-
ment of, 682; use of digitalis in,
684.

Aortic sinuses, the, position, 41, 45.

Aortic stenosis, ace Aortic obstruction.

Aortic valves, the, relations of, 41, 45, 117;
mode of action of, 457 ; aneurism of,
164 ; atrophy, 611 ; congenital disease
of, 615 ; endocardial inflammation of,
459 ; chronic changes in, 609.

Aortic valves, diseases of the, due to athe-
roma, 623 ; to rheumatic endocarditis,
212, 213 ; effects of, on the heart, 655 ;
a cause of hypertrophy of the heart, 9;
predisposes to endocarditis, 521.

Aortic vestibule, the, 42.

Apex of the heart, the, position of during
life, 79; after death, 17, 36, 110; a
common seat of aneurysmal dilatation,
155 ; change in the position of, caused
by respiration, 78 ; by habit of body
and nature of occupation, 86 ; by peri-
cardial effusion, 218, 866 ; by hyper-
trophy of the heart, 712.

Apex-beat of the heart, changes in, caused
by rheumatic endocarditis, 483 ; by
adherent pericardium 450, 454 ; by
dilatation of the heart, 747.

Apex murmurs, systolic, clinical significance
of, 640, 675 ; a sign of dilatation of
left ventricle, 748 ; sometimes present
in fibroid disease of the heart, 675,
794.

Apoplexy, cerebral, a consequence of hyper-
trophy of the heart, 717; pulmonary,
connection of, with embolism, 719.

A reus sinilis, value of, in diagnosis of
cardiac degeneration, 784.

Arterial pyaemia of Wilks, 651.

Arterial tension, increase of, during the
anginal paroxysm, 578.

Arteries, thickening of the walls of, in
Bright's disease, 702.

Arteritis deformnna of Virchow, 623.

Arsenic, value of, in the treatment of an-
gina pectoris, 597, 686.

Ascites, a cause of displacement of the
heart, 183 ; a consequence of chronic
heart disease, 668.

Aspirator, use of the, for tapping the peri-
cardium, 435.

Asthma, spasmodic, a cause of vertical dis-
placement of the heart, 127.

Asystolie of the heart, 664, 738 ; treatment
of, 683.

Atheroma, a cause of incompetence of the
cardiac valves, 623; a consequence of
hypertrophy of the heart, 716, 719 ; of
the coronary arteries, a cause of dilata-
tion of the heart, 733 ; of fatty degene-
ration of the heart, 770 ; of the pul-
monary artery, a consequence of mitral
stenosis, 664.

Atrophy of the heart, article on, 687 ;
including, —definition and history, 687 ;
varieties and causes, 688 ; pathological
anatomy, 689 ; symptoms, 690 ; treat-
ment, &c., 691.

Auricle, the left, position of, 94 ; move-
ments of, during life, 80 ; aneurism of,
162 ; signs of dilatation of, 749 ; of hy-
pertrophy of, 710, 720; hypertrophy of,
a consequence of mitral stenosis, 661.

Auricle, the right, position of, 25 ; dimen-
sions of, 31, 114 ; movements of, 77 ;
signs of dilatation of, 749.

Bacteria, found in the heart in acute
ulcerative endocarditis, 652 ; relation
of, to embolism, 654.

Bath, use of the, in rheumatic hyper-
pyrexia, 255, 262, 266.

Belladonna, value of, in the treatment of
angina pectoris, 598 ; of dilated heart,
756 ; external application of, in rheu-
matic endocarditis, 526, 528 ; in jwri-
carditis, 481 ; in chronic valvular dis-
ease of the heart, 686.

Blisters, value of, in the treatment of hy-
drops pericardii, 534 ; of pericarditis,
482.

Blood-letting, for the relief of angina pec-
toris, 594 ; in dilatation of the heart,
753 ; in hypertrophy of the heart, 724,
726 ; in chronic valvular disease, 684.

Brain, the, changes in, caused by dilata-
tion of the heart, 745 ; by embolism
due to valvular disease, 648 ; by capil-
lary embolism due to endocarditis, 291,
292.

Bright 's disease, effects of, on the heart,
740 ; a cause of endocarditis, 456, 517 ;
of pericarditis, 406 ; of hypertrophy
of the heart, 7, 701 ; complicating
angina pectoris, 5.47 ; predisposes to
hydrops pericardii, 532.

Bronchitis, a cause of disphicement of the
heart, 127; of hypertrophy of the
heart, 7.

Bronchus, the left, partial obstruction of,
by the left auricle from extreme mitral
stenosis, 665.

Calcification of the walls of the heart, 179;
a mode of cure of aneurism of the heart
161 ; of the valves of the heart, 607;
of the coronary arteries, see Atheroma.

Cancer of the heart, 169

INDEX.

799

Cancer, a cause of fatty degeneration of the
heart, 767 ; of hydrops pericardii, 532;
of pericarditis, 424.

Cardiac asthma of Stokes, 565 ; treatment
of, 589.

Cardiograph, the, indications of, in mitral
stenosis, 636, 662; in aortic stenosis,
658.

Carditis, article on, 529 ; including,— eti-
ology, 529 ; pathological anatomy, 530;
symptoms, diagnosis, Ac., 531.

Carotid artery, the left, position of, in the
chest, 80.

Chalmers, Dr., sudden death of, 554.

Chest, pain in the, a symptom of angina
pectoris, 537 ; of pericarditis, 234 ; of
chronic valvular disease, 669 ; shape of
the, affects the position of the heart,
86, 97.

Cheyne -Stokes, respiration, or rhythmical
dyspnoea, 567 (note), 780.

Chloral-hydrate, value of, in the treat-
ment of angina pectoris, 587 ; in dila-
ted heart, 757.

Chloric ether, inhalation of, for the relief
of pseudo-angina, 756.

Chloroform, use of, in the treatment of
angina pectoris, 589 ; danger of, in
fatty heart, 786 ; external application
of, in rheumatic pericarditis, 433 ; in
endocarditis 526.

Chords tendinea? of the heart, rupture of
the, 606.

Chorea, complicating rheumatic pericar-
ditis, 292 ; with non-rheumatic pericar-
ditis, 298 ; numerical summary, 301 ;
connection of, with cerebral embolism,
291 ; relation of, to endocarditis, 456,
511, 619.

Cirrhosis of the heart, 791.

Cirrhosis of the lung, a cause of displace-
ment of the heart, 141 ; of dilatation of
the right ventricle, 736 ; of tricuspid
regurgitation, 640.

Coma, occurrence of, in carditis, 531 ; in
rheumatism with endocarditis, 263 ;
with pericarditis, 255, 282; without
heart affection, 265, 283.

Concentric hypertrophy of the heart, 694,

707.

Congenital atrophy of the heart, 688.

Congenital disease of the valves of the
heart, 613.

Conus arteriosus, position of the, 34, 41,
43 ; relation of, to the lungs, 64.

Convulsions, a symptom of carditis, 531 ;
of pericarditis, 300.

Copaiba, value of, in dropsy from chronic
heart disease, 685, 759.

Coronary arteries, origin of the, 45 ; athe-
roma of, a cause of dilatation of the
heart, 733 ; of fattv degeneration of the
heart, 770 ; embolism of, a cause of
rupture of the heart, 787 ; ossification

of, a cause of angina pectoris, 544, 547,
% 561 (note).
Corrigan's pulse, 657.
Cough, a troublesome symptom in dilated

heart, 750.
Cupping, value of, in the treatment of

angina pectoris, 594 ; of dilated heart,

753, 758 ; in chronic valvular disease.

685.
Cysts in the heart, 171.

Death, mode of, affects the size of the
heart, 4,707 ; the position of the heart,
15,28.

Death, sudden, in cases of angina pectoris,
probable cause of, 579 ; from aneurism
of the heart, 161; from aortic regurgi-
tation, 679 ; from fatty heart, 763, 783;
from fibroid disease of the heart, 794 ;
from " heart disease " generally, 550 ;
from rupture of the heart, 789.

Delirium, a symptom of carditis, 531 ; of
endocarditis, 472 ; of dilated heart,
750 ; occurs in rheumatism with peri-
carditis, 256, 283 ; with endocarditis,
263, 284 ; without heart affection, 265,
284 ; melancholic, 283 ; in non-rheu-
matic pericarditis, 296.

Delirium tremens, complicating rheuma-
tism, 257, 273, 285.

Delusions, occurrence of, in rheumatic
patients, 286.

Diaphragm, the, movements of, affect the
position of the heart, 69 ; affections of,
causing pericarditis, 429.

Diarrhoea, in rheumatic hyperpyrexia, 270 ;
in dilated heart, 751, 758.

Diastole of the heart, see Heart, movements
of.

Diastolic murmurs, causes of, 633, 644.

Digitalis, value of, in the treatment of
chronic valvular disease of the heart,
683 ; in dilated heart, 754 ; in fatty
heart, 786 ; in hypertrophy of the
heart, 727.

Dilatation of the heart, article on, 729 ;
including, — definition and history, 729;
etiology, 731 ; pathological anatomy,
741 ; consequences, 743 ; symptoms,
747; diagnosis, 751; prognosis, 752;
treatment, 753.

Dimensions of the heart, in health, 5 ; in
disease, 8.

Diphtheria, a cause of endocarditis, 624 ; of
acute fatty degeneration of the heart,
769.

Diphtheritic endocarditis of Eberth, 658.

Diseases, constitutional, influence of, on
the size of the heart, 6 ; acute febrile,
a cause of fatty degeneration of the
heart, 768.

Diuretics, value of, in the treatment of
dilated heart, 759 ; of hydrops peri-

800

INDEX.

cardii, 584 ; of pericarditis, 437 ; of
valvular disease of the heart, 685.

Dropsy, a consequence of aneurism of the
heart, 159 ; of dilated heart, 744, 749 ;
of fatty heart, 782 ; of chronic valvular
disease, 669 ; symptoms of, 746 ; treat-
ment, 758.

Dropsy, ovarian, effect of, on the action of
the heart, 134.

Ductus arteriosus, patent, a rare cause of
cardiac murmurs, 646.

Dull loss on percussion, area of, from dila-
tation of the heart, 747, 752 ; from
hypertrophy of the heart, 712, 721 ;
from pericardial effusion, 329.

Duration of angina pectoris, 584 ; of fatty
degeneration of tne heart, 782 ; of dila-
tation of the heart, 758 ; of hyper-
trophy of the heart, 723 ; of rheumatic
pericarditis, 207 ; of effusion into the
pericardium, 218, 309.

Dysphagia, caused by pericardial di&ten-
sion, 239.

Dyspnoea, a symptom of heart disease, 670;
of angina pectoris, 539 ; of carditis,
531 ; of dilated heart, 750 ; of fatty
heart, 567, 763, 780 ; of hydrops peri-
cardii, 588 ; of hypertrophy of the
heart, 715 ; causes of, in pericarditis,
237 ; treatment of, 757.

Eccentric hypertrophy of the heart, 694 ;
pathology of, 708.

Electricity, use of, in the treatment of
angina pectoris, 594.

Embolism, a consequence of valvular dis-
ease of the heart, 647 ; pathology of,
C05, 648 ; a cause of pulmonary apo-
plexy, 665, 719 ; of the cerebral arteries,
a probable cause of chorea and rheu-
matic insanity, 2i)0, 291 ; connection
of, with hypertrophy of the heart, 717 ;
of the coronary arteries, a cause of
ruptureof the heart, 787.

Emphysema, pulmonaiy, a cause of dis-
placement of the heart, 125 ; of dila-
tation of the heart, 736 ; of hypertrophy
of the left ventricle, 700.

Empyema, a cau*e ol displacement of the
heart, 135.

Endarteritis deformans, 716 ; see Atheroma.

Endocarditis, article on, 4^6 ; including, —
pathological anatomy, 456 ; physical
»>igus aiid symptoms, 460 ; prognosis,
4i>9 ; diagnosis, 505 ; treatment, 525.

rnlocarditis diphtheritica, 653; maligna,
of Virchov, 650 ; secondary to acute
rheumatism, 456 ; to Bright's disease,
517 ; to chorea, 511 ; to pyemia, 516 ;
to chronic valvular disease of the heart,
506, 519, 607.

Endocarditis, rheumatic, comparative fre-
quency of, in relation to joint affection,
186, 526, 618 ; increased liability to,

after first attack, 208, 216 ; relation
of, to pericarditis, 212 ; predisposes to
aneurism of left ventricle, 149, 152.

Endocarditis, recurrent, pathology of, 519;
symptoms of, 523 ; diagnosis of, in
cases of old valvular disease, 507.

Endocarditis, ulcerative, etiology of, 621 ;
pathology of, 458, 605 ; symptoms, 650;
diagnosis, 651 ; treatment, 681 ; relation
of, to pyaemia, 620.

Entozoa in the heart, 172.

Epigastrium, pulsation at the, causes of,
126, 668 ; a sign of dilatation of right
ventricle, 749 ; of hypertrophy of right
ventricle, 718; of adherent pericardium,
451, 454 ; pain at the, a symptom of
pericarditis, 230.

Erysipelas, a cause of acute fatty degene-
ration of the heart, 768.

Ether, value of, in the treatment of angina
pectoris, 586 ; of dilated heart, 757 ;
m chronic valvular disease of the heart,
686.

Exercise, beneficial in cases of fatty heart,
768 ; an aid to diagnosis of heart dis-
ease, 674.

Expiratory type of chest, 87.

Face, the, expression of, in angina pectoris,
541 ; in endocarditis, 471, 494 ; in
rheumatic pericarditis, 243 ; cyanosis
of, from dilated heart, 749 ; from dis-
tended pericardium, 248 ; from chronic
valvular disease, 666 ; flushing of, in
hypertrophy of the heart, 715.

Fainting, see Syncope.

Fatty degeneration of the heart, article on,
764 ; including definition and history,
764 ; varieties, 765 ; etiology, 766 ;
pathological anatomy, 771 ; symptoms,
778 ; diagnosis, 783 ; prognosis and
treatment, 785.

Fatty overgrowth of the heart, article on,
760 ; including, — causes, 761 ; patho-
logical anatomy, 762 ; symptoms and
treatment, 763.

Fibrinous deposits in the heart, 176 ; on
the cardiac valves, 604.

Fibro-cartilage, the central, of the heart,
44.

Fibrocartilaginous degeneration of the

walls of the heart, 177.
Fibroid disease of the heart, article on,

791 ; including, — definition and history,

791 ; etiology and pathology, 792 ;

symptoms, &c, 798.
Fifth left costal cartilage, variations in

relative position of, 17.
Fingers, clubbing of the, a result of chronic

heart disease. 666.
First sound of the heart, see Sounds of the

h»»art.
Fluid in the pericardium, physical signs

if, 3*29 ; ♦•fleets of, on neightauring

INDEX.

801

organs, 306 ; on the heart itself, 307 ;
diagnosis of, from dilated heart, 752 ;
from hypertrophy of the heart, 330 ;
characters of the, in hydrops pericardii,
533.

Fremitus, the friction, of pericarditis, ace
Thrill.

Friction-sound, the, of pericarditis, time of
its appearance in acute rheumatism,
209, 348 ; auscultatory signs of, 345 ;
area of, 352, 361 ; spots of greatest
intensity, 364, 381 ; varieties, 353 ;
decline and disappearance of, 375, 384 ;
diagnostic characters of, 388 ; effects
of pressure on, 391 ; diagnosis of, from
endocardial murmurs, 346, 672 ; rela-
tion of, to amount of effusion, 329,
349 ; characters of, in pericarditis from
Bright' 8 disease, 413.

Friction, pleuritic, complicating pericar-
ditis, 232.

Furrow, the interventricular, 33, 104 ; the
auriculo-ventricular, 34, 58, 101.

Gaxorknr of the limbs from embolism,
649.

Granulations on the cardiac valves, in endo-
carditis, 458, 603 ; further changes in,
622.

Gout, chronic, a cause of fatty degeneration
of the heart, 769 ; predisposes to angina
pectoris, 547, 596.

Hallucinations, occurrence of, in rheu-
matic patients, 286, 289.

Headache, from dilated heart, 750 ; treat-
ment of, 757.

Head, oscillatory movements of the, a
rare symptom in pericarditis, 302.

Heart, the, abscess of, 530 ; acute aneurism
of, 580 ; lateral or partial aneurism of,
article on, 149.

Heart, adventitious products in the, article
on, 165 ; including, — tubercle in the
heart, 165 ; cancer, 169 ; cysts, 171 ;
entozoa, 172 ; fibrinous deposits, 176 ;
fibro-cartilaginous or osseous degenera-
tion, 177 ; polypoid growths, 179.

Heart, atrophy of the, article on, 687.

Heart, dilatation of the, article on, 729 ;
a cause of angina pectoris, 568 ; a con-
sequence of aortic regurgitation, 655 ;
diagnosis of, from pericardial effusion,
752.

Heart, dimensions of the, in health, 5 ; in
disease, 8.

Heart, displacement of the, due to, abdom-
inal distension, 15, 27 ; to angular cur-
vature of the spine, 6P9 ; to ascites,
183 ; to asthma, 127 ; to aortic aneu-
rism, 129, 148 ; to bronchitis, 127 ; to
cirrhosis of the lung, 141 ; to dia-
phragmatic hernia, 429; to deformities
of the thorax, 699; to pulmonary emphy-

sema, 125 ; to empyema, 135 ; to
hypertrophy of the heart, 712 ; to
enlargements of the liver, 29, 135 ; to
mediastinal tumours, 130, 144 ; to peri-
cardial effusion, 218, 308 ; to pleuritic
effusion, 130, 136, 141 ; to pneumotho-
rax, 141 ; to distension of tne stomach,
130; see also Heart, position of.

Heart, fatty diseases of the, article on, 760;
including, — fatty overgrowth, 760 ;
fatty degeneration, 764.

Heart, fatty degeneration of the, a cause
of angina pectoris, 545, 568 ; of sudden
death, 763 ; predisposes to rupture of
the heart, 786.

Heart, fibroid disease of the, article on
791 ; a cause of mitral regurgitation,
675.

Heart, gout in the, 547.

Heart, hypertrophy of the, article on, 692 ;
effects of, on size and weight of the
heart, 8 ; a consequence of aortic ste-
nosis, 655 ; relation of, to pericarditis
in Bright's disease, 410 ; predisposes
to pericarditis in acute rheumatism,
426 ; relation of, to dilatation o'f the
hrart, 739.

Heart, impulse of the, ate Impulse, cardiac.

Heart, movements of the, described, 65 ;
relation of, to the normal sounds and
to abnormal bruits, 632.

Heart, ossification of the, 774.

Heart, malpositions of the, article on, 115;
including, — vertical displacements, 125;
lateral, 135 ; forward, 148 ; backward,
148.

Heart, pain in the region of the, see Pain.

Heart, position of the, during life, 73 ;
variations in the, vertical, 14 ; lateral,
28 ; due to nge, 89 ; to position of
patient, 29 ; to respiration, 69, 97 ; to
sex, 89, ; to state of health and nature
of occupation, 86 ; to shape of thorax,
97 ; to mode of death, 15, 28.

Heart, rapid enlargement of the, 10 ; rela-
tion of, to spinal column, 94, 100, 122.

Heart, rupture of the, article on, 786 ; a
result of carditis, 530 ; of fatty degene-
ration of the heart, 779.

Heart, state of the, after death from angina
pectoris, 644, 580.

Heart, syphilitic affections of the, 176.

Heart, weight of the, in health, 4 ; iti
general diseases 7 ; when itself disease* I,
' 8 ; when atrophied, 689 ; when hyp* r-
trophied, 655, 7o9.

Hemiplegia, right, a common result of
cerebral embolism, 650.

Hereditary predisposition to dilatation of
the heart, 732 ; to fatty heart, 761, 765 ;
to rupture of the heart, 788.

Hunter, John, illness and sudden death of,
560.

Hydatid <-ysts in the heart, 173.

302

INDEX.

Hydropericardium, hydropericarditis, 532.

Hydro-pneumo-pericarditis, diagnosis of,
185.

Hydrops pericardii, article on, 532 ; in-
cluding,—etiology and pathology, 532 ;
symptoms, 533 ; treatment, 534.

Hyperesthesia, local cutaneous, in rheu-
matic pericarditis, 224.

Hyperpyrexia, occurrence of, in cases of
rheumatism with pericarditis, 254 ;
with endocarditis, 262 ; without heart
affection, 264 ; without delirium, 266;
general summary, 270, 284 : occurs
ilso in sunstroke, &c, 271.

Hypertrophy of the heart, article on, 692;
including, — definition and history, 692 ;
causes, 694 ; pathological anatomy,
706 ; symptoms, 712 ; diagnosis, 720;
prognosis, 722 ; treatment, 724.

Impulse, the, of the heart, character of,
in carditis, 531 ; in dilatod heart, 747,
751 ; in fatty heart, 778, 783 ; from
hypertrophy of left ventricle, 712 ; of
rignt ventricle, 718; changes in, caused
by adherent pericardium, 842, 385 ;
by endocarditis affecting mitral valve,
481 ; by pericarditis with effusion, 834,
371, 380 ; value of, in diagnosis, 720,
752.

Injury, local, a cause of acute rheumatism,
221.

Innominate artery, position of, in the chest,
80.

Insanity, temporary, a sequela of acule
rheumatism, 286.

Insomnia, from heart disease, treatment
of, 757.

Inspiration, effect of, on the heart, 72 ; sec
inspiration.

Inspiratory type of chest, 86.

Intra- thoracic tumours, a cause of displace-
ment of the heart, 144.

Iodide of potassium, value of, in the treat-
ment of angina pectoris, 598; of chronic
valvular disease of the heart, 680, 682.

Iron, value of, in the treatment of carditis,
531 ; of dilated heart, 754.

Jactitation, muscular, in pericarditis, 302.

Joints, the, first affected in acute rheuma-
tism, 221.

Jugular veins, pulsation in the, a sign of
tricuspid regurgitation, 666 ; fulness of
the, from distended pericardium, 242,
248 ; from dilatation of right ventricle,
749.

Kidneys, congestion of the, due to dilated
heart, 745, 751 ; to chronic valvular
disease of the heart, 668 ; treatment of,
# 758.

Kidneys, chronic disease of the, see
Blight's disease.

Labyngitis, a cause of displacement of the
heart, 127.

Leeches, use of, in tho treatment of dilated
heart, 757 ; of endocarditis, 526, 528 ;
of pericarditis, 431 ; in chronic valvular
disease of the heart, 685.

Liver, changes in the, caused by chronic
valvular disease, 668 ; by dilatation of
the heart, pathology of, 745 ; sym-
ptoms, 750 ; treatment, 757 ; enlarge-
ment of, a cause of displacement of the
heart, 29, 135, 146.

Lungs, the, relations of, to the heart, 60,
82 ; relative size of, 62, 113 ; relative
size of, affects the position of the heart,
28 ; abscesses in, from embolism, 651 ;
brown induration of, a consequence of
mitral stenosis, 665, 745 ; embolism of,
665, 719.

Lungs, cirrhosis of the, a cause of dis-
placement of the heart, 141 ; of dila-
tation of the right ventricle, 736; of
tricuspid regurgitation, 640

Mediastinum, tumours in the, affect the
position of the heart, 130, 144.

Melancholia, following acute rheumatism,
286.

Microscopical appearances in endocarditis,
603 ; in fatty degeneration of the heart,
771 ; in fibroid disease of the heart,
798.

Mitral orifice, the, circumference of, in
health, 5 ; in disease, 8 ; variations in
the position of, 53; anatomical relations
of, anterior, 85 ; posterior, 108.

Mitral valve, the, description of, 49 ; re-
lations of, 85, 118, 124 ; action of, 68,
457 ; aneurism of, 164 ; endocardial
inflammation of, 458 ; frequently at-
^ tacked by rheumatic endocarditis, 212.

Mitral disease, chronic, causes of, 624;
pathology of, 608 ; rarely congenital,
613 ; due to chorea, 513 ; a cause of
hypertrophy of the heart, 10 ; effect o£
on the cardiac impulse, 342 ; predis-
poses to secondary endocarditis, 521.

Mitral regurgitation, characters of murmur,
467, 476, 638 ; causes of, 641 ; diagnosis
of, 643, 674 ; diagnosis of murmur from
pericardial friction, 347, 478; not
always audible at back, 104 ; effects
of, on the heart, 740 ; guides to pro-
gnosis in early stage, 479 ; relation of,
to pericarditis, 426 ; treatment of, 683.

Mitral stenosis, frequency of, 609 ; charac-
ters of murmurs, 634 ; effects of, on
the heart, 740; diagnosis of, 678;
prognosis, 678 ; treatment, 684 ; see
also Presystolic murmurs.

Morphia, hypodermic injection of, in
angina pectoris, 590 ; in dilated heart,
756; in late stages of mitral disease,
686 ; caution necessary, 786.

INDEX.

803

Movements involuntary muscular, in peri-
carditis, 300.

Murmurs, endocardial, mode of produc-
tion, 627, 630 ; variability of, a sign of
endocarditis, 507 ; pericardial, charac-
ters of, 345, 386.

Muscular fibres of the heart, anatomical
arrangement of, 44.

Muscular strain, habitual or long-con-
tinued, a cause of dilatation of the
heart, 735 ; of hypertrophy of the
heart, 700 ; of chronic valvular disease,
623.

Mycosis endocardii, 652.

Myocarditis, acute, 529 ; chronic, 791 ; a
cause of fibrinous deposits in the walls
of the heart, 1 76 ; of irregular action
of the heart, 236 ; relation of, to fatty
degeneration, 768.

Nervous system, symptoms affecting the,
in angina pectoris, 541 ; in endocar-
ditis, 472 ; in non-rheumatic pericar-
ditis, 296 ; in rheumatism with pericar-
ditis, 249, 281 ; with endocarditis, 262,
282 ; without heart affection, 264,
282 ; connection of, with high tem-
perature, 254, 270 ; with remission of
joint affection, 259, 285 ; with sup-
pression of perspiration, 259, 263 ; with
alcoholism and nervous exhaustion,
273.

Nutmeg liver, the, a result of chronic
heart disease, 668, 745.

Obesity, effects of, on the action of the
heart, 133 ; predisposes to dilatation
of the heart, 733 ; to fatty heart,
761.

Occupation, influence of, on the position
ot the heart, 86 ; on the joints first
affected in acute rheumatism, 220 ;
predis]x>sing to angina pectoris, 549,
550 ; to dilatation of the heart, 732 ;
to fatty heart, 762, 766 ; to hyper-
trophy of the heart, 700 ; to acute
rheumatism, 189, 220 ; to rheumatic
pericarditis, 189, 200 ; to chronic val-
vular disease of the heart, 623.

(Esophagus, disease of the, a cause of peri-
carditis, 428 ; perforation of the, a
cause of pneumo-pericardium, 183,
184.

Opiates, value of, in the treatment of
angina pectoris, 586, 587 ; of dilated
heart, 756 ; of rheumatic endocarditis,
528 ; sec also Morphia.

Opisthotonos, in angina pectoris, 542 ; in
pericarditis with nervous complications,
803.

Orthopnea, from chronic valvular disease
of the heart, 670 ; from dilated heart,
750 ; su Dyspnoea.

Ossification of the heart, 177, 774 ; of the

coronary arteries, 544, 561.
Over-exertion, a cause of hypertrophy of

the heart, 8, 700 ; of chronic valvular

disease, 623, 681.

Pain, the, of angina pectoris, characters

of, 535 ; seat of, 537 ; causes of, 576.
Pain in left arm and shoulder, a symptom
of chronic valvular disease of the heart,
669.
Pain in the region of the heart, a sym-
ptom of carditis, 531 ; of dilatation of
the heart, 749 ; of endocarditis, 472,
510 ; of fatty degeneration of the heart,
779 ; of fibroid disease, 794 ; rare in
hypertrophy, 714 ; of rheumatic peri-
carditis, 210, 223, 231 ; sudden, from
rupture of the heart, 789, 790.
Palpitation of the heart, in rheumatic
pericarditis, 219 ; in dilatation of the
heart, 749 ; in hypertrophy, 714 ;
value of, as a sign of heart disease,
669.
Papillary muscles, tlit, of the heart, ar-
rangement of, 52, 55 ; relations of, 84,
85 ; action, 67.
Paracentesis pericardii, in acute pericar-
ditis, 433 ; in pericardial dropsy, 534 ;
mode of performing the operation, 436 ;
precautions, 437.
Patches, white, on the heart, origin of,

439.
Pericardial sac, tho average capacity of,

305, 588.
Pericardial friction, see Friction.
Pericarditis, article on, 186 ; including
rheumatic pericarditis, 186 ; renal, 400;
due to other causes, 295, 419.
Pericarditis, rheumatic, article on, 186 ;
including, —etiology, 187 ; relation of,
to other symptoms of rheumatism, 202;
to endocarditis, 212 ; pathological ana-
tomy, 217 ; symptoms, — pain, 228 ;
changes in pulse, respiration, Ac., 235;
in expression and general appearance,
243 ; symptoms affecting the nervous
system and hyperpyrexia, 249 ; phy-
sical signs, 304 : percussion, 309 ; in-
spection and palpation, 332; auscul-
tation, 345 ; diagnosis, 330, 846, 388 ;
relapses, 870 ; treatment, 430.
Pericarditis, relative frequency of, in acu*e
rheumatism, 186 ; relation of, to the
severity of the joint affection, 203 ; a
cause of aneurism of the heart, 152,
154 ; of carditis, 529 ; of fatty degene-
ration of the heart, 771 ; of fibroid
disease of the heart, 178, 792; of ad-
herent pericardium, 342.
Pericarditis, tubercular, 165.
Pericardium, adherent, article on, 488 ; a
cause of atrophv of the heart, 689 ; of
dilatation of the heart, 733, 788 ; of

804

INDEX.

hypertrophy, 10, 440, 447, 697; effect
of, on the cardiac impulse, 342, 385.

Pericardium, distension of the, a cause of
dyspnoea, 237 ; of dyHphagia, 239 : of
cardiac syncope, 236, 242 ; of lividity
of the face, 243.

Pericardium, dropsy of the, 532.

Pericardium, effusion into the, physical
signs of, 218, 309, 329, 345 ; process of
absorption and cure, 382 ; diagnosis of,
from dilatation of the heart, 752 ; from
hypertrophy of the heart, 721 ; relation
of, to joint affection in acute rheuma-
tism, 205 ; amount of, in pericarditis
from Blight's disease, 412.

Perspiration, profuse, a symptom of rheu-
matic endocarditis, 472 ; suppression
of, in rheumatic hyperpyrexia, 259,
263, 268, 288.

Phthisis, pulmonary, effects of, on the size
of the heart, 6 ; a cause of atrophy of
the heart, 689 ; of hypertrophy, 700 ;
of fatty degeneration of the heart, 767.

Phosphorus, use of, in the treatment of
angina pectoris, 598 ; chronic poison-
ing t>7» * cause of fatty degeneration of
the heart, 769.

Pleurisy, a cause of pericarditis, 427 ;
relation of, to pericarditis in Blight's
disease, 409.

Pleuritic pain, occurrence of, in pericar-
ditis, 224, 232.

Pneumonia, relation of, to pericarditis in
Blight's disease, 410.

Pneumopericardium, article on, 182 ; dia-
gnosis of, 184.

Pneumothorax, a cause of displacement of
the heart, 141.

Polypi in the heart, 179.

Position of the patient, the, affects the posi-
tion of the heart, *29 ; characteristic of
pericardial effusion, 334 ; of chronic
heart disease, 670, 750, 757.

Pregnancy, a cause of hypertrophy of the
heart, 701 ; predisposes to ulcerative
endocarditis, 621.

Pressure of stethoscope, effect of, on peri-
cardial friction sound, 357, 859, 391 ; a
cause of pulmonary murmur in children,
640.

Presystolic murmurs, explanation of 635 ;
relation of, to first sound of the heart,
686; to second sound, 637 ; diagnosis of,
672, 673 ; variuble character of, 674.

Prognosis, in rheumatic endocarditis, mm to
mitral disease, 479 ; us to aortic disease,
499.

Pfeeudo-angina pectoris, 571, 676.

Pulmonary apoplexy, pathology of, 665,
668 ; a consequence of pericardial dis-
tension, 242 ; relation of, to embolism,
719.

Pulmonary artery, the, relations of, 81, P0,
96; to vertebral column, 123; to the

aorta, 22, 96 ; variations in position of,
19, 21, 34, 111 ; in the length of, 20 ;
communication of, with the aorta, a
rare cause of murmur, 646 ; hyper-
trophy of, a consequence of mitral ste-
nosis, 664.

Pulmonary artery, orifice of the, size of in
health, 5 ; in disease, 8 ; congenital
contraction of, 10.

Pulmonary artery, valves of the, anato-
mical relations of, 83 ; results of dis-
ease of, 666.

Pulmonary artery, the, regurgitant mur-
mur in, 646 ; systolic murmur in, 368 ;
characters of, 488, 639 ; causes of, 489 ;
clinical significance of, 190 ; diagnosis
of, from pericardial friction, 347.

Pulmonary veins, anatomical relations of
the, 95, 101.

Pulsation, epigastric, set Epigastrium.

Pulse, characters of the, in aortic stenosis,
656 ; in aortic regurgitation, 657 ; in
angina pectoris, 540 ; in carditis, 531 ;
in dilated heart, 748 ; in fatty heart,
768, 779 ; in fibroid disease of the heart,
794 ; in hypertrophy of the heart, 715,
719 ; in hydrops pericardii, 534 ; in
mitral stenosis, 662 ; in mitral regurgi-
tation, 663 ; rheumatic endocarditis,
472; in rheumatic pericarditis, 241.

Pulse, the radial, an unsafe guide in the
diagnosis of cardiac murmurs, 673 ;
carotid pulse useful, 633.

Purgatives, value of, in chronic valvular
diseases of the heart, 685 ; in dilated
heart, 758.

Pyaemia, a cause of dilatation of the heart,
733 ; of simple endocarditis, 456, 516;
of ulcerative endocarditis, 621 ; of peri-
carditis, 423.

Relapses, occurrence of, in rheumatic
pericarditis, 370 ; symptoms of, 378 ;
effect of, on prognosis, 874.

Respiration, characters of the, in angina

Pectoris, 539 ; in rheumatic endocar-
itis, 472, 494; in endocarditis com-
plicating old valvular disease, 511 ; in
pericarditis, 237, 396 ; in Adherent
pericardium, 455 ; in rheumatic hyper-
pyrexia, 269 ; see also Dyspnoea.

Respiration, influence of, on the position
of the heart, 69 ; on pericardial friction
sound, 391 ; ratio of, to the pulse in
rheumatic pericarditis, 241.

Rest, importance of, in the after-treatment
of endocarditis, 622 ; in the treatment
of angina pectoris, 5P5 ; of dilated
heart, 753 ; of endocarditis, 526, 680 ;
of hypertrophy of the heart, 725 ; of
pericarditis, 43<\

l.i.t i in i-iinn, urine artkmlr.r, a cause of
dilatation of the Iwait, 733 ; of chronic

INDEX.

805

valvular disease, 617 ; relation of, to
chorea, 512, 514.

Risus sardonicus, occurrence of, in rheu-
matic pericarditis, 258, 260, 303.

Rupture of the heart, article on, 786 ; in-
cluding,—etiology and pathology, 786;
ByjnptomR and diagnosis, 789 ; treat-
ment, 790.

Rupture of aneurism of the heart, 161 ; oi
the valves of the heart, 625 ; of the
aortic valves, 9.

Scarlatina, a cause of endocarditis, 624.

Sclerosis, chronic, of the valves of the
heart, 607.

Sedentary habits predispose to angina pec-
toris, 650; to fatty hpart,. 762, 766.

Seneca, description of angina pectoris by,
552.

Senega, value of, in aortic regurgitation,
682.

Septum, the fibrous, of the heart, 43 ; the
interventricular, 44, 45.

Septicemia, a cause of carditis, 530 ; of
acute fatty degeneration of the heart,
768 ; see Pyaemia.

Servants, domestic, very liable to rheu-
matic pericarditis, 189, 198.

Sex, influence of, on the size and weight of
the heart, 5 ; on the position of the
heart, 89 ; on the area of pericardial
effusion, 331.

Sex, the, predisposing to aneurism of the
heart, 162 ; to angina pectoris, 548 ; to
dilatation of the heart, 732 ; to fatty
heart, 761, 766 ; to fibroid disease of
the heart, 792 ; to hypertrophy of the
heart, 694 ; to rheumatic pericarditis,
187, 200 ; to tubercular pericarditis,
169 ; to rupture of the heart, 788 ; to
valvular disease of the heart, 622.

Sound of the heart, the first, prolongation
of, an early symptom of endocarditis,
473 ; also a sequela of endocarditis,
492 ; diagnostic value of, 504.

Sound of the heart, the second, modifica-
tion of, in aortic regurgitation, 501 ;
accentuation of, in mitral regurgitation,
483 ; character of, a valuable guide in
mitral disease, 486 ; reduplication of, a
consequence of mitral disease, 487.

Sounds of the heart, the, relation of,
to the movements of the heart
in health and disease, 632 ; changes
in, caused by dilatation of the heart,
747, 752 ; by fatty degeneration,
779 ; by fibroid disease, 793 ; by hyper-
trophy, 713, 719 ; by pericarditis, 845.

Spasm, cardiac, a cause of the sudden

death in angina pectoris, 580.
Spasms, muscular, tetanic or choreic,
occurrence of, in angina pectoris, 542 ;
in rheumatism with pericarditis, 260,
285; with endocarditis, 263, 472;

without heart affection, 267 ; with
delirium or mania, 287, 292 ; in non-
rheumatic pericarditis, 298.

Sphygmograph, indications of the, in an-
gina pectoris, 572 ; in aortic stenosis,
658 ; in aortic regurgitation, 659 ; in
hypertrophy of the heart, 715 ; an aid
to prognosis in valvular disease, 660.

Spine, angular curvature of the, a cause of
endocarditis, 620.

Spleen, state of the, in acute ulcerative
endocarditis, 650 ; in chronic valvular
diseaso of the heart, 668.

Stenocardia, syn, for angina pectoris, 672,
575.

Stenosis of the heart, 792.

Sternum, relation of the, to the arch of the
aorta, 22 ; to the heart, 22, 26, 109 ;
to the pulmonary artery, 21 ; to the
vertebral column, 121.

Stimulants, value of, in the treatment of
angina pectoris, 586, 595 ; in dilated
heart, 757 ; in fatty heart, 786.

Stomach, collapse of the, a cause of dis-
placement of the heart, 127 ; .distension
of the, also causes displacement, 130.

Strain, long-continued muscular, a cause
of dilatation of the heart, 735 ; of
hypertrophy of the heart, 700; of
chronic valvular disease, 623.

Subclavian artery, the left, position of, in
the chest, 80.

Suspirious respiration, the, characteristic
of heart disease, 553 (note), 567.

Syncope, from fatty heart, 763, 780 ; from
dilated heart, 749 ; in rheumatic endo-
carditis, 472 ; in pericarditis, 235.

Syphilitic affections of the heart, 176.

Syphilis, a cause of fibroid disease of the
heart, 792 ; of valvular disease of the
heart, 625.

Systole, the, of the heart, described, 65,
95, 103.

Systolic endocardial murmurs, causes of,
638.

Swallowing, difficulty in, caused by peri-
cardial effusion, 239.

Temperature, elevation oi, in carditis,
531 ; in acute ulcerative endocarditis,
650 ; in acute fatty degeneration of the
heart, 783 ; see also Hyperpyrexia.

Tension, arterial, increase of, during the
anginal paroxysm, 572, 591 ; in Bnght's
disease, 702.

Tetanus, a rare complication of pericarditis,
299, 303.

Thickness of the parietes of the heart, 5,
8, 710.

Thrill, characters of the, due to pericardial
friction, 343, 414, 418 ; relative fre-
quency of, 353 ; late appearance of,
371 ; causes of, in chronic valvular
disease, 631.

806

INDEX.

Tricuspid orifice, the, relations of, 58, 84 ;
circumference of, in health and disease,
5, 8.

Tricuspid regurgitant murmur, characters
of, 463, 466, 688 ; causes of, 464, 640 ;
diagnosis of, from pericardial friction,
347, 467 ; clinical significance of, iu
cases of rheumatic endocarditis, 490.

Tricuspid stenosis, characters of murmur,
637,

Tricuspid valve, the, description of, 54 ;
relations of, 84, 119, 124 ; variations in
the position of, 59 ; action of, 68 ; in-
competence of, a result of endocarditis,
212, 213 ; not often thus diseased, 523.

Trismus, in rheumatic pericarditis, 261,
308.

Tympanitic distension of the abdomen, a
cause of displacement of the heart, 15,
27.

Typhus, a cause of acute fatty degenera-
tion of the heart, 769.

Tubercle in the heart, 165.

Tumours, abdominal, effect of, on the
action of the heart, 134 ; mediastinal,
a cause of displacement of the heart,
144 ; cancerous, also causing displace-
ment, 188.

Urine, state of the, in rheumatic hyper-
pyrexia, 269 ; in dilated heart, 751 ;
in fatty heart, 782; in hypertrophy of
the heart, 515 ; in chronic valvular
disease, 668.

Valve*, the, of the heart, aneurism of, 163,
458, 606 ; atheroma of, 623 ; calcifica-
tion of, 607 ; rupture of, 625.

Valves of the heart, diseases of the, article
on, 601 ; including, — pathological ana-
tomy, 603 ; etiology, 612 ; physical
signs, 627 ; symptoms, 647 ; diagnosis,
670 ; prognosis, 676 ; treatment, 680.

Valvular disease of the heart, chronic,
a frequent complication of cardiac aneu-
rism, 158 ; predisposes to recurrent
endocarditis, 519, 607 ; to ulcerative
endocarditis, 622 ; comparative fre-
quency of, after acute rheumatism, 212;
influence of, on prognosis in rheumatism,
216 ; predisposes to endocarditis, 506 ;
to pericarditis, 425 ; effect of, on area
of pericardial effusion, 332 ; on the
position of the impulse, 386 ; relation
of, to adherent pericardium, 446, 448.

Valvular disease of the heart, chronic,
guides to prognosis of, 675 ; relative
importance of the different forms, 677.

Vegetations on the cardiac valves, mode of
origin of, 459, 603.

Veins, the cervical, fulness of, from peri-
cardial effusion, 242, 248 ; from chronic
heart disease, 749 ; pulsation of, from
tricuspid regurgitation, 666.

Vena cava, inferior, relations of, in the
chest, 104 ; superior, relations of, 81,
99, 107 ; dilatation of, a consequence
of mitral disease, 666, 668.

Venesection, see Blood-letting.

Venous murmurs, in the neck, causes of,
629; varieties of, 632.

Ventricle, the left, dimensions of in health
and disease, 5, 8 ; breadth of, 85 ;
thickness of parietes, 710 ; relations
of, in the chest, 94, 101 ; movements of,
79.

Ventricle, the left, aneurism of the, article
on, 150 ; including, — nature and mode
of origin, 151 ; seat of the disease, 155;
form and size, 157 ; state of other parte
of the heart, 158 ; of other organs of
the body, 159 ; symptoms and cause of
death, 160.

Ventricle, the left, dilatation of, 748 ;
hypertrophy of, 712 ; most liable to
rupture, 788; changes in, caused by
mitral stenosis, 661 ; simple dilatation
of, may cause a murmur, 748.

Ventricle, the right, dimensions of, 5, 8 ;
breadth of, 32, 114; length of, 20, 25;
thickness of wall, 710 ; position of, 78,
95 ; action of, described, 79 ; not liable
to aneurismal dilatation, 149 ; signs of
dilatation of, 749 ; of hypertrophy of,
718 ; changes in, caused by mitral ste-
nosis, 665.

Ventricles, the, systole of, 65, 95, 108.

Veratrum viride, use of, in hypertrophy of
the heart, 727 ; in chronic valvular dis-
ease, 684.

Vertigo, a symptom of aortic regurgitation,
660 ; of dilated heart, 750.

Vestibule, the aortic, 42.

Virginian prune, bark of the, useful in
dilated heart, 728, 756.

Voice, loss of, in rheumatic pericarditis,
240.

Vomiting, a symptom -of rheumatic endo-
carditis, 472 ; of rupture of the heart,
789 ; of dilated heart, 750 ; treatment
of, 758.

Weight of the heart, normal, 4 ; affected
by general diseases, 7 ; by local dis-
eases, 8 ; when atrophied, 689 ; when
hypertrophied, 655, 709 ; general
remarks on, 11.

LIST OF CHIEF AUTHORS REFERRED TO IN

EACH ARTICLE.

LIST OF THE CHIEF AUTHORS REFERRED TO IN

EACH ARTICLE.

ADHERENT PERICARDIUM, Article on, by Francis Sibson,

M.D, F.R.S., p. 438.

AUTHOR* REFERRED TO.

Bouillaud, on the diaguo&is of adherent pericardium, 444.

Hope, on the physical signs of adherent pericardium, 442.

Kennedy, on adherent iwricardium as a cause of hypertrophy of the heart, 440, 447.

Skoda, description of the physical signs of adherent pericardium by, 444.

Stokes, on the effects of adherent pericardium on the heart, 447.

ANGINA PECTORIS AND ALLIED STATES, Article on, by

Professor Uairdner, M.D., p. 535.

AUTHORS REFERRED TO.

Anstie, on the relation of angina pectoris to the neuralgia*, 571 ; on the value of arsenic

in the treatment of angina, 597.
Hrinton, on gout at the heart, a form of angina. 547.
Brunton, L., on the character of the pulse in angina, as indicated by thesphygmograph,

572.
Forbes, Sir J., on the connection between angina pectoris and heart disease, 544 ; on the

etiology of angina, 548.
Heberden, angina fiectoris first described by, 535, 537 ; on sudden death in angina, 559 ;

his treatment, 586.
I^itham, on the pain of angina pectoris, 536.
Parry, on the pathology of angina pectoris, 541, 561.
Seneca, description of angina pectoris by, 552.

Stokes, on the peculiarity of the respiration during the anginal paroxysm, 567.
Trousseau, on thoracic aneurisms as a cause of anginal symptoms, 537, 544 ; on the relation

Iwtween angina pectoris and epilepsy, 542.
Walshe, on pseudo-angina, 571 ; on the influence of evident disease of the heart on the

prognosis of true angina, 583 ; on the duration of angina }»cctoiis, 584.

VOL. IV. 3 G

810 LIST OF CHIEF AUTHORS

ANEURISM OF THE HEART, LATERAL OR PARTIAL,
Article on, by Thomas Bevill Peacock, M.D., F.R.O.P., p. 149.

AUTHORS REFERRED TO.

Brescbet, on the origin of aneurisms of the left ventricle, 149, 150 ; on the situation of

aneurisms of the left ventricle, 155, 156.
Cniveilhier, on fibroid degeneration as a cause of aneurism of the heart, 151 ; on the chit

of aneurism of the left ventricle by calcification, 161.
Hope, on aneurisms of the base of the left ventricle, 156.
Rokitansky, on endocarditis as a cause of aneurism of the left ventricle, 149, 151, 152 ;

on aneurism of the mitral valve, 163.
Thurnam, on the pathology of aneurismal dilatations of the heart, 149, 150, 152 ; on the

size of aneurisms of the left ventricle, 157 ; on aneurisms of the left auricle, and of

the mitral valve, 168.

ENDOCARDITIS, Article on, by Francis Sibson, M.D., F.R.S.,

p. 456.

AUTHORS REFERRED TO.

Cheevers, Nonnan, on endocarditis in the foetus, 457.

Hasse, on the pathological anatomy of endocarditis, 456.

Moxon, on the pathological anatomy of endocarditis, 457, 460, 528 ; on endocarditis

secondary to chronic valvular disease, 519.
Payne, on the pathological anatomy of endocarditis, 457, 521.
Rindfleisch, on the pathological anatomy of endocarditis, 456, 453.
Rokitansky, on the pathological anatomy of endocarditis, 456.

HEART, ADVENTITIOUS PRODUCTS IN THE, Article ox,
by Thomas Bevill Peacock, M.D., F.R.C.R, p. 165.

AUTHORS REFERRED TO.

Andral, on hydatid cysts in the heart, 173, 174.

Aran, on polypi of the heart, 180.

Baillie, description of tubercular growths in the pericardium by, 165.

Bouill iud, on tubercle in the heart, 166.

Cobbold, on entozoa in the heart, 175.

Corvisart, on tubercular pericarditis, 166 ; on syphilitic growths in the heart, 176 ; on

fibrocartilaginous degeneration of the heart, 177.
CruveiHiier, on tubercular pericarditis, 166, 167 ; on fibrocartilaginous degeneration of

the heart, 178,
Jenner, Sir Win., on fibro-cartilaginous degeneration of the heart, 178, 179.
Laennec, on tubercles in the heart, 165 ; on syphilitic disease of the heart, 176.
Louis, on tubercle in the heart, 165 ; in the pericardium, 167.
Rillietand Barthez, on tubercular pericarditis in children, 166.
Rokitansky, on the rarity of tubercle in the heart, 165 : on hydatid cysts in the heart.

173, 174.
Virchow, on syphilitic degeneration of the heart, 177.
Walshe, on tubercular pericarditis, 167 ; on cancer of the heart, 169.

REFERRED TO IN EACH ARTICLE. 811

HEART, ATROPHY OF THE, Article on, by W. R. Gowers,

M.D., p. 687.

AUTHOR8 REFERRED TO.

Bouillaud, on the varieties of cardiac atrophy, 688.

Burns, Allan, description of atrophy of the heart by, 688.

Chomel, on atrophy of the heart, 688, 690.

Hayden, on atrophy of the heart, 688.

Quain, on atrophy of the heart in phthisis, 689, 690.

Rindfleisch, on the pathological anatomy of cardiac atrophy, 690.

Senac, on phthisis of the heart, 687.

Wakhe, on the varieties of atrophy of the heart, 688 ; on the symptoms, 690.

HEART, DILATATION OF THE, Article on, by W. R. Gowers,

M.D., p. 729.

AUTHORS REFER RED TO.

Beau, on asystolie of the heart, 738.

Bouillaud, on the pathology of dilatation of the heart, 730.

Corvisart, on aneurism of the heart, 730.

Gairdner, on adherent pericardium as a cause of dilatation of the heart, 733 ; on chronic
pulinouary emphysema as a cause of dilatation, 734.

Hayden, on the varieties of cardiac dilatation, 734 ; on the influence of adherent pericar-
dium on the production of dilatation, 733, 734.

Laennec, description of the physical signs of dilatation by, 730.

Niemeyer, on the pathology of cardiac dilatation, 732, 739, 741.

Stokes, on the pathology of dilatation of the heart, 730 ; on adherent pericardium as a
cause of dilatation, 733; on dilatation of the auricles, 74*2; on alterations of the
heart sounds from dilatation, 747, 748.

Walshe, on the physical signs of dilatation of the heart, 747, 748, 752.

Wilks, on the pathology of cardiac dilatation, 730, 734.

HEART, FATTY DISEASES OF THE, Article on, by W. R.

Gowers, M.D. p. 7G0.

AUTHORS REFERRED TO.

Hayden, on predisposition to fatty hypertrophy of the heart, 701 ; to fatty degenera-
tion of the heart, 766.

Laennec, on the pathological anatomy of fatty hypertrophy of the heart, 762, 768 ; of
fatty degeneration, 765.

Louis, on acute molecular degeneration of the heart, 768, 773.

Ormerod, on wasting diseases as a cause of fatty degeneration of the heart, 767.

Paget, Sir James, on the pathological anatomy of fatty degeneration of the heart, 765,

767.
Quain, on the causes of fatty hypertrophy of the heart, 761, 762 ; on the pathology of

fatty degeneration of the heart, 76'?, 770, 773 ; on fatty degeneration as a cause of

rupture of the heart, 787.
Rindfleisch, on the pathological anatomy of fatty degeneration of the heart, 772, 775.

812 LIST OF CHIEF AUTHORS

Roldtansky, on the microscopical appearances of fatty degeneration of the heart, 765,

775.
Stekcs, on acute molecular degeneration of the heart, 768, 773 ; on the physical signs o*

fatty degeneration of the heart, 779 ; on peculiarities of the respiration during

anginal paroxysms, 780.
Walshe, on the symptoms of fatty degeneration of the heart, 779 ; on the use of digitalis

in treatment, 786.

HEART, FIBROID DISEASE OF THE, Article on, by W. R

Gowers, M.D., p. 791.

AUTHORS REFERRED TO.

< 'orvisart, on the pathology of fibroid disease of the heart, 791, 793.
Hilton Fag^e, on the pathology of fibroid disease of the heart, 792, 793.
Pelvet, on hbroid disease as a cause of dilatation of the heart, 791, 793.
Chimin, on connective tissue hypertrophy of the heart, 791, 793.

HEART, HYPERTROPHY OF THE, Article on, by W. R.

Uowkks, M.D., p. 693.

AUTHORS RFFERRED TO.

Birtin, on the pathology of cardiac hypertrophy, 693, 707, 710.

Hiight, on chronic renal disease as a cause of hyjwrtrophy of the heart, 701.

Corvisart, on cardiac hypertrophy as a cause of aneurism of the aorta and of cerebral

apoplexy, 699, 717.
Cruveilhier, on the real nature of concentric hypertrophy, 707.
Laennec, on the physical signs of cardiac hypertrophy, 693, 713.
Quain, on hypertrophy of the heart in phthisis, 700 ; on hypertrophy of the heart as a

cause of apoplexy, 717.
Rindrleiseh, on the pathological anatomy of cardiac hypertrophy, 711.
Senac, on the connection between hypertrophy of the heart and arterial degeneration,

716 ; on the importance of rest in treatment, 725.
Walshe, on the physical signs of hypertrophy of the heart, 712, 713.

HEART, MALPOSITIONS OF THE, Article on, by Frantis

Sibson, M.D., F.R.S., p. 125.

AUTHORS HKFF.RRF.l) TO.

Bennett, on displacement of the heart by intra-thoracic tumours, 130, 135, 144.

(iairdner, on the displacement of the heart in pleurisy, 140.

Hope, on displacement of the heart by aneurism of the aorta, 148.

Stokes, on epigastric pulsation in bronchitis and emphysema, 126 ; on oncer of the lung
without displacement of the heart, 145.

Townshend, on displacement of the heart by empyema, 138, 140.

AValshe, on displacement of the heart by pleuritic effusion, 137.

"Wintrieh, on displacement of the heart by pleuritic effusion, 138, 139, 148 ; in pneumo-
thorax, 14 1.

REFERRED TO IN EACH ARTICLE. 813

HEART AND GREAT VESSELS, Position and Form of the,
Article on, by Francis Sibson, M.D., F.R.S., p. 14.

*
AUTHORS REFERRED TO.

Braun, on the relative position of the thoracic viscera, 92, 109.

iialler, on the valves or the heart, 37, 47.

Heath, description of the aortic si u uses, 48.

!<e G end re, on the anatomy of the thorax, 109.

Pirogoff, on the anatomy of the heart, 48, 84 ; on the relative position of the thoracic

viscera, 92, 109.
Keid, on the anatomy of the heart, 46.
Sibson, on the medical anatomy of the thorax, 50, 89, 91.
Thurnam, on the aortic sinuses, 46.

HEART, WEIGHT ANT) SIZE OF THE, Article on, by Thomas

Bevill Peacock, M.D., F.R.C.P., p. 3.

AUTHORS REFERRED TO.

Bouillaud, on the variations in the weight of the heart, 3, 4, 11.

Bright, on hypertrophy of the heart from chronic renal disease, 8.

Ciletidi lining, on the weight of the heart in health and disease, 3, 4, 6.

Laennec, on the size of the heart, 3.

Beid, on the weight and dimensions of the heart, 3, 4.

Cases by Bristowe, Vanderbyl, Church, &c, in the Pathological Transactions.

HYDROrERICARDIUM, Article o*, by W. R. Gowers, M.D.,

p. 532.

AUTHOR* REFERRED TO.

Corvisart, on the physical signs of pericardial dropsy, 533, 534.

(i raves, on effusion into the pericardium without evidence of inflammation, £33, 534.

Laennec, on the occurrence of pericardial effusion during the last hours of life, 532.

Stokes, on pericardial drojwy, 533, 534.

Walshe, on the causes of hydro -pericardium, 532.

PERICARDITIS, Article on, by Fkantis Sibson, M.I), F.R.S.,

p. 180.

AITIIORS REFERRED TO.

Allbutt, Clifford, on paracentesis pericardii, 434.

Buri I on -Sanderson, on the distribution of the nerves of the heart, 236* ; on the influence

of the sympathetic nerves on the circulation, 247.
Bouillaud, on pericarditis with nervous complications, 239, 296, 297.
Fuller, on delirium in pericarditis, 294.
Fox, Wilson, on the treatment of hyj>erpyrexia, 255, 2f>7, 261.

814 LIST OF CHIEF AUTHORS REFERRED TO.

Frerichs, on pericarditis from renal disease, 406.

Laennec, on paracentesis pericardii, 433.

Moxon, on pericarditis from pyaemia, 423.

Trousseau, on delirium in rheumatism, 285 ; on paracentesis pericardii, 433.

Watson, Sir Thomas, on nervous complications of aeute rheumatism, 286, 295.

PNEUMOPERICARDIUM, Article on, by J. Warburton Begbie,

M.D., p. 182.

AUTHORS REFERRED TO.

Bouillaud, on the diagnosis of pneumopericardium, 182.

Laennec, on the frequency of pneumo-pericardium, 182, 183 ; on the physical sigus of,

184.
Stokes, on a case of pneumo-pericardium, 182 ; physical signs of, 185.
Walshe, on the diagnosis of pneumo-pericardium, 183, 185.

VALVES OF THE HEART, DISEASE OF THE, Article on, by

C. Hilton Faggk, M.D., F.R.C.P. p. 601.

AUTHORS REFERRED TO.

Allbutt, C, on overwork as a cause of valvular disease, 623, 681.

Bouillaud, on the rheumatic origin of valvular disease of the heart, 617.

Corrigan, Sir D., on the mode of production of cardiac murmurs, 627 ; on the peculiar

pulse of aortic regurgitation, 657.
Chauveau, on the cause of blood murmurs, 628, 639.
Corvisart, on the pathological anatomy of valvular disease, 602 ; on rupture of the cardiac

valves, 625.
Friedreich, on endocarditis in infants, 613 ; on hepatic pulsation, 668 ; on the prognosis

of valvular disease, 677.
Gairdner, on auricular systolic murmurs, 635.
Hayden, on the murmur of tricuspid stenosis, 637.
Moxon, on endocarditis secondary to valvular disease, 605.
Peacock, on congenital valvular disease, 613, 615 ; on rupture of cardiac valves, 625,

626.
Rindfleisch, on the pathological anatomy of endocarditis, 603.
Walshe, on the relative importance of the different forms of valvular disea-.e, 677, 679.

LONDON :

R CLAY, SON*, AND TAYLOR, PRINTER*,

BREAD STREET RILL,

QUEEN YICTORIA RTREET.

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