Full text of "Arteriosclerosis and hypertension, with chapters on blood pressure"

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ARTERIOSCLEROSIS

AND

HYPERTENSION

if 1

With Chapters on Blood Pressure

LOUIS M. WARFIELD, A.B., M.D., (Johns Hopkins),

F.A.C.P.

FORMERLY PROFESSOR OF CLINICAL MEDICINE, MARQUETTE UNIVERSITY MEDICAL
SCHOOL ; CHIEF PHYSICIAN TO MILWAUKEE COUNTY HOSPITAL ; ASSOCIATE
MEMBER ASSOCIATION AMERICAN PHYSICIANS; MEMBER AMERI-
CAN ASSOCIATION PATHOLOGISTS AND BACTERIOLOGISTS;
AMERICAN MEDICAL ASSOCIATION, ETC., FELLOW
AMERICAN COLLEGE OF PHYSICIANS

THIRD EDITION

ST. LOUIS
C. V. MOSBY COMPANY

1920

Press of

C. V. Mosby Company
St. Louis

MY MOTHER

THIS VOLUME IS AFFECTIONATELY
DEDICATED

PREFACE TO THIRD EDITION

Several years have elapsed since the appearance of the
second edition of this book. During this time there has
been considerable experimentation and much writing on
arteriosclerosis. The total of all work has not been to add
very much to our knowledge of the etiology of arterial 'de-
generation. Points of view and opinions change from time
to time. It is so with arteriosclerosis. In this edition ar-
teriosclerosis is not regarded as a disease with a definite
etiologic factor. Rather it is looked upon as a degenerative
process affecting the arteries following a variety of causes
more or less ill defined. It is not considered a true disease.
Possibly syphilitic arteritis may be viewed as an entity, the
cause is known and the lesions are characteristic.

Much new material and many new figures have been
added to this edition. Some rearranging has been done.
The chapter on Blood Pressure has been much expanded
and some original observations have been included. The
literature has been selected rather than indiscriminately
quoted. Much that is written on the subject is of little
value.

It has always seemed to the author that there is not
enough of the personal element in medical writings. At the
risk of being severely criticized, he has attempted to make
this book represent largely his own ideas, only here and
there quoting from the literature.

New chapters on Cardiac Irregularities Associated with
Arteriosclerosis, and Blood Pressure in Its Clinical Appli-
cation have been added.

The fact that the book has passed through two editions is
very gratifying and seems to show that it has met with fa-
vor. The author takes this opportunity of thanking those
who have loaned him illustrations.. Wherever figures are
borrowed due credit is given.

16 PREFACE

It is hoped that the kind of reception accorded to the first
and second editions will also not be withheld from this pres-
ent edition.

Louis M. WARFIELD.

Milwaukee, Wise.

PREFACE TO THE SECOND EDITION

In this second edition so many changes and additions
have been made that the book is practically a new one. All
the chapters which were in the previous edition have been
carefully revised. Two chapters, ' * Pathology ' ' and ' ' Phys-
iology, ' ' have been completely rewritten and brought up to
date. It was thought best to add some references for those
who had interest enough to pursue the subject further.
These references have been selected on account of the read-
iness with which they may be procured in any library, public
or private. Two new chapters have been added one on
''The Physical Examination of the Heart and Arteries/'
the other on " Arteriosclerosis in Its Relation to Life In-
surance/' and it is hoped that these will add to the prac-
tical value of the book.

Arteriosclerosis can scarcely be considered apart from
blood pressure, and in the view expressed within, with
which some may not concur, high tension is considered to be
a large factor in the production of arteriosclerosis. As the
data on blood pressure have increased, the importance of it
has become more evident. The chapter on "Blood Pres-
sure" has been wholly rewritten, expanded so as to give
a comprehensive grasp of the essential features, and several
illustrations have been added in order to elucidate the text
more fully. The chief objects in view were to make clear
to the physician the technique and the necessity for estimat-
ing both systolic and diastolic pressures.

The author is grateful for the kindly reception accorded
the first edition. No one is more keenly aware of the im-

PREFACE 17

perfections than he. The necessity for a second edition is
taken to mean that the book has found a place for itself
and has been of use to some.

The author hopes that this new edition will fulfill ade-
quately the purpose for which he prepared the book-
namely, as a practical guide to the knowledge and appre-
ciation of a most important and exceedingly common
disease.

Louis M. WARFIELD.

Milwaukee, May, 1912.

PREFACE TO THE FIRST EDITION

It is hoped that this small volume may fill a want in the
already crowded field of medical monographs. The au-
thor has endeavored to give to the general practitioner a
readable, authoritative essay on a disease which is espe-
cially an outcome of modern civilization. To that end all
the available literature has been freely consulted, and the
newest results of experimental research and the recent
ideas of leading clinicians have been summarized. The au-
thor has supplemented these with results from his own
experience, but has thought it best not to burden the con-
tents with case histories.

The stress and strain of our daily life has, as one of
its consequences, early arterial degeneration. There can
be no doubt that arterial disease in the comparatively
young is more frequent than it was twenty-five years ago,
and that the mortality from diseases directly dependent
on arteriosclerotic changes is increasing. Fortunately, the
almost universal 'habit of getting out of doors whenever
possible, and the revival of interest in athletics for persons
of all ages, have to some extent counteracted the tendency
to early decay. Nevertheless, the actual average pro-
longation of life is more probably due to the very great
reduction in infant mortality and in deaths from infectious
and communicable diseases.

18 PREFACE

The wear and tear on the human organism in our mod-
ern way of living is excessive. Hard work, worry, and
high living all predispose to degenerative changes in the
arteries, and so bring on premature old age. The author
has tried to emphasize this by laying stress on the preven-
tion of arteriosclerosis rather than on the treatment of the
fully developed disease.

No bibliography is given, as this is not intended as a
reference book, but rather as a guide to a better apprecia-
tion and understanding of a most important subject. It
has been difficult to keep from wandering off into full dis-
cussions of conditions incident to and accompanied by
arteriosclerosis, but, in order to be clear in his statements
and complete in his descriptions, the author has to invade
the fields of heart disease, kidney disease, brain disease,
etc. It is hoped, however, that these excursions will serve
to show how intimately disease of the arteries is bound
up with diseases of all the organs and tissues of the body.

Some authors have been named when their opinions
have been given. Thanks are extended also to many oth-
ers to whom the writer is indebted, but of whom no indi-
vidual mention has been made.

The author also takes this opportunity of expressing
his appreciation of the kindness of Dr. D. L. Harris, who
took the microphotographs, and to the publishers for their
unfailing courtesy and consideration.

Louis M. WARFIELD.

St. Louis, August, 1908.

CONTENTS

PAGE

CHAPTER I

ANATOMY 25

Introduction, 25 ; Definition, 26 ; General Structure of the Arteries,
27; Arteries, 29; Veins, 30; Capillaries, 31.

CHAPTER II
PATHOLOGY 32

Syphilitic Aortitis, 44 ; Experimental Arteriosclerosis, 50 ; Arte-
riosclerosis of the Pulmonary Arteries, 63 ; Sclerosis of the Veins, 64.

CHAPTER III

PHYSIOLOGY OF THE CIRCULATION 65

Blood Pressure, 68; Blood Pressure Instruments, 70; Technic, 80;
Arterial Pressure, 85 ; Normal Pressure Variations, 88 ; The Aus-
cultatory Blood Pressure Phenomenon, 90; The Maximum and Mini-
mum Pressures, 94; Relative Importance of the Systolic and Dia-
stolic Pressures, 97; Pulse Pressure, 100; Blood Pressure Variations,
102; Hypertension, 106; Hypotension, 117; The Pulse, 123; The
Venous Pulse, 123; The Electrocardiogram, 126.

CHAPTER IV

IMPORTANT CARDIAC IRREGULARITIES ASSOCIATED WITH ARTERIOSCLEROSIS 131
Auricular Flutter, 131; Auricular Fibrillation, 133; Ventricular
Fibrillation, 138; Extrasystole, 138; Heart Block, 140.

CHAPTER V

BLOOD PRESSURE IN ITS CLINICAL APPLICATIONS 147

Blood Pressure in Surgery, 147 ; Head Injuries, 148 ; Shock and
Hemorrhage, 148; Blood Pressure in Obstetrics, 152; Infectious
Diseases, 153 ; Valvular Heart Disease, 155 ; Kidney Disease, 155 ;
Other Diseases, Liver, Spleen, Abdomen, etc., 156.

CHAPTER VI
ETIOLOGY 157

Congenital Form, 157; Acquired Form, 159; Hypertension, 159;
Age, Sex, Race, 161; Occupation, 162; Food Poisons, 163; Infec-
tious Diseases, 163; Syphilis, 165; Chronic Drug Intoxications, 166;
Overeating, 167; Mental Strain, 168; Muscular Overwork, 169;
Renal Disease, 169; Ductless Glands, 171.

20 CONTENTS

PAGE

CHAPTER VII

THE PHYSICAL EXAMINATION OF THE HEART AND ARTERIES ...'.. 172
Heart Boundaries, 172; Percussion, 174; Auscultation, 176; The
Examination of the Arteries, 177; Estimation of Blood Pressure,
179; Palpation, 180; Precautions When Estimating Blood Pres-
sure, 181; The Value of Blood Pressure, 181.

CHAPTER VIII

SYMPTOMS AND PHYSICAL SIGNS 183

General, 183; Hypertension, 185; The Heart, 188; Palpable Arter-
ies, 189; Ocular Signs and Symptoms, 190; Nervous Symptoms, 191.

CHAPTER IX

SYMPTOMS AND PHYSICAL SIGNS 194

Special, 194; Cardiac, 195; Renal, 199; Abdominal or Visceral, 201;
Cerebral, 203; Spinal, 205; Local or Peripheral, 207; Pulmonary
Artery, 209.

CHAPTER X

Diagnosis 210

Early Diagnosis, 210; Differential Diagnosis, 215; Diseases in Which
Arteriosclerosis is Commonly Found, 216.

CHAPTER XI
PROGNOSIS 218

CHAPTER XII
PROPHYLAXIS . . 224

CHAPTER XIII

TREATMENT . 229

Hygienic Treatment, 230 ; Balneotherapy, 233 ; Personal Habits,
234; Dietetic Treatment, 235; Medicinal, 238; Symptomatic Treat-
ment, 245.

CHAPTER XIV
ARTERIOSCLEROSIS IN ITS RELATION TO LIFE INSURANCE 249

CHAPTER XV
PRACTICAL SUGGESTIONS 256

ILLUSTRATIONS

FJG- PAGE

1. Cross section of a large artery 28'

2. Cross section of a coronary artery 36

3. Arteriosclerosis of the thoracic and abdominal aorta 39

4. Arteriosclerosis of the arch of the aorta 40

5. Normal aorta 41

6. Radiogram showing calcification of both radial and ulnar arteries . 42

7. Syphilitic aortitis of long standing 44

8. Diagrammatic representation of strain hypertrophy 48

9. Strain hypertrophy 49

10. Cross section of small artery in the mesentery 56

11. Enormous hypertrophy of left ventricle 58

12. Aortic incompetence with hypertrophy and dilatation of left ventricle 61

13. Cook's modification of Riva-Rocca's blood pressure instrument . . 72

14. Stanton's sphygmomanometer 73

15. The Erlanger sphygmomanometer with the Hirschfelder attachments 74

16. Desk model Baumanometor 75

17. Taught blood pressure instrument 76

18. Rogers' "Tycos" dial sphygmomanometer 77

19. Detail of the dial in the "Tycos" instrument 78

20. Faught dial instrument 79

21. Detail of the dial of the Faught instrument 79

22. The Sanborn instrument 80

23. Method of taking blood pressure with a patient in sitting position . 81

24. Method of taking blood pressure with patient lying down .... 82

25. Observation by the auscultatory method and a mercury instrument . 84

26. Observation by the auscultatory method and a dial instrument . . 85

27. Schema to illustrate decrease in pressure 86

28. Chart showing the normal limits of variation in systolic blood pressure 89

29. Tracing of auscultatory phenomena ... 94

30. Tracing of auscultatory phenomena ... 95

31. Clinical determination of diastolic pressure, fast drum 96

32. Clinical determination of diastolic pressure, slow drum 96

33. Venous blood pressure instrument 121

34. New venous pressure instrument 122

35. Events in the cardiac cycle 124

36. Simultaneous tracings of the jugular and carotid pulses .... 125

37. Jugular and carotid tracings I 25

38. Right side of the heart showing distribution of the two vagus nerves 127

39. Normal electrocardiogram ^ 128

40. Auricular flutter 132

41. Auricular fibrillation 134

22 ILLUSTRATIONS

FIG. PAGE

42. Auricular fibrillation 134

43. Pulse deficit . . . . 135

44. Ventricular fibrillation 137

45. Auricular extrasystoles 139

46. Ventricular extrasystole 139

47. Delayed conduction 141

48. Partial heart block 141

49. Complete heart block 142

50. Alternating periods of sinus rhythm and auriculoventricular rhythm 144

51. Auriculoventricular or il nodal" rhythm 144

52. Influence of mechanical pressure on the right vagus nerve .... 144

53. Schematic distribution of right and left vagus 145

54. Blood pressure record from a normal reaction to ether 149

55. Chart showing the method of recording blood pressure during an

operation 150

56. Method of using blood pressure instrument during operation . . . 151

57. Finger-tip palpation of the radial artery 178

58. Finger-tip palpation of the radial artery 178

59. Aneurysm of the heart wall 196

60. Large aneurysm of the aorta eroding the sternum 198

ARTERIOSCLEROSIS AND HYPERTENSION

CHAPTER I
ANATOMY

With the increased complexity of our modern life comes
increased wear and tear on the human organism. "A man
is as old as his arteries" is an old dictum, and, like many
proverbs, the application to mankind today is, if any-
thing, more pertinent than it was when the saying was
first uttered. Notwithstanding the fact that the average
age of mankind at death has been materially lengthened
the increase in years amounting to fourteen in the past
one hundred years of history clinicians and pathologists
are agreed that the arterial degeneration known as arterio-
sclerosis is present to an alarming extent in persons over
forty years of age. Figures in all vital statistics have shown
us that all affections of the circulatory and renal systems
are definitely on the increase. "Arterial diseases of va-
rious kinds, atheroma, aneurysm, etc., caused 15,685 deaths
in 1915, or 23.3 per 100,000. This rate, although somewhat
lower than the corresponding ones for 1912 and 1913, is
higher than that for 1914, and is very much higher than
that for 1900, which was 6.1."

The great group of cases of which cardiac incompetence,
aneurysm, cerebral apoplexy, chronic nephritis, emphysema,
and chronic bronchitis are the most frequent and important
appear as terminal events in which arteriosclerosis has
probably played an important part.

Thus, in the sense in which we speak of tuberculosis or
pneumonia as a distinct disease, we can not so designate the
diseased condition of the arteries.

Arteriosclerosis is not a disease sui generis. It is best

26 ARTERIOSCLEROSIS

I viewed as a degeneration of the coats of the arteries, both
large and small resulting in several different more or less
distinct types.

These types blend one into the other and in the same pa-
tient all types may be found. Thus the sclerosis of the
arteries is the result of a variety of causes, none of which
is definitely known in the sense of a bacterial disease. As
we shall see later, one type of arteriosclerosis has a special
pathology and etiology, the syphilitic arterial changes.

Bearing in mind that arteriosclerosis (called by some
"arteriocapillary fibrosis, " by others "atherosclerosis")
is not a true disease, it may, for convenience be defined as a
chronic disease of the arteries and arterioles, characterized
anatomically by increase or decrease of the thickness of the
walls of the blood vessels, the initial lesion being a Weak-
ening of the middle layer caused by various toxic or me-
chanical agencies. This weakness of the media leads to
secondary effects, which include hypertrophy or atrophy
of the inner layer and not infrequently hypertrophy of
the outer layer connective tissue formation and calcifi-
cation in the vessels./and the formation of minute aneu-
rysms along them. /The term arteriocapillary fibrosis has
a broader meaning, but is a cumbersome phrase, and con-
veys the idea that the capillary changes are an essential
feature of the process, whereas these are for the most part
secondary to the changes in the arteries. The veins do
not always escape in the general morbid process, and when
these are affected the whole condition is sometimes called
vascular sclerosis or angiosclerosis.

Upon the anatomical structure of the arteries depends,
as a rule, the character and extent of the arteriosclerotic
lesions. For the clear comprehension of the process, it is
necessary to keep in mind the essential histological dif-
ferences between the aorta and the larger and smaller
branches of the arterial tree.

The vascular system is often likened to a central pump,
from which emanates a closed system of tubes, beginning

ANATOMY 27

with one large distributing pipe, which gives rise to a series
of tubes, whose number is constantly increasing at the
same time that their caliber is decreasing in size. From
the smallest of these tubes, larger and larger vessels col-
lect the flowing blood, until, at the pump, two large trunks
of approximately the same area as the one large distribut-
ing trunk empty the blood into the heart, thus completing
the circle. This is but a rough illustration, and, while pos-
sibly useful, takes into account none of the vital forces
which are constantly controlling every part of the dis-
tributing system.

General Structure of the Arteries

The aorta and its branches are highly elastic tubes, hav-
ing a smooth, glistening inner surface. When the arteries
are cut open, they present a yellowish appearance, due to
the large quantity of elastic tissue contained in the walls.
The elasticity is practically perfect, being both longitudinal
and transverse. The essential portion of any blood vessel
is the endothelial tube, composed of flat cells cemented to-
gether by intercellular substance and having no stomata
between the cells. This tube is reinforced in different
ways by connective tissue, smooth muscle fibers, and fibro-
elastic tissue. Although the gradations from the larger to
the smaller arteries and from these to the capillaries and
veins are almost insensible, yet particular arteries pre-
sent structural characters sufficiently marked to admit of
histological differentiation.

The whole vascular system, including the heart, has an en-
dothelial lining, which may constitute a distinct inner coat,
the tunica intima, or may be without coverings, as in the
case of the capillaries. The intima (Fig. 1) consists typically
of endothelium, reinforced by a variable amount of fibro-
elastic tissue, in which the elastic fibers predominate. The
tunica media is composed of intermingled, bundles of elas-
tic tissue, smooth muscle fibers, and some fibrous tissue.
The adventitia or outer coat is exceedingly tough. It is

ARTERIOSCLEROSIS

usually thinner than the media, and is composed of fibro-
elastic tissue. This division into three coats is, however,
somewhat arbitrary, as in the larger arteries particularly
it is difficult to discover any distinct separation into layers.

The muscular layer varies from single scattered cells, in
the arterioles, to bands of fibers making up the body of the
vessel in the medium-sized arteries and veins.

There is elastic tissue in all but the smallest arteries,

Fig. 1. Cross section of a large artery showing the division into the three coats; in-

ima, media, adventitia. The intima is a thin line composed of endothelial cells. The

wavy elastic lamina is well seen. The thick middle coat is composed of muscle fibers

.ndfibroelastic tissue. The loose tissue on the outer (lower portion of cut) side of the

edia is the adventitia. (Microphotograph, highly magnified.)

and it is also found in some veins. It varies in amount
from a loose network to dense membranes. In the intima
of the larger arteries the elastic tissue occurs as sheets,
which under the microscope appear perforated and pitted,
the so-called fenestrated membrane of Henle.

The nutrient vessels of the arteries and veins, the vasa
vasorum, are present in all the vessels except those less

ANATOMY 29

than one millimeter in diameter. The vasa vasorum course
in the external coat and send capillaries into the media,
supplying the outer portion of the coat and the externa
with nutritive material. The nutrition of the intima and
inner portion of the media is obtained from the blood cir-
culating through the vessel. Lymphatics and nerves are
also present in the middle and outer layers of the vessels.

Arteries

The structure of the arteries varies notably, depending
upon the size of the vessel. A cross section of the thoracic
aorta reveals a dense network of elastic fibers, occupying
practically all of the space between the single layer of
endothelial cells and the loose elastic and connective tis-
sue network of the outer layer. Smooth muscle fibers are
seen in the middle coat, but, in comparison with the mass
of elastic tissue, they appear to have only a limited func-
tion.

In a cross section of the radial artery one sees a wavy
outline of intima, caused by the endothelium following the
corrugations of the elastica. The endothelium is seen as
a delicate line, in which a few nuclei are visible. The
media is comparatively thick, and is composed of muscle
cells, arranged in flat bundles, and plates of elastic tissue.
Between the media and the externa the elastic tissue is
somewhat condensed to form the external elastic mem-
brane. The adventitia varies much in thickness, being bet-
ter developed in the medium-sized than in the large arter-
ies. It is composed of fibrous tissue mixed with elastic
fibers.

"Followed toward the capillaries, the coats of the artery
gradually diminish in thickness, the endothelium resting
directly upon the internal elastic membrane so long as the
latter persists, and afterward on the rapidly attenuating
media. The elastica becomes progressively reduced until
it entirely disappears from the middle coat, which then be-
comes a purely muscular tunic, and, before the capillary is
reached, is reduced to a single layer of muscle cells. In

30 AETEFvIOSCLEROSIS

the precapillary arterioles the muscle no longer forms a
continuous layer, but is represented by groups of fiber cells
that partially wrap around the vessel, and at last are re-
placed by isolated elements. After the disappearance of
the muscle cells the blood vessel has become a true capil-
lary. The adventitia shares in the general reduction, and
gradually diminishes in thickness until, in the smallest ar-
teries, it consists of only a few fibroelastic strands outside
the muscle cells." (Piersol's Anatomy.)

The large arteries differ from those of medium size
mainly in the fact that there is no sharp line of demarca-
tion between the intima and the media. There is also much
more elastic tissue distributed in firm bundles throughout
the media, and there are fewer muscle fibers, giving a
more compact appearance to the artery as seen in cross
section. The predominance of elastic tissue permits of
great distention by the blood forced into the artery at
every heartbeat, the caliber of the tube being less markedly
under the control of the vasomotor nerves than is the case
in the small arteries, where the muscle tissue is relatively
more developed. The adventitia of the large arteries is
strong and firm, and is made up of interlacing fibroelastic
tissue, of which some of the bundles are arranged longi-
tudinally.

Veins

The walls of the veins are thinner than those of the ar-
teries; they contain much less elastic and muscular tissue,
and are, therefore, more flaccid and less contractile. Many
veins, particularly those of the extremities, are provided
with cup-like valves opening toward the heart. These
valves, when closed, prevent the return of the blood to the
periphery and distribute the static pressure of the blood
column. The bulgings caused by the valves may be seen
in the superficial veins of the arm and leg. There are no
valves in the veins of the neck, where there is no necessity
for such a protective mechanism, gravity sufficing to drain
the venous blood from the cranial cavity.

ANATOMY 31

Capillaries

These are endothelial tubes in the substance of the or-
gans, the tissue of the organ giving them the necessary
support. They are the final subdivisions of the blood ves-
sels, and the vast capillary area offers the greatest amount
of resistance to the blood flow, thus serving to slow the
blood stream 'and allowing time for nutritive substances
or waste products to pass from and to the blood. Usually
the capillaries are arranged in the form of a network,
the channels in any one tissue being of nearly uniform size,
and the closeness of the mesh depending upon the organ.

As far back as 1865, Strieker observed contraction of the
capillaries. This observation was apparently forgotten un-
til revived again by Krogh recently. The latter finds that
the capillaries are formed of cells which are arranged in
strands encircling the vessel. The capillaries are rarely
longer than 1 mm., and, according to Krogh, are capable of
enormous dilatation.

The rate of flow through any capillary area is very incon-
stant, and the usual explanation has been that the capilla-
ries were endothelial tubes the blood flow of which was de-
pendent upon the contraction or dilatation of the terminal
arterioles. The actual fact that in an observed capillary
area some capillaries are empty renders the above explana-
tion untenable. The color of a tissue depends upon the state
of filling of the capillaries with blood.

It would seem that all the evidence now leads us to be-
lieve that the capillaries themselves are contractile and it
is even possible that they may be under vasomotor control.
If the anatomic structure as stated above, is correct, it
would take but a slight contraction of the encircling cell to
shut off completely the capillary. When the enormous cap-
illary bed is considered, it is not inconceivable that circu-
lating poisons may act on large areas and produce a true
capillary resistance to the onflow of blood which might
express itself, if long continued, in actual hypertrophy of
the heart.

CHAPTER II

PATHOLOGY

The whole subject of the pathology of arteriosclerosis has
been much enriched by the study of the experimental lesions
produced by various drugs and microorganisms upon the
aortas of rabbits. Simple atheroma must not be confused
with the lesions of arteriosclerosis. The small whitish or
yellowish plaques so frequently seen on the aorta and its
main branches, may occur at any age, and have seemingly
no great significance. Such plaques may grow to the size
of a dime or larger, and even become eroded. They repre-
sent fatty degeneration of the intima which, at times, has
no demonstrable cause; at times . follows in the course of
various diseases, and undoubtedly is due to disturbances of
nutrition in the intima. Except for the remote danger of
clot formation on the uneven or eroded spot, these places
are of no special significance, and are not to be confused
with the atheroma of nodular sclerosis.

The lesions of arteriosclerosis are of a different char-
acter. It has been customary to differentiate three types:
(1) nodular; (2) diffuse; (3) senile. It must be understood
that this is not a classification of distinct types. As a rule
in advanced arteriosclerosis, lesions representing all types
and all grades are found. The nodular type, however, may
occur in the aorta alone, the branches remaining free. This
is most often found in syphilitic sclerosis where the lesion is
confined to the ascending portion of the arch of the aorta.

The retrogressive changes of advancing years can not
be rightly termed disease, yet it becomes necessary to re-
gard them as such, for the senile changes, as we shall see,
may be but the advanced stages of true arteriosclerosis.
Much depends on the nature of the arterial tissue and much

PATHOLOGY 33

on the factors at work tending to injure the tissue. A man
of forty years may therefore have the calcified, pipe stem
arteries of a man of eighty. Our parents determine, to
great extent, the kind of tissue with which we start life.
The arteries are elastic tubes capable of much stretching
and abuse. In the aorta and large branches there is much
elastic tissue and relatively little muscle. When the vessels
have reached the organs, they are found to be structurally
changed in that there is in them a relatively small amount
of elastic tissue but a great deal of smooth muscle. This
is a provision of nature to increase or decrease the supply
of blood at any point or points.

The aorta and the large branches are distributing tubes
only. It is after all in the arterioles and smaller arteries
that the lesions of arteriosclerosis do the most damage. A
point to be emphasized is that the whole arterial system is
rarely, if ever, attacked uniformly. That is, there may be
a marked degree of sclerosis in the aorta and coronary
arteries with very little, if any, change in the radials. On
the contrary, a few peripheral arteries only may be the seat
of disease. A case in point was seen at autopsy in which
the aorta in its entirety and all the large peripheral
branches were absolutely smooth. In the brain, however,
the arteries were tortuous, hard, and were studded with
miliary aneurysms. It is not possible to judge accurately
the state of the whole arterial system by the stage of the
lesion in any one artery; but on the whole one may say that
an undue thickening of the radial artery indicates analogous
changes in the mesenteric arteries and in the aorta.

So far as the anatomical lesions in the aorta and
branches are concerned, there is much uniformity even
though the etiologic factors have been diverse. The only
difference is one of extent. To Thoma we owe the first
careful work on arteriosclerosis. He regarded the lesion
in arteriosclerosis as one situated primarily in the media;
there is a lack of resistance in this coat. His views are

34 ARTERIOSCLEROSIS

now chiefly of historical interest. As the author under-
stands him, he considered a rupture in the media to be the
cause of a local widening and consequently the blood could
not be distributed evenly to the organ which was supplied
by the diseased artery or arteries. Moreover, there was
danger of a rupture at the weak spot unless this were
strengthened. It was essential for the even distribution of
blood that the lumen be restored to its former size. Na-
ture's method of repair was a hypertrophy of the subin-
timal connective tissue and the formation of a nodule at
that point. The thickening was compensatory, resulting
in the establishment of the normal caliber of the vessel.
Thoma showed that by injecting an aorta in the subject of
such changes, with paraffin at a pressure of 160 mm. of mer-
cury, these projections disappeared and the muscle bulged
externally. He recognized the fact that the character of
the artery changed as the years passed, and to this form
he gave the name, primary arteriosclerosis. To the group
of cases caused by various poisonous agents, or following
high peripheral resistance and consequent high pressure,
he gave the name, secondary arteriosclerosis. This is a
useful but not essential division, as the changes which age
and high tension produce may not be different from those
produced in much younger persons by some circulating
poison. And most important to bear in mind, octogena-
rians may have soft, elastic arteries.

As the body ages, certain changes usually take place in
the arteries leading to thickening and inelasticity of their
walls. This is a normal change, and in estimating the pal-
pable thickening of an artery, such as the radial, the age
of the individual must always be considered.

Thayer and Fabyan, in an examination of the radial
artery from birth to old age, found that, in general, the
artery strengthens itself, as more strain is thrown upon it,
by new elastica in the intima and connective tissue in the
media and adventitia. Up to the third decade there is only

PATHOLOGY 35

a strengthening of the media and adventitia. During the
third and fourth decades there is also distinct connective
tissue thickening in the intima. ' * In other words, the strain
has begun to tell upon the vessel wall, and the yielding tube
fortifies itself by the connective tissue thickening of the
intima and to a lesser extent of the media. " By the fifth
decade the connective tissue deposits in the intima are
marked, there is an increase of fibrous tissue upon the
medial side of the intima and, in lesser degree, throughout
the media. "Finally, in these sclerotic vessels degenerative
changes set in, which are somewhat different from those
seen in the larger arteries, consisting, as they do, of local
areas of coagulation necrosis with calcification, especially
marked in the deep layers of the connective tissue thicken-
ings of the intima, and in the muscle fibers of the media,
particularly opposite these points. These changes may
. . . go on to actual bone formation." The mesenteric
artery differs in some respects from the radial, but in the
main, the changes brought about by age are the same.
Thayer and Fabyan note two striking points of difference:
" (1) calcification is apparently much less frequent than in
the radials; (2) in several cases plaques were seen with
fatty softening of the deeper layers of the intima and super-
ficial proliferation a picture which we have never seen in
the radial." (See Fig. 2.)

Aschoff's studies of the aorta show that, "in infancy the
elastic laminae of the media stand out sharply defined, well
separated from each other by the muscle layers, which are
well developed. . . . From childhood there is to be observed
a slowly progressive increase in the elastic elements of the
media. Not only do the individual lamellae seen in cross-
sections become thicker, but also they afford an increasing
number of fine secondary filaments feathering off from these
and crossing the muscle layer, so that now they are no
longer sharply defined, but more ragged upon cross-section.
This progressive increase attains its maximum at or about

ARTERIOSCLEROSIS

the age of thirty-five, and from now on for the next fifteen
years the condition is relatively stationary. After fifty
there is to be observed a slowly progressive atrophy of
the elastica. The media becomes obviously thinner and
presumably weaker. " (Adami.) It has also been found
(Klotz) that after the age of thirty-five, the muscle of the
media begins to exhibit fatty degeneration which after fifty

Fig. 2. Cross-section of a coronary artery, x50, showing nodular sclerosis. Note the
heaping up of cells in the intima, the fracture of the elastica, and the destruction of the
media beneath the nodule. The primary lesion evidently was in the media. The thick-
ened intima is the effort on the part of nature to heal the breach. At such places as
shown here aneurysms may form. (Microphotograph.)

years is well marked. The fatty degeneration may then
give place to a calcareous infiltration or the fibers may un-
dergo complete absorption. It would appear that the thin-
ning of the aortic media is due not so much to the atrophy
of the elastic tissue as to that of the muscle tissue. The
elastic tissue does lose its specific property and the artery
thus becomes practically a connective tissue tube.

PATHOLOGY 37

Scheel has made very careful measurements of the
ascending, the thoracic, and the abdominal aorta, and the
pulmonary artery. He found that from birth to sixty
years, the aorta became progressively wider and lost its
elasticity. The pulmonary changed little, if at all, after
thirty to forty years, and where before it was wider than
the aorta, it now was found to be smaller. In chronic
nephritis both were widened. The continuous increase of
width and length of the aorta stands in reverse relationship
to the elasticity of its walls.

Although the division of the lesions into nodular, diffuse,
and senile has been the usual one, it is better to separate
three groups into (1) nodular, (2) diffuse or senile, and (3)
syphilitic. There is more known about the histology of
the syphilitic form and the lesions which consist of pucker-
ings and scars seen on opening an aorta just above the
valves, and on the ascending portion of the arch are charac-
teristic. A macroscopic examination suffices in most cases
for a definite diagnosis.

In the nodular form, the lesions are found on the aorta
and large branches particularly at or near the orifices of
branching vessels. These nodules may increase in size,
forming rather large, slightly raised plaques of yellowish-
white color. They are, as a rule, irregularly scattered
throughout the aorta and branches and tend to be more
numerous and larger in the abdominal aorta. The initial
lesion is in the media, consisting of an actual dissolution of
this coat with rupture of the elastic fibers and infiltration
with small round cells. There is thus a weak spot in the
artery. Hypertrophy of the intimal cells takes place,
layer upon layer being added in an attempt to strengthen
the vessel at the injured place. Coincidently with this,
there is thickening by a connective tissue growth in the
adventitia. The process begins, at least in syphilis, around
the terminals of the vasa vasorum. It will be recalled that
the blood supply of the inner portion of the media comes

38 ARTERIOSCLEROSIS

from within the vessel itself. As the intimal growth in-
creases, the blood supply is cut off. The inevitable result
is softening of the portion farthest from the lumen of the
vessel. As a rule there has been a sufficient growth of con-
nective tissue in the media and adventitia to repair the
damage done to the media. This softening and dissolution
gives rise to a granular debris composed of degenerated
cells and fat. This is the so-called atheromatous abscess.
There are no leucocytes as in ordinary pus. These " ab-
scesses " are frequent and in rupturing leave open ulcers
with smooth bases, the atheromatous ulcer. A further
change which often takes place is calcification of the bases
of the ulcers and calcification of the softened spots before
rupture takes place. This only occurs in advanced cases.
(See Fig. 3.)

Bather contrary to what one would expect, there are no
new capillaries advancing from the media to the intima in
the nodular form of arteriosclerosis, consequently there is
no granulation tissue to heal and leave scars. It must be
borne in mind that these changes rarely, if ever, are the
only ones found throughout the arterial system. Never-
theless, the manifold changes, as will be shown within, ap-
pear to be but stages of one primary process.

The character of the changes which are known as diffuse
arteriosclerosis seems to have, at first sight, little in com-
mon with those of the nodular sclerosis. The aorta may
or may not have plaques of nodular sclerosis, while the
arteries, such as the radial or temporal, may be beaded or
pipe stem in hardness. In spite of these far advanced
peripheral lesions the aorta may appear smooth but it is
markedly dilated, particularly the thoracic portion, it is
noticeably thinned even on macroscopic examination, it
has elongated as evidenced by its slight tortuosity, and it
has lost the greater part of its elasticity. The abdominal
aorta is not so extensively affected, although this, too, shows
some elongation and slight thinning. This is considered by

PATHOLOGY 39

some pathologists to be the uncomplicated form of the so-
called senile arteriosclerosis. It is more of the nature of a

Fig. 3. Arteriosclerosis of the thoracic and abdominal aorta, showing irregular
nodules, atheromatous plaques, denudation of the intima, thin plates of bone scattered
throughout with spicules extending into the lumen of the vessel. Note the contraction
of the openings of the large branches, the rough appearance of the aorta and the greater
degree of sclerosis of the upper two-thirds, i. e., of the aorta above the diaphragm.
This aorta in the recent state was much thickened and almost inelastic.

degenerative change, it is true, but, as will be shown later,
it has its beginnings, at times, in comparatively young per-

ARTERIOSCLEROSIS

sons and its etiology is not simple. This type has been
studied most carefully by Moenckeberg, who showed that on
the large branches of the aorta there were depressions due

Fig. 4. Arteriosclerosis of the arch of the aorta. Numerous calcified plaques,
thickening and curling of the aortic valves, giving rise to insufficiency of the aortic
valves. The aortic ring is rigid and not much dilated. (Milwaukee County Hospital.)

to a degeneration of the middle coat. These depressions
encircled the vessel to a greater or lesser extent, causing

PATHOLOGY 41

small bulgings at such places and giving to the vessel a
beaded appearance. On viewing such an artery held to the
light, the sacculated spots are seen to be much thinner than
the contiguous normal artery. Associated with such

Fig. 5.- Normal aorta. Compare with Fig. 3. Note the perfectly smooth, glossy ap-
pearance of the intima. The openings of all the intercostal arteries are distinctly seen.
In the recent state this artery was highly elastic, capable of much stretching both
transversely and longitudinally.

changes in the aorta and large branches is marked sclerosis
of the smaller arteries. Intimal fibrosis is common, together
with hypertrophy and fibrosis of the middle coat. Not in-
frequently periarterial thickening is also seen. Calcification

ARTERIOSCLEROSIS

Fig. 6. Radiogram of a man aged seventy-five, showing calcification of both radial and

Xllnar arteries.

PATHOLOGY 43

of the media is found and is said to be preceded by hyper-
trophy of the middle coat.

Pure cases of this, the so-called Moenckeberg type, are
seen but seldom. Most commonly there are nodules and
plaques in the aorta and large branches together with thin-
ning and sacculation of other portions of the vessels' walls.
While the two processes appear at a glance to be so differ-
ent from each other, it is possible for them to have a
common origin. The initial lesion is in the media but the
resulting sclerotic changes depend upon the kind of vessel,
the strength of the coats, the pressure in the vessel, and
other causes.

Thus the sclerosis of the radials of such an extent that
these arteries are easily palpable, appears to be a different
process from that of the sclerosis in the aorta, yet funda-
mentally it is the same. The difference lies in the ana-
tomic structure of the two vessels, and possibly also in the
degree of stretching and strain to which the vessels are
subjected at every heart beat. In the radial artery the
media as usual is affected first. The muscle cells undergo
degeneration and either marked thickening takes place or
sacculation results, depending upon the severity of the ex-
citing cause. Calcification of the media is common. This
occasionally takes the form of rings encircling the vessel,
and gives to the examining finger the sensation of feeling
a string of fine beads. There may be calcification of the
subintimal tissue without deposits of lime salts in the me-
dia, but this is more commonly found in the larger arteries.
When the calcification occurs in plates through the media,
the well known pipe stem vessel is produced. (Fig. 6.)

The senile sclerosis found in old people is usually a com-
bination of the Moenckeberg type in the large and medium-
sized arteries, and the nodular type in the aorta, leading
eventually to calcareous intimal deposits, and widened,
elongated, inelastic aorta.

ARTERIOSCLEROSIS

Syphilitic Aortitis

The seat of election of the syphilitic poison is in the aorta
just above the aortic valves, Fig. 7, and in the ascending

Fig. 7. Syphilitic aortitis of long standing. The aortic valves are curled and
thickened, the heart is enlarged and the cavity of the left ventricle is dilated. (Mil-
waukee County Hospital.)

portion of the arch. There are semitranslucent, hyaline-like
plaques which have a tendency to form into groups and,

PATHOLOGY 45

instead of undergoing an atheromatous change as in the or-
dinary nodular form of arteriosclerosis, they are prone to
scar formation with puckering, so that macroscopically the
nature of the process may, as a rule, be readily diagnosed.
Microscopically the process is found to be a subacute in-
flammation of the media, which has been called a mesaorti-
tis. There is marked small celled infiltration around some
of the branches of the vasa vasorum and there appears to be
actual absorption of the tissue elements of the middle coat.
This is accompanied by hypertrophy of the intimal tissue.
There follows degeneration in the deeper portions of this
new tissue and new capillaries are formed which have their
origin in the inflammatory area in the media. As is every-
where the case throughout the body, granulation tissue in
the process of healing contracts and forms scars. This ex-
plains the scar formation in the aorta. When the process
is more acute, instead of there being a reparative attempt
on the part of the intima, there is actual stretching of the
wall at the weakened spot and there results an aneurysmal
dilatation. Spirochetae pallidae have been found in the de-
generated media and in small gummata which were situated
beneath the intima. Within the past years it has been
found that a large percentage of patients with cardiovascu-
lar disease give the Wassermann reaction. In cases of
aortic insufficiency, the reaction is present in almost every
case. This is in marked contrast to the cases of diffuse en-
docarditis where the reaction is rarely present.

According to Adami the effects of syphilis upon the aorta
are the following: (1) the primary disturbance is a granu-
lomatous, inflammatory degeneration of the media; (2) this
leads to a local giving way of the aorta; (3) if this be
moderate it results in a strain hypertrophy of the intima
and of the adventitia, with the development of a nodose in-
timal sclerosis; (4) if it be extreme, there results, on the
contrary, an overstrain atrophy of the intima and aneurysm
formation; (5) the intimal nodosities are here not of an

46 ARTERIOSCLEROSIS

inflammatory type and are nonvascular, although, with the
progressive laying down of layer upon layer of connective
tissue on the more intimal aspect of the intima, the earlier
and deeper-placed layers of new tissue gain less and less
nourishment, and so are liable to exhibit fatty degeneration
and necrosis; (6) these products of necrosis exert a chemo-
tactic influence upon the nearby vessels of the medial gran-
ulation tissue, with, as a result, (a) a secondary and late
entrance of new vessels into the early and deeply-placed
atheromatous area, (b) absorption of the necrotic products,
(c) replacement by granulation tissue, (d) contraction of
the granulation tissue, and (e) depression and scarring of
the sclerotic nodules so characteristic of syphilitic sclerosis.
In the smaller arteries and arterioles the arteriosclerotic
process appears on superficial examination to be a different
process from that in the aorta and large arteries, but the
difference is only apparent. It will be recalled that there
is relatively much more muscle tissue in the arterioles than
in the large arteries. The size, of course, is much less.
Large nodular plaques are not possible. The atheromatous
degeneration is not marked. In the smaller muscular
arteries is seen the intimal proliferation, the stretching of
the Moenckeberg type, and the calcification of the media
rather than the intima. The media is thinned beneath the
marked intimal proliferation so that the artery exhibits
translucent areas when held to the light. Again, there is
seen degeneration of the muscle and replacement by con-
nective tissue with or without hypertrophy of the intima.
In the arterioles three kinds of changes occur: a muscular
hypertrophy ; a fibrosis of all the coats ; or a marked prolif-
eration of the intimal endothelium. The last two are
probably the same process, the connective tissue having its
origin in the proliferated endothelial cells. Such a deposi-
tion of layer upon layer of cells in an arteriole and the re-
sulting fibrosis leads to the condition of disappearance of
the lumen of the vessel, endarteritis obliterans, This ob-

PATHOLOGY 47

literating endarteritis is not, of course, due alone to
syphilis. Syphilis is only a type of poison which produces
such changes as have been described above. It is in the
organs such as the kidney, liver, spleen, and intestines that
one sees the most perfect examples of this obliterating
endarteritis. Endarteritis deformans is a term applied to
the condition of the arteries as a result of irregular thick-
enings and deposits of lime salts in the walls. These
changes give rise to marked tortuosity of the vessels.

Occasionally such an obliterating process takes place in
a larger artery. A thrombus forms and by a process of
central softening, new channels permeate the thrombus,
thus restoring to some extent the function of the vessel.

That the same process leads at one time to thinning and
at another time to thickening of the arterial walls has been
noted above. Prof. Adami holds that the regular develop-
ment of layer upon layer of new connective tissue is non-
inflammatory.. He calls it a "strain hypertrophy. " It is
analogous to the localized hypertrophy of bone where the
muscle tendons are attached, as is so frequently seen in
athletes. The increased tension on connective tissue, pro-
vided that it is not overstrained, leads to its overgrowth,
but only when there is sufficient nourishment. Such con-
ditions are adequately fulfilled in the arteries. When a
local giving way under pressure occurs in the media, the
intima is put on the stretch (see Fig. 8), and there results
a hypertrophy of the intima until the volume of the new
tissue and the resistance which this affords to the mean dis-
tending force, balances the loss sustained by the weakened
media. When the balance is struck, the hypertrophy is
arrested. The youngest tissue is thus found directly be-
neath the endothelium. Now should this local weakening of
the media have an acute origin, instead of a stimulus to
growth there is overstrain, and there is, in consequence, not
hypertrophy but atrophy. The beginning process is here
a mesaortitis, but the acuteness of the poison, and the pres-

ARTERIOSCLEROSIS

sure from within the artery so stretches the artery that
there is no compensatory hypertrophy, but a thinning, and
the ground is prepared for aneurysmal dilatation or pouch-
ing.

Again, one not infrequently encounters intimal nodosities
when the underlying media appears of normal thickness.
The explanation of this apparent exception is that the me-
dia in the living aorta is actually thinned, but the layers of
subintimal tissue deposited over the weak spot due to strain
hypertrophy become bulged inward when the pressure is

Fig. g. J ) media weakened at M' with overgrowth of intima filling in the depression.
II, with postmortem rigor and contraction of the muscles of the media and removal
of the blood pressure from within, the stretched media at M" contracts; the intimal
thickening thus projects into the arterial lumen. (After Adami.)

relieved, as at postmortem. The media has not lost all of
its elasticity (see Fig. 9), hence it contracts and there is
the appearance of a nodule on the intima beneath which is a
media equal in thickness to that of the healthy surrounding
media.

The essential lesion in arteriosclerosis of the aorta and
large arteries is a degeneration in the middle coat. This
may be brought about by a variety of poisons circulating in
the body. In syphilis, for example, the initial lesion has

PATHOLOGY

been shown to be a mesaortitis. The media seems to be dis-
solved, the artery is consequently thinned, there is actual
depression along the level of the vessel. The elastic fibers
disappear and small-celled infiltration takes its place. The

- Met/.

Fig. 9. Schematic representation of the increased strain brought to bear upon the
cells of the intirna, Int., when the media, Med., undergoes a localized expansion through
relative weakness. (After Adami.)

intima hypertrophies, layer upon layer being added in an
attempt to restore the strength of the vessel. There is also,
as a rule, rather pronounced hypertrophy of the adventitia.

50 ARTERIOSCLEROSIS

Experimental Arteriosclerosis

Within the past few years many workers have attempted
by various means, to produce arterial lesions in animals,
chiefly rabbits and dogs. The present status is somewhat
chaotic, some affirming and some denying that arterial
changes follow the various methods employed. Following
the injection of small, repeated doses of adrenalin over a
certain period of time, changes occur in the arteries of
rabbits which are arteriosclerotic in type, the essential
lesion being a degeneration of the muscular and elastic tis-
sue of the media with the consequent production of aneu-
rysm in the vessel. This is said by some to be quite like
the type of arteriosclerosis in man which has been so well
described by Moenckeberg. The degenerations in the ar-
teries following the experimental lesions are of the nature
of a fatty metamorphosis, and later proceed to calcification.
Barium chloride, digitalin, physostigmin, nicotin and other
substances, as well as adrenalin, have been found to exert
a selective toxic action on the muscle cells of the middle
coat of the aorta. The infundibular portion of the pituitary
body, the portion which is developed from the infundibulum
of the brain, possesses an internal secretion, which, injected
intravenously, causes a marked rise of blood pressure and
slowing of the heart beat. So far as I know, this active
principle of the gland has not been used in an attempt to
produce experimentally the lesions of arteriosclerosis.

Wacker and Hueck succeeded in producing aortic dis-
ease in rabbits which they considered to be in many points
quite like human arteriosclerosis. They injected the rab-
bits intravenously with cholesterin. They feel that this is
of great importance in view of the fact that exercise (mus-
cle metabolism) dyspnea, certain poisons, as well as adren-
alin, and even adrenal extirpation occasion a high choles-
terin content of the blood. Anitschow's experiments are
confirmatory. He fed rabbits on large amounts of choles-

PATHOLOGY 51

terin-containing substances (yolk of egg, brain tissue) and
pure cliolesterin and found changes in the intima and inner
portion of the media consisting of fatty infiltration between
the muscle and elastic fibres, advent of small round cells
and large phagocytic cells containing fat droplets of choles-
terin esters. The elastic fibres were dissolved, broken up
into fibrillse and these seemed to be absorbed. The internal
elastic lamina as such disappeared and the inner layer of
the aorta fused with the middle coat. He considers these
changes to be quite analogous to those found in human
aortas.

Oswald Loeb produced changes in the arteries of rabbits
by feeding them sodium lactate (lactic acid). His controls
fed on other acids became cachectic, but showed no arterial
changes. He further found that in 100 gm. of human blood
there was normally from 15 to 30 mg. of lactic acid. After
heavy work, he found as much as 150 gm. He considers
that after adrenalin or nicotin injections, the function of the
liver is so disturbed that lactic acid is not bound. The ar-
teriosclerosis is actually due to the presence of free lactic
acid in the circulation. He succeeded, also, in producing
lesions of the intima in a dog fed for a long time on pro-
tein poor diet, plus lactic acid and sodium lactate.

Another investigator, Steinbiss, fed rabbits on animal
proteins only, a .diet totally foreign to their natural habits.
He succeeded, however, in keeping some alive for three
months. He also tried various substances and in the general
conclusions says that no aortic changes could be produced
in animals kept in natural living conditions by any mechan-
ical means, increase of blood pressure, digital compression,
hanging by hind legs, etc. In infectious diseases, especially
septic, widespread sclerotic changes occurred in the aorta.
A most suggestive conclusion in this "the most important
result of feeding rabbits with animal proteins is, along with
a constant glycosuria, disease of the aorta and peripheral
arteries which is identical with changes in the aorta pro-

52 ARTERIOSCLEROSIS

duced by injections of adrenalin. The degree of disease of
the circulatory system increases with the duration of the
experiment. ' '

By a small addition of vegetable to the protein diet, the
lives of the animals were prolonged at will. With this
modification of the experiment, the findings in the vessel
walls were noticeably altered. The changes affected chiefly
the intima, to less degree the media, and histologically were
very much like human intimal disease.

I have been unable to produce the slightest arterial le-
sions in rabbits by intravenous injections of lead. Froth-
ingham had no success feeding animals with lead. In a
study of autopsy material from persons up to 40 years, who
died of infectious disease, he found changes in the arteries
of those who had succumbed to infection with the pus cocci
or to very severe infectious disease. These changes were,
however, localized, and Avere not like those of the general
diffuse arteriosclerosis.

Adler has recently reported experiments on dogs, to
which he fed or injected intravenously various -substances
supposed to induce arteriosclerotic changes. He was una-
ble to find any arterial lesions comparable to human arterio-
sclerosis.

The difficulty experienced by experimenters is not sur-
prising when the character of the changes is considered.
Arteriosclerosis is not an acute process. In its very nature,
it is of months' or years' standing, the specific changes are
of slow growth, and more in the nature of degeneration. It
would seem that a very careful study of the histories of
those with arteriosclerosis and a final examination upon the
actual tissue might eventually give us data for the etiology.

The most frequent site of disease in these experimental
lesions is the thoracic aorta, and it is there also that the
most severe changes are seen. While the toxic action is felt
in the vessels all over the body, the lesions are, as a rule,
scattered and small. The thoracic aorta stands the brunt

PATHOLOGY 53

of the high pressure, and this combined with the poisonous
action of the drug or drugs, results in the formation of a
fusiform aneurysmal dilatation which stops at the dia-
phragmatic opening. The aortic opening in the diaphragm
seems to act as a flood gate, allowing only a certain amount
of blood to flow through, and thus the abdominal aorta is
protected to a great extent from the deleterious effects of
increased pressure. Focal degenerative lesions are, how-
ever, found in the abdominal aorta.

Changes somewhat analogous lu those found in the human
aorta as the result of intimal proliferations, are produced
in animals by the toxins of the typhoid bacillus and the
Streptococcus pyogenes. Clinically, Thayer and Brush
have found that the arteries of those who have recovered
from an attack of typhoid fever are more palpable than the
arteries of average individuals of equal age who have never
had the disease.

Experimentally, the changes caused by the toxins above
noted are proliferations of cells in the intima and subintimal
tissues, and a breaking up of the internal elastic laminae
into several parallel layers which stretch themselves among
the proliferating cells. The diphtheria toxin, on the con-
trary, produces a lesion more like that caused by adrenalin.
All pathologists are not agreed as to whether the experi-
mental lesions produced by blood pressure raising drugs
are similar to the arteriosclerotic changes in the arteries
of man.

Some of the work on rabbits has been discredited for the
reason that arteriosclerosis appears spontaneously in about
fifteen per cent of all laboratory rabbits. Furthermore,
comparatively young rabbits have been found with arterio-
sclerosis. 0. Loeb, however, denies this. He has examined
in the course of eight years 483 healthy rabbits and never
found arterial changes. The spontaneous lesions can not
be distinguished histologically from those due to adrenalin.

54 ARTERIOSCLEROSIS

They differ macroscopically in that the lesion is usually
limited to a few foci near the origin of the aorta.

Lesions produced by the drugs enumerated above repre-
sent one type of experimental arteriosclerosis. More in-
teresting and important are the experiments which seem to
show that high tension alone is capable of producing lesions
in arteries which in all respects correspond to Adami's
strain hypertrophy and overstrain theory. It has been
shown that when a portion of vein is placed under condi-
tions of high arterial pressure, as in a transplantation of a
portion of vein into a carotid artery, the vein undergoes
marked connective tissue hypertrophy which includes all
the coats. This is evidently strain hypertrophy. Again, it
has been demonstrated that by suspending a previously
healthy rabbit by the hind legs for three minutes daily over
a period of three to four months, there results hypertrophy
of the heart with thinning and dilatation of the arch and the
upper part of the thoracic aorta. No change was found in
the abdominal aorta. The carotids, however, were larger
than normal and they showed typical intimal sclerosis with
connective tissue thickening.

Neither I nor others have been able to confirm this ex-
periment, so it is very doubtful whether mechanical pres-
sure alone can produce true arteriosclerosis. Some evi-
dence is adduced to bear on this point, however, in the fact
that sclerosis of the pulmonary artery follows often upon
mitral stenosis. Yet we do not know but that factors other
than pressure alone produce the arteriosclerotic change in
such cases, so we are forced back on .our conclusion ex-
pressed above; viz., that experiments on animals fail to
sustain the purely mechanical origin of arteriosclerosis.

The changes in the intima constitute the effort on the
part of nature to repair a defect in the vessel wall which is
to compensate for the weakened media and the widened
lumen. This applies only to true arteriosclerosis, not to

PATHOLOGY 55

the condition produced experimentally by the toxin of the
typhoid bacillus, for example.

When an artery loses its elasticity and begins to have
connective tissue deposited in its walls, the pressure of the
blood stretches the vessel which is now no longer capable of
retracting when the pulse wave has passed, and, in conse-
quence, the artery is actually lengthened. This necessarily ;
causes a tortuosity of the vessel which can be easily seen in
such arteries as the temporals, brachials, radials, and other
arteries near the surface of the skin.

The exact mechanism of increase of blood pressure is not
satisfactorily explained. The smaller arteries all over the
body are supplied with vasoconstrictor and vasodilator
nerve fibers from the sympathetic nervous system. Nor-
mally when an organ is actively functionating the vessels
are widely dilated and the flow of blood is rapid. Among
the many factors which influence blood pressure and blood
supply must be reckoned the psychic.

We know that normally there is a certain resistance
offered to the propulsion of blood through the arteries by
the contraction of the heart. This tonus is essential to the
maintenance of an equalized circulation. The muscular
arterioles throughout the body by their tonus serve to keep
up the normal blood pressure and to distribute the blood
evenly to the various organs. Contraction of a large area
of -arterioles increases the blood pressure and, strangely
enough, the arteries respond to increased arterial pressure,
not by dilatation, but by contraction. It would appear that
rise of blood pressure tends to throw increased work upon
the musculature of the arterioles. This may be sufficient
only to cause them to hypertrophy, but further strain may
easily lead to exhaustion and to dilatation. "As a result
strain hypertrophy of the intima shows itself with thicken-
ing, and it may also be of the adventitia, resulting in chronic
periarteritis. And now with continued degeneration of the
medial muscle in those muscular arteries, fibrosis of the

ARTERIOSCLEROSIS

media may also show itself. I would thus regard muscular
hypertrophy of the arteries and fibrosis of the different
coats as different stages in one and the same process.
Whether these peripheral changes are the more marked, or
the central, depends upon the relative resisting power of

Fig. 10. Cross-section of a small artery in the mesentery. Note that the vessel ap-
pears capable of being much widened. The internal elastic lamina is thrown into folds
somewhat resembling the convolutions of the brain. Note also that the middle coat
of the artery is composed almost entirely of muscle. The enormous number of such
vessels in the mesentery and intestines explains the ability of the splanchnic area to
accommodate the greater part. of the blood in the body. Universal constriction of these
vessels would naturally render the intestines anemic. The vasomotor control of these
vessels plays an important role in the distribution of the blood. Small arteries in the
skin and in other organs, possibly the brain, have a similar function. (Microphotograph,
highly magnified.)

the elastic and muscular arteries of the individual respec-
tively." (Adami.)

It is conceivable that in one section of the body the vessels

PATHOLOGY 57

may be markedly contracted, but if there is dilatation in
some other part there will be no increased work on the part
of the heart, and theoretically, there should be no rise of
blood pressure. The vascular system, however, while lik-
ened to a system of rubber tubes, must be regarded as a
very live system, every subsystem having the property of
separate control.

For blood tension to be raised all over the body, condi-
tions must favor the generalized contraction of a large area
of arterioles. Some authors consider that the so-called
viscosity of the blood also is a factor in the causation of
increased tension. The usual cause for the high tension is
probably the presence in the blood of some poisonous sub-
stance.

It is held by some authors that the great splanchnic area
is capable of holding all the blood in the body and in respect
of its liability to arteriosclerosis, it is second only to the
aorta and coronary arteries. The enormous area of the
skin vessels could probably contain most of the blood.
The tone of the vasoconstrictor center controls the distribu-
tion of blood throughout the body. The fact that the ves-
sels in the splanchnic area are frequently attacked by
sclerotic changes means, as a rule, increase of work for
the heart.* The resistance offered to the passage of the
blood must be great and signifies that, for blood to travel at
the same rate that it did before the resistance set in, more
power must be expended in its propulsion. In other words,
the heart must gradually become accustomed to the changed
conditions, and, as a result of increased work, the muscle
hypertrophies. (See Fig. 11.)

In diffuse arteriosclerosis accompanied by chronic nephri-
tis the heart is always hypertrophied. This is a result, not

*Longcope and McClintock, however, conclude that permanent constriction of the
superior mesenteric artery and celiac axis, as well as gradual occlusion of one or both
of these vessels, may be present in dogs for at least five months without giving rise to
definite and constant elevation of blood pressure 'or to hypertrophy of the heart. Further,
they have been unable to find at autopsy on man a definite association between sclerosis
of the abdominal aorta and great splanchnic vessels and cardiac hypertrophy.

ARTERIOSCLEROSIS

a cause of the condition. In the pure type, there is hyper-
trophy only of the left ventricle without dilatation of the
chamber. The muscle fibers are increased in number and in
size, and there are frequently areas of fibrous myocarditis
due to necrosis caused by insufficient nutrition of parts of
the muscle. In these cases the coronary arteries share in
the generalized arteriosclerotic process. The openings of
the arteries behind the semilunar valves may be very small.

Fig. 11. Enormous hypertrophy of left ventricle probably due to prolonged in-
creased peripheral resistance. Note that the whole anterior surface of the heart is occu-
pied by the left ventricle. The right ventricle does not appear to be much affected.
x2/3.

There is often thickening and puckering of the aortic valves
and of the anterior leaflet of the mitral valve leading, at
times, to actual insufficiency of the orifice. Later, when the
heart begins to weaken, there is dilatation of the chambers
and loud murmurs result, caused by the inability of the non-
distensible valves to close the dilated orifices. Until the
compensation is established, it is impossible to say whether
or not true insufficiency is present.

PATHOLOGY 59

In senile arteriosclerosis there is the physiologic atrophy
of the media to be reckoned with. This change has already
been referred to. When such degeneration has taken place,
the normal blood pressure may be sufficient to cause stretch-
ing of the already weakened media with or without hyper-
trophy of the intima. The arteries may be so lined with
deposits of calcareous matter that they appear as pipe
stems. More frequently there are rings of calcified material
placed closely together or irregular beading, giving to the
palpating finger the impression of feeling a string of very
fine beads. The arteries are often tortuous, hard, and are
absolutely nondistensible. At times no pulse wave can be
felt.

The larger arteries such as the brachials and femorals
are most affected. The walls become thinned and show
cracks, and areas apparently, but not actually denuded of
intima. Yellowish-white, irregular, raised plaques are scat-
tered here and there. Interspersed among these areas are
irregularly shaped clean-cut ulcers having as a rule a
smooth base, and frequently on 'the base is a thin plate of
calcified matter. The color of these denuded areas is usu-
ally brownish red or reddish brown. White thrombi may
be deposited on these areas. The danger of an embolus
plugging one of the smaller arteries is great and probably
happens more often than we think. The collateral circula-
tion is able to supply the thrombosed area. Should the
thrombus be on the carotid arteries, hemiplegia may result
from cerebral embolism. On microscopic examination of
the arteries there is seen extreme degeneration of all the
coats, the degeneration of the media leading almost to an
obliteration of that coat, On seeing such arteries as these
one wonders how the circulation could have been main-
tained and the organs nourished. Senile atrophy of the
internal organs naturally goes hand in hand with such
arterial changes.

There is, as a rule, no increase in arterial tension; on the

60 ARTERIOSCLEROSIS

contrary, the pressure is apt to be low. This is readily
understood when the heart is seen. This organ- is small,
the muscle is much thinned, it is flabby and of a brownish
tint, the so-called "brown atrophy." Microscopically,
there is seen to be much fragmentation of the fibers with
a marked increase of the brown pigment granules which
surround the cell nuclei. Cases are seen, however, in which
blood pressure increases as the patient grows older. The
hearts in such cases are more or less hypertrophied and
show extensive areas of fibroid myocarditis.

From what has been said, it follows that hypertension
alone may be the cause of arteriosclerosis; that certain
poisons in the blood which attack the media and cause it
to degenerate and weaken cause arteriosclerosis without
increased blood pressure; that the normal blood pressure
may be, for the artery which is physiologically weakened in
an individual over fifty, really hypertension, and arterio-
sclerosis may result. Our observations lead us to believe
that the process is at bottom one and the same. The dif-
ferent types noted clinically depend upon the nature of the
etiologic factors and the kind of arterial tissue with which
the individual is endowed. This view at least brings some
order out of previous chaos, and corresponds well with our
present knowledge of the disease.

There are many cases of arteriosclerosis which lead to
definite interference with the closure of the valves of the
heart, particularly the aortic and the mitral. It has been
said that puckerings of the valves frequently occur (Fig.
12). This arteriosclerotic endocarditis at times leads to
very definite heart lesions, chiefly aortic or mitral insuffi-
ciency, or both with, at times, murmurs of a stenotic char-
acter at the base. There is rarely true aortic stenosis,
however. The murmur is caused by the passage of the
blood over the roughened valves and into the dilated aorta.
Aortic stenosis is one of the rarest of the valvular lesions
affecting the valves of the left heart, and should be diag-

PATHOLOGY

nosed only when all factors, including the typical pulse
tracings, are taken into consideration.

The kidneys, as a rule, show extensive sclerosis. They
are small, firm, and contracted and not always to be dif-
ferentiated from the contracted kidneys of chronic inflam-
mation. The lesions of the arteriosclerotic kidney are due
to narrowing and eventual obstruction of the afferent ves-

Fig. 12. Aortic incompetence with hypertrophy and dilatation of left ventricle, the
result of arteriosclerosis affecting the aortic valves. Note how the valves have been curled,
thickened, and shortened, the edges of valves being a half inch below the upper points
of attachment. The anterior coronary artery is shown, the lumen narrowed. (Reduced
one-half.)

sels. The organs are usually bright red or grayish red in
color. At times there is marked fatty degeneration of
cortex and medulla, giving _to them a yellowish streaking.
The capsule is here and there adherent, the cortex is much
thinned and irregular. The surface presents a roughly

62 ARTERIOSCLEROSIS

granular appearance. The glomeruli stand out as whitish
dots and the sclerosed arteries are easily recognized, as
their walls are much thickened. The process does not, as
a rule, affect the whole kidney equally, but rather affects
those portions corresponding to the interlobular arteries.
The replacement of the normal kidney tissue by connective
tissue and the resulting contraction of this latter tissue
leads to the formation of scars. As the process is not reg-
ular, the scarring is deeper in some places than in others,
with the result that localized rather sharply depressed
areas appear on the surface. The pelvis is relatively large
and is filled with fat. The renal artery is often markedly
sclerosed and the whole process may be due to localized
thickening of the artery, or as part of a general arterioscle-
rosis. The latter is the more frequent. Microscopically,
it is seen that the tubules are atrophied, the Bowman's
capsules are, as a rule, thickened, and the glomeruli are
shrunken or have been replaced by fibrous tissue. In places
they have fallen out of the section. There is marked pro-
liferation of connective tissue in cortex and medulla. The
arterioles are thickened, the sclerosis being either of the
intima or media or of both. There is even occlusion of
many arterioles.

Changes in other organs as the result of arteriosclerosis
of their afferent vessels occur, but are not so characteristic
as in the kidney. In the brain the result of gradual thick-
ening of the arterioles is a diminished blood supply, soften-
ing of the portion supplied by the artery, and later a con-
nective tissue deposit. The occurrence of thrombi is fa-
vored and, now and again, a thrombus plugs an artery
which supplies an important and even vital part of the
brain. The arteries of the brain are end arteries, hence
there is no chance for collateral circulation. It is there-
fore evident how serious a result may follow the disturb-
ance in or actual deprivation of blood supply to any of the
brain centers or to the internal capsule.

PATHOLOGY 63

Arteriosclerosis of the Pulmonary Arteries

There have been a number of cases of sclerosis of the
pulmonary arteries, either alone, or associated with general
systemic arteriosclerosis.

A primary and a secondary form are recognized, the for-
mer in conjunction with congenital malformations of the
heart, the latter as the result of severe infection or of mi-
tral stenosis. These two causes seem to be the most impor-
tant in the production of the arterial changes. The cases
thus far described have revealed widespread thickening
of the pulmonary arteries. If one may judge by the de-
scription of the pathologic changes, the condition is quite
similar to that produced in a vein by transplantation along
the course of an artery. The diffuse form with connective
tissue thickening of all coats has been generally described.
There is also obliterating endarteritis of the smaller ves-
sels. In the etiology of the condition severe infection seems
to play a prominent role. The constant presence of right
ventricular hypertrophy is interesting, the heart dullness
extends, as a rule, far to the right of the sternum. In some
of the cases no demonstrable changes were observed in the
bronchial arteries or in the pulmonary veins.

Sanders has described a case of primary pulmonary ar-
teriosclerosis with hypertrophy of the right ventricle.

Recently Warthin* has reported a case of syphilitic
sclerosis of the pulmonary artery which places the lesion
in exactly the same category as that of syphilis in the sys-
temic arteries. There was also aneurysm of the left upper
division present and, to settle the etiologic nature of the
process, Spirochete pallida were found in the wall of the
aneurysm sac and in that of the pulmonary artery. The
microscopic picture in the pulmonary artery could not be
told from that in a syphilitic aorta.

*Warthin, A. S. : Am. Jour. Syph., 1918, i, 693.

64 ARTERIOSCLEROSIS

Sclerosis of the Veins

Phlebosclerosis not infrequently occurs with arterioscle-
rosis. It is seen in those cases characterized by high blood
pressure. Such increased pressure in the veins is due, for
example, to cirrhosis of the liver which affects the portal
circulation, or to mitral stenosis which affects the pulmo-
nary veins. The affected vessels are usually dilated. The
intima shows compensatory thickening especially where the
media is thinned. As a rule all the coats are involved in the
connective tissue thickening. Occasionally hyaline degen-
eration or calcification of the new-formed tissue is seen.
" Without existing arteriosclerosis the peripheral veins
may be sclerotic usually in conditions of debility, but not in-
frequently in young persons." (Osier.)

In many cases of arteriosclerosis, the pathologic changes
are not confined to the arteries, but are found in the veins
as well as in the capillaries. Such cases could be called
angiosclerosis.

CHAPTER III

PHYSIOLOGY OF THE CIRCULATION

No attempt will be made to cover the entire subject of
the physiology of the circulation. Only in so far as it re-
lates to arteriosclerosis and blood pressure and has a bear-
ing on the probable explanation of blood pressure phe-
nomena will it be discussed.

"The heart and the blood vessels form a closed vascular
system, containing a certain amount of blood. This blood
is kept in endless circulation mainly by the force of the
muscular contractions of the heart; but the bed through
which it flows varies greatly in width at different parts of
the circuit, and the resistance offered to the moving blood
is very much greater in the capillaries than in the large
vessels. It follows, from the irregularities in size of the
channels through which it flows, that the blood stream is
not uniform in character throughout the entire circuit-
indeed, just the opposite is true. From point to point in
the branching system of vessels the blood varies in regard
to its velocity, its head of pressure, etc. These variations
are connected in part with the fixed structure of the system
and in part are dependent upon the changing properties of
the living matter of which the system is composed." (W.
H. Howell.)

If the vascular system were composed of a central pump,
projecting at every stroke a given amount of liquid into
a series of rigid tubes, the aggregate cross sections of which
were equal to the cross section of the main pipe, then the
velocity at the openings would be the same as at the source
(making allowances for friction). The problem would then
be a simple one. In the circulation of the blood no such
simple condition obtains. The capillary beds is an enormous

66 ARTERIOSCLEROSIS

area through which the blood flows slowly. From the
time the blood is thrown into the aorta the velocity begins
to diminish until it reaches its minimum in the capillaries.
In no two persons is the initial velocity at the heart the
same, nor in the same person is it the same at all times of
day. The size of the heart, the actual strength of the
muscle, the amount of blood ejected at every beat, and the
size and elasticity of the aorta are some of the factors which
determine the velocity of blood at the aortic orifice. When
to these factors are added the differences in arterial tissue,
the activity or resting stage of the various organs, etc., the
question becomes exceedingly complicated. In spite of
these many disturbing elements, attempts more or less suc-
cessful have been made to estimate the velocity of the blood
in animals. Thus, in the carotid of the horse the velocity
was found to be 300 mm. per second (Volkman) and 297
mm. (Chauveau); in the carotid of the dog, 260 mm.
(Vierordt). In the jugular vein of the dog Vierordt found
the velocity to be 225 mm. per second. These figures do
not represent the actual velocity of the blood in all horses
or all dogs, but they do give us some general idea of the
rate of flow of the blood. For man it has been calculated
that the velocity in the aorta is about 320 mm. per second.
The velocity is not uniform in the large arteries, where at
every heart beat there is a sudden increase followed by a
decrease as the heart goes into diastole. The farther away
from the heart the measurements are made the more even
is the flow.

Observations by W. H. Luedde with the Zeiss binocular
corneal microscope on the rate of flow in the conjunctival
capillaries must modify somewhat our former conceptions.
He finds that "The rate varies in the different arteries,
capillaries, and veins from a barely perceptible motion to
a little more than 1 mm. per second. Further, some parts
of the capillary network are ordinarily supplied with blood
elements only occasionally. This is shown by the passage

PHYSIOLOGY OF THE CIRCULATION 67

of a column of corpuscles along a certain line, followed
after an interval of seconds, during which no corpuscles
pass, by another column in the same line as before."

The vessels of the conjunctiva probably are quite like
superficial vessels in the skin and mucous membranes.
Therefore, we must be free to admit that the circulation
in them is not absolutely steady. Luedde found further that
in syphilitics there were tortuosities, irregularities, minute
aneurysmal dilatations and even obliterations of capillaries.
Some of the changes occurred as early as one month after
infection.

The rate in the capillaries of man is estimated to be be-
tween 0.5 mm. and 0.9 mm. per second. As the blood is
collected into the veins and the bed becomes smaller, the
velocity increases until at the heart it is almost the same
as in the aorta. That the velocity could not be exactly the
same is evident from the fact that the cross section of the
veins, which return the blood to the right auricle, is greater
than is the cross section of the aorta.

The volume of the bed is subject to rapid and wide
fluctuations, which are dependent on many causes, both
physiologic and pathologic. The call of an actively func-
tionating organ or group of organs causes a widening
of a more or less extensive area, and the velocity necessarily
varies. In states of great relaxation of the vessels there
may be a capillary pulse. In order to force blood at the
same rate through dilated vessels as through normal ves-
sels, there must be more blood or there must be a more
rapid contraction of the central pump. What actually
happens, as a rule, is an increase in the rate of the heart
beat. There are conditions such, for example, as aortic
insufficiency where actually more blood is thrown into
the circulation at every beat, so that the rate is not
changed.

It has been calculated that the average amount of blood
thrown into the aorta at every systole of the heart is from

68 ARTERIOSCLEROSIS

50 to 100 c.c. This is forcibly ejected into a vessel already
filled (apparently) with blood. In order to accommodate
this sudden accession of fluid, the aorta must expand. The
aortic valves close, and during diastole the blood is forced
through the vascular system by the forcible, steady contrac-
tion of the highly elastic aorta. Other large vessels which
branch from the aorta also have a part in this steady pro-
pulsion of blood. From seventy to eighty times a minute
the aorta is normally forcibly expanded to accommodate
the charge of the ventricle. It is not difficult to under-
stand the great frequency of patches of sclerosis in the arch
when these facts are borne in mind.

What relationship the viscosity of the blood has to the
rate and volume of flow is not fully understood. As yet
there is not much known about the subject, and no one has
devised a satisfactory means of measuring the viscosity.
It is thought by some that an increased viscosity assists in
producing an increased amount of work for the heart.

Blood Pressure

Blood pressure is the expression used for a series of
phenomena resulting from the action of the heart. As every
heart beat is actual work done by the heart in overcoming
resistance to the outflow of blood, this force is approx-
imately measurable in a large artery such as the brachial.
It has been determined that the pressure in the brachial
artery is almost equal to the intraventricular pressure in
the left ventricle. In animals it is easy to attach manom-
eters to the carotid artery and to measure the blood pres-
sure accurately. Formerly the method consisted in attach-
ing a tube and allowing the blood to rise in the tube. The
height to which the blood rose measured the maximum pres-
sure. This is a crude method and has been replaced by
the U-tube of mercury with connection made to the artery
by saline or Ringer's solution. This apparatus is familiar
to all physiologists.

PHYSIOLOGY OF THE CIRCULATION 69

In man the measurement is most conveniently made from
the brachial artery. There is some difference in the pres-
sure in the femoral and the brachial and some use both
arteries. However, the difficulty of adjusting instruments
to the upper leg, the great force which must be used to com-
press the femoral artery and the relative inaccessibility of
the leg as compared to the arm, make the leg an inconveni-
ent part for use in blood pressure determinations. It is
not to be recommended.

Blood pressure is a valuable aid in diagnosis and of ma-
terial help in many cases in prognosis, but it is not infalli-
ble neither can it be used alone to diagnose a case. Blood
pressure is only one of many links in a chain of evidence
leading to diagnosis. It has been badly used and much
abused. It has been condemned unjustly when it did not
furnish all the evidence. It has been made a fetish and
worshipped by both doctors and patients. A sane concep-
tion of blood pressure must be widely disseminated lest
we find it being discarded altogether.

Blood pressure consists of more than the estimation of
the systolic pressure. The blood pressure picture consists
of (1) the systolic pressure, (2) the diastolic pressure, (3)
the pulse pressure which is the difference between the
systolic and diastolic pressure, (4) the pulse rate. Ex-
pressed in the literature it should read thus: 120-80-40; 72.
That tells the whole story in a brief, accurate form. This
is recommended in history reporting. It must be ever kept
in mind that a blood pressure reading represents the work
of the heart at the moment ivJien it was taken. Within a
few minutes the pressure may vary up or down. There is
no normal pressure as such, but an average pressure for
any group of people of the same age living under similar
conditions. The habit of speaking of any systolic figure as
normal should be broken. A pressure picture may be nor-
mal but a systolic reading, whatever it may be, is not ac-
curately designated as normal. This distinction is worth
insisting upon.

70 ARTERIOSCLEROSIS

Blood Pressure Instruments

There are several instruments which are in common use
for the purpose of recording blood pressure in man.

Historically, the determination of blood pressure for man
began with the attempt of K. Vierordt in 1855 to measure
the blood pressure by placing weights on the radial pulse
until this was obliterated. The first useful instrument,
however, was devised by Marey in 1876. He placed the
hand in a closed vessel containing water connected by tub-
ing with a bottle for raising the pressure and by another
tube with a tambour and lever for recording the size of the
pulse waves. He maintained that when pressure on the
hand was made, the point where oscillations of the lever
ceased was the maximal pressure, the point where the oscil-
lations of the recording lever was largest, was the minimal
pressure.

This pioneer work was practically forgotten for twenty-
five years. It was not until 1887 that V. Basch devised an
instrument which was used to some extent. This instru-
ment recorded only maximum pressure. It consisted of a
small rubber bulb filled with water communicating with a
mercury manometer. The bulb was pressed on the radial
artery until the pulse below it was obliterated and the
pressure then read off on the column of mercury. V. Basch
later substituted a spring manometer for the mercury
column. Potain modified the apparatus by using air in the
bulb with an aneroid barometer for recording the pressure.
These instruments are necessarily grossly inaccurate.
Moreover, they do not record the diastolic pressure.

In 1896 and 1897 further attempts were made to record
blood pressure by the introduction of a flat rubber bag
encased in some nonyielding material, which was placed
around the upper arm. Riva-Rocci used silk, while Hill
and Barnard used leather. The latter used a bulb or
Davidson syringe to force air into the cuff around the arm

PHYSIOLOGY OF THE CIRCULATION 71

and palpated the radial artery at the wrist, noting the point
of return of the pulse after compression of the upper arm,
and reading the pressure on a column of mercury in a tube.

Except that the width of the cuff has been increased from
5 cm. to 12 cm., this is the general principle upon which all
the blood pressure instruments now in use are based.
Most of the apparatuses make use of a column of mercury
in a U-tube to record the millimeters of pressure. As the
mercury is depressed in one arm to the same extent as it
is raised in the other arm the scale where readings are made
is .5 cm. and the divisions represent 2 mm. of mercury but
are actually 1 mm. apart.

The cuff was made 12 cm. in diameter because it was
shown (v. Eecklinghausen) that with narrow cuffs much
pressure was dissipated in squeezing the tissues. Jane-
way has shown that with the use of the 12 cm. cuff
accurate values are obtained independently of the amount
of muscle and fat around the brachial artery. In other
words if an actual systolic blood pressure of 140 mm. is
present in two individuals, the one with a thin arm, the
other with a thick arm, the instrument will record these
pressures the same where a 12 cm. arm band is used. We
need have no fear of obtaining too high a reading when
we are taking pressure in a stout or very muscular individ-
ual. Janeway also was the first to call attention to the fact
that the diastolic or minimal pressure was at the point
where the greatest oscillation of the mercury took place.
This is difficult to estimate in many cases as the eye can
not follow slight changes in the oscillation when the pres-
sure in the cuff is gradually reduced. Practically this is
the case in small pulses.

The Eiva-Eocci instrument was modified by Cook. (See
Fig. 13.) He used a glass bulb containing mercury into
which a glass tube projected. The bulb was connected by
outlet and tubing to the cuff and syringe. The glass tube
was marked off in centimeters and millimeters and for con-

ARTERIOSCLEROSIS

venience was jointed half way in its length. The instru-
ment could be carried in a box of convenient size. This
instrument is fragile and more cumbersome, although
lighter in weight, than others and is very little used at
present.

Stanton's instrument (Fig. 14) is practically Cook's
made more rigid in every way but without the jointed tube.
The cuff has a leather casing, the pressure bulb is of heavy
rubber, the glass tube in which the mercury rises is fixed

Fig. 13. Cook's modification of Riva-Rocci's blood pressure instrument.

against a piece of flat metal and there are stopcocks in a
metal chamber introduced between the bulb and mercury
with which to regulate the in- and out-flow of air. The
pressure can be gradually lowered conveniently without re-
moving the pressure bulb.

The most accurate mercury manometer is that of Er-
langer. (Fig. 15.) The instrument is bulky and is not
practicable for the physician in practice. The principle is
that used by Riva-Rocci. There is an extra T-tube intro-

PHYSIOLOGY OF THE CIRCULATION 73

duced between the manometer and air bulb connecting with
a rubber bulb in a glass chamber. The oscillations of this
are communicated to a Marey tambour and recorded on
smoked paper revolving on a drum. There is a compli-
cated valve which enables the operator to reduce the pres-
sure with varying degrees of slowness. The mercury is
placed in a U-tube with a scale alongside it. The instru-
ment is expensive and not as easy to manipulate as its

Fig. 14. Stanton's sphygmomanometer.

advocates would have us believe. Hirschfelder has added
to the usefulness (as well as to the complexity) of the Er-
langer instrument, by placing two recording tambours for
the simultaneous registering of the carotid and venous
pulses. In spite of its complexity and necessary bulkiness,
very valuable data are obtained concerning the auricular
contractions.

AKTERIOSCLEROSIS

One of the best of the mercury instruments is the Brown
sphygmomanometer. In this (Fig. 16) the mercury is in
a closed, all-glass tube so that it can not spill under any

Fig. 15. The Erlanger sphygmomanometer with the Hirschf elder attachments by
means of which simultaneous tracings can be obtained from the brachial, carotid, and
venous pulses.

PHYSIOLOGY OF THE " CIRCULATION

sort of manipulation. It is in this sense ' ' fool-proof. ' ' The
cuff, however, is poorly constructed. It is too short and
there are strings to tie it around the arm. I have found
that this causes undue pressure in a narrow circle and ren-

Fig. 16. Desk model Baumanometer.

ders the reading inaccurate. In the clinic we use this mer-
cury instrument with a long cuff like that provided by the
Tycos instrument.

The Faught instrument (Fig. 17) is larger than the
Brown, but is less easily broken and is not too cumbersome

76 ARTERIOSCLEROSIS

to carry around. The substitution of a metal air pump for
the rubber makes the apparatus more durable.

The v. Recklinghausen instrument is not employed to
any extent in this country. It is both expensive and cum-
bersome, and has no advantages over the other instruments.

Several other instruments have been devised and new ones
are constantly being added io the already large list. With
those employing mercury the principle is the same. The
aim is to make an instrument which is easily carried, dura-
ble, and accurate.

In all the mercury instruments the diameter of the tube

Fig. 17. The Faught blood pressure instrument. An excellent instrument which is
quite easily carried about and is not easily broken.

is 2 mm. One would suppose that there would be notice-
able differences in the readings of the different mercury
instruments depending upon the amount of mercury used
in the tube. By actual weight there is from 35 to 45 gms.
of mercury in the several instruments. After many trials,
no noticeable differences in blood pressure readings can be
made out between a column weighing 35 gm. and one weigh-
ing 45 gm.

There is, however, the inertia of the mercury to be over-

PHYSIOLOGY OF THE CIRCULATION 77

come, friction between the tube and the mercury, and vapor
tension. The mercury is therefore not as sensitive to rapid
changes of pressure in the cuff as a lighter fluid would be.
The mercury must be clean and the tube dry so that there
is no more friction than what is inherent between the mer-
cury and glass. In making readings on a rapid pulse the
oscillations of the mercury column are apt to be irregular
or to cease now and then, due to the fact that the downward
oscillation coincides with a pulse wave, or an upward oscil-
lation receives the impact of two pulse waves transmitted
through the cuff. Instruments have been devised to obviate
this difficulty, but they have not come into favor. They are

Fig. 18. Rogers' "Tycos" dial sphygmomanometer.

usually too complicated and at present can not be recom-
mended.

An instrument devised by Dr. Rogers (the "Tycos")
has met with considerable popularity. (Fig. 18.) This is
not an instrument which operates with a spring and lever.
The instrument is composed essentially of two metal discs
carefully ground and attached at their circumferences to
the metal casing below the dial. There is an air chamber
between these discs through the center of which air is
forced by the syringe bulb. When air is forced into the
space between these two discs, they are forced apart to a
very slight extent, with the highest pressures only 2-3 mm.
of bulging occurs. From data gathered after extensive use

ARTERIOSCLEROSIS

for five years these discs were not found to have sprung.
A lever attached to a cog which in turn is attached to the
dial needle magnifies to an enormous extent the slightest
expansion of the discs. Every dial is handmade and every
division is actually determined by using a U. S. govern-
ment mercury manometer of standard type. No two dials
therefore are alike in the spacing of the divisions of the

Fig. 19. Detail of the dial in the "Tycos" instrument.

scale but every one is calibrated as an individual instru-
ment. There is no doubt in the author 's mind that for the
general practitioner the instrument has some advantages
over the mercury instruments. It reveals the slightest
irregularity in force of the heart beat. The oscillation of
the dial needle is more accurately followed by the eye than
is that of the column of mercury. The needle passes di-
rectly over the divisions of the scale, while with usual mer-

PHYSIOLOGY OF THE CIRCULATION

cury instruments the scale is an appreciable distance (some-
times .5 cm.) from the column of mercury at the side. (Fig.
19.) The diastolic pressure is more easily read on the

Fig. 20. Faught dial instrument.

Fig. 21. Detail of the dial of the Faught instrument.

80 ARTERIOSCLEROSIS

1 ' Tycos. " It is where the maximum oscillation of the nee-
dle occurs as the pressure is slowly released from the cuff.
Although it does not appear that this instrument, if prop-
erly made and standardized, could become inaccurate,
nevertheless it is advisable to check it every few months
against a known accurate mercury manometer instrument.

Another perfectly satisfactory dial instrument is the
Faught (Figs. 20 and 21). The general plan of this differs
in some minor points from the ' ' Tycos. ' ' I have compared
the two and have found no difference in the readings. Both
can be recommended.

One or two other cheaper dial instruments are on the
market. The Sanborn seems to be quite satisfactory. (Fig.

Fig. 22. The Sanborn instrument.

22.) It is cheaper than the other dial instruments. There
is this much to be said, no instrument using a spring as re-
sistance to measure pressure can be recommended.

Technic

The same technic applies to all the mercury instruments.
The patient sits or lies down comfortably. The right or left
arm is bared to the shoulder, the cuff is then slipped over
the hand to the upper arm. (See Fig. 23.) At least an inch
of bare arm should show between the lower end of the cuff
and the bend of the elbow. The rubber is adjusted so that
the actual pressure from the bag is against the inner side

PHYSIOLOGY OF THE CIRCULATION

8.1

of the arm. The straps are tightened, care being taken not
to compress the veins. The upper part of the cuff should
fit more snugly than the lower part. The part of the in-
strument carrying the mercury column is now placed on a
level surface ; the two arms of the mercury in the tube must
be even, and at on the scale. With the fingers of one hand
on the radial pulse, the bag is compressed until the pulse
is no longer felt. (See Fig. 24.) One should raise the pres-
sure from 10-12 mm. above this, and close the stopcock

Fig. 23. Method of taking blood pressure with a patient in sitti

ng position.

between the bulb and the mercury tube. In a good instru-
ment the column should not fall. If it does there is a leak
of air in the system of tubing and arm bag. Now with the
finger on the pulse, or where the pulse was last felt, grad-
ually allow air to escape by turning the stopcock so that
the column of mercury falls about 2 mm. (one division on
the scale) for every heart beat or two. One must not allow
the column of mercury to descend too slowly as it is un-

ARTERIOSCLEROSIS

comfortable for the patient and introduces a psychic ele-
ment of annoyance which affects the blood pressure. On the
other hand, the pressure must not be released too rapidly,
else one runs over the points of systolic and diastolic pres-
sure and the readings are grossly inaccurate. It is impossi-
ble to say how rapidly the mercury must fall. Every opera-
tor must find that out for himself by practice. The first per-
ceptible pulse wave felt beneath the palpating finger at the
wrist, represents on the scale the systolic pressure. This
can be seen to correspond to a sudden increase in the magni-

Fi^. 24. Method of taking, blood pressu

h patient lying down.

tude of the oscillation of the mercury column. The systolic
pressure, thus obtained, is from 5-10 mm. lower than the
real systolic pressure. The more sensitive the palpating
finger, the more nearly does the systolic pressure reading
approach that found by using such an instrument as Er-
langer's, where the first pulse wave is magnified by the
lever of the tambour.

The pressure is now allowed to fall, until the palpating

PHYSIOLOGY OF THE CIRCULATION 83

finger feels tire largest possible pulse wave, which is coinci-
dent with the greatest oscillation of the mercury. This is
the diastolic pressure. Beyond this point there is no oscil-
lation of the mercury column. The difference between the
two is the pulse pressure. Thus the pulse is felt after com-
pression at 120 on the scale, and the maximum oscillation
occurs at 80. The systolic pressure is 120 mm., the dias-
tolic is 80 mm., and the pulse pressure is 40 mm.

With the "Tycos" or Faught the arm band is snugly
wound around the arm, the bag next to the skin and the end
tucked in, so that the whole band will not loosen when air
is forced into the bag. The cuff is blown up until the pulse
is no longer felt. One should raise the pressure not more
than -10 mm. above the point of obliteration of the pulse.
The valve is then carefully opened so that the needle grad-
ually turns toward zero. At the first return of the pulse
wave felt at the wrist, the needle is sure to give a sudden
jump. This is the systolic pressure and is read off on the
scale. The needle is now carefully watched until it shows
the maximum oscillation. This is the diastolic pressure.
The difference between the two is, as above, the pulse pres-
sure.

In taking pressure one should take the average of several,
three or four. Moreover, one must not take consecutive
readings too quickly and one must be sure that between
every two readings all the air is out of the cuff and that the
mercury or dial is at zero. It has been repeatedly shoivn
that in a cyanosed arm the systolic pressure is raised so
that even slight cyanosis between readings must be care-
fully avoided.

The only accurate method of determining both the sys-
tolic and diastolic pressure, but especially the diastolic, is
by the so-called auscultatory method. (See Fig. 25.) The
cuff is adjusted in the usual way and one places the bell
of a binaural stethoscope over the brachial artery from
one to two centimeters below the lower edge of the

ARTERIOSCLEROSIS

cuff.* Care must be taken that the bell is not pressed too
firmly against the arm and that the edge of the bell nearest
the cuff is not pressed more firmly than the opposite end.
For this purpose, one can not use the ordinary Bowles
stethoscope or any of the other much lauded steth-
oscopes, because the surface of the bell is too large. The
diameter of the bell must not be more than twenty-five mil-
limeters, twenty is still b'etter. It is advisable before be-
ginning the observation to locate with the finger the pulse

Fig. 25. Observation by the auscultatory method and a mercury instrument. One hand
regulates the stop cock which releases air gradually.

in the brachial artery just above the elbow, so that the
stethoscope may be placed over the course of the artery.
(Fig. 26.) The first wave which comes through is heard as
a click, and occurs at a point on the manometer or dial scale
from 5-10 mm. higher than can usually be palpated at the
radial artery. This is the true systolic pressure. By keep-

*A firm makes a stethoscope so that the bell is clamped on the arm leaving both the
operator's hands free.

PHYSIOLOGY OF THE CIRCULATION

ing the bell of the stethoscope over the brachial artery
while the pressure is falling, one comes to a point when all
sound suddenly ceases. This is said to be the diastolic pres-
sure. This is incorrect as will be shown later.

Fig. 26. Observation by the auscultatory method and a dial instrument. The right
hand holds the bulb and regulates the air valve.

Arterial Pressure

The arterial pressure in the large arteries undergoes ex-
tensive fluctuations with every heart beat. The maximum
pressure produced by the systole of the left ventricle of the
heart is known as the maximum or systolic pressure. It
practically equals the intraventricular pressure. The mini-
mum pressure in the artery, the pressure at the end of dias-
tole, is called the diastolic pressure. The difference be-
tween the systolic and diastolic pressures is known as the
pulse pressure. There is yet another term known as the
mean pressure. For convenience, this may be said to be the

86 ARTERIOSCLEROSIS

arithmetical mean of the systolic and diastolic pressures.
Actually, however, this can not be the case, owing to the
form of the pulse wave, which is not a uniform rise and fall
the upstroke being a straight line, but the downstroke be-
ing broken usually by two notches. We do not make use of
the mean pressure in recording results. It is of experimen-
tal interest and needs only to be mentioned here.

It has been shown that the mean pressure is quite con-
stant throughout the whole arterial system. The maximum
pressure necessarily falls as the periphery of the vascular
system is approached. In general it may be said that

Fig. 27. Schema to illustrate the gradual decrease in pressure from the heart to the
vena cava: (a), arteries; (c), capillaries; (v), veins; (A), aorta, pressure 150 mm.;
(B), brachial artery, pressure 130 mm.; (F), femoral vein, 20 mm.; (IVC), inferior
vena cava, 3 mm. (Modified from Howell.)

the minimal pressure is quite constant. Too little attention
is paid to minimal and pulse pressure. The minimal pres-
sure is important, for it gives us valuable data as to the
actual propulsive force driving the blood forward to the
periphery at the end of diastole.

It is readily understood how the maximum pressure falls
as the periphery is approached, until in the arterioles the
maximum and minimum pressures are about equal. The
pressure then in these arterioles is practically the same as
the diastolic pressure. Actually it is a few millimeters
less. The diastolic blood pressure would, therefore, meas-
ure the peripheral resistance and, as the maximum for
systolic pressure represents approximately the intraven-

PHYSIOLOGY OF THE CIRCULATION 87

tricular pressure, the difference between the two, the pulse
pressure, actually represents the force which is driving the
blood onward 'from the heart to the periphery. It is hence
very evident that the mere estimation of the systolic pres-
sure gives us but a portion of the information we are
seeking.

The pulse pressure is subject to wide fluctuations but as
a rule for any one normal heart it remains fairly constant
as the rate varies. In a rapidly beating heart the -diastole
is short and the diastolic pressure rises. If the systolic
pressure does not also rise, as in a normal heart following
exercise, we will say, the pulse pressure falls. We know
that when the pulse rate is constant, vasodilatation causes a
fall in diastolic pressure and a rise in pulse pressure. On
the contrary, vasoconstriction causes a rise in diastolic
pressure and a fall in pulse pressure.

It is very probably the case that with two individuals of
equal age and equal pulse rate, and equal systolic pressure
of 160 mm., the one with a diastolic pressure of 110 mm.
and, therefore, a pulse pressure of 50 mm. is much worse
off than the other with a diastolic pressure of 90 mm. and a
pulse pressure of 70 mm. The latter may be normal for the
age of the person especially when certain forms of fibrous
arteriosclerosis accompanied by enlarged heart are present.

The former is not normal for any age. Low pulse pres-
sure usually means a weak vasomotor control and is only
found in failing circulation or in markedly run down states,
such as after serious illness or in tuberculosis. Therefore,
it is most important to estimate accurately the diastolic
pressure as well as the systolic pressure, for only in this
way can we obtain any data of value regarding the driving
power of the heart and the condition of the vasomotor sys-
tem. A high systolic pressure does not necessarily mean
that a great deal of blood is forced into the capillaries. Ac-
tually it may mean that very little blood enters the periph-
ery. The heart wastes its strength in dilating constricted

88 ARTERIOSCLEROSIS

vessels without actually carrying on the circulation ade-
quately.

Normal Pressure Variations

The systolic pressure varies considerably under condi-
tions which are by no means abnormal. Thus, the average
for men at all ages is about 127 mm. Hg. (All measure-
ments are taken from the brachial artery, with the individ-
uals in the sitting posture.) For women the average, is
somewhat lower, 120 mm. Hg. The pressure is lowest in
children. In children from 6-12 years the average systolic
pressure is 112 mm. Normally, there is a gradual increase
as age comes on, due, as will be shown in the succeeding
chapter, to physiologic changes which take place in the
arteries from birth to old age. In the chart here appended
is graphically shown the normal variations in the blood
pressure at different ages compiled from observations made
on one thousand presumably normal persons. (Fig. 28.)

The diastolic pressure has been estimated to be about 35
to 45 mm. Hg lower than the systolic pressure, and conse-
quently these figures represent the pulse pressure in the
brachial artery of man. This is equivalent to saying that
every systole of the left ventricle distends this artery by a
sudden increase in pressure equal to the weight of a column
of mercury 2 mm. in diameter and 35 to 45 mm. high. Nat-
urally, at the heart the pressure is highest. As the blood
goes toward the capillary area the pressure gradually de-
creases until, at the openings of the great veins into the
heart, the pressure is least. At the aorta (A) the pressure
(systolic) is approximately 150 mm. Hg, at the brachial
artery (B) it is 130 mm., in the capillary system (C) it is
30 mm., in the femoral vein (F) it is 20 mm., at the opening
of the inferior vena cava (I) it is 3 mm.

Attention has been called to the normal systolic pressure
at different ages. This is not the only cause for variations
in the blood pressure. Normally, it is greater when in the

PHYSIOLOGY OF THE CIRCULATION

erect position than when seated, and greater when seated
than when lying down. During the day there are well-
recognized changes. The pressure is lowest during the
early morning hours, when the person is asleep. In women
there are variations due to menstruation. Muscular exer-

AGES

VtR

Fig. 28. Chart showing the normal limits of variation in systolic blood pressure. (After

Woley.)

cise raises the blood pressure markedly. The effect of a
full meal is to raise the blood pressure. The explanation
is that during and following a meal there is dilatation of
the abdominal vessels. This takes blood from other parts
of the body, provided that the other factors in the circula-

90 ARTERIOSCLEROSIS

tion remain constant. A fall of pressure would necessarily
occur in the aorta. To compensate for this, there is in-
creased work on the part of the heart, which reveals itself
as increased pressure and pulse pressure. It is well known
that the interest in the process taken by an individual upon
whom the blood pressure is estimated for the first time tends
to increase the rate of the heart and to raise the blood pres-
sure. For this reason the first few readings on the instru-
ment must be discarded, and not until the patient looks
upon the procedure calmly can the true blood pressure be
obtained. As a corollary to this statement, mental excite-
ment, of whatever kind, has a marked influence on the
pressure. The patient must remain absolutely quiet. Kais-
ing the head or the free arm causes the pressure to rise.
Another important physiologic variation is produced by
concentrated mental activity. This tends to hurry the heart
and increase the force of the beat. In short, it may be
stated as a general rule that any active functioning of a
part of the body which naturally requires a great excess of
blood tends to elevate the blood pressure. At rest the pres-
sure is constant. Variations caused by the factors men-
tioned act only transitorily, and the pressure shortly re-
turns to normal.

The Auscultatory Blood Pressure Phenomenon

Since the first description of the auscultatory blood pres-
sure sounds by Korotkov in 1905, this method has been more
and more employed until today it is the standard, recog-
nized method of determining the points in the blood pres-
sure reading. When one applies the 12 cm. arm band over
the brachial artery and listens with the bell of the stetho-
scope about one cm. below the cuff directly over the bra-
chial artery near the bend of the elbow, one hears an inter-
esting series of sounds when the air in the cuff is gradually
reduced. The cuff is blown up above the maximum pres-
sure. As the air pressure around the arm gradually is

PHYSIOLOGY OF THE CIRCULATION 91

lowered, the series of sounds begins with a rather low-
pitched, clear, clicking sound. This is the first phase. This
only lasts through a few millimeters fall when a murmur
is added and the tone becomes louder. This click and mur-
mur phase is the second phase. A few millimeters more of
drop in pressure and a clear, sharp, loud tone is audible.
Usually this tone lasts through a greater drop than any of
the other tones. This is the third phase. Kather suddenly
the loud, clear tone gives place to a dull muffled tone. In
general the transition is quite sharp and distinct. This is
the fourth phase. The tone gradually or quickly ceases
until no tone is heard. This is the fifth phase (Ettinger.)

The first phase is due to the sudden expansion of the
collapsed portion of the artery below the cuff and to the
rapidity of the blood flow. This causes the first sharp
clicking sound which measures the systolic pressure.

The second, or murmur and sound phase, is due to the
whorls in the blood stream as the pressure is further re-
leased and the part of the artery below the cuff begins to
fill with blood.

The third tone phase is due to the greater expansion of
the artery and to the lowered velocity in the artery. A
loud tone may be produced by a stiff artery and a slow
stream or by an elastic artery and a rapid stream. This
tone is clear cut and in general is louder than the first
phase.

The fourth phase is a transition from the third and be-
comes duller in sound as the artery approaches the normal
size.

The fifth phase, no sound phase, occurs when the pressure
in the cuff exerts no compression on the artery and the
vessel is full throughout its length.

It is generally conceded that the sounds heard are pro-
duced in the artery itself -and not at the heart.

The tones vary greatly in different hearts. A very
strong third tone phase or prolongation of this phase usu-

92 ARTERIOSCLEROSIS

ally means that the heart which produces the tone is a
strongly acting one, although allowances must be made for
a sclerosed artery in which there is a tendency to the pro-
duction of a sharp third phase.

Weakness of the third phase, as a rule, indicates weak-
ness of the heart and this dulling of the third phase may be
so excessive that no sound is produced. Goodman and
Howell have carried this method further by measuring the
individual phases and calculating the percentage of each
phase to the pulse pressure. Thus, if in a normal individ-
ual the systolic pressure is 130 mm., the diastolic 85 mm.,
and the pulse pressure 45 mm., the first phase lasts from
130 to 116 or 14 mm., the second from 1.16 to 96, or 20 mm.,
the third from 96 to 91 or 5 mm., the fourth from 91 to 85, or
6 mm. The first phase would then be 31.1 per cent of the
total pulse pressure, the second phase 44.4 per cent, the
third phase 11.1 per cent, and the fourth phase 13.3 per
cent. They consider that the second and third phases rep-
resent cardiac strength (C. S.) and the first and fourth rep-
resent cardiac weakness (C. W.). They believe that C. S.
should normally be greater than C. W. In the example
above C. S.:C. W.=- 55.5:44.4. In weak hearts, especially in
uncompensated hearts, the conditions are reversed and C.
W. > C. S. This is often the case. As a heart improves
C. S. again tends to become greater than C. W. They think
that the phases should be studied in respect to the sounds
and also to the encroachment of one sound upon another.

These observations are interesting but we have not found
the division into phases as helpful as it was thought to be.
We spent a great deal of time on this question. All that
can be said, in my opinion, is that a loud, long third phase
is usually evidence of cardiac strength.

A further interesting feature which can be heard in all
irregular hearts is a great difference in intensity of the in-
dividual sounds. Goodman and Howell call this phenom-
enon tonal arrhythmia. Irregularities can be made out by

PHYSIOLOGY OF THE CIRCULATION 93

the auscultatory method which can not be heard at the
heart.

In anemia the sounds are very loud and clear and do not
seem to represent the actual strength of the heart.

The general lack of vasomotor tone in the blood vessels
together with some atrophy and flabbiness of the coats
probably explains the loud sounds.

In polycythemia the sounds have a curious, dull, sticky
character and can not be differentiated accurately into
phases, a condition which was predicted from the knowl-
edge of the sharp sounds in anemia.

In not all cases can all phases be made out. It is usually
the fourth phase which fails to be heard.

In such cases the loud third tone almost immediately
passes to the fifth phase or no sound phase. The importance
of this will later be taken up.

"In arteriosclerosis, with hardening and loss of elasticity
of the vessel walls, the auscultatory phenomena, according
to Krylow, are apt to be more pronounced, since the back
pressure at the cuff probably causes some dilatation of the
vessel above it, while the lumen of the vessel is smaller
than normal. Both of these factors cause an increased
rapidity in the transmission of the blood wave when pres-
sure in the cuff is released, which in time favors the vibra-
tion of the vessel walls.

"In high grade thickening of the arterial walls, how-
ever, especially where calcification had occurred, Fischer
found that the sounds were distinctly less loud )than nor-
mal, the more so in the arm, which showed the greater
degree of hardening. According to Ettinger's experience,
the rapidity of the flow distinctly increases the auscultatory
phenomenon/' (Gittings.)

The sounds depend upon the resonating character of the
cuff, upon the size and accessibility of the vessel, upon the
force of the heart beat, and upon the velocity of the blood.

94 ARTERIOSCLEROSIS

The Maximum and Minimum Pressures

The maximum (systolic) pressure is read at the point
where the first audible click is heard after the cuff is blown
up and the pressure gradually reduced by means of the
needle valve in the hand bulb or on the upright of the
glass containing the mercury. All are agreed upon this
point. There has been some dispute as to the place where
the diastolic pressure should be read. Korotkov considered
that the diastolic pressure should be read at the fourth

Fig. 29. Tracing of auscultatory phenomena. (See explanation in legend of .Fig. 30.)

phase when the loud tone suddenly becomes dulled. Others
held that the diastolic pressure should be read at the fifth
phase, the absence of all sound. Experiments carried out
to determine this point were made by me with the assist-
ance of Prof. Eyster and Dr. Meek at the Physiological
Laboratory of the University of Wisconsin. We arranged
apparatus making it possible to hold the pressure in the
carotid artery of dogs at maximum or minimum. A femoral

PHYSIOLOGY OF THE CIRCULATION 95

artery was then dissected and an instrument devised to
compress the artery with a water jacket. The whole was
connected up with a kymograph. A time marker was put
in so as to record the place where changes in sound were
heard while listening below the cuff around the femoral
artery. Two sets of records were taken. One with pres-
sure greater than minimum pressure and a falling pres-
sure over the femoral artery (Fig. 29), the other with
pressure at zero and gradually raised to minimum pres-
sure (Fig. 30). Both sets of records showed the same re-

Fig. 30. Figures are to be read from left to right. The top line records the points
where sounds were heard, the figures above the short vertical lines refer to tones (see
text). MX. B. P., maximum blood-pressure. M. I. P., minimum blood-pressure. P. B.,
pressure bulb recorder. It was impossible to lower and raise this bulb by hand without
obtaining the great irregular oscillations of the attached lever above the mercury manom-
eter. B. L., base line.

suit; viz., that at a point corresponding to the sudden
change of tone the pressure on the artery corresponded to
the minimum pressure. It was therefore concluded that
experimentally in dogs the point where diastolic pressure
should be read is at the tone change from clear to dull,
not at the point where all sound disappears.

Erlanger showed some years ago, that with his instru-
ment, the point at which diastolic pressure should be read
was at the instant when the maximum oscillation of the

ARTERIOSCLEROSIS

lever suddenly became smaller. While checking up the
graphic with the auscultatory method using Erlanger's in-
strument, it was noticed that the disappearance of all sound
did not correspond with the sudden diminution of the os-
cillation of the lever connected with the brachial artery. A
series of records were carefully made on patients. It was
seen that during the period of the third tone phase the os-

Fig. 31. Fast drum. Sudden decrease in size of pulse wave at 4, marking the change
from clear sharp tone to dull tone.

Fig. 32. Slow drum. Sudden decrease in amplitude at 4.

dilations of the lever on the drum reached a maximum
(Fig. 31) and remained at approximately the same height
for some millimeters while the pressure was gradually fall-
ing. At a point at which the third tone, clear and distinct,
became dull, there was an appreciable decrease in the height
of the pulse wave. From this point to the disappearance
of all sound there was a gradual diminution of the size of
the pulse waves.

PHYSIOLOGY OF THE CIRCULATION 97

For normal pressures the difference between the fourth
(dull) tone and the fifth (disappearance of all tone) phase,
amounted to 4 to 10 mm. Occasionally the difference was
so little, the change from sharp third tone through fourth
dull tone to disappearance of all sound was so abrupt, that
one could take the disappearance of all sound as the dias-
tolic pressure, with an error of not more than 2 to 4 mm.
This is within the limits of normal error and practically
may be used by those who have difficulty in noting the
change from third to fourth phase. For high pressures,
however, the difference between fourth and fifth phases was
never less than 8 mm., and was found as much as 16 mm.
The diastolic, therefore, should always be taken at the
fourth phase if possible.

It was found that with the dial instrument the greatest
fling of the lever corresponded to the third phase and the
sudden lessened amplitude of the 'oscillation was at the
fourth phase and was coincident with the change of tone
from sharp to dull. Thus the diastolic pressure may be
read off on the dial scale by watching the fling of the hand
and with some practice one might acquire considerable ac-
curacy. It is better, simpler, and, for most observers, more
accurate to use the stethoscope and hear the change of
sound.

The Relative Importance of the Systolic and Diastolic

Pressures

The systolic pressure represents the maximum force of
the heart. It is measured by noting the first sound audible
over the brachial artery using the auscultatory method.
It is the summation of two factors largely; the force ex-
pended in opening the aortic valves (potential) and the
force expended from that point to the end of systole, the
force which is actually driving the blood to the periphery
(kinetic). To start the blood in motion, the heart must
overcome a dead weight equal to the sum of all the forces

98 ARTERIOSCLEROSIS

holding the aortic valves closed. This sum of factors,
called the peripheral resistance, must be reached and passed
by the force of the ventricular beat before one drop of
blood is set in motion along the aorta. This factor of re-
sistance assumes a great importance.

The systolic pressure is always fluctuating as it depends
upon so many conditions, and the calls of the body except
during sleep are many and various. In a study of diurnal
variations in arterial blood pressure it has been found that
(1) A rise of maximum pressure averaging 8 mm. of Hg.
occurs immediately on the ingestion of food. A gradual
fall then takes place until the beginning of the next meal.
There is also a slight general rise of the maximum pressure
during the day. (2) The range of maximum pressure
varies considerably in different individuals, but the highest
and lowest maximum pressures are practically equidistant
from the average pressure of any one individual.*

The pressure is lowest during sleep and gradually rises
near the end of sleep, so that on awakening the pressure
was the same as before sleep.

Physiologically there are many conditions which modify
the systolic pressure. Sleep, position, meals, exercise, emo-
tional states cause often wide fluctuations which may be
very sudden. It should be constantly borne in mind, that
the systolic pressure reading which is made, is the maxi-
mum effort of the heart at that moment only.

The diastolic pressure measures the peripheral resistance.
It measures the work of the heart, the potential energy, up
to the moment of the opening of the aortic valves. It is
the actual pressure in the aorta. The diastolic pressure is
not very variable; it is not subject to the same influences
which disturb the systolic pressure. It fluctuates as a rule,
within a small range. It is not affected by diet, by mental
excitement, by subconscious psychic influences, to anything
like the extent to which the systolic pressure is affected by

Weyse, A. W., and Lutz. B. R.: Diurnal Variations in Arterial Blood Pressure,
Am. Jour. Physio!., 1915, xxxvii, 330.

PHYSIOLOGY OF THE CIRCULATION 99

the action of these factors. The diastolic pressure is de-
termined by the tone in the a'rterioles and is under the con-
trol of the vasomotor sympathetic system. Any agent
which causes chronic irritation of the whole vasomotor sys-
tem produces increase in the peripheral resistance with con-
sequent rise in the diastolic pressure. Any agent which
acts to produce thickening of the walls of the arterioles,
narrowing their lumina, produces the same effect.

Such states naturally result in increased work on the
part of the heart, which as a result, hypertrophies in the
left ventricle. The increase in size and strength is a com-
pensatory process in order to keep the tissues supplied
with their requisite quota of blood. Conversely, paralysis
of the vasomotor system produces fall of diastolic pressure
which, if long continued, results in death.

The diastolic pressure then is of importance for the fol-
lowing reasons:

1. It measures peripheral resistance.

2. It is the measure of the tonus of the vasomotor system.

3. It is one of the points to determine pulse pressure.

4. Pulse pressure measures the actual driving force, the
kinetic energy of the heart.

5. It enables us to judge of the volume output, for pulse
pressure which is only determined by measuring both sys-
tolic and diastolic pressure, is such an index.

6. It is more stable than the systolic pressure, subject to
fewer more or less unknown influences.

7. It is increased by exercise.

8. It is increased by conditions which increase periph-
eral resistance.

9. The gradual increase of diastolic pressure means
harder wbrk for the heart to supply the parts of the body
with blood.

10. Increased diastolic pressure is always accompanied
by increased pulse pressure, and increased size of the left
ventricle, temporarily (exercise) or permanently.

100 ARTERIOSCLEROSIS

11. Decreased diastolic pressure goes hand in hand with
vasomotor relaxation, as in fevers-, etc.

12. Low diastolic pressure is frequently pathognomonic
of aortic insufficiency.

13. When the systolic and diastolic pressures approach,
heart failure is imminent either when pressure picture is
high or low.

When all these factors are taken into consideration, it
becomes apparent that the diastolic pressure is most im-
portant, if not the most important part of the pressure
picture.

Up to within a very brief time all the statistical evidence
of blood pressure was based on systolic readings alone.
This data is most valuable and much has been learned as
to diagnosis and prognosis, but it is a mass of data based
on a one-sided picture and can not be as valuable as the
statistics which will undoubtedly be published later when
all the pressure picture figures can be analyzed.

Pulse Pressure

The pulse pressure is the actual head of pressure which
is forcing the blood to the periphery. At every systole a
certain amount of blood 75-90 c.c. (Howell) is thrown vio-
lently into an already comfortably filled aorta. The sud-
den ejection of this blood instigates a wave which rapidly
passes down the arteries as the pulse wave. The elastic
recoil of the aorta and large arteries near the heart con-
tract upon the blood and keep it moving during diastole.
Normally the blood-vessels are highly elastic tubes with
an almost perfect coefficient of elasticity. The pulse pres-
sure varies under normal conditions from 30 to 50 mm. Hg.
There is a very definite relationship between the velocity
of blood and the pulse pressure which is expressed thus;
velocity = pulse rate x pulse pressure.*

*Erlanger and Hooker: An Experimental Study of Blood Pressure and of Pulse
Pressure in Man, Johns Hopkins Hosp. Rep., 1904, xii, 145.

PHYSIOLOGY OF THE CIRCULATION 101

Further it has been demonstrated that under normal con-
ditions and during various procedures the pulse pressure
is a reliable index of the systolic output.*

Increased pulse pressure therefore goes hand in hand
with greater systolic output. Physiologically this is most
ideally seen during exercise. Following exercise the pulse
rate increases, the systolic pressure rises greatly, the dias-
tolic slightly or not at all. The pulse pressure therefore is
increased. The velocity also is much increased. The call
comes for more blood and the heart responds. In the chronic
high pulse pressures there are four correlated conditions
which, so far as I have studied them, are always present.
These are: (1) An increase in size of the cavity of the left
ventricle. The ventricle actually by measurement contains
more blood than normal, and therefore throws out more
blood at every systole. The volume output is greater per
unit of time. (2) There is actual permanent increase in
diameter of the arch of the aorta. This is a compensating
process to accommodate the increased charge from the left
ventricle. (3) There are on careful auscultation over the
manubrium, particularly the lower half, breath sounds
which vary from bronchial to intensely tubular, depending
upon the anatomic placing of the aorta, the shape of the
chest, and the degree of dilatation. Often there is very
slight impairment of the percussion note as well. (4)
There is increase in size of all the large distributing ar-
teries, carotids, brachials, femorals, renals, celiac axis, etc.,
with fibrous changes in the media, loss of some elasticity,
and increase in size of the pulse wave. Increased pulse
pressure means increased volume output, but does not al-
ways mean increased velocity. The proper distribution of
blood to the various organs of the body is regulated by the
vasomotor system acting upon the small arteries which con-
tain considerable unstriated muscle. When fibrous ar-
teriosclerosis is present there is loss of elasticity in the dis-

*Dawson and Gorham: The Pulse Pressure as an Index of Systolic Output, Jour.
Exper. Med., 1908, x, 484.

102 ARTERIOSCLEROSIS

tributing arteries and a greater volume of blood must be
thrown out by the ventricle at every systole in order that
every organ shall have its full quota of blood. A force
which is sufficient to send blood through elastic normal dis-
tributing tubes becomes totally insufficient to send the same
amount of blood through tortuous and more or less inelastic
tubes.

It is evident then that pulse pressure is exceedingly im-
portant. It can only be determined by measuring both the
systolic and diastolic pressure. The pulse rate must also
be known in order to compute the velocity. It is essential
to have the whole pressure picture for all cases if correct
conclusions are to be drawn.

In an irregular heart, especially in the cases due to myo-
cardial disease, it is quite impossible to determine the true
diastolic pressure. One can only approximate it and say
that the pulse pressure is low or high. As a matter of fact
the real systolic pressure can not be determined. For this
figure the place on the scale where most of the beats are
heard may be taken for the average systolic pressure. No
one can seriously maintain that he can measure the dias-
tolic pressure under all circumstances.

By means of the auscultatory method of measuring blood
pressure we are able to determine irregularities of force in
the heart beats more easily than by listening to the heart
sounds. A pulsus alternans is readily made out. The ir-
regular tones heard over the brachial artery in cases of ir-
regular heart action have been called "tonal arrhythmias."

Blood Pressure Variations

A recent study of diurnal variations in blood pressure has
shown that while the maximum pressure rises after the in-
gestion of food and steadily rises slightly throughout the
day, the minimum blood pressure is very uniform through-
out the day, and is little affected by the ingestion and di-
gestion of meals. When it is affected, a rise or a fall may

PHYSIOLOGY OF THE CIRCULATION 103

take place. Throughout the day, it tends to become slightly
lower. The pulse pressure then is greater towards evening.
Weysse and Lutz in a study of this question draw^ the fol-
lowing conclusions:

1. A rise of maximum pressure averaging 8 mm. of Hg
occurs immediately on the ingestion of food. A gradual
fall then takes place until the beginning of the next meal.
There is also a slight general rise of the maximum pressure
during the day.

2. The average maximum blood pressure for healthy
young men in the neighborhood of 20 years of age is 120
mm. of Hg. This pressure obtains commonly one hour
after meals. The higher maximum pressures occur imme-
diately after meals, and the lower, as a rule, immediately
before meals.

3. The range of maximum pressure varies considerably in
different individuals, but the highest and lowest maximum
pressures are practically equidistant from the average pres-
sure of any one individual.

4. The minimum blood pressure is very uniform through-
out the day, and is little affected by the ingestion and diges-
tion of meals. When it is affected a rise or fall may take
place. There is a tendency for a slight general lowering
of the minimum pressure throughout the. day.

5. The average minimum blood pressure for healthy
young men in the neighborhood of 20 years of age is 85 mm.
of Hg. Thus we get an average pulse pressure of 35 mm.
of Hg.

6. Pulse pressure, pulse rate, and the relative velocity
of the blood floAV are increased immediately upon the inges-
tion of meals. They attain the maximum, as a rule, in
half an hour, and then decline slowly until the next meal.
There is a general increase in each throughout the day.

These measurements were made upon persons at rest.
Almost any form of exercise would have made the varia-
tions much greater. No account is taken of the psychic

104

ARTERIOSCLEROSIS

THE AVERAGE DIURNAL BLOOD PRESSURE EECORD OF THE TEN SUBJECTS

TIME

MAXI-
MUM

MINT-
MUM

MEAN

PULSE
PRES-
SURE

PULSE
RATE

PP X PR

NOTES

4:30 p.m
5:00 p.m
6-00 p m

mm. Hg
119.5
117.7
118

mm. Hg

84.1
83.5

mm. Hg

101.8
100.6
101

mm. Hg
35.4
34.2
34

72.0
71.1

74 Q

2549
2432
2547

6:45 p.m
7:00 p.m
7*30 p m

127.2
124.7
122

88.2
87.7
83 4

107.7
106.2

102 7

39.0
37.0

38 6

78.1
76.0
7fi

3046
2812
2934

After dinner

8-00 p m. .

122 4

85 5

103 4

36 9

2527

8:30 p.m
9:00 p.m
9-30 p.m. .

120.0
120.5
118 2

85.0
84.7
844

102.5
102.5
101 6

35.0
35.8
33 8

69.7
65.2
64 4

2439
2334
2177

7:30 a.m
8:00 a.m
8:30 a.m

118.4
116.4
124.2

87.6
86.4

854

103.0
101.4
104.8

30.8
30.0
38 8

70.3
69.8
79 4

2165
2094
3081

Before breakfast
After breakfast

9:00 a.m
10-00 a.m

123.8
118.2

84.4
83 6

104.1
100.9

39.4
34 6

84.1

70 7

3313
2446

11:00 a.m
12-00 m .

116.2
1144

84.8
83 2

100.5

98.8

31.4
31 2

67.7

66 2

2126
2065

Before luncheon

12:30 p.m
1:00 p.m
2:00 p.m
3:00 p.m. .

122.8
122.3
118.4

118.8

83.2
82.0
81.4
82.6

103.0
102.1
99.9
100.7

39.6
40.3
37.0
362

70.9
79.7
77.6
75 1

2808
3212
2871
2719

After luncheon

4:00 p.m
5:00 p m

115.8
117.2

82.0
83.4

98.9
100.3

33.8
33 8

71.9
69 6

2420
2352

6:00 p.m
6 *45 p m

117.4
124.6

84.4
83 1

100.9
103.8

33.0
41.5

72.8
804

2402
3337

Before dinner
After dinner

7:00 p.m
7:30 p.m

125.2
122.0

84.2
84.0

104.7
103.0

41.0
38.0

76.1
73.7

3120
2801

8:00 p.m

119.6

85.0

102.3

34.6

72.3

2502

8:30 p.m. .

119.7

84.0

101.3

34.7

69.0

2394

9:00 p.m

120.0

86.2

103.1

33.8

68.0

2298

Average. .

120.0

85.0

102.5

35.0

72.0

2550

(Taken from Weysse and Lutz.)

variations which for the physician are the most important
to bear in mind. Neglect to take this variation into ac-
count will inevitably lead to false conclusions.

In some experiments to determine the changes upon the
blood pressure induced by hot and cold applications on and
within the abdomen, Hammett, Tice and Larson found that
heat applied to the outside of the abdomen raises the blood
pressure. The application of cold produces no change. Ei-
ther hot or cold saline introduced within the abdomen
causes a fall in blood pressure.

PHYSIOLOGY OF THE CIRCULATION 105

Experimentally, certain drugs such as adrenalin, barium
chloride, nicotine, digitalis, strophanthus and the infundib-
ular portion of the pituitary body known as pituitrin raise
the maximum pressure. In the clinic it is difficult to con-
clude always whether the drug alone is responsible for rise
in maximum pressure. Adrenalin given intravenously will
raise the pressure. So will digitalis and strophanthus. I
have watched the maximum pressure rise within three min-
utes following an intravenous injection of gr. Vioo (0.0006
gm.) strophanthin 20 mm. of Hg. I have seen the subcu-
taneous injection of 10 minims of adrenalin repeated sev-
eral times daily for six months fail to have the least effect
on the blood pressure picture.

Elevation of the foot of the bed about nine inches proved
so efficacious in steadying failing hearts in acute infectious
diseases, particularly typhoid, that a study was made of
the effect upon blood pressure. Many observations were
made, but no instrumental proof of rise in blood pressure
could be adduced.

Exercise always raises blood pressure, the maximum
much more than the minimum. In athletes the minimum
pressure may actually fall, the maximum rise so that a
greater volume output results from the greater pulse pres-
sure.

Shock and hemorrhage lower it. Hemorrhage lowers
also the pulse pressure, and it may be possible to prognos-
ticate internal hemorrhage by frequent estimations of the
systolic and diastolic pressures (Wiggers). Compression
of the superior inesenteric artery or the celiac axis in dogs
raises the blood pressure measured in the carotid artery
for a period of at least an hour. This seems to be depend-
ent on purely mechanical causes, and is not a reflex vaso-
motor phenomenon. (Longcope and McClintock.)

Experimentally blood pressure can be increased by di-
rect compression of the brain as Gushing has shown. It was
thought at one time that in man the same effect would re-

106 ARTERIOSCLEROSIS

suit from tumor of the brain or especially from subdural
or extradural hemorrhage following head injuries. This,
however, is not the case. No information of great value
can be obtained by the measurement of blood pressure in
these states. We do know that too high and too prolonged
compression of the medulla brings about exhaustion of the
cardiac center accompanied with rapid pulse, low pressure
and eventual death.

Hypertension

All the conflict during the past few years over the sub-
ject of blood pressure has revolved around this much over-
worked word. Hypertension means high pressure, and yet
it carries with it a suggestion of high pressure which is
harmful to the individual. As a matter of fact hyperten-
sion is a compensatory process, it is often a saving process
in spite of the fact that it carries possibilities of harm in
its possessor. It has been made a fetish, a god to fall down
before and worship and it has been the means of holding a
torch of fear over a patient which has not been lost on the
charlatans. Popularization of blood pressure has brought
its crop of evils, no one of which has been as fruitful in
dollars to unprincipled quacks as hypertension.

Hypertension is the expression on the part of the circu-
lation to meet new conditions in the tissues so that all tis-
sues will be nourished and all will be enabled to function.
Looked at from that point of view it is a conservative proc-
ess and in many cases it is. It is not an average normal
state, but it is normal state for the man who has it in
chronic form. Hypertension should be viewed rationally
and its proper place in the whole make-up of the patient de-
termined. Hypertension is a relative term. What might
be high pressure in a man of sedentary habits who reaches
the age of fifty, might not be high pressure in a full blooded
formerly athletic man of the same age. Temporary hyper-
tension due to excitement, exercise, etc., must be kept in

PHYSIOLOGY OF THE CIRCULATION 107

mind. It is not intended to convey the impression that
hypertension is of no moment. It is a matter for investi-
gation, but not a matter to worship as the all-in-all.

Hypertension is, after all, a physiologic response on the
part of the organism in order to maintain the circulation in
equilibrium in the face of conditions which tend to produce
vasoconstriction in large areas and, therefore tend to de-
prive these areas of blood. That there must be some sub-
stance in the blood stream which causes this constriction
seems certain. What it is, is not at present known. Ee-
cently, Voegtlin and Macht* have isolated a crystalline sub-
stance from the blood of man and other mammals which
they regard as a lipoid and closely related to cholesterin.
This substance was recovered by them from the cortex of
the adrenal gland. This becomes of added interest in the
light of observations made by Gubar (quoted by Voegtlin
and Macht). He noted "that the vasoconstricting proper-
ties of blood serum vary in different pathologic conditions,
being increased in nephritis, 'for instance, and diminished
in others/' In some experiments made in the summer of
1913, we found there was no marked difference in the ana-
phylactic shock produced in half-grown rabbits by the in-
jection of normal and uremic blood serum. As lipoids do
not cause anaphylaxis, there should be no difference in the
reaction of normal and uremic sera unless in one there was
some form of protein not in the other. This does not seem
to be the case. The presence of something in the circula-
tion, therefore, produces constriction of vessels. This calls
for more force in contraction on the part of the heart. This
substance may be of lipoid nature. The continued presence
of this hypothetical substance naturally would lead to hy-
pertrophy of the heart.

What makes hypertension of significance is not the hy-
pertension itsel-f, but the fact that it is the expression of

*Isolation of a New Vasoconstrictor Substance from the Blood and the Adrenal Cor-
tex, Jour. Am. Med. Assn., 1913, Ixi, 2136.

108 ARTERIOSCLEROSIS

processes going on in the body which demand exhaustive
investigation. To attach a blood pressure cuff to the arm,
find the pressure, and diagnose hypertension is like putting
a thermometer under the tongue, noting a rise in the mer-
cury, and diagnosing fever. What causes the hyperten-
sion! Can the causes be removed? Those are the really
vital questions after the symptom hypertension has been
discovered.

All states of hypertension are accompanied by more or
less increase of pulse pressure. In other words the systolic
pressure is always increased to greater degree than the di-
astolic pressure. In studies carried out in the wards and
Pathological Laboratory of the Milwaukee County Hospi-
tal, Milwaukee, we found that in all of the cases of chronic
high blood pressure with resulting high pulse pressure four
correlated factors were found. If any one of these factors
is present, the other three are found.

1. In all high pulse pressure cases there is increase in the
size of the cavity of the left ventricle. The ventricle actu-
ally contains more blood when it is full, and throws out,
therefore, more blood at each systole. The actual volume
output is greater per unit of time. Such hearts always
show increase in thickness of the ventricular wall. I quite
agree with Stone,* who says, "It is merely to be empha-
sized that when the pulse pressure persistently equals the
diastolic pressure (high pressure pulse, in other words)
with a resulting 50 per cent, overload, which means the ex-
penditure of double the normal amount of kinetic energy on
the part of the heart muscle, cardiac hypertrophy has oc-
curred." They are found in aortic insufficiency, in chronic
nephritis, in the diffuse fibrous type of arteriosclerosis, and
in some cases of exophthalmic goiter. Such a condition
occurs temporarily after exercise.

*Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of Hyperarterial
Tension in Vascular Diseases, Arch. Int. Med., November, 1915, p. 775.

PHYSIOLOGY OF THE CIRCULATION 109

2. In all high pulse pressure cases there is actual per-
manent increase in diameter of the arch of the aorta. This
is a compensating process to accommodate the increased
charge from the left ventricle. Smith and Kilgore* have
shown this to be true in cases of chronic nephritis with hy-
pertension. Their research confirms my own observations.
They found dilatation of the arch in (1) syphilis (that is,
aortitis) ; (2) age over 50 (that is, probable factor of ar-
teriosclerosis); (3) other serious cardiac enlargement, and
(4) hypertension (with more or less hypertrophy, as in
chronic nephritis).

In ten cases showing arches at the upper limit of normal
(that is, 6 cm. in diameter) and hypertrophy of the heart,
three were chronic mitral endocarditis; one was chronic
aortic endocarditis; three were chronic mitral and aortic
endocarditis, and there was one each of hyperthyroidism,
pericarditis 'and adherent pericardium.

In fourteen cases of hypertension (highest systolic 270
mm., average systolic, 215 mm.), all showed cardiac hy-
pertrophy. "All but three of these cases had great ves-
sels whose transverse diameters measured over the normal
limit of 6 cm., and in one of those measuring 6 cm. the
Roentgen-ray diagnosis was ' slight dilatation 7 of the
arch. ' ' Smith and Kilgore are at a loss to explain the three
exceptions. They did not give diastolic pressures, so pulse
pressures are not known. Possibly the three exceptions
were cases of high diastolic pressure in which the pulse
pressure possible was not over 60 mm. Such cases might
show "slight dilatation of the arch," but not marked dila-
tation, such as was found in the other, evidently high pulse
pressure cases.

We have found that only the high pulse pressure cases
show dilatation of the arch. Certain high tension cases
which have had a very high diastolic pressure do not re-
veal any accurately measurable . dilatation of the aortic

*Smith, W. H., and Kilgore, A. R. : Dilatation of the Arch of the Aorta in Chronic
Nephritis with Hypertension, Am. Jour. Med. Sc., 1915, cxlix, 503.

110 ARTERIOSCLEROSIS

arch. An empty aorta after death is quite different from a
functionating aorta during* life. Hence the dilatation
which is found postmortem must have been considerable
during life. And conversely, a dilatation which was pres-
ent during life might not be looked on as such after death.

3. In all high pulse pressure cases one will find on care-
ful auscultation over the manubrium, particularly its lower
half, breath sounds which vary from bronchial to intensely
tubular. At times the percussion note will be slightly im-
paired, as McCrae* has shown in dilatation of the arch of
the aorta. This auscultatory sign is evidence of some more
or less solid body in the anterior mediastinum which is
lying on the trachea and permits the normal tubular breath-
ing in the trachea to be audible over the upper part of the
sternum. It is found in cases of dilated aortic arch. Flu-
oroscopic examination has confirmed the findings on auscul-
tation.

4. In all high pulse pressure cases, in which the pulse
pressure is over 70 mm. of mercury, there is increase in
the size of all large distributing arteries, carotids, brachials,
femorals, renals, celiac axis, etc., with fibrous changes in
the media, loss of some of the elasticity, and in the palpable
superficial arteries, increase in size of the pulse wave.

Increased pulse pressure means increased volume output,
but does not always mean increased velocity. The proper
distribution of blood to the various organs of the body is
regulated by the vasomotor system acting on the small ar-
teries which contain considerable unstriated muscle. In
order that there may be enough blood at all times and under
varying conditions of rest and function, there must be a
proper supply coming through the distributing vessels, the
large arteries, those containing much elastic tissue, and
only a very small amount of unstriated muscle tissue or
none whatever. Fibrous sclerosis of these vessels causes
them to become enlarged and tortuous and to lose much

*McCrae, Thomas: Dilatation of the Arch of the Aorta, Am. Jour. Med. Sc., 1910
cxl, 469.

PHYSIOLOGY OF THE CIRCULATION 111

of their elasticity, which is essential for the even distribu-
tion of blood. A greater blood volume is therefore neces-
sary in order that the organs may receive their quota of
blood. A force which is sufficient to send blood through
elastic normal distributing tubes becomes totally insufficient
to send the same amount of blood through tortuous and
more or less inelastic tubes. As a compensatory process
the pulse pressure increases. For this to increase, the left
ventricular cavity dilates, the arch dilates, and as a greater
force must be exerted to keep the increased mass in motion,
the heart responds by hypertrophy of its left ventricle and
becomes itself the subject of fibrous changes in the myo-
cardium. The mass movement of blood is therefore greater
in high pulse pressure cases than in cases of normal pulse
pressure.

In cases of chronic interstitial nephritis contracted
granular kidney it may w T ell be that the sclerosis of the
arteries is a secondary process caused, as Adami thinks,
by the hypertension itself. In aortic insufficiency the situ-
ation is somewhat different. The high pulse pressure is due
to a very low diastolic pressure, for in my experience with
uncomplicated aortic insufficiency the systolic pressure is,
as a rule, not much increased above the normal for the in-
dividual's age. Here peripheral resistance is so low that
a capillary pulse is common. The volume output per unit
of time is greatly increased, the arch of the aorta is dilated,
and the pulse is large. The fact that a large part of the
blood regurgitates during diastole back into the ventricle,
and the fact that the diastolic pressure is low means that
there is no increased resistance to overcome, and the sys-
tolic pressure is not raised.

Stone* has divided the cases of hypertension into the cere-
bral and cardiac types. He finds that there is a difference
in prognosis and in the mode of death in the two groups.
He has further attempted to judge of the work placed upon

*Stone, W. J.: Arch. Int. Med., 1915, xvl, 775.

112 ARTERIOSCLEROSIS

the heart by calculating what he calls the heart load or pres-
sure-ratio. For example, he takes a normal pressure at
120-80-4Q. The relation between 80 and 40 is y 2 or 50 per
cent. That he considers normal. When the heart load in-
creases so that the pulse pressure equals or exceeds the
diastolic pressure, the heart load is 100 per cent or more,
he considers the danger of myocardial exhaustion graver
than when the heart load is normal or less than 50 per cent.

It is his opinion, in which I heartily concur, "that an
individual with a systolic pressure of 200 and a diastolic
pressure of 140, is in greater danger of cerebral death than
an individual with a systolic pressure of 200 and a diastolic
pressure of 100." He is "likewise certain that the indi-
vidual with a systolic pressure of 200 and a diastolic of
90 to 100 is in greater danger of a cardiac death. It is
apparently the constant high diastolic pressure rather than
the intermittently high systolic pressure which predisposes
to cerebral accident."

I have not been able to confirm all of Stone 's conclusions.
His contention holds good for some cases, but not, in my
experience, for the great majority of the hypertension cases.
I feel that in the classification of the chronic high pressure
case we can go one step farther and split his first group
into two usually differentiate groups. Syphilis is not an
etiological factor in any of these groups. It is not consid-
ered that these groups are absolutely distinct and can al-
ways be rigidly separated. There are variations and com-
binations which render an exact separation impossible.
But bearing this in mind the following classification is pro-
posed as a working classification.

Group A. Chronic nephritis.

Group B. Essential hypertension.

Group C. Arteriosclerotic hypertension.

Group A. Chronic Nephritis. These are the cases with
a high-pressure picture, that is to say, high systolic (200+)
and high diastolic (120-140 +). The pulse pressure is much

PHYSIOLOGY OF THE CIRCULATION 113

increased. The palpable arteries are hard and fibrous.
There is puffiness of the under eyelids, which is more pro-
nounced in the morning on arising. Polyuria with low
specific gravity and nycturia are present. There are almost
constant traces of albumin in the urine, with hyaline and
finely granular casts.

Functionally these kidneys are much under normal. The
functional capacity determined by Mosenthal's modification
of the Schlayer-Hedinger method shows a marked inability
to concentrate salts and nitrogen. The phthalein output
is below normal. As the case advances the phthalein output
becomes less and less, until a period is reached when there
are only traces or complete suppression at the end of a two-
hour period. Such patients may live for ten weeks (one of
our cases) or longer, all the time showing mild uremic
symptoms, and suddenly pass into coma and die.

The natural end of patients in this group is either uremia
or cardiac decompensation (so-called cardiorenal disease).
Cerebral accidents may happen to a small number. It is
only to this group, in my opinion, that the term cardiorenal
disease should be applied. Formerly I believed that all high
systolic pressure cases were cases of chronic nephritis of
some definite degree. From the purely pathologic stand-
point that is true, but from the important, functional stand-
point it is far from being the true state of the cases.

In this group there is marked hypertrophy and moderate
dilatation of the left ventricle with dilatation and nodular
sclerosis of the aorta. The kidneys are firm, red, small,
coarsely granular, the cortex much reduced, the capsule
adherent. Cysts are common. It is the familiar primary
contracted kidney. Mallory calls this capsular-glomerulo-
nephritis. The etiology is obscure. Often no cause can be
found. Again, there is a history of some kidney involve-
ment following one of the acute infectious diseases, or it
may follow the nephritis of pregnancy. Usually, however,

114 A&TERlOSCLEtiOSlS

these cases fall into the group of secondary contracted kid-
neys, chronic parenchymatons nephritis.

Illustrative Case. E. Z., a woman, aged thirty-six years, was seen July 26,
1916, in coma. There was a history of typhoid fever at nineteen years, but no
other disease. She had had nine full-term pregnancies, the last one thirteen
months previously. For a week before the onset of the present illness she had
complained of severe headaches and dizziness. There were no heart symptoms.
For the past year she has had nycturia. Physical examination revealed tubular
breathing beneath the manubrium, a few rales in the chest, an enlarged heart
(left side), with a systolic murmur over the aortic area. Blood pressure was
178-125-53, the pulse rate 96, leucocytes 27,250. Venesection of 500 c.c. of
blood and intravenous injections of 500 c.c. of 5 per cent NaHCO 3 in normal
saline were employed. Lumbar puncture withdrew 60 c.c. of clear fluid under
pressure with 6 cells per cubic millimeter. The eye grounds showed distinct
haziness of the disks and dilatation of the veins. Blood pressure after vene-
section was 164-122-42, pulse 76, but in a few days rose to 222-142-80, pulse 70.
A second venesection of 400 c.c. and proctoclysis of 1000 c.c. saline solution
was tried. The blood-pressure now was 198-140-58. The pH of the blood was
7.6, the alkaline reserve was 35 volume per cent (van Slyke), and the CO 2
tension of the alveolar air (Marriott) was 25 mm. The phthaleiii on the day
following the second venesection was 45 per cent in two hours. The urine
at first showed 500 c.c. in twenty-four hours, specific gravity 1016, albumin
and casts. Later she passed 1300 to 1600 c.c. with specific gravity around
1010. The blood-pressure fluctuated considerably, reaching as low as 138-98-
40, pulse 88. She was discharged improved September 10, 1916. She had
constant headache but managed to keep up. In June, 1917, she suddenly
died in an uremic coma.

Group B. This one might designate as the hereditary
type, although there is not always a history in the ante-
cedent. This group includes the robust, florid, exuberantly
healthy people. They often are heard to boast that they
have never had a doctor in their lives. They are usually
thick-set or very large, fleshy people. The pressure pic-
ture is exceedingly high. The pulse pressure is moderately
increased. The arteries are rather large, fibrous, and often
quite tortuous, although this is not always the case. Some
persons have hard, small, fibrous arteries. There is no
puffiness beneath the eyes, no polyuria, and no nycturia as
a rule. The urine is of normal amount, color, and specific
gravity. Albumin is only rarely found and then in traces,
but careful search of a centrifuged specimen invariably re-

PHYSIOLOGY OF THE CIRCULATION 115

veals a few hyaline casts. The phthalein excretion is nor-
mal or only slightly reduced. The kidneys excrete salt and
nitrogen normally. It is in this group that apoplexy is
found most frequently. The rupture of the vessel occurs
when the victim is in perfect health, often without any
warning. Occasionally when such a case recovers suffi-
ciently to be around, cardiac decompensation sets in later
and he dies then of the cardiac complications.

Pathologically the hearts of such persons are found to
have the most enormous hypertrophy of the wall of the left
ventricle. The cavity is somewhat enlarged, as is always
the case when the pulse-pressure is increased, but the size
of the cavity is not the striking feature. The aorta is
fibrous, thick walled, and the arch is slightly dilated. There
are patches of arteriosclerosis. One such case seen only
at autopsy had a rupture of the aorta just above the sinus
of Valsalva and died of hemopericardium. The kidneys
are of normal size, dark red, firm, the capsule strips readily,
the surface is smooth or finely granular, the cortex is not
decreased. The pyramids are congested and red streaks ex-
tend into the cortex. Microscopically the capsules of the
glomeruli are a trifle thickened; a few show hyaline
changes. There is rather diffuse, mild, round-cell infiltra-
tion between the tubules. The tubular epithelium shows lit-
tle or no demonstrable changes. The arterioles are gener-
ally the seat of a moderate thickening of the intima and me-
dia, but it is not usual to find obliterating endarteritis.
There is evidently a diffuse fibrous change which has not
affected either the tubules or glomeruli to any great extent.

Illustrative Case. L. C., a man, aged fifty-six years, stonemason by trade,
is a stocky, thick-necked individual. He had never been ill in his life until
a year ago, when he fell from his chair unconscious. He had a right-sided
hemiplegia which has cleared up so completely that except for a very slight
drag to his foot he walks perfectly well. He came in complaining of short-
ness of breath and cough. There was no swelling of the feet. Here evi-
dently was left-heart decompensation. Examination showed the blood pressure
to be 240-130-110, pulse irregular, 104 to the minute. There were cyanosis
and rales throughout both chests. The urine was normal in color, specific

116 ARTERIOSCLEROSIS

gravity 1025, small amount of albumin, few casts, hyaline and granular.
The phthalein elimination was 65 per cent in two hours. Under rest, purga-
tives, and digitalis he was much improved. He has since had two other
apoplectic strokes, the last of which was fatal.

When these patients are seen with acute cardiac decom-
pensation, there are, of course, much albumin and many
casts in the urine, and the phthalein output is, for the time
being, decreased.

Group C. This might be called the arteriosclerotic high-
tension group (Stone's cardiac group). The cases are usu-
ally over fifty years old. They are men and women who
have lived high and thought hard. Often they have had
periods of great mental strain. Many men in this group
were athletes in their young manhood. Many have been
fairly heavy drinkers, although never drinking to excess.
They are usually well nourished and inclined to stoutness.
The pressure picture is high systolic with normal or only
slightly increased diastolic and large pulse pressure. The
arteries are large, full, fibrous, usually tortuous. The heart
is very large, the apex far down and out. There is no poly-
uria ; nycturia is uncommon, quite the exception. The urine
is normal in color, amount, and specific gravity. Albumin
is only rarely found and hyaline casts are not invariably
present. The phthalein excretion is quite normal and the
excretions of salt and nitrogen are also normal. The ter-
minal condition in most of the patients in this group is car-
diac decompensation. They may have several attacks from
which they recover, but after every attack the succeeding
one is produced by less exertion than the preceding one, and
it becomes more and more difficult to control attacks.
Eventually the patients become bed- or chair-ridden, and
finally die of acute dilatation of the heart.

Occasionally patients in this group may have a cerebral
attack, but in my experience this is uncommon. Pathologi-
cally the heart is large, at times true cor bovinum, dilated
and hypertrophied. The cavity of the left ventricle is much
dilated. The aorta is dilated and sclerosed.

PHYSIOLOGY OF THE CIRCULATION 117

The kidneys are increased in size, are firm, dark red
in color, with fatty streaks in the cortex. The capsule strips
readily and the cortex is normal in thickness or only
slightly increased. The organ offers some resistance to the
knife. The microscope shows small areas scattered
throughout where the glomeruli are hyalinized, the stroma
full of small round cells, the tubules dilated, and the cells
are almost bare of protoplasm. Naturally the tubules are
full of granular cast material. Also the arterioles show
extensive intimal thickening, fibrous in character, with oc-
casional obliterating endarteritis. One gets the impression
that the small sclerotic lesions are the result of anemia and
gradual replacement of scattered glomeruli by fibrous tis-
sue. For the most part the kidney, except for the chronic
passive congestion, appears quite normal. One can readily
understand that in such a kidney function could not have
been much interfered with.

Illustrative Case. C. K., an active, stout, business man, aged fifty-six
years, consulted me on account of shortness of breath and swelling of the feet
in May, 1915. He had just returned from a hospital in another city, where
he had gone with what was apparently cardiac decompensation. In his early
manhood he had been a gymnast and a prize winner. He has worked hard,
often given way to violent paroxysms of temper, has eaten heavily but drunk
very moderately. The heart was greatly enlarged, the arch of the aorta
dilated, a mitral murmur was audible at the apex. The radials and temporals
were large, tortuous, and fibrous. The blood pressure picture ranged around
180-90-90. He was easily made dyspneic and had a tendency to swelling of
the lower legs. The urine was acid, of normal specific gravity, normal in
amount, normal phthalein, normal concentration of salt and nitrogen, con-
tained albumin only when he was suffering from decompensation of the heart.
Casts were always found. He finally died, after sixteen months, with all
the symptoms of chronic myocardial insufficiency. The heart was enormous,
a true cor bovinum. The kidneys were typical of this condition, possibly
somewhat larger than usual.

Hypotension

When the pressure is -constantly below the normal, it is
called hypotension. This may be transient as in fainting
it may be a normal state of the individual, it occurs in

118 ARTERIOSCLEROSIS

most fevers and in a great variety of diseases, including
anemias.

In arteriosclerosis, especially the diffuse (senile) type,
the blood pressure is invariably low, and may be spoken of
as hypotension. The heart in such a case is small, the
muscle is flabby, there is brown atrophy of the fibers, and
some replacement of the muscle cells by connective tissue.
The same causes which have produced general arterioscle-
rosis have also produced sclerosis of the coronary arteries,
and probably the lessened blood supply accounts for much
of the atrophy of the heart muscle.

In typhoid fever the maximum blood pressure during
beginning convalescence may be as low as 65 mm. Hg. I
have frequently seen hypotension of 80 mm. This is com-
mon.

Meningitis is the only acute infectious disease in which
the blood pressure is more often high than low. This is
accounted for by the increased intracranial tension.

Following large hemorrhages the blood pressure is re-
duced. In venesection the withdrawal of blood may not
affect the blood pressure. The procedure is done to relieve
overdistension of the heart.

In pleurisy with effusion and in pericarditis with effusion
there is hypotension.

Collapse, whether from poisoning by drugs or as the re-
sult of dysentery, cholera, or profuse vomiting from what-
ever cause, reduces the blood pressure.

In cachectic states, such as cancer, the blood pressure is
low. General wasting of the whole musculature includes
that of the heart and the heart muscle shows the condition
known as " brown atrophy."

A most interesting and important condition in which
hypotension occurs is pulmonary tuberculosis. Haven
Emerson has recently gone over the whole subject in a care-
ful piece of work and his summary is as follows:

"Hypotension or subnormal blood pressure is univer-

PHYSIOLOGY OF THE CIRCULATION 119

sally found in advanced pulmonary tuberculosis, in which
condition emaciation may play a part in its causation.
Hypotension is found in almost all cases of moderately ad-
vanced tuberculosis, or in early cases in which the toxemia
is marked except when arteriosclerosis, the so-called ar-
thritic or gouty diathesis, chronic nephritis, or diabetes
complicate the tuberculosis and bring about a normal pres-
sure or a hypertension. Occasionally the period just pre-
ceding a hemoptysis or during a hemoptysis may show hy-
pertension in a patient whose usual condition is that of
hypotension.

i 'Hypotension has been found by so many observers in
early, doubtful or suspected cases with or before physical
signs of the disease in the lungs, and is considered by com-
petent clinicians so useful a differential sign between vari-
ous conditions and tuberculosis, that it should be sought for
as carefully as it is the custom at present to search for
pulmonary signs.

"Hypotension when found persistently in individuals or
families or classes living under certain unhygienic condi-
tions should put us on our guard against at least a pre-
disposition to tuberculosis. Most unhygienic conditions,
overwork, undernourishment and insufficient air, are of
themselves causes of a diminished resistance, and it seems
likely that a failure of normal cardiovascular response to
exercise or change of position may be found to indicate this
stage of susceptibility, especially to tuberculous infection.

" . . . Hypotension, when it is present in tuberculosis, in-
creases with an extension of the process. Recovery from
hypotension accompanies arrest or improvement. Return
to normal pressure is commonly found in those who are
cured. Continuation of hypotension seems never to accom-
pany improvement. Prognosis can as safely be based on
the alteration in the blood pressure as on changes in the
pulse or temperature. . . ."

There are a few drugs which lower the blood pressure,

120

AKTERIOSCLEROSIS

but, as a rule, their effects are more or less transitory. We
know of no drug, unless it be iodide of potassium, which has
the property of causing changes in the blood (decrease in
viscosity!), which tends to reduce the blood pressure when
it is excessive. This drug fails us many times.

SOME DKUGS WHICH INFLUENCE THE BLOOD PKESSUBE

jections of the infundibular portion
of the pituitary body. Not in use
clinically.

Pressure Depressors

Nitroglycerine and amyl nitrite,
action transitory but rapid.

Sodium nitrite and erythrol tetra-
nitrate. Action somewhat more pro-
longed.

Aconite, veratrum viride, chloral,
etc. These depress the heart.

Purgatives, drastic and hydragogue.

Potassium and sodium iodide may
lower blood pressure. When they do,
the action is prolonged.

Diuretin and theocin-sodium-ace-
tate.

Pressure Raisers

Adrenalin, when injected directly
into a vein or deep into the muscles.
The action is transitory.

Caffeine, preferably in the form
of caffeine-sodium-benzoate. A good
drug.

Strychnine, which does not act di-
rectly but seemingly through the
higher centers.

Ergot, somewhat uncertain.

Nicotine, not used therapeutically.

Camphor, used in sterile olive oil
and injected deeply into the muscles.

Digitalis, when the cardiac tone is
low and decompensation is present.
Its action is prolonged but slow. In-

Venous Pressure

Comparatively little work has been done upon the de-
termination of the pressure in the veins in man. It is con-
ceivable that this procedure may, at times, be of great
value. A number of attempts have been made to measure
the venous pressure by compressing the arm veins and not-
ing on a manometer the force necessary to obliterate the
vein. As the pressure is so slight, water is used instead
of mercury, and readings have been given in centimeters
of water.

In the apparatus shown in the figure (Fig. 33), Drs.
Hooker and Eyster succeeded in making estimations of the
venous pressure. The box B is held in position by the tapes
A, so that the vein is visible through the rectangular open-
ing in the thin rubber covering the bottom. The box is con-
nected with the water manometer G, by a rubber tube,
from which a T-tube enters the rubber bulb E. When the
bulb E is compressed between the plates D, by the coarse

PHYSIOLOGY OF THE CIRCULATION

121

thumbscrew C, air is forced into the box B, exerting a pres-
sure on the vein lying exposed beneath. This pressure is
transmitted directly to the manometer G, and may be read
off in centimeters of water on the accompanying scale. The
veins of the back of the hand are used and there must be no

Rg.I

Fig. 33. Apparatus for estimating the venous blood pressure in man, devised by
Drs. Hooker and Eyster. The small figure is the detail of the box B. See explanation
in text.

obstruction between them and the heart. The rubber-cov-
ered box is accurately and lightly fitted over a vein and
pressure made until it is obliterated. By measuring the
distance above or below the heart level that the hand was
when the observation was made, and subtracting or adding

122

ARTERIOSCLEROSIS

these figures to the manometer reading, we obtain the
venous pressure at the heart level.

Eyster has modified this instrument so that it is now
much simpler to operate. He uses a small glass cup with a
flaring edge and a diameter of about 2 cm. This is sealed
to the skin directly over a vein on the back of the hand by
means of collodion. The stem of the cup has a rubber tube
leading to a small hand bulb and to the manometer tube

Fig. 34. New venous pressure instrument. (After Eyster.)

which contains colored water. Slight compression of the
hand bulb obliterates the vein which can be seen through
the glass cup. The pressure in centimeters of water is then
read off. (Fig. 34.) The principle is the same as in the
earlier instrument, but the application is easier.

Practically Hooker and Eyster found that the normal
variation in healthy subjects was from 3 to 10 cm. of water.
The pressure rose in cases of decompensated hearts with

PHYSIOLOGY OF THE CIRCULATION 123

dyspnea and venous stasis, and returned to normal with
improvement in the condition of the patient. It might be
possible with this instrument to foretell an oncoming de-
compensation by the rise in venous pressure.

The venous pressure may also be estimated roughly by
slowly elevating the arm and noting the instant at which
a particular vein collapses. By measuring the height of
the vein above the heart some idea may be obtained of the
pressure within the right auricle.

The Pulse

There is nothing characteristic about the pulse of a
person suffering from arteriosclerosis, except it be the dif-
ference in the pulse of high tension and of low tension.
The pulse of high tension has a gradual rise, a more or less
rounded apex, and the dicrotic wave is slightly marked and
occurs about half-way down on the descending limb. In
arteriosclerosis with low tension the radial artery is usually
so rigid that very little pulse wave can be obtained. The
general form of a low tension pulse is a sharp up-stroke, a
pointed summit, and a secondary wave on the base line,
which corresponds to the dicrotic wave. Such a pulse can
be easily palpated, and is known as a dicrotic pulse. How-
ever, such a pulse can occur only when the artery still re-
tains all or a large part of its elasticity; hence in arterio-
sclerotic low tension we would never see such a pulse as
the typical dicrotic.

The Venous Pulse

It would carry us too far to discuss fully the character
of the venous pulse, but a brief summary of the essential
features of the normal venous pulse is presented. The
venous pulse is a term used to express the tracing obtained
from the internal or external jugular vein at the root of
the neck. Normally a very characteristic curve is produced,
which can be readily analyzed into a series of waves corre-

124

ARTERIOSCLEROSIS

spending to the fluctuations in the cardiac cycle. To under-
stand these waves and their values, the accompanying
figure is helpful. (Fig. 35.)

Bachmann summarizes the normal waves in the venous
pulse tracing as follows:

"The physiological or so-called venous pulse consists of
three positive and three negative waves, bearing a more or

AORTIC AND PULMONARY
VALVES OPEN

Fig. 35. Semidiagrammatic representation of the events in the cardiac cycle: Jug.,
pulse in the jugular vein; Aur., contraction of auricle; V. Pr., intraventricular pres-
sure; Pap. M., contraction of the papillary muscles; Car., carotid pulse. Below are
given the times of occurrence of the heart sounds and of the opening and closing of
the heart valves. (After Hirschfelder.)

less definite relation to the events of the cardiac cycle, and
having their origin in the various movements of the cham-
bers and structures of the right heart. The first positive
wave (a) is presystolic in time, and is due to the contrac-
tion of the auricle, causing a slowing of the venous current
and producing a centrifugal wave through a sudden arrest
of the inflowing blood. The second positive wave (S) is
presystolic in time, and originates in the sudden projection

PHYSIOLOGY OF THE CIRCULATION

125

of the tricuspid valve into the cavity of the auricle during
the quick, incipient rise in the intraventricular pressure
occurring in the protosystolic period. The third positive
wave (v) occurs toward the end of ventricular systole. It
consists of two lesser waves separated by a shallow notch.
The factors entering into its formation are the relaxation

Carotid

Vlfo^^

Tim

Fig. 36. Simultaneous tracings cf the jugular and carotid pulses showing normal waves
in the venous pulse and relation to carotid pulse. (After Bachmann.)

Fig. 37. Jugular and carotid tracing from a normal individual with a well-marked
third heart sound showing a large "h" and a smaller pre-auricular wave "w." ? indi-
cates a small wave in mid-diastole following the "h" wave, occasionally found though
perhaps an artefact. (After Hirschfelder.)

of the papillary muscle at a time when the intraventricular
is still higher than the intraauricular pressure, resulting
in an upward movement of the tricuspid leaflets and a re-
turn of the auriculoveiitricular septum to its position of
rest.

126 ARTERIOSCLEROSIS

"The first negative wave (between positive wave a and
S) is due to the relaxing auricle. The second negative
wave (Af) occurs during the diastole of the auricle. It
is due to the dilatation of its walls, to the displacement of
the auriculoventricular septum toward the apex occurring
at the time of ventricular systole, and to the pull of the
papillary muscles on the tricuspid valve leaflets. The third
negative wave (F/) appears during ventricular diastole and
in the common pause of the heart chambers. Its cause is
found in the passage of the blood from the auricle into the
ventricle. It is somewhat modified possibly by the contin-
ual ascent of the auriculoventricular septum and by a wave
of stasis due to the accumulation of blood coming from the
periphery." (Fig. 3f>.)

Hirschf elder has described another wave .which he calls
the "h" wave, which is due to the floating up of the tricus-
pid valve by the blood in the ventricle before the complete
filling of the ventricle following the auricular systole. (Fig.
37.)

The Electrocardiogram

In the past few years an immense amount of work has
been done by numerous observers on the changes in the
electrical potential of the various portions of the heart
during contraction. The very elaborate and delicate elec-
trocardiograph with the string galvanometer devised by
Einthoven is used. It has been definitely determined that
the impulse to cardiac contraction originates in the sinus
node, a collection of differentiated nerve cells situated at
the junction of the superior vena cava with the right auricle.
From there the impulse travels in certain fibers in the in-
terauricular wall, passes through another node, the auric-
uloventricular or Tawara node, situated in the auricular
wall just above the auriculoventricular ring, thence via
the Y-bundle, or bundle of His to the ventricles. This se-

PHYSIOLOGY OF THE CIRCULATION

127

quence is orderly, regular, and normally invariable. (Fig.
38.)

The sino-auricular (s-a) node is the most irritable por-
tion of the heart, it is endowed with the greatest amount

Right
vagus

Centres of ventricular
contraction

Tawara's node
His' bundle

Centres of ventricular contraction

Fig. 38. Right side of the heart showing diagrammatically the distribution of the
two vagus nerves to different parts of the viscus. The impulse to contraction originates
at the sino-auricular node and passes over the wall of the auricle to Tawara's node, and
thence over His' bundle across the auriculoventricular septum to be distributed through-
out the ventricular wall. If the upper," sino-auricular, node is damaged, or if its im-
pulses fail to get across the wall of the auricle, Tawara's node acts in its place to start
off the ventricle. If a lesion at the base of the mesial segment of the tricuspid valve
damages His' bundle, so that Tawara's node is cut off from the ventricle, then the ven-
tricle may originate its own impulses to contraction. (Hare's Practice of Medicine.)

128

ARTERIOSCLEROSIS

Lead I (right arm left arm).

II"

1 J

IQl-fi

Lead II (right arm left leg).

Lead III (left arm left leg).
Fig. 39. Normal electrocardiogram. (After Hart.)

PHYSIOLOGY OF THE CIRCULATION 129

of rhythmicity as well. It is under the control of the vagus
nerve. Its inherent rate of rhythmicity is probably more
rapid than the usual numbers of impulses per minute, but
it is inhibited by the vagus. Paralysis of -the vagus endings
increases the rate of impulse formation and therefore the
rate of the heart.

The electrocardiogram is a graphic representation on a
photographic film or sensitive bromide paper of the changes
of electrical potential during muscular activity. The lines
are made by the highly magnified string of the galvanom-
eter as it moves across the slit in the photographic appa-
ratus in response to the induction currents set up in the
heart magnified by the special galvanometer.

The record is made in three so-called Leads.

Lead I
The electrodes are attached to right arm and left arm.

Lead II
The electrodes are attached to right arm and left leg.

Lead III
The electrodes are attached to left arm and left leg.

A series of regular figures is normally obtained in which
are depressions and elevations and regular spacing of these
elevations and depressions. The waves so-called have been
arbitrarily designated P, Q, R, S, T. There is some dif-
ference in the three leads. "The wave P is positive in all
leads. P to R interval varies slightly in the three leads.
All the waves of Lead II are greater than those of Leads I
and III. The wave R is positive in all leads. T is usually
positive in all leads, but is occasionally negative in Lead
III. Even in normal individuals there is a considerable
range of variation in the electrocardiogram which is within
the limits of the normal.' 7 (Hart.) (Fig. 39.)

The P wave is admitted to be the wave of auricular con-
traction. Q, R, S, is the ventricular complex caused, it is

130 ARTERIOSCLEROSIS

thought, by the current passing over the ventricles. T
wave is not yet definitely settled. It has been thought by
some that it represented actual ventricular contraction and
its height and shape had some meaning in heart force.
This is denied by others. Hart defines it as "The final ac-
tivity of the ventricle. ' ' The T wave is usually increased
in size during exercise.

The P-R interval is almost the most important feature
of the tracing. It is the actual conduction time in fractions
of a second of the impulse from s-a node to the ventricles.
Normally this is about 0.2 second or slightly less. Much
that was hoped for from the electrocardiograph in the clinic
has not been forthcoming. Its greatest value is in states
of abnormal conductivity, such as various grades of heart
block, extra-systoles, whether originating in auricles or in
either ventricle, abnormalities of rhythm, as flutter and
fibrillation. It has, however, aided materially in the in-
telligent interpretation of many phenomena heretofore not
well understood, and has enormously increased our knowl-
edge of the physiology and pathologic physiology of the
heart.

It is not possible to enter farther into the subject here.
This brief discussion must suffice. The reader is referred
to works on this subject in connection with diseases of the
heart.

CHAPTER IV

IMPORTANT CARDIAC IRREGULARITIES
ASSOCIATED WITH ARTERIOSCLEROSIS

Arteriosclerosis of the aorta, of the coronary arteries,
or of both, is practically always found in cases dying of
various cardiac irregularities other than those the result
of rheumatic cardiac lesions. It is not that arteriosclerosis
causes the cardiac lesions (although the thickening of the
walls of the coronary arteries does interfere mechanically
with the nutrition of the heart muscle), but the arterio-
sclerosis is a part of the tissue reaction in the arteries to
some set of causes affecting the whole body. It is true
when one boils down the question to its last analysis, gen-
eral arteriosclerosis may mechanically so interfere with the
blood supply to tissues that the tissue is thrown out of
function either in the reduction or even loss of function.
So it may be that occasionally the arteriosclerosis in the
arteries supplying the heart is really responsible for the
cardiac irregularity. The past few years have been fruit-
ful ones in increasing our knowledge of the various irregu-
larities of the heart. We can do no more than sketch
briefly some of them in relation to arteriosclerosis.

The chief irregularities are (1) auricular flutter, (2)
auricular fibrillation, (3) ventricular fibrillation, (4) au-
ricular extrasy stole, (5) ventricular extrasystole, (6) heart
block, partial or complete.

Auricular Flutter

Auricular flutter is an abnormal rhythm characterized by
very rapid, but rhythmic auricular contractions usually 250
to 300 per minute. The auricular contractions are so rapid
that the ventricle can not respond, so that an electrocar-

131

132

ARTERIOSCLEROSIS

diagram of a heart in such a state (Fig. 40) shows the
ventricle beating regularly but at a much slower rate than
the auricle.

The majority of cases exhibiting this peculiar rhythm are
over 40 years of age. In many cases sclerosis of the coro-

;

3E:

Lead III (auricular flutter).
Fig. 40. (After Hart.)

nary arteries as a part of general arteriosclerosis has been
found. Auricular flutter can be suspected when the pulse
is regular or not particularly irregular and a fluttering,
rapid pulsation is seen in the jugular vein on the right side.
One can only be sure of the condition by making graphic
records of the heart.

IMPORTANT CARDIAC IRREGULARITIES 133

Attacks usually come on suddenly and may disappear as
suddenly, suggesting paroxysmal tachycardia. The patient
feels a commotion in his chest, dyspnea, precordial distress,
etc. The attack may last for weeks or months, in which
case the patient may carry on his usual work but be con-
scious of palpitation in his chest. One may safely assume
that the flutter is a sign of a failing myocardium and sooner
or later the heart will pass to the graver stage of auricular
fibrillation.

Auricular Fibrillation

In this condition the auricle is widely dilated and over its
surface are countless twitchings of individual muscles giv-
ing to the auricle the appearance of a squirming bunch of
worms. Such a condition may be readily produced in a
dog's exposed heart by direct faradization of the auricle.
It should be seen by every physician in order fully to ap-
preciate the passive, dilated sac part which the auricle
plays when in such a state. There is no auricular wave on
the electrocardiogram (Figs. 41 and 42) only a series of fine
tremulous lines, and the ventricles beat irregularly with
many dropped beats and variations in the size and force of
individual beats. Extrasystoles are also frequent. The heart
is absolutely irregular. Such a condition is readily recog-
nizable as the state of broken compensation. Graphic rec-
ords are not essential as in auricular flutter to establish
the condition. Inspection of the root of the neck for jugular
pulsations and examination of the pulse with the patient's
evident dyspneic, cyanotic, edematous condition settles the
diagnosis.

In no case of auricular fibrillation is the heart muscle
free from extensive fibrous changes. These may be the re-
sult of general arteriosclerotic changes or may result from
toxic changes. It is the general consensus of opinion that
auricular fibrillation may persist for months or even years.
Some hold that the state of perpetual irregular pulse is
associated with auricular fibrillation. If that is true, then

134

ARTERIOSCLEROSIS

Fig. 41. Electrocardiogram showing auricular fibrillation in Leads I (upper) and II
(middle and lower). (Courtesy of Dr. G. C. Robinson.)

Fig. 42. Auricular fibrillation. (After Hart.)

IMPORTANT CARDIAC IRREGULARITIES

135

auricular fibrillation may last for many years. Patients
may go about their work but always live with the imminent
danger of a sudden dilatation of the ventricle and symp-
toms of acute cardiac decompensation.

In these cases the blood pressure is of particular interest.
It is often stated that the blood pressure is lowered as com-
pensation returns and digitalis has exhibited its full action.
As a matter of fact this statement needs some modification.
If one takes the highest pressure at the strongest beat,
which may be only one in a dozen or more, that may be true,
but that does not represent the action of the much em-

Fig. 43. The shaded area represents the pulse deficit; the upper edge is the apex
rate, the lower edge the radial rate. The broken line indicates the "average systolic
blood pressure." (Compare these \ 7 alues with the figures at the bottom of the chart,
which show the systolic blood pressure determined by the usual method.) (After Hart.)

barrassed heart. We know that the circulation is much in-
terfered with, that there is hypostatic congestion, that the
mass action is slow. The pulse pressure is greatly dis-
turbed and the head of pressure which should force the
blood to the periphery is so little that the circulation almost
ceases.

A count of the cardiac contractions heard with the steth-
oscope and a count of the pulse shows a great discrepancy
in number. This has been called, the ' ' pulse deficit ' ' ( Hart ) .
In order to arrive at the true average systolic pressure the
following procedure is done. "The apex and radial are

136 ARTERIOSCLEROSIS

counted for one minute, at the same time by two observers,
(if possible) then a blood pressure cuff is applied to the
arm, and the pressure raised until the radial pulse is com-
pletely obliterated; the pressure is then lowered 10 mm.,
and a second radial count is made; this count is repeated
at intervals of 10 mm. lowered pressure until the cuff -pres-
sure is insufficient to cut off any of the radial waves (be-
tween each estimation the pressure on the arm should be
lowered to zero). From the figures thus obtained the
average systolic blood pressure is calculated by multiplying
the number of radial beats by the pressures under which
they came through, adding together these products and
dividing their sum by the number of apex-beats per minute,
the resulting figure is what we have called the i average
systolic blood pressure.' (Fig. 43.)

For example: "B. S., April 29, 1910, Apex 131; radial, 101; deficit, 30.

BRACHIAL PRESSURE RADIAL COUNT

100 mm. Hg.

90 mm. 13 13x90 = 1170

80 mm. 47 - 13 = 34 x 80 2720

70 mm. 75-47= 28x70 = 1960

60 mm. 82 - 75 7 X 60 = 420

50 mm. 101 - 82 19 X 50 = 950

Apex = 131)7220

Average systolic blood-pressure 55 plus

B. S., May 11, 1910, Apex 79; radial, 72; deficit 7.

BRACHIAL PRESSURE RADIAL COUNT

120 mm. Hg.

110 mm. 44 44x110 = 4840

100 mm. 64-44 = 20x100 = 2000

90mm. 72-64= 8x 90= 720

Apex = 79) 7560"
Average systolic blood-pressure 95 plus ' '

The diastolic pressure in these cases can not be deter-
mined except approximately. This may be done by using
an instrument with a dial and noting the pressure where
the oscillations of the dial hand show the maximum excur-
sion. The diastolic pressure is not at all important under
such conditions of acute cardiac breakdown. It would
make no difference in treatment whether the case was one

IMPORTANT CARDIAC IRREGULARITIES

137

5-.G

is.

1 s -

3 '

138 ARTERIOSCLEROSIS

of pure cardiac disease or one of the hypertension groups.
After the heart has rallied and the circulation is reestab-
lished, then a careful determination of the diastolic pres-
sure can be made and the prognosis will rest on what is
found at the compensated stage.

Ventricular Fibrillation

Ventricular fibrillation as its name implies, is fibrillation
of the ventricle analogous to that of the auricle, but the
condition is rarely observed as it is incompatible with life.
It has been shown that hearts at the time of death at times
enter a state of fibrillation of the ventricles and that cases
of sudden death may be due to this condition. Recently
G. Canby Robinson* has seen and made electrocardiograms
of a case of ventricular fibrillation. (Fig. 44.) The case
was that of a woman forty-five years old, "who had a se-
ries of attacks of prolonged cardiac syncope, closely re-
sembling Stokes-Adams syndrome, from which she recov-
ered. ' ' During an attack of unconsciousness in which there
was no apex beat for about four minutes, the electrocardio-
gram was taken. Following this the tracings showed an
almost regular heart beating at the rate of 85 to 100 per
minute. The patient had three convulsions and died with
edema of lungs about 30 hours after the attack of ventricu-
lar fibrillation.

Autopsy revealed chronic fibrous endocarditis of aortic
and mitral valves, arteriosclerosis, bilateral carcinoma of
the ovaries, and signs of general chronic passive congestion.

It is possible that the syncopal attacks in this case were
the result of sclerosis of the vessels supplying the heart
muscle although careful microscopical examination did not
throw much light on the ultimate cause.

Extrasystole

Whenever there is a dropped beat or an intermittent pulse
one may be sure that it is the result of an extrasystole.

*Robinson, G. C, and Bredeck, J. F.: Arch. Int. Med., 1917, xx, 725.

IMPORTANT CARDIAC IRREGULARITIES

139

Such extrasystoles are produced in the ventricle at some
point other than the regular path of conduction of impulses.
The extrasystole may have its origin in either the auricle
or the ventricle. If there is auricular extrasystole it can
not usually be recognized except by graphic methods. (Fig.
45.) The ventricular extrasystole on the contrary is com-
monly seen and readily recognized. Most of those seen in

Fig. 45. Electrocardiogram showing auricular extrasystoles (P). Courtesy of Dr. G. C.

Robinson.)

Fig. 46. Electrocardiogram showing ventricular extrasystole. Heart rate 56-60
beats per minute. Note that diastolic pause in which extrasystole occurs is practically
equal to two normal diastolic pauses. (Courtesy of Dr. G. C. Robinson.)

the clinic have their origin in some part of the ventricular
wall. Their two characteristics are that they occur too
early and that they are followed by a pause longer than the
normal diastolic pause. (Pig. 46.)

When one listens over the chest to a heart when extra-
systoles are occurring, one suddenly hears a weak beat

140 ARTERIOSCLEROSIS

which has taken place rather too early after the previous
systole to be strong enough to effect the opening of the
aortic valves. Consequently there is no pulse, the blood
does not move, and that beat is lost to the circulation.
Moreover, when the next regular stimulus comes from the
s-a node it finds the ventricle in a refractory condition,
having just ceased a contraction, and it is not until the next
sinus impulse that the ventricle responds normally. (Fig.
46.)

Patients who have occasional extrasystoles will say that
all of a sudden the heart turns upside down in the chest.
Sometimes there is slight sharp twinge of pain. Patients
are at times quite alarmed about their condition. Provided
there is no evidence of gross myocardial lesion, the extra-
systole itself is of no great significance.

While many cases showing pathologic causes for extra-
systoles have more or less marked arteriosclerosis, there
are other states in which no arteriosclerosis i$ found where
the extrasystole is present.

Heart Block

As heart block occurs frequently in cases characterized
by extensive arteriosclerosis, a brief discussion of the essen-
tial features will be given. It is, however, probable that
arteriosclerosis is not the cause of any of the cases of heart
block directly, but it is only a result of the same etiological
conditions which produce the lesion or lesions which result
in heart block. We may define heart block as the condi-
tion in which the auricles and ventricles beat independently
of each other. There may be delayed conduction (Fig. 47),
partial (Fig. 48), or complete heart block (Fig. 49). In
the former there are ventricular silences, during which the
auricles beat two, three, four, five, even up to nine times,
with only one ventricular contraction. It is believed by
most physiologists that the essential factor in the produc-
tion of heart block is an interference in the conduction of

IMPORTANT CARDIAC IRREGULARITIES

141

impulses from the auricles to the ventricles through the
band of tissue known as the auriculoventricular bundle.
The bundle of muscles described by His in. 1905, con-

Fig 47. Electrocardiogram showing delayed conduction (lengthening of P-R
val). These P-R intervals are quite regular. When irregular there is apt to be
systole of ventricle or occasional blocking of impulse going to ventricle. (Court
Dr. G. C. Robinson.)

inter-
extra-
tesy of

Fig. 48. Electrocardiogram showing partial heart-block in the three leads. Note
the variability of P-R interval calculated in seconds in Lead II. (Courtesy of Dr.
G. C. Robinson.)

necting the auricles and ventricles, has been definitely
shown to be the path through which impulses having their
origin in the orifices of the great veins pass to the ventri-

142

ARTERIOSCLEROSIS

cles. The situation and size of this bundle has been thus
described in man by Eetzer :

"When viewed from the left side, the bundle lies just
above the muscular septum of the ventricles and below the
membranous septum. In some hearts the muscular septum
is so well developed that it envelops the bundle. It is then
difficult to find, but occasionally it can be seen directly
by means of transmitted light. From the left side the bun-

Fig. 49. Complete heart block. (Courtesy of Dr. G. C. Robinson.)

die can be followed no farther posteriorly than the right
fibrous trigone, for here the connective tissue becomes so
dense that it is difficult to dissect it away. The impression
is, therefore, received that this mass of connective tissue
forms the insertion of the bundle. The bundle may be fol-
lowed anteriorly until it becomes intimately mixed with the
musculature of the ventricles.

IMPORTANT CARDIAC IRREGULARITIES 143

"When viewed from the right side of the heart, the
bundle can not be seen, because it is covered by the mesial
leaflet of the tricuspid valve, whose line of attachment
passes obliquely over the membranous septum. Then, if
the endocardium is removed from the posterior part of the
septum of the auricle up to the membranous septum, the
posterior part of the auriculoventricular bundle will be ex-
posed. If, in addition, the membranous septum be removed,
the bundle may be traced from the point to which it could
be followed when viewed from the left side as it passes
posteriorly over the muscular septum. In the region of the
auriculoventricular junction it loses its compactness, the
fibers divide, and the bundle seems to fork. One branch
passes into the superficial part of the valve musculature
which descends from the auricles, and the other branch
passes directly into the musculature of the auricle.

"Briefly, the auriculoventricular bundle runs posteriorly
in the septum of the ventricles about 10 mm. below the
posterior leaflet of the aortic semilunar valves ; with a gen-
tle curve it passes posteriorly just over the upper edge of
the muscular septum and sends its fibers into the muscula-
ture of the right auricle and of the auricular valves. In
the heart of the adult the bundle is 18 mm. long, 2.5 mm.
wide, and 1.5 mm. thick." (Erlanger.)

All normal impulses have their origin in the sino-auric-
ular node at the junction of the superior vena cava with
the right auricle (Fig. 50). From there the impulse travels
in the wall of the auricle in the interauricular septum to the
node of Tawara or A-V node (Fig. 51), thence through the
bundle of His to be distributed to the fibers of the right and
left ventricles. This sequence is orderly and perfectly
regular.

It has also been shown that the independent auricular
and ventricular rates vary somewhat, that of the auricle
being in general faster than that of the ventricle. A strip
of mammalian ventricle placed outside of the body in

144

ARTERIOSCLEROSIS

proper surroundings will begin to beat automatically at
the rate of about 40 beats a minute. Experimentally various
grades of heart block have been produced in the dog's

Fig. 50. Showing alternating periods of sinus rhythm and auriculoventricular rhythm.
(After Eyster and Evans.)

Fig. 51. Period of auriculoventricular or "nodal" rhythm following exercise in sitting
posture. (After Eyster and Evans.)

Fig. 52. Influence of mechanical pressure on the right vagus nerve. (After Eyster

and Evans.)

heart by more or less compression of the bundle at the A-V
ring. The block may be partial, when two to nine auricular
beats occur to every one of the ventricle, up to absolute

IMPORTANT CARDIAC IRREGULARITIES

145

RIGHT

VAG04

SYMPATHETIC

LEFT

SYMPATHETIC

Fig. 53. Schematic distribution of right and left vagus. (After Hart.)

complete block when tlie auricles and ventricles beat inde-
pendently of one another.

In any stage of partial block, pressure on the vagus nerve

146 ARTERIOSCLEROSIS

in the neck produces certain specific changes. (Fig. 52.)
Robinson and Draper* have found qualitative differences
in the two vagi. The right vagus sends most of its fibers to
the s-a node (Fig. 53) and has a more evident influence on
the rate and force of the cardiac contractions. The major-
ity of fibers from the left vagus are distributed to the A-V
node so that its most evident action is upon the conductiv-
ity of the impulse. Pressure then on the right vagus will
have a tendency to slow the whole heart. Pressure on the
left vagus will have a tendency to prolong the P-R interval
until even complete block occurs. Even when the heart
block is complete, stimulation of the accelerator nerve, as a
rule, increases the rate jof both auricles and ventricles.

If the block is functional, depending upon some tempo-
rary overstimulation of the vagus nerve, atropin, which
paralyzes the endings of the vagus, will naturally lift the
block. If the block is due to some actual lesion of the bun-
dle of His, such as fibrosis, gumma, or other lesion, then
atropin will have no influence to terminate the block. In
this manner we are able to distinguish between functional
and organic heart block.

*Jour. Exper. Med., 1911, xiv, 217.

CHAPTER V

BLOOD PRESSURE IN ITS CLINICAL APPLICATIONS

It is well to bear constantly in mind the point made over
and over in this work, that blood pressure is only one of
many methods of acquiring information. He who worships
his sphygmomanometer as a thing apart and infallible will
sooner or later come to grief. Judgment must be used in
interpreting changes in blood pressure just as judgment is
essential in properly evaluating any instrumental help in
diagnosis. One must not forget the personal equation
which enters into even accurate instrumental recording in
medicine and surgery.

In this chapter there will be no attempt to quote largely
from what others have said or thought. Every one has
his own opinion as to the value of certain methods after he
has worked with them for a long time. The ideas here ex-
pressed, except in cases where no opportunity has offered
to make personal studies, are those gathered from personal
experience.

Blood Pressure in Surgery

Careful estimation of the blood pressure in surgical cases
has, at times, great value. In all surgical diseases the most
important fact to know is not the systolic pressure, but the
pulse pressure. If the pulse pressure keeps within the
range of normal, does not drop much below 30 mm. in an
adult, then so far as we can tell the circulation is being
carried on. When the systolic pressure is gradually fall-
ing and the diastolic remains the same, the circulation is
failing and unless the pulse pressure can be established
again the patient will die. Again we see the value of the
pulse pressure.

147

1 48 ARTERIOSCLEROSIS

All prolonged febrile diseases tend to produce a lowering
of the blood pressure picture. The diastolic does not fall to
the same extent as the systolic so that there is a pulse pres-
sure smaller than normal. This is to be expected from what
we know of the general depression of the circulation in
fevers. The blood pressure reading is only a graphic rec-
ord of what we have long known, and enables us from day
to day accurately to measure the general circulation.

Head Injuries

It was claimed that in fracture of the skull or in con-
cussion much could be gained by frequent estimations of
the blood pressure. This seemed probable in the light of
experiments on compressing the brains of dogs by the use
of bags inserted through trephine openings (Gushing). In
the clinic, however, it has not been found of any material
value. It has a value in differentiating a simple fracture,
let us say, from a case of uremia which is picked up on the
street with a bump on the head. There the high pressure
usually found would at once direct attention to the kidneys
and the newer methods of blood examination would at once
settle the question. Naturally uremics may also have skull
fracture. There the diagnosis would be complicated. A
decompression done at once would be indicated. If the
skull fracture happened in a uremic, the decompression
would probably do no harm. In fact, there are some who
advise decompression for uremia.

Shock and Hemorrhage

In shock the blood pressure picture is low but the pulse
pressure drops to abnormally low figures. It seems to me
that the blood pressure instrument has its greatest value
in surgery in the warning it gives to the operating surgeon
in cases of impending shock.

It is well known that the first effect of ether, the com-

BLOOD PRESSURE
HOSPITAL _/ / \jt> VVAUK E E tjouiHTy

NO. a. 3 * a. y

ANAESTHESIA CHART

149

NflR l

J. P. 1 I -

^ DATE OF nPFRATTON M A R C H I 3. _ I 1

.BLEEDER LOOSE TEETH-

PRELIM. TREAT.

POST OP._ ------ URINE; ALB

URINE; AT.R N R E Po It TTASTS
WATER ,

TOTAL AMOUNT ANAESTHETIC USED

PRELIM DRUGS

ETHER^
OXYGEN

B P

RESP

PULSE

/( ,

y<>

MM HC

190

rfl

22O

170

21O

1i30

ISO

190

14O

...

530

-J

ISO

120

17O

110'

^ 1^

100

r f

*i"

"r 1

^ ^

-i

CODE: FULSE

K i OT 6r*\

PATH. GROSS.
PATH. MIC

ANAESTHETIST-

Fig. 54. Blood pressure record from a normal reaction to ether. Note that the
systolic and diastplic rise and fall together. At the end of the anesthetization the pulse
pressure is practically the same as at the beginning. Compare this with the record in
Fig. 55 ? where the operation had to be discontinued on account of the onset of shock.

HOSPITAL

sSet

ANAESTHESIA CHART

.- _____ J}"T. -. -.-- ________________________ , AGE__.1_3-_. DATE OF OPERATION- ..."^Llvt _____ U.-.-A^

AMicaV ..HEART-CX*""* ^"* B - p ------------ - _______ BLEEDER ------ ........... LOOSE TEETH. .Tf\OA ft

... URINE; AeB^eaO^W.- ...CASTS _____________ SUGAR _____________ ACETONE ............ -ACIDITY

PRELIM. TREAT: WATER ___________ - ___________________ .-SUGAR ------------------ ............ ALK ..... ----- ...........

POST OP ______ _____ URINE ALB --------------- CASTS- ------------- SUGAR ------------- ACETONE ------------- ACIDITY

/ GAS ___________________________ PRELIM DRUGS

TOTAL AMOUNT ANAESTHETIC USED

,.. ,

FATH. GROSS
PATH. MIC

CLOSURE. ____________________ ..... ._,_. ________________________ ANAESTHETIST _ .JOf.. _ -L .Q,

REMARKS. "!\xcK>on .%W\ou) ftwi-io*vi -------- Qo\\ \c,\*&&Y Jound

Fig. 55. Beginning of operative shock. Chart showing the method of recording blood pres-
sure during operation.

Note that the pulse and respiration show no remarkable changes, but the blood pressure
steadily fell, the systolic more than the diastolic so that the pulse pressure was gradually reaching
the danger point. Further work on this case was stopped following the warning given by the
blood pressure. The patient was returned to the ward and a week later anesthesia was again
given, the operation was completed, and the patient had a satisfactory convalescence,

BLOOD PRESSURE 151

monly used anesthetic, is to raise the blood pressure and
quicken the pulse rate. The whole blood pressure picture
is at first elevated (Fig. 54). Soon the whole pressure falls
slightly but continues at a higher level than normal. The-
diastolic pressure drops back nearly to normal and the in-
creased pulse pressure is due almost entirely to the slight
rise in the systolic pressure. Now the whole duty of the an-
esthetist is to administer the ether so that this ratio of sys-
tolic and diastolic is maintained throughout the operation.

Fig. 56. Showing method of using blood pressure instrument during operation with-
out interfering with the operator or assistants. Sheet thrown back to show cuff on
arm of patient. Anesthedst has chart on table beside him, dial pinned to pad in full
view, bulb near hand. 3ixtra tubing must be put on the blood pressure instrument.

Warning comes to him of impending shock before it comes
to any one in the neighborhood (Fig. 55). Any sudden
change in the pressure is a signal for increased watchful-
ness. Should the pressure all at once drop he can imme-
diately notify the surgeon and institute measures to resus-
citate the patient.

A method which is widely used is as follows : The anes-
thetist wraps the cuff of one of the dial instruments around
the patient's arm, and arranges the dial so that it can easily

152 ARTERIOSCLEROSIS

be seen by him at all times. This does not in any way inter-
fere with the work of the surgeon. Over the brachial ar-
tery below the cuff is the bell of a binaural stethoscope held
in place by the strap attachment now on the market. The
tubes of the stethoscope are long enough to reach conven-
iently to the ear pieces. A watch is pinned to the sheet of
the table. He has a chart, as illustrated (Fig. 56) on a
board and makes a dot in every space for five minute inter-
vals. By joining the lines a curve is obtained which tells
at a glance what the circulation is doing. I feel sure that
more attention and care exercised on the part of the anes-
thetist would be the means of conserving many lives lost
from shock following operation.

A sudden drop in the pressure picture may mean a large
hemorrhage. The gradual return of the pressure picture
means that the vasomotor mechanism has acted to keep up
the pulse pressure. Should the diastolic pressure contin-
ually fall, it may mean that the hemorrhage is still taking
place (Wiggers).

Blood Pressure in Obstetrics

One might affirm almost without fear of contradiction
that the constant determination of blood pressure during
pregnancy is more important than the examination of the
urine. Within recent years a number of observers having
access to a large material, have given the results of their
findings. There is a striking unanimity of opinion, al-
though now and then a difference in minor details.

The blood pressure should be taken frequently during
pregnancy. The usual and highly essential precautions in
taking pressure in general apply most particularly in these
cases. Towards the end of pregnancy the pressure should
if possible be taken daily and oftener if necessary.

Pressure in women is usually below 120 mm. Many pa-
tients have a temporary rise in blood pressure during preg-
nancy, due oftenest to constipation, without developing

BLOOD PRESSUKE 153

other symptoms. This is common to all conditions and has
no significance. Some think that an abnormally low pres-
sure, that is, a systolic below 90 mm., suggests that the
patient is likely to react unduly to the strain of labor. This
is denied by others. Among 1000 cases (Irving) the pres-
sure was below 90 in only one case. A gradually rising
pressure precedes albuminuria, as a rule. If there is al-
bumin without change in pressure the albumin may usually
be disregarded. Some think that a pressure over 130 mm.
systolic should be carefully watched. The danger limit
is set by some at 150 mm. If the blood pressure from the
very first is high, it may mean only that that was the pa-
tient's normal pressure. This calls for increased watchful-
ness. It is held by some that high blood pressure favors
hemorrhage and probably explains the hemorrhagic lesions
in the placenta and some viscera in eclampsia and albumi-
nuria.

All are agreed that the most significant change is the
gradual but sure rise from a low pressure. "When this is
combined with albuminuria the danger of toxemia is im-
minent. The high blood pressure in those under thirty
years of age seems to be a more certain sign of approach-
ing toxemia than the same pressure in those older. The
pressure falls within a few days to its normal after delivery
in the toxic cases.

Although the emesis gravidarum is held to be a sign of
a toxemia of some unknown nature, the blood pressure is
never raised even in the pernicious form.

Infectious Diseases

In all infectious diseases the blood pressure tends to be
lower than normal. During chills the systolic may rise to
great height due to the violent muscular contractions.

We found the blood pressure of great value in giving
information concerning the circulation. Again we repeat

154 ARTERIOSCLEROSIS

that it is not the systolic alone or the diastolic alone but the
pulse pressure which we wish to keep informed about. In
pneumonia we have tried out Gibson's law only to discard
it. This so-called law is that in pneumonia the systolic
pressure in millimeters should remain above the figure for
the pulse rate. When the figure in mm. of pressure is
equalled by or exceeded by the pulse rate the prognosis is
grave.

In typhoid fever we have made many estimations at va-
rious stages of the disease. We can only say that the pres-
sure picture tends to fall during the course. The systolic
falls more than the diastolic so that it is not uncommon
to see pulse pressures of 20 mm. at the beginning of con-
valescence in spite of the high caloric feeding practiced.
At the time of perforation the systolic pressure may be
raised. This is only the reflex from the initial pain. Soon
the pressure falls and if peritonitis sets in, the pressure is
exceedingly low and the pulse pressure gradually falls un-
til the circulation can no longer be carried on. In large
hemorrhage the pressure suddenly falls. If only one hem-
orrhage has occurred a gradual rise takes place, but the
general pressure picture remains at a lower level for days,
gradually returning where it was before the hemorrhage.

In beginning failure of the circulation we found ele-
vation of the foot of the bed about nine inches to be of such
value that we felt there must be some increase in blood pres-
sure. Numerous readings were made covering a period of
several months. Although we felt certain that the circula-
tion was improved, we rarely needed cardiac stimulation,
we never could prove any increase of blood pressure with
the sphygmomanometer.

In all infectious diseases there is no help offered by blood
pressure estimations in diagnosis. The sole and important
use is that of keeping track of the circulation.

BLOOD PRESSURE 155

Valvular Heart Disease

No rules can be laid down for blood pressure in valvular
heart disease. Aortic stenosis, the rarest of the valvular
lesions, is practically always accompanied by high pressure
picture. Mitral stenosis on the contrary usually shows a
low pressure picture. Mitral insufficiency may show an
exceedingly low picture or an exceedingly high picture.
Aortic insufficiency also may be accompanied by a high
systolic or by a normal systolic pressure. It depends on the
etiology. Practically all the rheumatic cases have low pres-
sure, the syphilitic cases have a high pressure. It is char-
acteristic of all cases of aortic insufficiency that the dias-
tolic pressure is low, even as low as 30 mm. The pulse
pressure is invariably high. Usually there is no difficulty
in determining the diastolic pressure. The intense third
tone suddenly becomes dull at the point of diastolic pres-
sure and frequently the dull sound can be distinctly heard
over the artery down to the zero of the scale. If difficulty
is found in reading the diastolic as the pressure is reduced,
the estimation may be reversed and the pressure gradually
increased from zero to the point where the dull tone sud-
denly becomes loud and clear. These points always coin-
cide.

Kidney Diseases

This has already been discussed somewhat fully in Chap-
ter III and will receive more consideration later. It might
be remarked in passing that in a case of seeming coma
where albumin is found in the urine but where the blood
pressure is low or normal, I have found at autopsy in sev-
eral cases pyonephrosis and not chronic nephritis. The
blood pressure may be useful in differentiating uremic coma
from the coma of pyonephrosis. Also in the cases of coma
with anasarca, either the acute, subacute or chronic form
the blood pressure is not raised as a rule. Other diseases
of the kidney, as tuberculosis, cancer, infection with pyo-

156 ARTERIOSCLEROSIS

genie .organisms, are not accompanied with any notable
changes in blood pressure.

Other Diseases, Liver, Spleen, Abdomen, etc.

Blood pressure is only of value in the above diseases in
affording information concerning the state of the circula-
tion. There is nothing characteristic about the pressure
in any of these diseases.

CHAPTER VI

ETIOLOGY

The causes of arteriosclerosis are many and varied. No
two persons have the same resisting power toward poisons
that circulate in the blood. Some go through life exposed
to all the infectious diseases without ever becoming in-
fected, while others fall easy victims to every disease that
comes, no matter how careful they may be, and it is quite
the same in regard to the resistance of the arterial tissues.
If the tubing is of first class quality and the individual does
not place too much strain on it, he may live to the biblical
three-score years and ten, and possess arteries which have
undergone such slight changes that they are not palpable.
Such a person is, however, the exception. On the other
hand, if the tissue is of poor quality, even the ordinary
wear and tear of life causes early changes in the vessels,
and a person of forty may have hard arteries.

We have described in a previous chapter the changes
which normally occur in the arteries as age advances. An
artery that is normal for a man of fifty years w r ould be
distinctly abnormal for a boy of fifteen.

Two broad divisions of arteriosclerosis may be made:
(1) congenital, or the result of inherited tendency; (2)
acquired.

Congenital Form

When Dr. 0. W. Holmes was asked how to live to the age
of seventy, he replied that a man should begin to pick his
ancestors one hundred years before he was born. Our
parents determine the character of the tissues with which
we start in life, and this determines our general resistance.
We might properly speak of congenital arteriosclerosis

157

158 ARTERIOSCLEROSIS

where the affected individual had poor arterial tissue with
which to begin life, for that, in a sense, is a congenital de-
fect, and arterial tissue that is poor in quality is prone to
disease.

The author is more and more impressed with the part that
heredity plays in the determination of arterial degenera-
tion. Especially does syphilis in the parents or grand-
parents leave its stigma in the succeeding generations in
the shape of poor arterial tissue which is prone to early
degeneration. Recently W. W. Graves has called atten-
tion to a malformation of the vertebral border of the scap-
ula which consists in a concavity instead of the normal
convexity of the bone. To this malformation he has given
the name, scaphoid scapula. He considers this to be but
one manifestation of a general lack of development in the
individual. He speaks of this maldevelopment as a blight
and considers that syphilis in the ancestors is responsible
for the condition in the offspring. He finds that even in
children, the subjects of the scaphoid scapula, the arteries
are very definitely thickened. While confirmation of his
observations is lacking, there is no doubt that we must lay
the blame for much of the arteriosclerosis in our patients
to the poor quality of arterial tissue transmitted by an-
cestors who have acquired some constitutional disease. It
may have been syphilis, it may have been the degeneration
produced by alcohol or other drug. We can not ignore the
part which heredity plays. The various factors to be con-
sidered in the production of the acquired form of arterio-
sclerosis appear to me to be but contributory factors to
a very great extent, the essential and fundamental factor
being the quality of arterial tissue with which the individ-
ual is endowed.

Arteriosclerosis may occur in infants. Cases have been
reported of calcification of the arteries in infants and chil-
dren. The arteriosclerosis may occur without nephritis or
rise of blood pressure. Cerebral hemorrhage in a child

ETIOLOGY 159

of two years lias been seen. Heredity in these cases plays
a most important role. In many of the reported cases there
was no question of congenital syphilis. Aneurysms, single
or multiple, have been found in the arteries of children,
and even the pulmonary artery may show sclerotic changes.

Acquired Form

As a rule the cases usually seen belong in this group
because it seems as if a connection could be established al-
most always between one or more of the etiologic factors
to be described and the disease. While this apparently is
the case, we must never lose sight of the part which the
quality of the tissue plays. When we leave this out of our
calculations we undoubtedly make many false deductions.
When two men of the same age who have been exposed to
the same conditions as far as we can learn, are found to
have quite different arteries, the one normal, the other
thickened, we must postulate congenitally poor tissue on
the part of the latter. Such tissue readily becomes dis-
eased following conditions which would very likely have
produced no noticeable effect on perfectly normal, healthy
tissue.

Hypertension

Hypertension must still be reckoned with in the etiology
of arteriosclerosis although the role that it was thought to
play does not seem so important. Changes of blood pres-
sure alone are not considered by many to be sufficient for
the production of arteriosclerosis. This may play some
part, but there are many other factors mostly unknown
which determine in any case the production of arterial
lesions. i i \ t

With every systole of the heart, blood is forced out into
the arterial system against a certain amount of resistance
represented by the tonicity of the capillary area, and the
amount of cohesion between the viscous blood and the walls

1 60 ARTERIOSCLEROSIS

of the arterioles. When a dilatation of the capillaries over
any large area takes place, the blood pressure falls, pro-
vided there is no compensatory contraction in other areas
to make up for the decreased resistance in the dilated ves-
sels. The viscosity of the hlood, as such, probably has
very little effect on the resistance to the flow. With the
systole of the heart there is a sudden dilatation of the arch
of the aorta, and a wave of expansion follows, which is
transmitted to the periphery and is lost only in the capil-
laries.

The blood pressure is constantly changing. Physio-
logically there are relatively wide variations in the pres-
sure in a perfectly normal individual. There are some
persons who have hypotension, a blood pressure much be-
low the normal. Such persons have usually small hearts,
small aortas, and they seem to have but little resistance
to disease. Many diseases, especially the prolonged fevers,
diminish markedly the blood pressure. Whether the hyper-
tension is the cause of the structural changes that are found
in the walls of the vessels, or is the result of the diminished
area of the arterial tree through which the same amount
of blood has to be driven as before the vessel walls became
narrowed, is still disputed. As has been stated, experi-
mental evidence would tend to place the initial blame upon
the poisons circulating in the blood, which first damage the
vessel walls. The subsequent changes then produce thick-
ening and inelasticity. Some think (Allbutt) that the
hypertension is primary. There are cases seen clinically
that lend support to this view and there is experimental
evidence also (v. Chap. II). Not infrequently individuals
in middle life begin to show increase of arterial blood pres-
sure without discoverable cause. In such case it may be
that there is slowly progressing chronic nephritis. The
urine if examined only superficially in single specimens may
not reveal any abnormalities. Careful functional examina-
tion by means of the newer tests may reveal functional

ETIOLOGY 161

deficiency. It must not be supposed that all cases of in-
creasing hypertension are cases of chronic nephritis. The
opinion has already been expressed (Chap. Ill) concerning
this point. Experience has convinced me that the opinion
expressed in former editions is not altogether correct.

Age

No age is exempt from the lesions of arteriosclerosis if we
consider the two groups. However, the disease is seen for
the most part in persons past middle life. The relative
frequency with which it is found in the different decades
depends on so many factors that it is of no value to tabulate
them. As has been stated, arteriosclerosis of all types is
an involution process that advances with age. Longevity
is a question of the integrity of the arterial tissue, and no
one can tell what sort of " vital rubber'' (Osier) any one
of us has. However, many with poor tubing may make
such use of it that it will outlast good tubing that is badly
treated. Unfortunately we have no way of telling early
enough with just what sort of arterial tissue we are start-
ing life.

Sex

There is no doubt that men are far more prone to arterial
disease than women are ; all statistics are in accord on this
point. This is explained by the greater exposure of men
to those conditions of life which tend to produce circulatory
strain, and so to produce arteriosclerosis, or vice versa.
Arteriosclerosis in women is not often seen until after the
fiftieth year. Cases of the most extreme grade of pipe
stem arteries are, however, seen in old women, and calcified
arteries are not hard to find among the inmates of an old
woman's home.

Race

Some of the most beautiful examples of arteriosclerosis
in this country are seen in the negro. Not only is this

162 ARTERIOSCLEROSIS

disease more frequent in the black race, but the age of onset
is much earlier than in the Caucasian. The accidents of
arteriosclerosis, viz., aneurysm, cerebral hemorrhage, etc.,
are more common among the negro males. The etiologic
factors that are most often found in the history are the
prevalence of syphilis and hard physical labor.

Occupation

Certain occupations have a distinct causal relationship to
arteriosclerosis; among such are particularly those entail-
ing prolonged muscular exercise, especially if much lifting
is necessary. Every one is familiar with the phenomena
accompanying the exertion of lifting. The breath is drawn
in, the glottis is closed, and the muscles of the chest wall
are held rigidly while the exertion lasts. This causes a
great increase in blood pressure, and constant repetition
of this will produce permanent high tension. In hospitals,
the stevedores as a class have marked arteriosclerosis, and,
almost without exception, they are comparatively young
men. Occupations that are accompanied with prolonged
mental strain, such as now occur to the heads of large man-
ufacturing and financial institutions, also predispose to
early arterial changes. Psychic activity, especially when it
is accompanied by worry, is a potent factor in the produc-
tion of the increased blood pressure which is the chief factor
in producing arterial disease. It has been suggested that
sexual continence in high-strung men produces changes in
the nervous system which can conceivably lead to the pro-
duction of high tension and further to arteriosclerosis. This,
however, I can not think has any foundation in fact except
in so far. as such men are prone to live at high speed and
wear themselves out sooner than the normal person. The
sexual continence per se is not harmful. There are, how-
ever, men who seem not to be harmed by the constant wear
and tear of our modern life. These are the exceptions.

Workers in factories where paint is made and the in-

ETTOLOGY 163

gredients hand-mixed, are prone to develop arteriosclerosis
early in life. It lias been found that the laborers most apt
to be victims of lead intoxication are those who are careless
in their habits of cleanliness, particularly in regard to the
fingernails. The continuous absorption of lead into the-
system, brings about a condition of hypertension that has
its inevitable results.

The fact is that any occupation which entails either the
absorption of toxic substances, or prolonged muscular la-
bor, will hasten markedly the onset of arterial disease.

Food Poisons

The opinion that arteriosclerosis is due in large part to
poisoning by end products or by-products of protein di-
gestion is now receiving much support. Experiments on
dogs and rabbits have lent some confirmation to chemical
observations. It has been shown that dogs fed for a long
time on putrefied meat developed inflammation and degen-
eration of the adventitia and media, with hyperplasia and
calcification of the intima of many arteries. In the pul-
monary and carotid arteries, in the vena cavas and myo-
cardium, there were extensive necroses and hyaline degen-
eration. Moreover, injections of sodium urate and ergot
caused necroses in the muscularis and elastica of the aorta,
pulmonary artery, vena cavas inferior and heart muscle, but
there w^as no calcification. Guinea pigs which were fed
indol in small doses by the mouth over a long period showed
atheromatous degeneration of the aorta.

Infectious Diseases

As more study has been given to the arteries in persons
who have died of the acute infectious diseases, more has
come to light concerning the effects of the toxins of these
diseases on the vessel walls. In the arteries of children
who have died of measles, scarlet fever, diphtheria, cere-

164 ARTERIOSCLEROSIS

brospinal meningitis, etc., degenerative changes in the ar-
teries occur, modified only by the length of time that the
toxins have acted.

Thayer has shown that the arteries of those who have
passed through an attack of moderately severe or severe
typhoid fever are as a rule more readily palpable than are
the vessels of persons of corresponding years who have
never had the disease. Clinically the typhoid toxin appears
to cause the early production of arteriosclerosis. The
changes in the arteries occur for the most part, and always
earlier, in the peripheral arteries, and the media is chiefly
affected. Minute yellowish patches are found on the aorta,
carotids, and coronaries. In persons who have passed
through an attack of one of the fevers, and have later died
from some other cause, regenerative changes are sometimes
found to have taken place in the arteries, consisting of an
ingrowth of elastic fibers from the intact adventitia to the
diseased media.

That there are some other factors than the infectious dis-
ease which are concerned in the production of arterial
changes seems evident from a study* made recently among
a group of almshouse inmates ranging in age from 38 to
90 years. The study included 500 persons of both sexes.
Careful histories were taken to determine the presence of
antecedent infectious disease. The radial artery was pal-
pated to determine the presence of sclerosis. Among the
cases giving a history of one infectious disease the follow-
ing table gives the results :

DISEASE

NO.

+-H-

POSITIVE

NEGATIVE

Measles

Infectious arthritis

Pneumonia

Typhoid

Scarlet fever

Smallpox

Miscellaneous

178 33 37 30 100 78

'Warfield, L,. M.: Jour. I^ab. and Clin. Med., November, 1917.

ETIOLOGY 165

A summary of the cases showed: 252 cases without sclero-
sis; 248 with sclerosis; 147 cases with infections but no
sclerosis; 180 cases with infections and sclerosis.

This study failed to throw any positive light on the ques-
tion. Infectious diseases undoubtedly play a certain role,
particularly those continuing a long time and certain par-
ticular infectious diseases, as measles.

Syphilis

Syphilis is one of the most important of the etiologic
factors in the production of arteriosclerosis. It has been
shown that in 85 per cent of cases of aortic insufficiency in
persons, usually males, over forty-five years, who did not
have chronic infective endocarditis, the Wassermann re-
action was positive. Acute aortitis affecting the ascending
and transverse portions of the arch of the aorta is very
commonly seen, and the irregular, scattered, slightly raised,
yellowish-white patches of sclerosis in the arch which are
found years after the syphilitic lesion, are considered by
some to be very characteristic of syphilis. Mesaortitis is
the primary lesion and acts as a locus minoris resistentice
where an aneurysm forms.

Hypertensive cardiovascular cases have been serologi-
cally studied, and a positive Wassermann reaction found
in a large percentage of one series. In fifty cases, 90 per
cent either gave a positive Wassermann reaction or luetin
test, were known to have syphilis, or had children with
hereditary syphilis. This suggests what might be called
"familial cardiovascular syphilis."

Hypertensive disease is possibly one of the common so-
called "late" manifestations of syphilis. That syphilis is
responsible for the arterial disease in the vessels of the
brain, resulting in apoplexy or sudden cardiac death in mid-
dle life, has long been known. In fact, it is claimed (Osier)
that all aneurysms occurring in persons under thirty years

166 ARTERIOSCLEROSIS

of age are due to syphilitic aortitis. In the late stages of
syphilis the arterial lesions may be of a diffuse character.

Chronic Drug Intoxications

Lead, tobacco, and according to some, tea and coffee, are
to be classed as causal factors in the production of arterio-
sclerosis. Certain it is that all these substances have a
tendency to raise the arterial pressure, but whether the
drug itself causes first a degeneration, and later a hyperten-
sion results, or vice versa, is not yet positively known.
We have just mentioned that lead particularly has a marked
effect in producing arterial lesions. Other drugs as ad-
renalin, barium chloride, physostigmin, etc., while produc-
ing experimental arteriosclerosis, hardly could produce
the disease in man. Alcohol has been blamed for much, and
as an etiologic factor in the production of arteriosclerosis
formerly was accorded a first place. More recently much
doubt has been thrown on this supposition by the work of
Cabot, who showed that the mere drinking of even large
quantities of spirits had no effect in producing arterial
disease.

This observation has been recently substantiated by
Hultgen, who carefully studied clinically 460 cases of
chronic alcoholism. He says, " There are no cardiovascu-
lar symptoms which might be termed characteristic of
chronic alcoholism, unless it be the peculiar fetal qualities
of the heart sounds which we know as embryocardia. I
find this very frequent among drinkers, but I can offer only
a tentative explanation for it, namely the following: Em-
bryocardia can only occur with low tension blood pres-
sure, and in the absence of renal insufficiency. Hence it
might be considered as a useful condition of no pathologic
significance at all. That alcohol is a sclerogenic pharmakon
and productive of arteriosclerosis with its usual train of
symptoms may be a fact, but its demonstration would be

ETIOLOGY 167

difficult and is really not shown by my tabulations. There
were cardiovascular changes, such as myocarditis, aortitis,
valvular heart disease and arteriosclerosis in chronic alco-
holics in 54.3 per cent of 461 cases, but this by no means
constitutes a proof of the causal relationship between these
lesions and the abuse of liquors. I believe it, nevertheless,
to be good reasoning to ascribe the bulk of cardiovascular
symptoms to the sclerogenic action of alcohol, while ab-
staining from an interpretation of its pathogenesis." Just
what role tobacco plays is difficult to say. My own opinion
is, that of itself when used in moderation, it has no ill
effects. However, as tobacco is a drug that may raise the
blood pressure, excessive use must be held responsible for
the production of arteriosclerosis. It is difficult to sepa-
rate its effects from those produced by eating and drinking.

Overeating 1

There can be no doubt but that the constant overloading
of the stomach with rich or difficultly digestible food is
responsible for a large number of cases of arteriosclerosis.
Every one must have noted the increase in force and volume
of the heart beat after the ingestion of a large meal. The
constant repetition of such processes conceivably can lead
to damage to the vessel walls through hypertension.

In the metabolism of food in the intestines there are sub-
stances produced which are poisonous when absorbed di-
rectly into the circulation. Ordinarily these substances
are rendered harmless either before absorption or are de-
toxicated in the liver to harmless substances. It is con-
ceivable that a constant overproduction of such poisons
would eventually damage the defensive mechanism of the
body to such an extent that some of the poisons would
circulate in the blood. An expression of a surplus of one,
at least, of these decomposition products is the appearance
of indican in the urine. It is not believed that indicanuria
has the importance attached to it which some authors would

168 ARTERIOSCLEROSIS

have us believe. It is found too often and in too many vary-
ing conditions, nevertheless it undoubtedly does reveal the
presence of perverted metabolism.

In how far the toxins absorbed from the intestinal tract
are responsible for the production of arterial disease, it is
not possible to say. Some observers lay great stress on
this factor as a cause of arteriosclerosis. The author be-
lieves that the role played by the absorption of products of
perverted intestinal metabolism is an important one. The
primary change is an increased tension in the arterioles
which later leads to thickening of the coats of the vessels
and to the other consequences of arterial disease. A vi-
cious circle is thus established which has a tendency to be-
come progressively worse.

Mental Strain

More and more does one become impressed with the fact
that patients with arteriosclerosis are very often those who
take life too seriously and either from ambition or from an
exalted sense of duty lead especially strenuous lives. Not
always are these persons addicted to drug or liquor habit.
Many are rather abstemious in their habits. It is not so
often that we see as a victim of arteriosclerosis, the care-
free person who laughs his way through life without worry-
ing about the morrow. He is not so prone to arteriosclero-
sis. Worry is a far more potent cause of breakdown than
actual manual work. It is the rule to find thickened arteries
among neurasthenics. This may be only part of a general-
ized degeneration of all tissue in the body. The blood pres-
sure in such persons is usually low. So many men of our
better class live under a continuous mental strain in the
business world. The increase in arteriosclerosis cases is
real, not apparent. The intense mental strain seems to cause
a marked increase in blood pressure (for short periods of
mental effort this has been proved) over a period of time

ETIOLOGY 169

sufficient to cause permanent changes in the vessel walls.
The same sequence of events repeats itself; high tension,
arterial strain, compensatory thickening, hypertrophied
heart, etc.

Certainly the character of the arterial tissue has much to
do with the determination of degenerative changes which
may result from the action of one or more of the etiologic
factors.

Muscular Overwork

Muscular overwork is to be reckoned with as an etiologic
factor. One sees it especially among the laboring class in
both whites and negroes. Possibly other factors, as alco-
hol and coarse heavy food, contribute to the early arterial
degeneration. Hypertrophy of the heart occurs in athletes,
and statistics gathered among the oarsmen especially, show
a relatively high mortality at the different decades trace-
able to the high tension produced while in training. This
question deserves more consideration than has been ac-
corded it.

Renal Disease

Chronic disease of the kidneys (contracted red kidney) is
one of the most certain producers of hypertension; in fact,
some maintain that high tension, even without demonstra-
ble kidney lesions, as revealed by careful urine examina-
tions, is a valuable sign pointing to chronic nephritis. This
is doubted by others, myself among them. Just what causes
the increase in blood pressure sometimes to over 270 mm.
of Hg, is not definitely known. It seems most probable that
it is some poison elaborated by the diseased kidneys and
absorbed into the general circulation. There it acts pri-
marily on the musculature of the arterioles causing tonic
contraction and an increase of work on the part of the heart
to force the blood through iiarrowed channels. One fact is
certain. We see patients in coma due to renal disease with

170 ARTEKIOSCLEROSIS

blood pressure much over 200 mm. of Hg. As these cases
clear up, the pressure may fall, and should they seemingly
recover, the recovery is accompanied with a marked de-
crease in blood pressure, finally reaching the normal for
the individual. Moreover, in the course of a severe acute or
sub-acute nephritis, hypertension is associated with head-
ache, partial or total blindness, and drowsiness. When the
pressure is reduced, all these symptoms disappear.

There is also the chronically shrunken and scarred kid-
ney known pathologically as the arteriosclerotic kidney.
It is probable that there are two groups of cases which we
may designate: (1) primary; (2) secondary. In the pri-
mary group the kidney disease antedates the sclerosis of
the arteries, and the sclerosis is most probably dependent on
the constant high tension. We know that prolonged hyper-
tension will produce severe forms of arteriosclerosis. The
arterial disease in this group is caused by the renal disease.

In the second group the kidney changes are apparently
due to the general arteriosclerosis which, affecting the kid-
ney vessels, causes changes leading to atrophy and subse-
quent fibrous tissue ingrowth of scattered areas. These
cases are not necessarily associated with hypertension; on
the contrary there is more apt to be hypotension. Where
the first group occurs for the most part in young and active
middle-aged people, the second group is the result of in-
volutionary processes which accompany advanced age.

However careful a urinalysis may be, there is no assur-
ance that one can predict the pathologic state of the kidney.
Often so-called normal urine will be secreted by a badly
diseased kidney, whereas a urine which contains considera-
ble albumin and many casts may be secreted by a kidney
which is only temporarily the seat of inflammation. What
matters after all is not the state of the kidney which the
pathologist describes, but the actual functional response
of the kidney in the body to the various tests now well
known.

ETIOLOGY 171

Ductless Glands

At the present time the tendency among some writers
is to make the ductless glands the responsible agents in
almost all diseases. Arteriosclerosis is no exception to this
tendency. Sajous, for example, divides the morbid process
producing arteriosclerosis into three types; (1) autolytic,
(2) adrenal, (3) denutrition. In the first type he finds
the pancreas to be the most important gland. It supplies
an internal secretion which " takes a direct part in the pro-
tein metabolism of the tissue cells, and also in the defensive
reactions within these cells, as well as in the phagocytes and
in the blood stream." This being the case exaggeration of
this digestive process has tissue destruction as its result,
arteriosclerosis among them.

In the adrenal type Sajous argues that adrenalin pro-
duces lesions experimentally, therefore the adrenal gland
has a profound influence by its internal secretion in connec-
tion with the sympathetic system in producing degenera-
tions leading to arteriosclerosis.

The denutrition type has as its particular gland the thy-
roid. The sclerotic process in the arteries is due to the lack
of thyroid as in cases of myxedema. After a long resume
of his ideas he concludes "that arteriosclerosis is the result
of excessive or deficient activity of certain ductless glands,
the thyroid and adrenal in particular."

No one can dogmatically deny the part which the ductless
glands may play in the production of arteriosclerosis, but it
hardly seems that there is enough actual experimental evi-
dence to show T that they take such an important part as Sa-
jous believes. Until further and more convincing evidence
is offered by competent investigators, I prefer to look with
some skepticism upon the ductless gland theory of the caus-
ation of arteriosclerosis. The field lends itself too easily
to speculation and imagery. Some are already allowing
themselves the mental debauch of this nature.

CHAPTER VII

THE PHYSICAL EXAMINATION OF THE HEART
AND ARTERIES

Heart Boundaries

In order to be able to estimate the departures from nor-
mal in the boundaries of the heart, it is essential that there
be a definite appreciation of the boundaries of the normal
heart in relation to the chest wall.

It is frequently stated that the right limit of cardiac dull-
ness is normally, in the adult, just at the right border of
the sternum. This is not strictly accurate. Careful dis-
sections at the autopsy table and x-ray plates of the chest
made at a distance of two meters from the tube show that
the border of the right auricle is from one to one and a
half and even two centimeters from the edge of the sternum
at the level of the fourth rib, and on the living subject this
can be also demonstrated. The right border of the heart
usually is from 3 to 4 cm. from the midsternal line at the
level of the fourth rib.

Again there is a term used in defining the apex, known as
the point of maximum impulse. As this does not always
coincide with the apex beat and with the outer lower left
border of the heart, it would be better to use the term apex
beat.

Normally, then, the cardiac dullness, the so-called relative
cardiac dullness, begins above at the upper border of the
third costal cartilage, as a rule, and taking a somewhat
curved line with the concavity inward, descends to the fifth
interspace or beneath the fifth rib from 9 to 10 cm. from a
line drawn through the center of the sternum parallel to its
length, the midsternal line. This seems to me to be a bet-
ter method of recording the size of the heart than by the

172

PHYSICAL EXAMINATION OF HEART AND ARTERIES 173

lines commonly used; viz., the nipple, or midclavicular, or
parasternal line. Below, the cardiac dullness is merged into
the tympany from the stomach and the dullness from the
liver. At the sixth right costosternal articulation there is
a sharp turn upwards forming at that point with the liver
the cardiohepatic angle. At the fourth right cartilage or
the third interspace, the dullness is from one to two centi-
meters from the edge of the sternum. We have then a some-
what pear-shaped area or triangular area with the apex at
the apex of the heart. The so-called absolute cardiac dull-
ness does not appear to me to be of any great significance.
In reality it is the limit of lung resonance and may be
greater or less, not so much on account of variations in the
size of the heart, as of variations in size of the lungs and
shape of the chest wall.

The really crucial question which should always be asked
is, Is the heart enlarged or decreased in size ? The position
of the apex beat alone can not determine this, neither can the
limit to the right of the sternum. The distance between
these two points and the depth of the dullness at a distance
of 5 cm. from the midsternal line on the left side, will give
the size of the heart as nearly as can be obtained in the liv-
ing subject. A series of measurements in normal adults
average 13 to 14 cm. and 9 to 10 cm. respectively. For
women they are about 1 cm. less in each direction.

The elaborate mechanism known as the orthodiagraph is
probably the best means of determining the actual limits
of the heart, but few men have such an expensive instru-
ment, and, moreover, at the bedside such an instrument
could not be used. From comparative measurements I con-
cur in the belief of those who affirm that careful percussion
will furnish equally as accurate limits.

The first step in making an examination of the heart is to
expose the patient's chest in a good light, and, sitting at his
right side, carefully inspect the chest. The position of the
apex beat, heaving, bulging, retraction of interspaces, etc.,

174 ARTERIOSCLEROSIS

can easily be seen if visible. After careful inspection lias
given all the data which it is possible to obtain, one next
lays the palm of the hand over the heart and attempts to
palpate the apex beat. The thrust of the apex in a hyper-
trophied heart can readily be felt, and one can feel whether
the heart is regular, irregular, intermittent, or has other
change in rhythm. The shock of the closing valves, particu-
larly the aortic, can be felt, and that and the forcible apical
impulse are very suggestive signs of hypertrophy and
hypertension. Thrills may also be felt and can be timed
in relation to the heart cycle.

Percussion

It is to percussion that we next proceed, and for the data
in regard to the size of the heart, it is, for our purpose, the
most valuable of all the physical methods of heart examina-
tion.

First and foremost we wish by percussion to learn the
actual size of the heart, in other words what is ordinarily
called the relative cardiac dullness. With the absolute dull-
ness we are not concerned. That irregular area represents,
as has been said, actually the limits of lung resonance. The
heart may or may not be covered with lung; there may or
may not be the incisura cardiaca. What I wish to insist
upon is that the size of the area of absolute dullness can
give us no data in regard to the size of the heart. What we
must endeavor to learn is the actual size of the heart as
nearly as our crude means will permit.

Light, very light, almost inaudible percussion, what Gold-
scheider called * ' Schwellungsperkussion, " must be prac-
ticed. Use the middle finger of the right (left) hand as the
hammer and the last joint of the middle finger of the left
(right) hand pressed firmly against the chest, as pleximeter.
I believe it is better to place the pleximeter finger parallel
to the boundary to be limited although some place the finger
perpendicularly, that is, pointing toward the boundary.

PHYSICAL EXAMINATION OF HEART AND ARTERIES 175

Now and then it helps to bend the pleximeter finger at the
second joint, hold it perpendicularly to the chest wall, and
strike the joint directly in line of the finger. This in my
hands has been of great assistance in percussing the limits
of the heart dullness. Pottenger's "light touch palpation"
is a modification of the light palpation and, to my mind, has
no very special advantages. Auscultatory percussion is of
great value at times. The bell of the stethoscope is placed
over the portion of heart uncovered by lung (should such
be the case), and with this point as a center the chest is
lightly and quickly tapped along radii converging toward
the stethoscope. One soon learns to recognize the change
of pitch as the tapping reaches the border of the heart. It
is well to use all methods, especially in difficult cases, and
to compare the results. Personally I have found that by
light percussion I can limit with much accuracy the upper,
right, and left borders of the heart.

There is much to be gained by using light percussion.
Strong blows set in vibration not only the underlying struc-
tures, but also more or less of the chest wall. We wish to
avoid this source of error, we do not wish to differentiate by
pitch alone. Finally one's pleximeter finger becomes, after
long practice, so sensitive to changes in the resonance of
structures lying below it, that there is actual feeling of im-
pairment to the slightest degree. This delicate touch is
what we should endeavor to cultivate.

It is at times of advantage to use immediate percussion.
This is done by bending the fingers of the striking hand,
bringing the tips in a line and striking the chest lightly with
the four fingers as one finger. Some find it easier to per-
cuss the dullness due to the heart in this way than by medi-
ate percussion.

The little hammer and hard rubber, celluloid, bone, or
ivory pleximeter does not seem to me to be nearly as good
as the fingers. Moreover, one always has his hands, but
may forget his hammer and pleximeter.

176 ARTERIOSCLEROSIS

Auscultation

In auscultating the heart I prefer the binaural stetho-
scope of the Ford pattern. The recent substitution of an
aluminum bell for the hard rubber bell is an improvement.
Personally I do not favor the phonendoscope or any of the
new patent non-roaring instruments now for sale by urgent
instrument makers. The phonendoscope has its uses, for
example in auscultating the back when a patient is lying
in bed or in listening to the heart sounds when a patient is
under an anesthetic; but for differentiating the murmurs
and for heart diagnosis, I much prefer the regular bell
stethoscope.

In arteriosclerosis the two places over which it is impor-
tant to listen are the apex and the second right cartilage,
the aortic area. Over the former, one gains data in regard
to the strength of the heart as indicated by the first sound,
over the latter point, one learns of the tension in the aorta
by the character of the sound produced when the aortic
valves close.

The hypertrophy of the heart in arteriosclerosis is in-
variably due to the enlargement and thickening of the left
ventricle. From the nature of the position which the heart
assumes in the thorax, this enlargement is downward and
to the left. The apex beat will therefore be found in the
fifth or sixth interspace, and definitely at an increased dis-
tance from the midsternal line. As stated above, it is
most important that this distance be accurately measured
and put down in the notes of the case for future reference.
No satisfactory prognosis can be given unless this is done,
for the gradual increase or the decrease under treatment in
the size of the heart can thus be definitely known, and,
knowing the other factors, a prognosis may be given which
will be of some value to the patient.

PHYSICAL EXAMINATION OF HEART AND ARTERIES 177

The Examination of the Arteries

It is exceedingly difficult at times to affirm definitely that
an artery, the radial for example, is actually sclerosed.
Much depends on the sensitiveness of the fingers of him
who palpates, and much upon the relation of the palpated
artery to the surrounding, chiefly underlying, structures.
In the examination of arteries it is well to inspect the body
for the pulsations caused by them. Frequently an exceed-
ingly tortuous artery, such as the brachial, may be seen
throughout its whole extent and yet the radial appear lit-
tle, if any, thickened by palpation. Again the artery of a
pulse of high tension which is small in size but full between
the beats, may not be as sclerosed as one which collapses
and feels much softer. It is difficult to obtain accurate data
in regard to the tension in an artery by feeling it with the
fingers of one hand. One should use both hands. With the
middle finger of the right (left) hand the artery is com-
pressed peripherally, that is, nearest the wrist. The blood
is then pressed out of the artery with the middle finger of
the left (right) hand, so as to obliterate completely the
pulse wave and the two or three inches between the middle
fingers are felt with the index fingers. By holding the fin-
ger firmly on the artery near the wrist so as to block any
wave that may come through the palmar arch by anastomo-
sis with the ulnar artery and by releasing pressure on the
proximal middle finger, some idea may be had of the degree
of pulse tension. However, no amount of practice can more
than approximate the tension and when one is surest that
he can tell how many millimeters of pressure there are, he
is apt to be farthest wrong when he checks his guess with
the sphygmomanometer.

Much may be learned from carefully palpating the periph-
eral arteries, and, as a rule, the sclerosis of these arteries
means general arteriosclerosis, although there are many
exceptions to this.

178

ARTERIOSCLEROSIS

A more recent method, and one which in the author's
hands has been found to be valuable, is that proposed by
Wertheim-Salomonson who palpates the artery not with
the ball of the finger but with the fingernail. The finger is

Fig. 57. A method of finger-tip palpation of the radial artery. (Graves.)

Fig. 58. Another method of finger-tip palpation of the radial artery. (Graves.)

held so that the nail is perpendicular to the surface of the
skin and the artery is felt with the end of the nail. The sen-
sation is perceived at the root and makes use of all the sensi-
tive nerve endings there. In this way it is possible to feel

PHYSICAL EXAMINATION OF HEART AND ARTERIES 179

the arterial wall distinctly, and a little practice will enable
one to determine whether or not the vessel wall is thickened.
It is also possible to determine with a considerable degree of
accuracy the diameter of the artery and the size of the wall
when the current is cut off by pressure on the proximal side
of the artery. It is best to have a firm background when
this " fingernail ?? palpation is used. This may be obtained
by palpating the radial artery against the lower end of the
radius.

Probably the best method of palpating the arteries, es-
pecially the radial, to determine the degree of sclerosis and
thickening, is to use the tip of the finger and roll it care-
fully over the artery. The tip of the finger is exceedingly
sensitive and, moreover, it is a firmer palpating surface
than the ball, thus enabling one to appreciate degrees of
sclerosis which could not be differentiated by palpation
with the soft yielding ball. This finger tip palpation is well
illustrated in the figures here shown. (Figs. 57 and 58.)

Estimation of Blood Pressure

It must be borne in mind at the outset that arteriosclero-
sis and high blood pressure are not always associated. As
a matter of fact in the severest grades of senile arterio-
sclerosis the blood pressure is usually below the normal
for the individual's years. However, as high tension is a
frequent factor in the production of arterial thickening,
blood pressure readings are of importance.

The instrument which one uses is of minor importance
provided it is properly standardized. The most important
feature of the instrument is the cuff. This must be 12 cm.
wide and be long enough to wrap around the arm several
times so that the pressure is evenly distributed over the
whole arm and not over a small portion. One mercury in-
strument we had in the hospital was reported to be at great
variance with a dial instrument. This mercury instrument
was provided with a cuff which was short and was tied

180 ARTERIOSCLEROSIS

around the arm by means of a piece of tape. This caused
a tight constriction over a small area and rendered the es-
timation too high. A new, long tailed cuff easily remedied
the apparent defect in the instrument.

In taking blood pressures the difference from day to day
of 10 or even 15 mm. of systolic pressure has no great sig-
nificance. Fluctuations of the systolic pressure alone, it is
insisted upon, have very little meaning. One must take the
whole pressure picture into consideration and determine
how the picture changes in order to draw any conclusion in
regard to the state of the blood pressure. Failure to pay
attention to this evident point has caused much futile work
to be written and published.

It is well to emphasize again the point that the blood
pressure picture consists of the systolic, the diastolic, the
pulse pressure and the pulse rate.

Palpation

Hoover has called attention to the direct palpation of the
femoral artery just below Poupart's ligament as a more ac-
curate index of the pressure in the aorta than the palpation
of the radial artery. Possibly one can obtain a more ac-
curate estimate of the blood pressure in this way. This,
however, is open to dispute. To estimate the blood pres-
sure by palpating the radial artery is most deceptive. In
about 75 per cent of cases one can tell fairly well whether
the pressure is abnormally high or abnormally low. Small
variations are impossible to determine. Unquestionably it
is most advantageous to get into the habit of palpating the
femoral artery and checking the result with the sphyg-
momanometer so that the fingers may be trained to appre-
ciate as accurately as possible changes of pressure.

It may be that one day when the instrument is needed it
is not at hand. A well-trained touch then becomes a great
asset.

PHYSICAL EXAMINATION OF HEART AND ARTERIES 181

Precautions When Estimating Blood Pressure

There are certain precautions which must be strictly ob-
served when deductions are drawn from the manometer
readings. The psychic factor must be reckoned with. Any
emotion may cause marked variations in the pressure. Ex-
citement and anger are especial sources of error. Even the
slight excitement arising from taking the first blood pres-
sure on a nervous patient especially is apt to give false
values. Usually the readings must be taken many times at
the first sitting and the first few may have to be set aside.
Worry is a potent factor in raising the pressure. A walk
to the physician's office, especially if rapid, has its effect.

The position of the patient when the blood pressure is
taken is important. Usually in the office the pressure is
taken when the patient sits in a chair. He should assume a
relaxed, comfortable attitude. The readings should be
made at the same time of day and at the same interval be-
tween meals. The pressure in both arms should be
measured and comparisons should be made only between
readings on the same arm. These precautions may seem
useless and even somewhat trivial, and the conditions dif-
ficult to control. But unless they are carefully observed the
readings will be false, no comparisons can be drawn be-
tween the readings on different days, and the instrument
will most probably be blamed. I have known this to hap-
pen so often that I can not emphasize too strongly the im-
portance of controlling all the essential conditions which
go to make accurate work.

The Value of Blood Pressure

In the past few years there has been a veritable ava-
lanche of blood pressure instrument salesmen who have
covered the country, sold instruments, and have made many
startling claims for the instrument. They have emphasized
its value out of proportion to what the instrument can do

182 ARTERIOSCLEROSIS

even in the hands of one familiar with all the defects. Con-
sequently it is not necessary to emphasize the value of blood
pressure. It seems best to utter a few words of caution in
regard to its interpretation.

The value lies not in the occasional estimation compared
with some other one reading, but in the frequent estimation
and in the visualization of the blood pressure picture. For
the great majority of diseases the blood pressure has no
particular value except to show that the circulation is not
materially disturbed. The limits of normal are rather wide,
so that consideration of the patient's age, sex, build, etc.,
will give us some idea of a base line, so to speak, for any one
person. Wide departures from relatively normal figures
are important, but are not diagnostic or, rather, pathogno-
monic. I can not help but feel that the diastolic pressure is
the most important part of the blood pressure picture. Per-
sistent high diastolic pressure means increased work for the
heart, which, if acting for a long time against the high
peripheral resistance, must eventually hypertrophy. The
arteries become thickened, lose their wonderful elasticity,
fibrous tissue is deposited in their walls, and the vicious
circle is established which leads to pathologic hypertension.

Blood pressure readings must be intimately mixed with
brains in order to be of any great value in diagnosis or
prognosis.

CHAPTER VIII
SYMPTOMS AND PHYSICAL SIGNS

General

Well developed arteriosclerosis shows four pathogno-
monic signs: (1) hypertrophy of the heart; (2) accentua-
tion of the aortic second sound; (3) palpable thickening ofi
the arteries; and (4) heightened blood pressure. However^
it must not be inferred that these signs must be present iir
order to diagnose arteriosclerosis. It has already been said
that a very marked degree of thickening, with even calcifi-
cation of the palpable arteries, may occur with absolutely
no increase of blood pressure, and at autopsy a small flabby
heart may be found.

While arteriosclerosis is usually a disease which is of
slow maturation, nevertheless cases are occasionally seen
which develop rather rapidly. The peripheral arteries have
been noticed to become stiff and hard in as relatively brief
a time as two years from the recognized onset of the disease.

Since involution processes are physiologic, as has been
described (vide infra), arteriosclerosis may assume an
advanced grade and run its course devoid of symptoms
referable to diseased arteries. It is doubtful whether the
sclerosis itself could produce symptoms, except in cases
later to be described, were it not that the organs supplied
by the diseased arteries suffer from an insufficient blood
supply and the symptoms then become a part of the symp-
tom-complex of any or all the affected organs.

There are cases, however, in comparatively young per-
sons where a combination of certain ill-defined symptoms
gives a clue to the underlying pathologic processes. These
symptoms of early arteriosclerosis are the result of slight

183

184 ARTERIOSCLEROSIS

and variable disturbances in the circulation of the various
organs. Normally there are frequent changes in the blood
pressure in the organs, but the vasomotor control of normal
elastic vessels is so perfect that no symptoms are noted by
the individual. When the arteries are sclerosed, they are
less elastic and the blood supply is, therefore, less easily
regulated. At times symptoms occur only after effort. The
patient may tire more readily than he should for a given
amount of mental or bodily exercise ; he is weary and de-
pressed, and occasionally there is noted an unusual intol-
erance of alcohol or tobacco. Vertigo is common, especially
on rising in the morning or in suddenly changing from a
sitting to a standing position. Some complain of constant
roaring or ringing in the ears. There may be dull head-
ache that the accurate fitting of glasses does not alleviate.
Unusual irritability or somnolency with a disinclination
to commence a new task may be present. Sometimes the
effort of concentrating the attention is sufficient to increase
the headache. This has been called "the sign of the pain-
ful thought." Numbness and tingling in the hands, feet,
arms, or legs are also complained of, and neuralgias, not
following the course of the nerves but of the arteries, also
occur. It is important to remember that the train of symp-
toms resembling neurasthenia in a person over forty-five
years old may be due to incipient arteriosclerosis. This
tardy neurasthenia frequently accompanies cancer, tubercu-
losis, diabetes, and incipient general paralysis, as well as
incipient arteriosclerosis.

Bleeding from the nose, epistaxis, taking place frequently
in a middle-aged person, sometimes is an early symptom.
The bleeding may be profuse, but is rarely so large as to be
positively harmful. In fact, it may do much good in reliev-
ing tension. Slight edema of the ankles and legs is seen.
Dyspnea on slight exertion is not uncommon. Dyspeptic
symptoms are not infrequent, pyrosis (heartburn), a feel-
ing of fullness after meals with belching or a feeling of

SYMPTOMS AND PHYSICAL SIGNS 185

weight in the epigastrium. The dyspeptic symptoms may
be so marked that one might almost speak of a variety of
arteriosclerosis, the dyspeptic type. For quite a while be-
fore any symptoms that would definitely fix the case as one
of undoubted arteriosclerosis, the patient complains that
foods which previously were digested with no difficulty now
give him gastric distress/ The examination of the stomach
contents of a patient presenting gastric symptoms reveals
usually a subacidity. The total acidity measured after the
Ewald test meal may be only 20 and the free HC1 may be
absent. Attention has been called to an unnatural pallor
of the face in early arteriosclerosis. Progressive emacia-
tion is sometimes seen in cases of arteriosclerosis and may
be the only symptom of which the patient complains.

Hypertension

Not all cases of arteriosclerosis are accompanied by in-
creased arterial tension. As has been stated in a previous
chapter, the blood pressure in the arterial system depends
chiefly on two factors; viz., the degree of peripheral (capil-
lary) resistance, and the force of the ventricular contrac-
tion. The highest arterial pressures recorded with the
sphygmomanometer occur not in pure arteriosclerosis but
in cases where there is concomitant chronic interstitial dis-
ease of the kidneys. When this is found there is always
arteriosclerosis more or less marked. In cases where the
arteries are so sclerosed that they feel like pipe stems there
may be an actual decrease in the blood pressure. Hence
the clinical measuring of the pressure in the brachial artery
alone is not sufficient for a diagnosis of arteriosclerosis. A
persistent high blood pressure even with normal urinary
findings is not a sign of arteriosclerosis. The high tension
later may lead to the production of sclerosis of the arteries,
but in these cases the kidney may be primarily at fault.

The impression must not be gained that hypertension in

186 ARTERIOSCLEROSIS

itself always constitutes a disease or even a symptom of dis-
ease. Hypertension itself is practically always a compen-
satory process. That is to say, it is the attempt on the part
of the body to equalize the distribution of blood in the body
when there is some poison causing constriction of the small
arteries. In this sense hypertension is not only essential,
but actually life-saving. A heart which is so diseased that
it can not respond to the call for increased action by hyper-
trophy of its fibers, would shortly wear out. The very fact
that the heart becomes enlarged and the tension in the
arteries becomes high, indicates that in such a heart there
was great reserve power. But while hypertension is largely
an effort at adjustment among the various parts of the cir-
culation, it nevertheless tends to increase, provided the
cause or causes which produced it act continuously. More-
over, as has been said (Chap. II), the arterioles do not re-
spond to increased work on the part of the heart by expand-
ing, but by contracting. A vicious circle is thus maintained
which eventually must lead to serious consequences.

Hypertension is then, if anything, only a symptom which
may or may not demand treatment. That hypertension
leads to the production of sclerosis of the arteries has been
repeatedly affirmed here. In certain cases it is good and
should not be experimented with. In other cases it is bad
and some treatment to reduce the tension must be tried.
The main point is to regard hypertension as one regards a
compensated heart lesion.

Prof. T. Clifford Allbutt divides the causes of arterio-
sclerosis clinically into three classes: (1) The toxic class
the results of poisons of the most part of extrinsic or-
igin, chiefly those of certain infections. In some of these
diseases, the blood pressures, as for example, in syphilis,
are ordinarily unaffected; in others, as in lead poisoning,
they are raised. (2) The class he calls, hyperpietic,* in

*From trieaia to squeeze, oppress or distress. Ilyperpiesis, therefore, signifies excessive
pressure.

SYMPTOMS AND PHYSICAL SIGNS 187

which an arteriosclerosis is the consequence of tensile
strength, of excessive arterial blood pressure persisting for
some years. A considerable example of this class is the
arteriosclerosis of granular kidney, but in many cases kid-
ney disease is, clinically speaking, absent. (3) The involu-
tionary class, in which the change depends upon a senile, or
quasisenile degradation. This may be no more than wear
and tear, a disposition of all or of certain tissues to pre-
mature failure partly atrophic, partly mechanical un-
der ordinary stresses; or it also may be toxic, a slow poison-
ing by the " faltering rheums of age." In ordinary cases
of this class the blood pressures for the age of the patient
are not excessive. Although the toxins of the specific
fevers, notably typhoid, as stated above, and influenza, have
been shown to produce arteriosclerosis, this, under favor-
able circumstances he believes tends to disappear. This
has been shown by Wiesel.

As the blood pressure is dependent on the resistance
offered by the capillaries and arterioles, there are only two
ways in which increased pressure can be brought about;
either by rendering the blood more viscous, or by the gen-
eration of some poison from the food taken into the body
which, acting on the vasomotor center or directly on the
finer vessels, arteriolar or capillary, sets up a constriction
over any large area, and mainly in the splanchnic area. In
regard to the liability to arteriosclerosis, this area stands
second only to the aortic and coronary areas. He believes
that arteriosclerosis itself has little effect in raising arterial
pressure. Many cases are seen in which with extreme ar-
teriosclerosis there was no rise in blood pressure, and some
in which pressures have been rising even long before the
appearance of arterial disease. Prof. Allbutt also believes
that in the hyperpietic cases the arteries undergo a tran-
sient thickening, which can be removed if the causes can be
reached and overcome.

Clinically speaking, then, hyperpietic arteriosclerosis is

1 88 ARTERIOSCLEROSIS

not a disease, but a mechanical result of disease. If the nar-
rowing of the arterioles is brought about by thickening due
to arteriosclerosis, then it would seem a priori that such
obliteration should cause a rise in pressure. Were the
vascular system a mere mechanical set of tubes and a pump,
this would happen, but other factors of great importance
must be taken into consideration besides the mechanical
factors; viz., chemical and biological factors. Thus, whole
parts may be closed and with compensatory dilatation in
other parts there would be little or no change in pressure,
unless there were hyperpiesis. In established hyperpiesis,
we note two conditions in the radial artery : first, a compara-
tively straight vessel with a small diameter; secondly, a
larger, more tortuous vessel, "the large leathery artery."
In the cases of the first group, hyperpiesis is often more
marked, although not appearing so to the examining finger,
than in the second class. In view of the difficulty of esti-
mating by touch alone the amount of hyperpiesis in a con-
tracted hard artery, it is often overlooked until a ruptured
vessel in the brain startles us to a realization of our mis-
take. The " narrow " artery is more dangerous than the
tortuous one, for with every change in pressure the passive
vessels of the brain must receive blood that under normal
conditions would go to other parts of the circulation.

In involutionary sclerosis there is a gradual thickening
and tortuosity of the vessel, which although it may be
greater than in the hyperpietic cases, yet is never so danger-
ous to life. The heart in hyperpiesis hypertrophies and
dilates, but such a heart is the result, not an integral part,
of the arterial disease.

The Heart

When the arterial tree becomes narrowed and the resist-
ance offered to the flow of blood thereby is increased, more
muscular work is required of the left ventricle and accord-

SYMPTOMS AND PHYSICAL SIGNS 189

ing to the general laws which govern muscles the ventricle
hypertrophies. There is an actual increase in number of
fibers as well as an increase in the size of the individual
fibers. Some of the best examples of simple hypertrophy
of the left ventricle are found under such circumstances.
The chambers as a rule do not dilate until the resistance be-
comes greater than the contraction can overcome, when
symptoms of broken compensation of the heart take place.
The hypertrophy of the left ventricle brings more of this
portion of the heart toward the anterior chest wall. The
enlargement is toward the left, also, consequently the apex-
beat is found below and to the left of its usual site, even an
inch or more beyond the nipple line. The impulse is heav-
ing, pushing the palpating hand forcibly up from the chest
wall. The visible area of pulsation may occupy three inter-
spaces and the precordium is seen to heave with every sys-
tole. On auscultation the second sound at the aortic carti-
lage is ringing, clear, and accentuated. Not infrequently,
too, the first sound is loud and booming, but has a curious
muffled sound that may even be of a murmurish quality.
The leaflets of the mitral valve may be the seat of sclerosis,
the edges are slightly thickened and do not quite approxi-
mate, thus causing a definite murmur with every systole.
This murmur may be transmitted out into the axilla and be
heard at the inferior angle of the left scapula.

Palpable Arteries

Not every artery that can be felt is the subject of arterio-
sclerosis, and, as has been stated, palpable arteries being
more or less a condition of advancing years, judgment as
to whether the artery is pathologically or physiologically
thickened may be a matter of individual opinion. A radial
artery that lies close to the lower end of the radius and can
actually be seen to pulsate when the hand is held slightly
extended on the back of the wrist, is easily felt, but must

190 ARTERIOSCLEROSIS

not, therefore, be considered a sclerosed artery. The radial
may he so deeply situated in the wrist of a fat subject that
it is difficultly palpable. Yet the two cases just described
may have arteries of identical structure, there being no
more "retrogressive changes in the one than in the other.
"Experience is fallacious and judgment difficult."

The small, contracted, wiry artery of a chronic nephritic
may feel like a pipe stem, but if properly felt the mistake
will not be made of considering such an artery an unusually
sclerosed one. When the wave is pressed out of such a
high tension artery, it is found that what seemed to be a
firm sclerosed vessel, was in reality an artery tightly
stretched over the column of blood.

Ocular Signs and Symptoms

It would not exaggerate too much to say that the exami-
nation of the eye grounds with the ophthalmoscope is the
most important aid in the early diagnosis of arteriosclero-
sis. Long before there are any subjective symptoms,
changes can be seen in the blood vessels of the retina which,
while not always diagnostic, at least call attention to a be-
ginning chronic disease. As I become more proficient in the
use of the ophthalmoscope, I am impressed with the impor-
tance of the ocular signs of arterial disease. I would urge
practitioners to familiarize themselves with this instrument.
The electrically lighted instruments on the market now have
so simplified the technic that any physician should be able
to see the grosser changes which take place in the arteries
and veins of the retina and in the disc. Frequently the
ophthalmologist is the first to recognize early arteriosclero-
sis. In the fundus are seen increased tortuosity of the reti-
nal vessels and their terminal twigs with more or less bend-
ing of the vessels at their crossings. The arteries are termi-
nal ones, and small patches of retinitis are therefore found.
The changes have been divided into (1) suggestive, (2)
pathognomonic.

SYMPTOMS AND PHYSICAL SIGNS 191

Under (1) are:

(a) Uneven caliber of the vessels,

(b) Undue tortuosity,

(d) An unusually light color of the breadth of the
artery.

Under (2) are:

(a) Changes in size and breadth of the retinal arteries
so that they look beaded,

(b) Distinct loss of translucency,

(d) Most important of all, the indentation of the veins
by the stiffened arteries.

There is yet another sign which appears to be pathogno-
monic. The arteries are pale, appear rigid and through the
center, parallel to the course, is a rather bright, fine thread-
like line. The appearance is known as the " silverwire ? '
artery. It is particularly constant in hypertension where
the most beautiful examples are seen.

Moreover, there is the arcus senilis, the fine translucent
to opaque circle surrounding the outer portion of the iris.
Practically every one with a well-marked arcus senilis has
arteriosclerosis, but vice versa not every one with even
marked arteriosclerosis has an arcus senilis.

In general, the symptoms are gradual loss of acute vision,
and attacks of transient loss of vision. The explanation
which has been offered for these phenomena is the contrac-
tion in a diseased central artery.

Nervous Symptoms

The onset of arteriosclerosis is, in the majority of cases,
so insidious that certain nervous manifestations, due in all
probability to disturbances in blood pressure, are present
long before the actual sclerosis of the arteries can be felt.

192 ARTERIOSCLEROSIS

These nervous symptoms are at times the sign posts to show
us the way to accurate diagnosis. There may be grad-
ual increase in irritability of temper, inability to sleep,
vertigo even extending to transient attacks of unconscious-
ness. Loss of memory for details frequently is an early
symptom of sclerosis of the cerebral arteries. Nervous in-
digestion may be present. Various paresthesias as numb-
ness, tingling, a sense of coldness or of heat or burning, a
sense of stiffness or even actual stiffness or weakness may
occur in the arms and legs, more frequently in the legs.
The pain complained of may be due to occlusion of an ar-
tery, although evidence for this is lacking. It has been
thought by some that the pain in angina pectoris might be
due to this cause. /

Several curious and interesting diseases which have
been thought by some to have arteriosclerosis as a basis are
accompanied by pain. Such are erythromelalgia, Ray-
naud's disease, "dead fingers," and intermittent claudica-
tion.

Erb has reported a large series of intermittent limp
(claudication) from his private practice. He finds that the
large majority of the cases occur in men. The abuse of
tobacco was evidently the main etiologic factor in about
half of the cases. Eepeated exposure to cold and the abuse
of alcohol were responsible for most of the other cases.
Curiously enough he finds that a history of syphilis was
present in only a small proportion of his cases. It is his
firm conviction that intermittent limping which he thinks
should be called angio sclerotic dysbasia is frequently in-
correctly diagnosed. It is mistaken for other troubles and
treated wrongly. As gangrene may develop this is par-
ticularly dangerous. The affection generally develops grad-
ually, although he has seen cases where the onset was rather
acute. The partial or complete lack of the pulse in the foot
is the one striking sign, together with the varying behavior
of the pulse, its disappearance when the feet are cold and

SYMPTOMS AND PHYSICAL SIGNS 193

its return after a warm foot bath or under other treatment.
Signs of general arteriosclerosis were present in nearly
every case. When there is a tendency to the development
of intermittent limp he finds that a valuable sign is the man-
ner in which the leg blanches when it is lifted repeatedly
while the patient is recumbent and becomes hyperemic later
when placed horizontally. In health this change occurs
more rapidly.

CHAPTER IX
SYMPTOMS AND PHYSICAL SIGNS

Special

Our conception of arteriosclerosis as a degenerative proc-
ess affecting the vascular tree rather than a disease, re-
moves the possibility of discussing special symptoms. As
a matter of fact, we know of very few organs where even
profound pathologic changes in the vascular system pro-
duced during life any symptoms which could be laid to
these arterial changes. Kind nature has given to us such
an excess of organs of every kind that the destruction of
large portions of any organ seems to affect the function
but little. So only particular groups of organs, which show
symptomatic changes as the result of arteriosclerotic proc-
esses, will be discussed. It is realized that this may not
give Teutonic completeness to the discussion, but it cer-
tainly saves paper and has a distinct practical value to the
long suffering reader.

Although arteriosclerosis is a disease which affects the
whole arterial system, it nevertheless never reaches the
same grade all over the body. The difference in the struc-
ture and functions of the various organs determines to great
extent the eventual symptomatology. Endarteritis obliter-
ans of a small sized artery in the liver or leg would lead to
no marked symptoms, as the circulation is so rich that the
anastomoses of the blood vessels would soon establish a
collateral circulation that would be perfectly competent to
sustain the function of the part. Quite different would it
be should one of the small arteries of the brain, the lenticulo-
striate, for example, which supplies the corpus striatum,
become the seat of a thrombosis or embolism caused by
arteriosclerosis. The arteries of the brain are terminal

194

SYMPTOMS AND PHYSICAL SIGNS 195

arteries and the blood supply would be cut off entirely with
a resulting anemic necrosis of the part supplied by the
artery and a loss of function of the part. What would be
of no moment in the leg or arm might prove even fatal in
the brain.

The further symptomatology, therefore, of arterioscle-
rosis depends entirely on the organ or organs most affected
by the interference with the blood supply. The following
groups may be recognized:

1. Cardiac.

2. Eenal.

3. Abdominal.

4. Cerebral.

5. Spinal.

6. Local vasomotor effects.

7. Pulmonary.

Cardiac

Most cases of arteriosclerosis sooner or later present
symptoms referable to the heart. When the organ is hyper-
trophied and is already working against an enormous
peripheral resistance, a slight excess of work put upon it
may cause a dilatation of the chambers with the resulting
broken compensation. There is dyspnea on slight exertion,
possibly some precordial distress, slight edema of the ankles
and lower legs and possibly scanty urine. With proper
care, a patient with such symptoms may recover, but the
danger of another break in compensation is enhanced. The
next attack is more severe. The edema is greater, there
may be signs of edema of the lungs, effusions into the serous
cavities may occur. The heart shows marked dilatation.
There is gallop or canter rhythm and there are loud mur-
murs at the apex. When a patient is first seen in this stage,
it may be quite impossible to state whether or not there is
true valvular disease of the heart. The muscle is usually
diseased in that there is fibroid degeneration of more or

196

ARTERIOSCLEROSIS

less extensive character. This factor causes the heart to
lose much of its elasticity and increases the tendency to
permanent dilatation. Such cases must be watched before
one can say that true valvular insufficiency is not present.
The fatal termination of such a case is quite like that of

Fig. 59. Aneurysm of the heart wall. (Milwaukee County Hospital.)

true valvular disease. There is increasing dyspnea, in-
creasing anasarca, and the patient usually succumbs to
edema of the lungs, drowned in his own secretions.

A very rare complication of the fibroid degeneration of
the heart muscle is aneurysm of the heart wall. (Fig. 59.)

SYMPTOMS AND PHYSICAL SIGNS 197

The apex of the left ventricle is most commonly the site of
the aneurysm and rupture occasionally occurs. Such an ac-
cident is rapidly fatal. In the arteriosclerotic process which
occurs at the root of the aorta, the coronary arteries become
involved both at the openings and along the courses of the
vessels. A branch or branches or even one artery may
become blocked as a result of obliterating endarteritis.
The arteries of the heart are not terminal vessels but as a
rule blocking of a large branch leads to anemic infarct.
These areas become replaced by fibrous tissue which in the
gross specimen appears as streaks of whitish or yellowish
color in the musculature. Anemic infarcts may not occur.
In such cases the anastomosis between branches of the cor-
onary arteries is unusually free. Through arteriosclerosis
of the coronary vessels extensive fibrous changes may oc-
cur that lead to a myocardial insufficiency with its attend-
ing symptoms dyspnea, irregular and intermittent heart,
gallop rhythm, edema, etc. One of the most distressing
and dangerous results of sclerosis of the coronary arteries
and of the root of the aorta is angina pectoris. While in
almost every case of angina pectoris there is disease of the
coronary arteries, the contrary does not hold true, for most
extensive disease, even embolism, of the arteries is fre-
quently found in persons who never suffered any attacks of
pain. This symptom group is more common in males than
in females and as a rule occurs only in adult life. "In men
under thirty-five syphilitic aortitis is an important factor."
(Osier.)

Since the valuable experiments of Eiianger on heart
block, considerable attention has been paid to lesions of the
Y-shaped bundle of fibers, a bundle arising at the auric-
uloventricular node and extending to the two ventri-
cles, known also as the auriculoventricular bundle of His.
Interference with the transmission of impulses through this
bundle gives rise to the, symptom group known as the
Stokes- Adams syndrome, which is characterized by: (a)

198

ARTERIOSCLEROSIS

slow pulse, (b) cerebral attacks vertigo, syncope, tran-
sient apoplectiform and epileptiform seizures, (c) visible
auricular impulses in the veins of the neck. Many of the
cases which occur are in elderly people the subjects of
arteriosclerosis.

So far as we now know all cases of the Stokes-Adams
syndrome are caused by heart block which is only another

Fig. 60. L,arge aneurysm of the aorta eroding the sternum. Death from rupture through
the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)

name for disease in the auriculoventricular bundle. Of
interest here is the fact that besides gummata, ulcers, and
other lesions of the bundle, definite arteriosclerotic changes
have been found.

"The investigation of a typical case of Stokes-Adams dis-
ease has shown that the symptoms of this case are caused
by some lesion in the heart which gives rise to the condi-

SYMPTOMS AND PHYSICAL SIGNS 199

tion now generally termed heart block. Practically all de-
grees of heart block have been observed, namely, complete
heart block and partial block with 4:1, 3:1, and 2:1 rhythm,
and occasionally ventricular silences. These stages oc-
curred during recovery.

"Experiments testing the reaction of the heart to various
extrinsic influences demonstrate that when the block is com-
plete the ventricles do not respond to influences presumably
of vagus origin, although the auricles still respond nor-
mally to such influences, that effects exerted upon the heart
presumably through the accelerators still influence the rate
of the ventricles as well as that of the auricles.

"When the block is partial the rate of the ventricular con-
traction varies proportionally with the rate of the auricular
contractions but only within certain limits. When these
limits are exceeded the block becomes more complete, i. e.,
a 2:1 rhythm may be changed into a 3:1 rhythm, this into
a 4:1 rhythm, and this into complete block, and vice versa.

' i The syncopal attacks are, in all probability, directly de-
pendent upon a marked reduction of the ventricular rate.
Such reductions of the ventricular rate are always asso-
ciated with an increase of the auricular rate, and it is
believed that the latter is the cause of the former." (Er-
langer. )

The epileptiform seizures of the syndrome may be caused
by the anemia of the brain resulting from failure of the
heart to supply a sufficient quantity of blood.

The apoplectiform attacks are most probably caused by
venous congestion when the slowing of the ventricular con-
tractions is not sufficient to cause convulsions, but will just
cause complete unconsciousness.

Renal

Chronic nephritis, hypertension, arteriosclerosis form a
most important trinity. Some stoutly affirm that in all
cases of high tension there is chronic renal disease. Cer-

200 ARTERIOSCLEROSIS

tainly the very highest blood pressures which we see occur
in the chronic interstitial forms of kidney disease. The
cause is most probably to be sought in some poison which
is elaborated in the kidney, is absorbed into the circula-
tion and acts powerfully either on the vasoconstrictor cen-
ter as a stimulus, or directly on the musculature of the
small arteries all over the body. Usually hypertension is
progressive but it may be temporary.

A man, 43 years old, entered the Milwaukee County Hos-
pital in uremic coma. The systolic blood pressure was
280-290 mm. Hg, the diastolic pressure 220 mm. ( Janeway
instrument). Under treatment his blood pressure gradu-
ally 4 became lower, at the same period the albumin and
casts gradually disappeared from the urine. In two weeks
from admission he seemed perfectly well, there were no
albumin or casts found in the urine, and the systolic blood
pressure was 136 mm., not a high figure for a muscular man
of the laboring class. It must be admitted, however, that
such cases are the exception, not the rule.

Patients suffering from the association of chronic nephri-
tis with hypertension die slowly, usually. There is gradual
development of anasarca. Headache is frequent and
severe. Pains all over the body may occur. The sight
may suddenly become dim or may even be lost. Dizziness
may be complained of and dyspnea is usually marked.
Cyanosis comes on, the pulse becomes weak, irregular or
intermittent, heart failure sets in, and the patient dies with
edema of the lungs.

Another class of renal arteriosclerosis is characterized
by a small granular kidney in which fibrous changes of a
patchy character have taken place. These scattered areas
are the result of obliterating endarteritis of renal arteries
here and there with consequent anemia, death of cells, and
replacement by fibrous tissue. It occurs as part of a gen-
eralized arteriosclerosis in which the whole arterial system
is the seat of diffuse (senile) sclerosis. The palpable ar-

SYMPTOMS AND PHYSICAL SIGNS 201

teries are usually beaded or even encircled with calcareous
deposits and the aorta is the seat of an extensive nodular
and ulcerating sclerosis. The heart is usually small, shows
extensive fibrous and fatty changes and possibly the condi-
tion known as " brown atrophy ;" the blood pressure is low.
Such cases do not show any special symptoms. They are
anemic, short of breath on exertion, have the appearance
and show the signs of senility.

In the first group it is, at times, difficult to say whether
the kidney disease or the arterial disease is the most im-
portant. From a clinical standpoint the decision is not
essential as the end results are much the same in both.
However, when actual uremic symptoms dominate the
picture, it becomes evident that the disease of the kidney is
the chief feature in the causation of the symptoms.

Abdominal or Visceral

There is an important group of cases to which but little
attention has been paid until quite recently. This is the
abdominal or visceral type of arteriosclerosis. It has been
stated that arteriosclerosis of the splanchnic vessels almost
invariably causes high tension. Among others, Janeway
has shown that general arteriosclerosis without marked
disease of the splanchnic vessels does not cause as a rule
increase of blood pressure.

There are cases in which the brunt of the lesion falls upon
the abdominal vessels. Such cases have been called
"angina abdominalis. " It has been suggested (Harlow
Brooks) . that this type of arteriosclerosis may be deter-
mined by constant overloading of the stomach with food,
especially rich and spiced food. This causes overwork of
the special arteries connected with digestion and so leads
to sclerosis of the vessels of the stomach, pancreas, and in-
testines. Personal habits probably influence to great ex-
tent the production of this more or -less localized condition.

The organs supplied by the diseased arteries suffer from

202 AKTERIOSCLEROSIS

changes analogous to those occurring in general or local
malnutrition, such as starvation, old age, or local anemias.
These changes are atrophy with hemachromatosis (brown
atrophy) or fatty infiltration and degeneration. Following
the degenerative changes there result connective tissue
growth and further limitation of the functionating power of
the affected organs.

Pain is a more or less constant symptom of visceral
sclerosis. In the early stages there may be only a sense
of oppression, of weight, or of actual pressure in the abdo-
men or pit of the stomach. There may be only recurring
attacks of violent abdominal pain accompanied by vomiting.
In some cases symptoms of tenderness in the epigastrium,
pains in the stomach after eating, vomiting and backache
may suggest gastric ulcer. There may be dyspnea and a
sense of anguish accompanied with a rapid and feeble pulse.
Hematemesis may make the symptom group even more like
ulcer of the stomach, and only the course of the disease
with the failure of rigid ulcer treatment and the substitu-
tion of treatment directed toward relief of the arterial
spasm with resulting betterment, enables one to make a
diagnosis. The condition may be present for years and the
symptoms only epigastric tenderness with dizziness and
sweating on lying down after dinner, as in one of Perutz's
patients. The attacks are probably due to spasmodic con-
traction of the sclerosed intestinal vessels with a resulting
local rise in blood pressure. The pains are most probably
due to the spasm of the intestinal muscles, and some think
they are located in the sympathetic and mesenteric plexuses.

This result of arteriosclerosis is not so uncommon, and
by keeping this cause of obscure abdominal pain in mind
we are now and then enabled to save a patient from opera-
tion.

An autopsy on a case which for many years had attacks
of abdominal pain and cramp-like attacks, with high blood
pressure and heart hypertrophy, showed extensive sclerosis

SYMPTOMS AND PHYSICAL SIGNS 203

of the abdominal aorta, superior mesenteric and iliacs.
These vessels were calcified. Hypertrophy of the left
ventricle was found. The kidneys were microscopically
normal. There were no changes in the ascending aorta but
in the descending portion there were scattered nodules and
small calcified plaques.

The attacks of pain from which this patient suffered for
many years, the hypertrophy of the left ventricle and the
increased blood pressure were thought to be directly due
to the sclerosis of the abdominal vessels.

Cerebral

It has been stated that arteriosclerosis is a general dis-
ease, yet certain systems of vessels may be affected far
more than others, and indeed there may be marked sclerosis
at one part of the body and none demonstrable at another
part.

In advanced sclerosis there may be one or more of a series
of accidents due to embolism, thrombosis, or rupture of the
vessels. Such conditions as transient hemiplegia, mono-
plegia or aphasia may occur. The attacks may come on
suddenly and be over in a few minutes; what Allbutt calls
"Larval apoplexies/' They may last from a few hours
up to a day, and are very characteristic. A patient aged
64 years with pipe stem radials and tortuous hard temporals
would be lying quietly in bed when suddenly he would
stiffen, the eyes would become fixed and the breathing
cease. In a few seconds consciousness returned, the patient
would shake himself, pass his hand over his brow and ask,
' ' Where am I ! Oh, yes, that 's all right. ' ' He had as many
as thirty of these attacks in twenty-four hours, none of
them lasting over one minute. To just what such attacks
are due, it is hard to say. Some have attributed them to
spasm of the smaller blood vessels of the brain, but there
have never been demonstrated in the vessels any constrictor
fibers.

204 ARTERIOSCLEROSIS

There is a well recognized form of dementia caused by
arteriosclerosis. In general paralysis of the insane and
in senile dementia the blood vessels are always diseased.
Milder grades of psychic disturbances are accompanied by
such symptoms as mental fatigue, persistent headaches,
vertigo, memory weakness and fainting. Aphasia, periods
of excitement and mental confusion occur in some. Later
stages are at times accompanied by inclination to fabulate,
loss of judgment, disorientation, narrowing of the external
interests, episodes of confusion and hallucinatory delirium.

The hemiplegias, monoplegias and paraplegias may oc-
cur again and again and last for one or two days. Unless
there has been rupture of the vessels, there is complete re-
covery as a rule.

In persons who have arteriosclerosis with high tension
attacks of melancholia are seen. There are at the same
time fits of depression, insomnia, irritability, fretfulness,
and a generally marked change in disposition. When the
tension is reduced by appropriate treatment these symp-
toms disappear, to recur when the tension again becomes
high. On the contrary, attacks of mania are accompanied
by low blood pressure. The dizziness and vertigo in cere-
bral arteriosclerosis are probably due to the stiffness of the
vessels which prevents them from following closely the va-
riations of pressure produced by position, and thus, at
times, the brain is deprived of blood and a transient anemia
occurs.

Arteriosclerosis of the cerebral vessels is always a seri-
ous condition. The greatest danger is from rupture of a
blood vessel. Another of the dangers is gradual occlusion
of the arteries bringing about necrosis with softening of the
brain substance. The latter is more apt to be associated
with psychic changes, dementia, etc.; the former, with
hemiplegia. It is curious that a small branch of the Sylvian
artery, the lenticulo-striate, which supplies the corpus stria-
turn, should be the one which most frequently ruptures.

SYMPTOMS AND PHYSICAL SIGNS 205

Where the motor fibers from the whole cortex are gathered
together in one compact bundle, a very small hemorrhage
may and does cause very serious effects. A comparatively
large hemorrhage in the silent area of the brain may cause
few or no symptoms.

Spinal

It is conceivable that arteriosclerosis of the vessels of
the spinal cord might cause symptoms which would be re-
ferred to the areas of the cord where the process was most
advanced. The lesions would be scattered and conse-
quently the symptoms might be protean in character.

True epileptic convulsions dependent on arteriosclerotic
changes are also seen and are not so uncommon.

This is on the whole a rare condition, much less common
than arteriosclerosis of the cerebral vessels. Collins and
Zabriskie report the following typical case :

"H., a fireman, fifty-one years old, was in ordinary good health until to-
ward the end of 1902. At that time he noticed that his legs were growing
weak and that they tired easily. Later he complained of a jerking sensation
in different parts of the lower extremities and at times of sharp pain, which
might last from several minutes to two or three hours. The legs were the
seat of a heavy, unwieldy sensation, but there was no numbness or other
paresthesia. About the same time he began to have difficulty in holding the I
urine, a symptom which steadily increased in severity. These symptoms con-
tinued until March, 1903, i. e., for three months, then he awakened one morn-
ing to find that he was unable to stand or walk, and the sphincters of the
bowels and bladder relaxed. There was no complaint of pain in the back or
legs, no difficulty in moving the arms, in swallowing or in speaking. He says
he was able to tell when his lower extremities were touched and he could
feel the bed and clothes. He was admitted to the City Hospital three weeks
later and the following record was made on April 21, 1903.

"The patient was a frail, emaciated man of medium height, who had the
appearance of being 55-60 years of age. He was unable to stand or walk.
When he was lying, he could flex the thigh and the legs slowly and feebly.
There was slight atrophy of the anterior and inner muscles, more of the left
than of the right side. The knee jerks and ankle jerks were absent. Irri-
tation of the soles caused quite a typical Babinski phenomenon. The patient
had fair strength in the upper extremities, but the arms tired very soon, he
said. The grip was moderate and alike in each hand. The motility of the
face, head, and neck was not noticeably 'impaired. There was no difficulty

206 ARTERIOSCLEROSIS

in swallowing, and articulation was not defective. Tactile sensibility was
slightly disordered in the lower extremities, although he could feel contact of
the finger, the point of a pin, and the like. Sensibility was not so acute as
normal; there was a quantitative diminution. Sensory perception was not
delayed. There was a distinct zone of slight hyperesthesia about as wide as
the hand above the femoral trochanters. Above that, sensibility was normal.
There was no discernible impairment of thermal sensibility. No part of the
body was particularly tender on pressure. A bedsore existed over the sacrum,
and there was excoriation of the genitals from constant dribbling of urine.

''Examination of the chest showed shallow respiratory movements. The
heart was regular, weak, there were no murmurs, the second sound was ac-
centuated. Examination of the abdomen showed that the liver and spleen
were palpable, but were not enlarged. The abdominal reflexes, both upper and
lower, were sluggish. The patient was slow of speech, likewise apparently of
thought. He did not seem to show an adequate interest in his condition, still
he was fully oriented and seemed to have a fair memory. His mental reflex
was slow. There were indications in the peripheral blood vessels and heart of
a moderate degree of general arteriosclerosis. The peripheral vessels
such as the radial, were palpable, the walls thickened, the blood pressure
increased.

' ' The patient did not complain of pain while he was in the hospital, a
period of four weeks, nor was there any particular change in the patient's
symptoms, subjective and objective, during this time. His mental state re-
mained clear until forty-eight hours before death, when he became sleepy,
stuporous, and comatose, dying apparently of cardiac weakness, which had set
in simultaneously with the clouding of consciousness."

At autopsy, except for a few small hemorrhages in the posterior horns of
the lower dorsal segments on the right side and a similar condition of the left
anterior horns, there was nothing noticed. On microscopic examination, there
was found widespread sclerosis of the vessels of the cord to a marked degree
with only slight thickening of the vessels of the brain. There were secondary
degenerations of ascending and descending type particularly marked at the
ninth dorsal segment. They included portions of all the tracts, the pyramidal
tract as well. The symptoms in brief were: (1) weakness and easily induced
fatigue of the legs; (2) peculiar sensations in the lower extremities, de-
scribed as jerky, numbness, heaviness, and occasionally sharp pain; (3)
progressive incontinence of urine; (4) progressive paraplegia.

Since one of the chief manifestations of syphilis is sclero-
sis of the arteries, neurologic cases characterized by irregu-
lar symptoms and signs which can not be placed in any of
the definite system disease groups, are possibly due to
irregularly scattered areas of sclerosis throughout the
spinal cord caused by obliterating arteritis. Such cases
are not so very uncommon. Several have come under my

SYMPTOMS AND PHYSICAL SIGNS 207

observation. Further studies of the spinal cords of these
cases at autopsy are necessary before a final opinion can
be given as to their dependence on arteriosclerosis of the
spinal vessels.

Local or Peripheral

When the arteriosclerosis in the peripheral arteries
reaches a stage where endarteritis obliterans supervenes,
there is usually no chance for a compensatory or collateral
circulation to be established. The area supplied by the ves-
sel undergoes dry gangrene. A portion of a toe or finger or
a whole foot or hand may shrivel up. It is more common to
see the spontaneous amputation take place in the lower ex-
tremities. The same effect may be produced by the plug-
ging of a vessel with a thrombus. There may be much pain
connected with the sudden blocking, whereas the gradual
obliteration of the blood supply of a toe or foot is not as a
rule at all painful. The condition is at times revealed more
or less accidentally when a patient injures his toe or foot
and discovers that there is no sensation in the part and that
the wound instead of healing is inclined to grow larger.

Other interesting vasomotor phenomena are frequently
connected with arteriosclerosis. Such a one is the curious
condition known as Raynaud's disease, a vascular disorder
which is divided into three grades of intensity: (1) local
syncope, (2) local asphyxia, (3) local or symmetrical gan-
grene. This is not the place to describe this condition ex-
cept to say that the condition called "dead fingers" is the
most characteristic feature of the first stage. Chilblains
represent the mildest grade of the second stage. The parts
are intensely congested and there may be excruciating pain.
Any one who has ever had chilblains knows how painful
they can be. The general health is not impaired as a rule,
although the attacks are apt to come on when the person is
run down. The third stage may vary from a very mild

208 ARTERIOSCLEROSIS

grade, with only small necrotic areas at the tips of the
fingers, to extensive multiple gangrene.

Another and very rare condition in which chronic endar-
teritis was the only constant finding is the disease described
by S. "Weir Mitchell and called by him erythromelalgia (red
neuralgia). This is "A chronic disease in which a part or
parts usually one or more extremities suffer with pain,
flushing, and local fever, made far worse if the parts hang
down." (Weir Mitchell.)

Probably the most frequently seen result of arteriosclero-
sis in the leg arteries is the remarkable condition, first de-
scribed by Charcot, known as intermittent claudication.
Persons the subject of this disease are able to walk if they
go slowly. If, however, any attempt be made to hurry the
step, there results total disability accompanied at times by
considerable cramp-like pain. The condition is much more
prone to occur in men than in women, and Hebrews seem
more frequently affected. The cause is most probably to
be sought in the anemia which results from the narrowing
of the channels through which the blood reaches the part.
The stiff, much narrowed arteries allow sufficient blood to
pass along for the nutrition of the part at rest or in quiet
motion. Just as soon as more violent exercise is taken,
calling for more blood, an ischemia of the part supervenes,
for the stiff vessels can riot accommodate themselves to
changes in the necessary vascularity of the part. A rest
brings about a gradual return of blood and the function of
the part is restored. Pulsation may be totally absent in the
dorsal arteries of the feet and when the legs are allowed to
hang down there is apt to be deep congestion.

In this connection a curious case reported by Parkes
Weber will not be out of place. The patient, a male, aged
42 years, complained of cramp-like pains in the sole of the
left foot and calf of the leg occurring after walking for a
few minutes and obliging him to rest frequently. When
the legs were allowed to hang over the side of the bed, the

SYMPTOMS AND PHYSICAL SIGNS ' 209

distal portion of the left foot became red and congested
looking. No pulsation could be felt in the dorsal artery of
the left foot or in the posterior tibial artery. There was no
evidence of cardiovascular or other disease. An ulcer on
the little toe had slowly healed, but cramp-like muscular
pains still occurred on walking. The disease had lasted
about five years without the appearance of gangrene.

Weber calls this case one of arteritis obliterans with in-
termittent claudication.

Pulmonary Artery

In the symptomatology of sclerosis of the pulmonary
artery the clinical signs and symptoms are mostly referable
to the obliterating endarteritis of the smaller vessels, while
the physical signs are more apt to reveal the involvement of
the main trunk. A history of severe infection in the past
is frequent, especially smallpox, and accompanying aortic
sclerosis with insufficiency of the mitral valve or stenosis of
this valve is the rule. Striking cyanosis is an early symp-
tom, while there is little if any dyspnea and edema. Inter-
mittent dyspragia is common. There seems to be no
tendency to clubbed fingers. Repeated hemorrhages from
the lungs without the formation of infarcts may occur.
There is usually an area of dullness at the upper left mar-
gin of the sternum and nearby parts, sensitive to pressure
and to percussion, and the heart dullness extends unusually
far towards the right. The diagnosis of the right ventricu-
lar hypertrophy may be substantiated by a fluoroscopic ex-
amination.

CHAPTER X
DIAGNOSIS

Early Diagnosis

Arteriosclerosis is essentially a disease of middle life
and old age. It is not unusual, however, to find evi-
dences of the disease in persons in the third decade and
even in the second decade. Hereditary influences play
a most important role, syphilis and the abuse of alcohol
in the family history are particularly momentous. The
recognition of the early changes in the arteries among
young persons depends largely upon how carefully these
changes are looked for. The difference in the point of view
of one man who finds many cases in the comparatively
young, and another man who rarely finds such changes early
in life, at times, depends upon the acuity of perception and
observation and not upon the fact that one man has had a
series of unusually young arteriosclerotic subjects. The
diagnosis of arteriosclerosis may be so easily made that the
tyro could not fail to make it. It is, however, the purpose
of this volume to lay stress on the earliest possible diagnosis
and, if possible, to point out how the diagnosis may be ar-
rived at. It is obviously much to the advantage of the pa-
tient to know that certain changes are beginning in his
arteries, which, if allowed to go on, will inevitably lead to
one or more of the symptom groups described in the pre-
ceding chapters.

The combination of (1) hypertrophied heart, (2) in-
creased blood pressure, (3) palpable arteries, and (4)
ringing, accentuated second sound at the aortic cartilage is,
in reality, the picture of advanced arteriosclerosis. If the
individual is in good condition much may be done by judi-

210

DIAGNOSIS 211

cious advice and treatment to ward off complications and
prolong life with a considerable degree of comfort. But we
should not wait until such signs are found before making a
diagnosis and instituting treatment. As in all forms of
chronic disease the early diagnosis is all important.

The history of the case is the first essential. Often a care-
ful inquiry into the personal habits of a patient, with the
record of all the preceding infectious diseases will give us
valuable information and may be the means of directing the
attention at once to the possible true condition. Particu-
larly must we inquire into the family history of gout and
rheumatism. An individual who comes of gouty stock is
certainly more prone to arterial degeneration than one who
can show a healthy heredity. Alcoholism in the family also
is of importance because of the fact that the children of
alcoholics start in life with a poor quality of tissue, and
conditions that would not affect a man from healthy stock
might cause early degeneration of arterial tissue in one of
bad ancestry.

What infectious diseases has the patient had? Even the
exanthemata may cause degenerations in the arteries, but,
as has been shown, such lesions probably heal completely
with no resulting damage to the vessel. Should the patient
have passed through a long siege of typhoid fever the prob-
lem is quite different. Here (vide supra) (Thayer), the
palpable arteries do appear to be sclerosed permanently.
Probably the length of time that the toxin has had a chance
to act determines the permanent damage to the vessel wall.
More potent than all other diseases to cause early arterio-
sclerosis is syphilis, and hence very careful inquiry should
be made in regard to the possibility of infection with this
virus. Not only the fact of actual infection but the dura-
tion and thoroughness of treatment are important matters
for the physician to know.

What is the patient's occupation? Has he been an
athlete, particularly an oarsman f Has he been under any

212 ARTERIOSCLEROSIS

severe, prolonged, mental strain? Is he a laborer? If so,
in what form of manual labor is he engaged? Such ques-
tions as these should never be overlooked, as they form the
foundation stones of an accurate diagnosis, and early, ac-
curate diagnosis, we repeat, is essential to successful
therapy.

We have called attention to the factor of sustained high
pressure in the production of arteriosclerosis. Constant
overstretching of the vessels leads to efforts of the body to
increase the strength of the part or parts. The material
which is used to strengthen the weakened walls has a higher
elastic resistance than muscle and elastic tissue, but a lower
limit of elasticity, and is none other than the familiar con-
nective tissue. In athletes, laborers, brain workers who are
under constant mental strain, and in those whose calling
brings them into contact with such poisons as lead, there is
every factor necessary for the production of high tension
and consequently of arteriosclerosis.

Another question in regard to personal habits is how
much tobacco does the patient use and in what form does he
use it? Our experience is that the cigar smoker is more
prone to present the symptoms- of arteriosclerosis than the
cigarette smoker, the pipe smoker, or the one who chews the
tobacco. A very irritable heart results not infrequently
from cigarette smoking but such is almost always found in
young men in whom the lesions of arteriosclerosis are ex-
ceedingly rare. The probabilities are that the arterioscle-
rosis in cigar smoking results from the slowly acting poison
which causes a rapid heart rate with an increase of pressure.

Last but not least, and perhaps the most important ques-
tion is, has the patient been a heavy eater? This I believe
to be a potent cause of splanchnic arteriosclerosis with the
resulting indigestion, cramp-like attacks, high blood pres-
sure, etc. In a joking manner we are accustomed to re-
mark, "Overeating is the curse of the American people."
There is, however, much truth in that sentence. Osier, than

DIAGNOSIS 213

whom there is 110 keener observer, states that he is more
and more impressed with the fact that overloading the
stomach with rich or heavy or spiced foods is today one of
the first causes of arterial degeneration. It stands to rea-
son that this is true. We know that organs exposed con-
stantly to hard work undergo hypertrophy, and that the
blood tension in those organs is high. Blood tension is,
after all, dependent on capillary resistance, and if the capil-
laries are distended with blood, the resistance is great.
The digestive organs can be no exception to this rule. In-
creased work means an increase of blood. This inevitably
causes distension of the capillaries with stretching of the
arteries and consequent damage to the walls. Once arterio-
sclerosis is present a vicious circle is established.

A man about forty-five consults us and says that he has
noticed recently that he gets out of breath easily; in tying
his shoes he experiences some dizziness. He finds that he
has palpitation of the heart and possibly pain over the
^precordial region now and then. He notices also that he is
irritable, that is, his family tell him he is, and he notices
that things that formerly did not annoy him, now are almost
hateful to him. On examination, one finds a palpable ra-
dial, a somewhat hypertrophied heart and slightly accen-
tuated second aortic sound. The blood pressure may be
high. The urine may or may not reveal any abnormalities.
Not infrequently, although no albumin may be found, there
are hyaline casts. Such a case of arteriosclerosis is evi-
dently not to be regarded as early. Then the question
arises, How are we to recognize early arteriosclerosis? I
do not believe that the solution of this problem lies entirely
in the hands of the physician. Some men are fortunate
enough to come up for an examination for life insurance
before an observant doctor who recognizes the palpable
artery, makes out the beginning heart hypertrophy and the
slightly accentuated second aortic sound. The patient will
tell you that he never felt better hi his life. He gets up at

214 ARTERIOSCLEROSIS

seven, works all day, plays golf, drinks his three to six
whiskies, and is proud of his physical development. But
the great mass of people are not fortunate from this stand-
point. They do not seek the advice of the physician until
they are stretched out in bed. They boast of the fact that
for twenty years they have never had a doctor. One may
well say that it is a problem how to reach such persons. It
seems to me that there can be but one way to do this. The
people must be taught that the duty of a physician is just
as much to keep them in health as it is to bring them back
to health when they are ill. To that end people should be
taught that at least twice a year they should be carefully
examined. I do not mean that the patient should present
himself to the doctor and, after a few questions the doctor
say cheerfully, "You are all right. " The patient should
be systematically examined. That means a removal of the
clothing and examination on the bare skin. Such coopera-
tion on the part of patient and doctor would save the pa-
tient years of active life and make of the doctor, what his
position entitles him to be, the benefactor to the community.
Too often careless work on the physician's part lulls the
patient into a false sense of security and he wakes up too
late to find that he has wasted months or years of life.
Early diagnosis of arteriosclerosis is only possible in excep-
tional cases unless people present themselves to the physi-
cian with the thought in mind that he is the guardian of
health as well as the healer.

There are patients who go to the ophthalmologist for
failing vision. Physically they feel quite well. They have
been heavy eaters, hard workers, men and women who have
been under great mental strain. On examination of the
fundus of the eye there is found slight tortuosity of the ves-
sels with possibly areas of degeneration in the retina. A
careful physical examination will usually reveal the signs
of arteriosclerosis elsewhere. We have mentioned fre-
quently high tension as an early sign. This must be taken

DIAGNOSIS 215

with somewhat of a reservation, for this reason: not infre-
quently a persistent high tension is the earliest sign of
chronic nephritis. The arteries may be pipe stem in char-
acter and the heart small and flabby. However, if one
watches for the palpably thickened superficial arteries (al-
ways bearing in mind the normal palpability as age ad-
vances) and the high tension, he can not go far wrong in his
treatment whether the case is one of chronic nephritis or of
arteriosclerosis.

There is also this to bear in mind. Arteriosclerosis may
be marked in some vessels and so slight in the peripheral
vessels that it can not with certainty be made out. But
when the radials are sclerosed, it is usually the case that
similar changes exist in other parts. Then too, there may
be marked changes at the root of the aorta leading to
sclerosis of the coronary vessels alone, and the first intima-
tion that the patient or any one else has that there is dis-
ease, may be an attack of angina pectoris. Except for
symptoms on the part of the heart there is no way to make
the diagnosis of sclerosis of the coronary arteries.

Differential Diagnosis

In arriving at a diagnosis, when the question is whether
or not arteriosclerosis is the main etiologic factor, the
most important fact to know is the age of the patient.
Other points that have been dwelt on fully must of necessity
also be borne in mind.

Possibly the chief conditions that may be confused with
some of the results of arteriosclerosis are pseudo angina
pectoris which may be mistaken for true angina pectoris,
and ulcer of the stomach, appendicitis (!) or other inflam-
matory abdominal condition which may be mistaken for
ansrina abdominalis.

Differential tables are sometimes of value in fixing the
chief points of difference graphically.

216

ARTERIOSCLEROSIS

Pseudo angina pectoris.

Etiology rather certain; hysteria,
neurasthenia, toxic agents, and reflex
irritations.

No age is exempt. Usually in
young people, chiefly females.

Paroxysms of pain occur spontane-
ously, are periodic and often noctur-
nal.

Pain, while severe, is diffuse and
sensation is of distension of heart.
No sense of real anguish.

Duration may be an hour or more.

Kestlessness and emotional symp-
toms of causative conditions are
prominent.

Usually no increase in arterial ten-
sion.

Prognosis favorable.

True angina pectoris.

Etiology not certain but almost al-
ways associated with arteriosclerosis
of the coronary arterie's and also
aortic regurgitation.

Age is important factor. Bare be-
fore forty, and males usually affected.

Paroxysms brought on by overex-
ertions or excessive mental emotion.
Barely periodic.

Intense pain, radiating down arm;
heart felt as in a vise. Sense of an-
guish and impending dissolution.

Duration from few seconds to sev-
eral minutes.

Silent and fixed attitude, rigidity
rather than restlessness.

Arterial tension is as a rule in-
creased.

Prognosis most unfavorable.

In differentiating between ulcer of the stomach and
angina abdominalis the following points may be of service:

Ulcer.

Occurs as a rule in young persons,
more often females.

Pain of boring character increased
by food and by certain positions with
food in stomach. Felt through to
left of spine.

Occult blood found in stools.

Considerable anemia apt to be
present.

Arterial tension usually low.

Angina abdominalis.

Only occurs in adults over forty
who have been heavy eaters and
drinkers, mostly males.

Pain cramplike, diffuse, although
more localized in epigastrium. Not
necessarily any connection with food.

No occult blood in stools.
Anemia more often absent.

Arterial tension high. (Splanch-
nic sclerosis.)

Diseases in Which Arteriosclerosis Is Commonly Found

There are certain more or less chronic diseases in which
arteriosclerosis is found either as a separate disease or as
a result of the chronic disease itself, or the sclerosis may be
the cause of the disease. As examples of the first class
are diabetes mellitus and cirrhosis of the liver. As exam-

DIAGNOSIS 217

pies of the second class are chronic nephritis, gout, syphilis,
and lead poisoning. Examples of the third class have al-
ready been fully described. Then certain rare diseases
that have been briefly described in this chapter, viz. : Eay-
naud's disease and erythromelalgia are frequently associ-
ated with demonstrable arteriosclerosis.

CHAPTER XI

PROGNOSIS

In a disease that presents as many vagaries as arterio-
sclerosis, it is not possible to give a certain prognosis.
Unfortunately we do not as a rule see the arteriosclerotic
until the disease is well advanced, or even after some of the
more serious complications have taken place. By that time
the condition is progressive, and while the prognosis is
grave the individual may live a number of years.

It is fortunate for the arteriosclerotic that mild grades
of the disease are compatible with a fairly active life. The
disease in this stage may become arrested and the patient
may live many years. Not only in the mild grades is this
possible. Even patients with advanced sclerosis may enjoy
good health provided the organs have not been so damaged
as to render them unfit to perform their functions. The
frequency with which we see advanced arteriosclerosis at
the postmortem table as an accidental discovery, attests
the truth of the foregoing statement. Yet how often does
it happen that individuals, apparently in the best of health,
suddenly succumb to an asthmatic or uremic attack, an
apoplexy, cessation of the heart beat, or a rupture of the
heart due to arteriosclerosis!

In order to arrive at an intelligent opinion in regard to
prognosis certain factors must be taken into consideration,
chief of which are: the seat of the sclerosis; the probable
stage; the existing complications; and, last and most impor-
tant, the patient himself. The whole man must be studied
and even then our prognosis must be most guarded.

It is much more dangerous for the patient when the
process is in the ascending portion of the arch of the aorta
than when it has attacked the peripheral arteries. Here,
at the root of the aorta, are the openings of the coronary

218

PROGNOSIS 219

arteries and the arteries supplying the brain are close by.
The coronary arteries here control the situation. When
loud murmurs are heard at the aortic orifice and the heart
is evidently diseased, it is useful to divide the endocarditis
into two types, the arteriosclerotic and the endocarditic.
The etiology of the former is sclerosis and the prognosis is
grave because of the liability, nay the probability, that the
orifices of the coronary arteries will become narrowed.
The etiology of the second type is in most cases rheumatic
fever or some other infectious disease, and the prognosis
is far better than in the first type. True, the two may be
combined. In such a case, the prognosis is entirely de-
pendent upon the course of the arteriosclerosis.

The involvement of the arteries in the kidneys is of con-
siderable importance, for it is usually bilateral and wide-
spread. As a rule, the disease makes but slow progress
provided that the general condition of the patient is good,
but at any time from a slight indiscretion or for no assign-
able cause, symptoms of renal insufficiency may appear and
may rapidly prove fatal.

It must not be thought that because the localization of
the arteriosclerosis in the peripheral arteries is usually the
most favorable condition that it is therefore devoid of ill
effects. On the contrary, very serious, even fatal, results
may be brought about by interference with the circulation
with resultant extensive gangrene of the part supplied by
the diseased arteries. The amputation of a portion of a
leg, for instance, may relieve, to some extent, an over-
burdened heart and prove life-saving to the patient, but the
neuritic pains are not necessarily relieved. The torture
from these pains may be excruciating.

No stage of the disease is exempt from its particular
danger. In the early stages of the disease before the
artery or arteries have had time to become strengthened by
proliferation of the connective tissue, there is the danger of
aneurysm. Later, the very same protective mechanism
leads to stiffening and narrowing of the arteries and hence

220 ARTERIOSCLEROSIS

to increased work on the part of the heart with all of its
consequences. Thrombosis is favored, and where- atherom-
atons ulcers are formed, embolism is to be feared.

As the complications and results of arteriosclerosis come
to the front every one must be considered by itself and as
if it were the true disease. There may be a slight apoplec-
tic attack from which the patient fully recovers, but the
prognosis is now of a grave character, as the chances are
that another attack may supervene and carry off the subject.
Yet, after an apoplectic attack, patients have lived for many
years. Probably the most noted illustration of this is the
life of Pasteur. He had at forty-six hemiplegia with grad-
ual onset. He recovered with a resulting slight limp, did
some of his best work after the stroke, and lived to be
seventy-three years old. Yet the exception but proves the
rule and the prognosis after one apoplectic stroke should
always be guarded.

The first attack of cardiac asthma is to be looked upon
as the beginning of the end. The end may be postponed
for some time, but it comes nearer with every subsequent
attack. One may recover from what appears to be a fatal
attack of cardiac asthma accompanied by edema of the lungs
and irregular, intermittent, laboring heart, but the recov-
ery is slow and the chances that the next attack will be the
fatal one are increased.

The significance of albuminuria is difficult to determine.
The kidneys secrete albumin under so many conditions that
the mere presence of albumin in the urine may have but
little prognostic value. Many cases are seen where there is
no demonstrable albumin, and yet the patient may suddenly
have a cerebral hemorrhage. As a general rule the urine
should be carefully examined, but not too much stress should
be laid on the discovery of albumin and casts. It is not
always possible to determine the extent of the kidney lesion
by the urinary examination, yet at any time a uremic attack
may appear and prove fatal.

PROGNOSIS 221

After all the most important fact for the patient is not
what the pathologist finds in his kidneys after he is dead,
but what the living functional capacity of the kidneys is.
This can now be determined in a variety of ways as the
result of extensive work carried out in quite recent years.
The simplest method of determining the functional capacity
of the kidneys is by the injection into the muscles of the
back of a solution containing 6 mg. of the drug phenol-
sulphonephthalein in one c.c. of fluid. This comes already
prepared in ampules, with full directions for its employ-
ment.* Some clinicians use indigo-carmine in place of
phthalein. The general consensus of opinion is in favor
of phthalein.

The nephritic test meal carefully worked out by Mosen-
thalf gives much valuable information. The determination
of the nonprotein nitrogen or the creatinin in the blood also
reveals the functional capacity of the kidney s.t

One might say that the appearance of albumin in the
urine of an arteriosclerotic where it had not been before,
is a bad sign, and in making a prognosis this must be taken
into consideration.

Bleeding from the nose is not infrequently seen in those
who have arteriosclerosis. It can hardly be called a dan-
gerous symptom as it can always be controlled by tampons.
There are times when epistaxis is decidedly beneficial as it
relieves headache, dizziness, and may avert the danger of
a hemorrhage into the brain substance. It is rare to have
nose bleed except in cases of high tension in plethoric
individuals. My experience has been that it has saved me
the trouble of bleeding the patient. It is always of serious
import in that it indicates a high degree of tension, but
there is scarcely ever any immediate danger from the nose
bleed itself.

Intestinal hemorrhage is always a grave sign. As has

*I have found the small colorimeter made by Hynson, Westcott and Dunning,
Baltimore, Mo., costing $5.00, a very practical instrument.
fMosenthal, II. O. : Arch. Int. Med:, 1915, xvi, 733.
JMyers and Lough: Arch. Int. Med., 1915, xvi, 536.

222 ARTERIOSCLEROSIS

been shown, arteriosclerosis of the splanchnic vessels not
infrequently occurs, and an embolus or thrombus may com-
pletely occlude the superior mesenteric artery. The
chances of the establishment of a collateral circulation are
small, as the arteries of the intestines are end arteries.
Necrosis of the part follows, blood is found in the stools,
and perforation or gangrene, or both, are apt to follow.
There may be blocking of small branches only, leading to
ulceration of the intestine. Under all conditions the prog-
nosis is serious.

The general condition of the patient, his build, physical
strength, powers of recuperation, etc., must be taken into
account in giving a prognosis. The more powerful the in-
dividual, the more favorable, as a rule, is the prognosis, with
this reservation always in mind, that the greater the body
development, the greater is the heart hypertrophy, and the
accidents from high tension must not be overlooked. Many
puny individuals with stiff, calcified arteries go about with
more ease than a robust man with thickened arteries only.
The differentiation as pointed out by Allbutt (page 186),
is well to keep in mind in giving a prognosis. It can not be
too strongly emphasized that it is the whole patient that we
must consider and not any one system that at the time hap-
pens to be the seat of greatest trouble, and by its group of
symptoms dominates the picture.

It is evident from what has been said that an accurate
prognosis in arteriosclerosis is no easy matter. Were
arteriosclerosis a simple disease of an acute character there
might be grounds for giving a more or less definite prog-
nosis. The most that can be said is that arteriosclerosis
is always a serious disease from the time that symptoms
begin to make themselves known. The gravity depends al-
together on the seat of the greatest arterial changes, and
is necessarily greater when the seat is in the brain than
when it is in the legs or arms.

The attitude of the patient himself also determines to a

PROGNOSIS 223

great extent the prognosis. Some men, especially those
who have always enjoyed good health, turn a deaf ear to
warnings and instead of ordering their lives according to
the advice of the physician, persist in going their own way
in the hope that the luck that has always been with them will
continue to stand at their elbows. Neither firmness nor
pleadings avail with some men. The only salve for the con-
science of the physician is that he has done his best to steer
the patient away from the shoals and breakers. In others
who realize their condition and take advantage of the advice
given as to the regulation of their lives, the prognosis is
generally favorable.

To sum up the chapter in a few words, I should say:
Always remember that the patient is a human being ; study
his habits and character and mode of life ; look at him as a
whole; take everything into consideration, and give always
a guarded prognosis.

CHAPTER XII

PROPHYLAXIS

Arteriosclerosis comes to almost every one who lives out
his allotted time of life. As has been noted within, many
diseases and many habits of life are conducive to the early
appearance of arterial degeneration. Decay and degenera-
tion of the tissues are necessary concomitants of advanc-
ing years and none of us can escape growing old. From
the period of adolescence certain of the tissues are com-
mencing a retrograde metamorphosis, and hand in hand
with this goes the deposit of fibrous tissue which later may
become calcified. The arterial tissue is no exception to this
rule, and we have already shown that certain changes nor-
mally take place as the individual grows older, changes
which are arteriosclerotic in type and are quite like those
caused in younger people by many of the etiologic factors
of the disease.

We are absolutely dependent upon the integrity of our
hearts and blood vessels for the maintenance of activity and
span of life. Respiration may cease and be carried on arti-
ficially for many hours while the heart continues to beat.
Even the heart has been massaged and the individual has
been brought back to life after its pulsations have ceased,
but such cases are few in number. We can not live without
the heart beat and the prophylaxis of arteriosclerosis con-
sists in the adjustment of our lives to our environment, so
that we may get the maximum amount of work accomplished
with the minimum amount of wear and tear on the blood
vessels.

The struggle for existence is keen. Competition in every
profession or trade is exceedingly acute, so much so that to
rise to the head in any branch of human activity requires

224

PROPHYLAXIS 225

exceptional powers of mind. Among those who are entered
in this keen competition, the fittest only can survive for any
period of time. The weaklings are bound to succumb. A
scion of healthy stock will stand the wear and tear far better
than will the progeny of diseased parentage.

It is only necessary to call attention to the part that
alcohol, syphilis and insanity play in heredity. These have
been discussed fully in the earlier part of this book.

We live rapidly, burning the candle at both ends. It is
not strange that so many comparatively young men and
women grow old prematurely. While heredity is a factor
as far as the prophylaxis of arteriosclerosis is concerned,
of far more importance is the mode of life of the individ-
ual. Scarcely any of us lead strictly temperate lives. If
we do not abuse our bodies by excessive eating and drink-
ing and so wear out .our splanchnic vessels and cause gen-
eral sclerosis by the high tension thereby induced, we abuse
our bodies by excessive brain work and worry with all their
multitudinous evils. The prophylaxis of arteriosclerosis
might well be labeled, "The plea for a more rational mode
of life. ' ' Moderation in all things is the keynote to health,
and to grow old gracefully is an art that admits of cultiva-
tion. Excesses of any kind, be they mental, moral, or
physical, tend to wear out the organism.

People habitually eat too much; many drink too much.
They throw into the vascular system excessive fluid com-
bined frequently with toxic products that cause eventually
a condition of high arterial tension. It has been shown how
poisonous substances absorbed from the intestines have
some influence on the blood pressure. Anything that causes
constant increase of pressure should be studiously avoided.

Mild exercise is an essential feature of prophylaxis. One
may, by judicious exercise and diet, make of himself a
powerful muscular man without, at the same time, raising
his average blood pressure. The man who goes to excess
and continually overburdens his heart, will suffer the con-

226 ARTEKIOSCLEROSIS

sequences, for the bill with compound interest will be
charged against him. It is a great mistake for any one to
work incessantly with no physical relaxation of any kind,
and yet, after all, it is not so much physical relaxation that
is necessary, as the pursuit of something entirely different,
so that the mind may be carried into channels other than
the accustomed routes. Diversification of interests is as a
rule restful. That is what every man who reaches adult
life should aim at. Hobbies are sometimes the salvation of
men. They may be ridden hard, but even then they are
helpful in bearing one completely away from daily cares
and worries. The man who can keep the balance between
his mental and physical work is the man who will, other
things being equal, live the longest and enjoy the best
health.

Nowadays the trend of medicine is toward prophylaxis.
We give the state authority to control epidemics so far as
it is possible by modern measures to control them.

We urge over and over again the value of early diagnosis
in all chronic diseases, for we know that many of them, and
this applies particularly to arteriosclerosis, could be pre-
vented from advancing by the recognition of the condition
and the institution of proper hygienic and medicinal treat-
ment.

It is the patent duty of every physician to instruct the
members of his clientele in the fundamental rules of health.
Recently the President of the American Medical Associa-
tion, in his address before the 1908 meeting, urged the
dissemination of accurate knowledge concerning diseases
among the laity. While this may be done by city and state
boards of health, it seems far better for the modern trained
physician to work among his own people. With concise
information concerning the modes of infection and the dan-
gers of waiting until a disease has a firm hold before con-
sulting the health mender, people should be able to protect
themselves from infections and be able to nip chronic proc-

PROPHYLAXIS 227

esses in the bud. But it is difficult to turn the average
individual away from the habit of having a drug-clerk pre-
scribe a dose of medicine for the ailment that troubles him.
It is really unfortunate that most of the pains and aches and
morbid sensations that one has speedily pass away with
little or no .treatment. Herein lies the strength of charla-
tanism and quackery. Unfortunate, yes, for a man can not
tell whether the trivial complaint from which he suffers is
any different from the one that was so easily conquered six
months ago. But instead of recovering, he grows worse.
Hope that springs eternal in the human breast, leads him
to dilly-dally until he at last seeks medical advice, only to
find that the disease has made such progress that little can
be done.

Instruct the public to consult the doctors tivice a year.
The dentists have their patients return to them at stated
intervals only to see if all is well. How much more rational
it ivould be if men and women past the age of forty had
a physical examination made twice a year to find out if all
is well.

The prophylaxis of arteriosclerosis is moderation in all
the duties and pleasures of life. This in no sense means
that a man has to nurse himself into neurasthenia for fear
that something will happen to him. As one grows in years
exercise should not be as violent as it was when younger,
and food should be taken in smaller quantities. Many forms
of exercise suggest themselves, particularly walking and
golf. Walking is a much neglected form of exercise which,
in these modern days with our thousand and one means of
locomotion, is becoming almost extinct. There is no better
form of exercise than graded walking. To strengthen the
heart selected hill climbing is one of the best therapeutic
methods that we have. The patient is made to exercise his
heart just as he is made to exercise his legs, and as with
exercise of voluntary muscles comes increase in strength,
so by fitting exercise may the heart muscle be increased in

228 ARTERIOSCLEROSIS

power. A warning should be sounded, however; against
over exercise. This leads naturally to hypertrophy with
all its disastrous possibilities. Men who have been athletes
when young should guard against overeating and lack of
exercise as they grow older. Many of the factors which
favor the development of arteriosclerosis are already there,
and a sedentary, ordinary life, such as office all day, club
in afternoon, a few drinks and much rich food, will inevi-
tably lead to well-advanced arterial disease.

Karl Marx in his famous Socialistic platform said: "No
rights without duties; no duties without rights. " So we
may paraphrase this and say: "No brain work without
moderate physical exercise in the open air ; no physical ex-
ercise without moderate brain work. ' '

There is yet one other point that is important, the com-
bination of concentrated brain work and constant whiskey
drinking. This is most often seen in men of forty-five to
fifty-five, heads of large business concerns who habitually
take from six to twelve drinks of whiskey daily, and with
possibly a bottle of wine for dinner. Such men appear
ruddy and in prime health but, almost invariably, careful
examination will reveal unmistakable signs of arterial dis-
ease. There is usually the enlarged heart and pulse of high
tension with or without the trace of albumin in the urine.
The lurking danger of this group of manifestations has so
impressed the medical directors of several of the large in-
surance companies that a blood pressure reading must be
made on all applicants over forty years of age. Should high
blood pressure be found, the premium is increased, as the
expectation of life is proportionately shorter in such men
than in normal persons.

Therefore, let every physician act his part as guardian
of health. Only in this way is the prophylaxis of arterio-
sclerosis possible.

CHAPTER XIII

TREATMENT

Although it has been rather dogmatically stated (vide
supra) that every one who reaches old age has arterioscle-
rosis, it must not be inferred that absolutely no exceptions to
this rule are found. Cases are known where persons of
ninety years even had soft arteries, and we have seen per-
sons of eighty whose arteries could not be palpated. When
infants and children are seen with considerable sclerosis,
it proves that, after all, it is the quality of the tissue even
more than the wear and tear, that is the determining factor
in the production of arteriosclerosis. It would be well if
those who can not bring healthy progeny into the world
were to leave this duty to those who can.

In general the treatment of arteriosclerosis is prophylac-
tic and symptomatic. In the preceding chapter I had some-
thing to say about prophylaxis in general; I must again
refer to it in detail.

Arteriosclerosis is essentially a chronic progressive dis-
ease, and the secret of success in the management of it is
not to treat the disease or the stage of the disease, but to
treat the patient who has the disease. To infer the stage
of the disease from the feeling of the sclerosed artery, may
lead to serious mistakes. Persons with calcined arteries
may be perfectly comfortable, while those with only moder-
ate thickening may have many severe symptoms. The
keynote is individualization. It is manifestly absurd to
treat the laboring man with his arteriosclerosis as one
would treat the successful financier. The habits, mode of
life, every detail, should be studied in every patient if we
expect to gain the greatest measure of success in the treat-
ment. One may treat fifty patients who have typhoid fever

229

230 ARTERIOSCLEROSIS

by a routine method and all may recover. Individualizing,
while of great value in the treatment of acute diseases, yet
is not absolutely essential in order that good results may
be obtained. Far different is it when treating a disease
like arteriosclerosis. One who relies on textbook knowl-
edge will find himself at a loss to know what to do. Text-
books can only outline, in the briefest manner, the average
case, and no one ever sees the average book case. At the
bedside with the patients is the place to learn therapeutics
as well as diagnosis. All that can be hoped for in outlining
the treatment of arteriosclerosis is to lay down a few prin-
ciples. The tact, the intuition, the subtle something that
makes the successful therapeutist, can not be learned from
books. So the man who treats cases by rule of thumb is a
failure from the beginning. There are certain general
principles that will be our sheet anchors at all times and
for all cases. The art of varying the application of these
fundamentals to suit the individual case, is not to be culled
from printed words.

Hygienic Treatment

Every man is more or less the arbiter of his own fate.
Granted that he has good tissue to begin life, his own habits
and actions determine his span of comfortable existence.
No one cares to live after his brain begins to fail, and the
failing brain is often due to disease of the cranial arteries.
The hygienic treatment resolves itself into advice in regard
to prophylaxis.

First and foremost is exercise. It has seemed to us that
the revival of out-of-door sports is one of the best signs of
promise of the preservation of a virile, hardy race. That
women, as well as men, indulge in the lighter forms of out-
of-door exercise should bring it about that the coming
generation will start in life under the most advantageous
conditions of bodily resistance.

Among all the forms of exercise, golf probably is the best.

TREATMENT 231

It is not too violent for the middle-aged man, yet it gives
the young athlete quite enough exercise to tire him. It is
played in the open. One is compelled to walk up and down
in pleasant company, for golf is essentially a companionable
game, while he reaps the full benefit of the invigorating ex-
ercise. The blood courses through the muscles and lungs
more rapidly; the contraction of the skeletal muscles serves
to compress the veins and so to aid the return of blood to
the heart: the lungs are rendered hyperemic, deeper and
fuller breaths must be taken; oxidation is necessarily more
rapid, and effete products, which if not completely oxidized
would possibly act as vasoconstrictors, are oxidized to
harmless products and eliminated without irritating the
excretory organs.

Other forms of out-door exercise that can be recom-
mended are tennis, canoeing, rowing, fishing, horseback rid-
ing, swimming, etc. Tennis is the most violent of all the
sports mentioned and might readily be overdone. Bowing
as practiced by the eights at college is undoubtedly too vio-
lent a form of exercise, and may be productive in later life
of very grave results. Canoeing is a delightful and in-
vigorating exercise. The muscles of the arms, shoulders,
and trunk are especially used, the leg muscles scarcely at
all. Nevertheless, the deep breathing that necessarily
comes with all chest exercises aerates every portion of the
lungs, and is of great benefit to the whole body.

Swimming as an exercise has much to recommend it. In
this sport all the muscles take part and at the same time the
chest is broadened and deepened.

All these methods of using the muscles to keep oneself in
trim, so to speak, are part and parcel of the general hygienic
mode of life that is conducive to a healthy old age. Exer-
cise can be overdone, as eating can be overdone. Both are
essential and yet both can be the means of hastening an in-
dividual to a premature grave.

When the arteriosclerosis has advanced so far that it is

232 ARTERIOSCLEROSIS

easily recognizable, certain forms of exercise should be abso-
lutely prohibited. Such are tennis, rowing and swimming.
Horseback riding to be allowed must be strictly supervised.
At times this may be an exceedingly violent exercise. As
an out-of-door sport, there is nothing that equals golf.
The physician, knowing the character of the course, and
the length of it, can say to his patient that he may play six,
nine, twelve, or eighteen holes, depending on the patient's
condition.

For those who are not able to get out, exercise in the
room with the windows open must take the place of out-of-
door sports. Here the use of chest weights is a most
excellent means of keeping up the tone of the muscles. By
adjusting the weights, the exercise may be made light,
medium, or heavy. Every physician should be familiar
with the chest weight exercises. They are not as good as
open air exercise but they undoubtedly have been the means
of saving years of life to many patients with arterial
disease.

There comes a time when all forms of exercise must be
prohibited on account of the dyspnea, edema, dizziness, etc.
It seems unwise to keep such a patient in bed, even though
the edema be considerable. Once on his back in bed he
becomes weak, and the danger of edema of the lungs or
hypostatic congestion of the bases, with subsequent bron-
chopneumonia, is very great.

Such patients may be allowed to sit up in a comfortable
chair with the legs supported straight out on a stool or
other chair. The half reclining position is not easy to as-
sume in bed. Considerable ingenuity must often be exer-
cised by the physician in making the patient comfortable
without increasing the symptoms from which the patient
suffers following the least amount of exercise. Although
such persons can not exercise actively, they should have
passive exercise in the form of massage, carefully given, so
that no injury is done to the rigid vessels. It is possible to

TREATMENT 233

rupture a vessel, the walls of which are encrusted with lime
salts, and full of small aneurysmal dilatations. Every pa-
tient must be watched carefully and measures instituted for
the individual.

Balneotherapy

As a tonic and invigorator, the cold or cool bath (shower
or tub), in the morning on arising can be highly recom-
mended. It promotes skin activity, is a stimulant to the
bowels and kidneys and to the general circulation, besides
being cleansing. We find today that the morning bath has
become such a necessity to the average American that all
new hotels are fitted with private baths, and old hotels, in
order to get patronage, are arranging as many baths con-
nected with sleeping rooms as is possible. Our generation
assuredly is a ruddy, clean-bodied one. What the actual
results of this out-door life and frequent bathing will be
for the race remains to be seen, but one can not but feel
that it must build up a stronger, more resistant race of
people, who not only enjoy better health than did their fore-
fathers, but enjoy it longer.

Not every one can stand a cold bath. It is folly to urge
it on one to whom it is distasteful, or on one who does not
feel the comfortable glow that should naturally result. For
the well, or those with a tendency to arteriosclerosis, or
those in whose families there have been several members
who had early arteriosclerosis, such proceedings as recom-
mended could not be improved upon. However, for the
person who has well recognized sclerosis, only warm baths
should be advised, and these not daily. The water should
be at a temperature of 90-95 F. Care should be taken
that persons sent to spas be cautioned against hot baths.
It is not inconceivable that the increased force of the heart
beat that accompanies a hot bath might be sufficient to rup-
ture a small cranial vessel. Hence, Turkish and Russian
baths should be most unqualifiedly condemned. As a mat-

234 ARTERIOSCLEROSIS

ter of fact, persons vary so in their habits with regard to
bathing that what might suit one person would do another
much harm.

Personal Habits

The personal habits of the individual, more than any
other factor, determine whether or not arteriosclerosis sets
in early in his life. The man or woman who is moderate in
eating and drinking, sees that the kidneys are kept in good
condition, and attends strictly to regularity of the bowels,
lays a good basis for the measure of health which is so
essential for happiness. It has been shown that sclerosis
of the splanchnic vessels may be due to constant irritation
of toxic products elaborated in digesting constantly enor-
mous meals. In obstinate constipation, many poisons, the
nature of which we do not know, are absorbed and circulate
in the blood. We have not sufficient data to prove that
constipation favors the production of arteriosclerosis, but
our impression has been that it does favor it. Constipa-
tion can often be relieved by a glass of water before break-
fast, a regular time to go to stool, and abdominal massage
or exercises. Some maintain that it is a bad habit only,
and can be readily overcome. Whatever is done, avoid
leading the patient into the drug habit, for the last state
of the patient will be worse than the first. Habits of sleep
are not of such great importance. Most persons get enough
sleep except when under severe mental strain. Most adults
need from seven to eight hours ' sleep, although some can
do all their work and keep in prime health on five or six
hours' sleep.

Tobacco has been accused of causing many ills and has
been thereby much maligned. We can not see that the use
of tobacco in any form in moderation is harmful to most
men. Undoubtedly the blood pressure is raised when mild
tobacco poisoning occurs, and individual peculiarities of re-
action to the weed are multitudinous. But to condemn off-

TREATMENT 235

hand its use is the height of folly. There is no reason why
the arteriosclerotic who has always used tobacco in modera-
tion, should not continue to use it, whether he smoke ciga-
rettes, cigars, or pipe. His supply should be decreased, but
there is no sense in depriving a man of one of the solaces of
life, unless, as is sometimes the case, abstinence is easier
for the patient than moderation.

As for alcohol, opinions differ widely.* Some see in al-
cohol one of the most frequent causes of arteriosclerosis;
others do not believe that the part played by alcohol is a
serious one, only in conjunction with other poisonous sub-
stances is it dangerous. Probably unreasoning fanaticism
has had much to do with the wholesale condemnation of
alcoholic beverages. The general effect of alcohol is to
lower the blood pressure by causing marked dilatation of
all the vessels of the skin. True, the alcohol circulates in
the blood, and is broken up in the liver, and this organ
would seem to bear the brunt of the harm done. Alcoholic
drinks in moderation, I do not believe have any deleterious
effect on health. On the contrary, I believe that they may
in some cases assist digestion and assimilation. Indiscrim-
inate indulgence is to be condemned, as is overindulgence
in exercise or eating. What may be moderate for A, might
be excessive for B. Every man is then the arbiter of his
own fortune and within his own limits can indulge moder-
ately (a relative term after all) without fear of doing him-
self harm. In advanced arteriosclerosis it is necessary to
decrease the supply of alcohol just as it is necessary to cut
down the food supply. This must rest entirely on the
judgment of the physician, who must not act arbitrarily,
but must have his reasons for every one of his orders.

Dietetic Treatment

Most persons eat too much. We not only satisfy our
hunger, but we satisfy our palates, and, instead of putting

*Discussion of alcohol at present has value only as it relates to the past. The present
is dry. The future is in the lap of the gods.

236 ARTERIOSCLEROSIS

substantial foodstuffs into our stomachs, we frequently take
unto ourselves concoctions that defy description.

Foodstuffs are composed of one or all of three classes:
(1) proteins, (2) fats, (3) carbohydrates. As examples
of the first are beef and white of egg; of the second, the
oils, butter, lard ; of the third, sugar, potato, beet, corn, etc.

The physiologists and chemists have shown us that both
endogenous and exogenous uric acid in excess will cause a
rise of blood pressure, but the bodies most concerned in
the production of elevated blood pressure are the purin
bodies, those organic compounds which are formed from
proteins and represent chemically a step in the oxidation
of part of the protein molecule to uric acid. Eed meat
contains more of the substances producing purin bodies
than any other one common foodstuff, and for this reason
the excessive meat eater is, ceteris paribus, more apt to
develop arteriosclerosis comparatively early in life.

The fats and carbohydrates contain practically no sub-
stances that react on the body of the ordinary individual
in a deleterious manner during their digestion. The extra
work that is put on the heart by the formation of many
new blood vessels in adipose tissue is the only harmful effect
of overindulgence in these foodstuffs.

It has been found that nitrogen equilibrium can be main-
tained at a wide range of levels. Formerly 135-150 gms.
of protein daily were considered necessary for a man doing
light work. Now it is known that half that amount is suf-
ficient to keep one in nitrogenous equilibrium, and to enable
one to keep his weight. A person at rest requires even less
than that. One who is engaged in hard physical labor burns
up more fuel in the muscles, and so must have a larger
fuel supply.

Although we habitually eat too much we drink too little
water. For those who have any form of arterial disease
an excess of fluid is harmful, as the vessels become filled
up and a condition of plethora results, which necessarily

TREATMENT 237

reacts injuriously on the heart and circulation. The drink-
ing of a glass of water during meals is, in the author's
opinion, good practice. The water must be taken mouthful
at a time, and not gulped down. If this is done, there
results sufficient dilution of the solid food to enable the
gastric juices successfully and rapidly to reach all parts
of the meal.

Some are in favor of a rigid milk diet for those who
have arteriosclerosis. Some men have lived on nothing
but milk for several years and have not only kept in good
health, but have actually gained weight and led at the
same time active lives. It has been held by others that rigid
milk diet is positively harmful on account of the relatively
large quantity of calcium salts that are ingested. This was
thought to favor the deposition of calcareous material in
the walls of the already diseased arteries. While possibly
there may be some danger of increased calcification, the
majority of clinicians are in favor of a milk cure given at
intervals. Thus the patient is made to take three to
four quarts daily for a period of a month. There is then a
gradual return to a general diet, exclusive of meat, for
several weeks, then another rigid milk diet period.

If we are bold enough to follow Metschnikoff in his theo-
ories of longevity, we might advise resection of the large
intestine, on the ground that it is an enormous culture tube
that produces prodigious amounts of poisonous substances
which are thrown into the general circulation. To combat
such a grave (?) condition as the carrying of several feet
of large intestine, we are recommended to take buttermilk
or milk soured by means of the b. acidus lacticus. Clinical
experience has taught that in arteriosclerosis buttermilk
is of great value, whether it be the natural product, or made
directly from sweet milk by the addition of the bacilli. The
latter is a smoother product and has, to my mind, a de-
lightful flavor. It may be diluted with Vichy or plain soda
water. Cases that can not take milk or any other food will

238 ARTERIOSCLEROSIS

often take buttermilk, and do well on this restricted diet.
From two to four quarts daily should be taken. It should
be drunk slowly as should milk.

Medicinal

It has long been thought that the iodides have some spe-
cific effect on the advancing arteriosclerosis, checking its
spread, if not really aiding nature to a limited restoration
of the diseased arteries. It is possible that the eulogies
upon the iodides owe their origin to the successful treat-
ment of syphilitic arteriosclerosis, in which condition these
drugs have a specific action. However that may be, there
I is no doubt that the administration of sodium or potassium
I iodide is good therapeutics in cases of arteriosclerosis.

Unfortunately many persons have such irritable stom-
achs that they can not take the iodides, even though they be
diluted many times. They may be made less irritating by
giving them with essence of pepsin. Unless the case is
syphilitic, it is doubtful whether it is of value to increase the
dose gradually until a dram or even more is taken three
times daily after meals. Usually a maximum dose of ten
grains seems to be quite sufficient. This may be taken three
times a day, well diluted, for three months. There follows
a month's rest, then the treatment is resumed for another
period of three months, and so on. Either sodium or potas-
sium iodide in saturated solution may be given. The so-
dium salt is possibly less irritating, and contains more free
iodine than the potassium salt, although the latter is more
generally used. The strontium iodide may also be used.

One sees a patient now and then who can not take the
iodides, however they may be combined. For such patients
one may obtain good results with iodopin, sajodin, or other
of the preparations put up by reputable firms. Personally I
have never yet seen a patient who could not take the ordi-
nary iodides in some form or other, and I am opposed to
ready made drugging.

TREATMENT 239

The action of the iodides is to lower the blood pressure,
and they are of greatest value when the blood pressure
is high, and when headache and precordial pain are present.

When the case is moderately advanced, very mild doses,
gr. y 2 , morning and evening, of the thyroid extract may be
given. It is generally believed that the internal secretion
of the thyroid and the adrenal are antagonistic. That the
thyroid secretion lowers blood pressure in certain forms of
hypertension is certain, possibly on account of its iodine
content. Some combinations of iodine and thyroid such as
the iodothyroidin have been used and have had some meas-
ure of success attributed to them.

Hypertension does not always demand active measures
for its reduction. Viewed from, the physiologic stand-
point, hypertension is but the expression of a compensating
mechanism which is designed to keep the blood moving-
through narrowed channels. Heart hypertrophy then is
absolutely essential to the maintenance of life. It has been
said that the highest blood pressures occur in chronic dis-
ease of the kidneys. The poisonous substances produced
in the kidneys must exert their action through absorption
into the general blood stream. This toxin may be com-
pletely eliminated, if we accept as our criterion the reduc-
tion of tension to normal together with the complete return
of the affected individual to health. A concrete example
is as follows: A man aged 44 years was brought to the
Milwaukee County Hospital in coma. His systolic blood
pressure was over 280 mm. Hg, diastolic 170 mm., his urine
contained considerable albumin and many casts. He had
general anasarca. Venesection was done at once and 300
c.c. blood obtained. Immediately following this operation
the pressure was 210-150, but within twelve hours it was
again above 280-170. He was given no medication to re-
duce pressure except that he was freely purged. He was
given a steam sweat bath daily. Frequent blood pressure
readings were taken. Within seven days the pressure was

240 ARTERIOSCLEROSIS

130-86. He had, in the meantime, completely recovered
from his symptoms. He was kept in the hospital for two
weeks longer assisting in the work on the ward, and he was
discharged with a pressure (systolic) between 130 and 136
diastolic 80-84. The treatment was rest in bed, free purg-
ing, venesection, and sweat baths, simple but exceedingly
effective.

Should there be actual indications for reducing the blood
pressure, I must admit that it can not always be done. The
majority of cases will do well on the sodium nitrite or
erythrol tetranitrate. However, these do not always lower
blood pressure and keep it within normal limits. When a
man has very high tension we do not wish to reduce it to
what it should normally be for the age of the patient, as
symptoms of collapse might set in at any time under such
conditions.

Observations made with the sphygmomanometer* show
that the effect of nitroglycerin is transient or of no effect
except in doses which are relatively enormous (one drop of
the one per cent solution given every hour). Sodium ni-
trite may lower the blood pressure but the effects will have
worn off in two hours. It is the same with erythrol tetrani-
trate. Sodium sulphocyanate in doses of from one to three
grains three times a day is highly recommended by some.
My own experience with it does not lead me to believe that it
is of any great value in hypertension. It, however, may be
tried. Benzyl benzoate has been used recently to reduce
the high blood pressure of hypertension. Macht has re-
ported some success. In the author's hands it has been
efficacious in a few cases. As long as the patient takes the
drug the pressure may be slightly reduced, but upon the
withdrawal of the drug the pressure returns to its former
level. It is well worth a trial and further experimentation

*Miller, Jos. L,. : Hypertension and the Value of the Various Methods for Its Re-
duction. Jour. Am. Med. Assn., 1910, liv, p. 1666.

TREATMENT 241

may reveal better methods of administration. The dose is
from 2 to 6 c.c. mixed with water at intervals.

In the hypertension of the menopause some have had
success with large doses of corpus luteum extract. As
a matter of fact the drug treatment of hypertension,
when it becomes necessary to treat this condition with
drugs, has suffered a notable set-back since more careful
control has been made with the blood pressure instruments.
In giving any of the depressor drugs their action should
be controlled by blood pressure measurements, for only
in this way can we be sure that the drug is exerting its
physiological effect and we may expect results. The indi-
vidual reaction to these drugs varies greatly and no rule
for dosage can be dogmatically laid down. The only suc-
cessful therapy is rigid individualization. This is the key-
stone to treatment in cases of arteriosclerosis and high
tension.

It must not be inferred from what has been said that the
nitrites are of no value. They are of decided value but
they have their limitations. The most evanescent of these
drugs is amyl nitrite. This is put up in the form of cap-
sules, or pearls, containing from one to three minims. When
it is desired to dilate the peripheral vessels suddenly, one
or two of these capsules are broken in a cloth held to the
nose. The effect is almost instantaneous. There is flush-
ing of the face and other peripheral vessels, particularly
near the head, denoting a relaxation and widening of the
bed of the blood stream, and a consequent decrease in pres-
sure in the arteries. These effects are over in a short
while. It is only used in attacks of cardiac spasm, as in
angina pectoris. Nitroglycerin, the Spiritus Glonoini of
the U. S. P., acts in about the same manner as amyl ni-
trite but the effects last usually a trifle longer. One drop
of the one per cent solution may be given every hour until
physiologic effects are produced. It may be given hypo-
dermically. This may be a means. of reducing pronounced

242 ARTERIOSCLEROSIS

high tension. This drug has been found of benefit espe-
cially in cases where arteriosclerosis combined with chronic
nephritis causes cardiac asthma. The other drug which
may be of service in these conditions, one whose sphere
of action is somewhat broader, because its effects are more
lasting, is sodium nitrite. This is given in water in doses
of one to three or five grains every four hours. Some
have objected to the use of this drug, but my experience
has made me place considerable confidence in its harmless-
ness, provided that the patient is carefully watched. This,
however, applies to all of the nitrite compounds. My ex-
perience with erythrol tetranitrate is not large. It may
be used 'in place of sodium nitrite.

For a mild case, one often finds that sweet spirits of
niter is sufficient to control the pressure and relieve the
distressing symptoms, and it is undoubtedly the least harm-
ful of all the nitrites. Drugs that are of great value, but
of which little is noted in textbooks, are aconite and vera-
trum viride. Both of these drugs are well known to be
marked circulatory depressors. Veratrum viride in my ex-
perience should be very cautiously used, and never used
unless a trained attendant is constantly at hand. With re-
gard to aconite I have no such feeling, and a mixture of
tincture of aconite and spiritus etheris nitrosi may be
given for several weeks with no fear of doing any harm.
Personally, of all the drugs mentioned, I prefer the nitrite
of sodium or the combination just given. They may be ad-
vantageously alternated.

My own feeling is that the most successful means of treat-
ment of acute high tension is without the use of drugs.
The most important measure is absolute rest in bed. This
often suffices to lower the blood pressure and to arrest the
symptoms produced by high tension. Venesection I believe
is also of value. True the arterioles appear to contract
almost immediately upon the lessened quantity of blood,
or there is immediate interchange of serum from the tissues

TREATMENT 243

which brings the blood volume back to the original amount.
Whatever happens the pressure is not greatly reduced, at
times not reduced at all, but often the symptoms are re-
lieved. Hot packs or sweat baths assuredly do reduce the
pressure in many cases. This seems to me to be an ex-
ceedingly valuable measure. Finally the diet should be
nourishing, but very light, not too much fluid should be
ingested, and the bowels should be freely opened.

With the fibrolysin of Merck, I have had no experience.
Some men assert that they have had good results from
its use, but on the whole the evidence is not highly favor-
able.

Morphine is invaluable. No drug is of such value in the
nocturnal dyspneic attacks that occur in the late stages of
arteriosclerosis when the heart or the kidneys are failing.
Morphine not only relaxes spasm and quiets the cerebral
centers, but is an actual heart stimulant under such condi-
tions, and should never be withheld, as the danger of the
patient's becoming addicted to its use is more fanciful than
real. However, morphine, at times, suppresses the secre-
tion of urine. So that if after trial the urine becomes
scanty and the edema increases, recourse must be had to
other drugs. The various hypnotics may be used with
caution. One which seems to be very useful is adalin.

As heart stimulants, one may use strychnine, spartein,
caffein, or camphor. In desperate cases, where a rapidly
diffusible stimulant is needed, a hypodermic syringeful of
ether may be given, and repeated in a short while.

Several years ago a so-called serum was brought out by
Trunecek which was said to have a favorable effect on the
metabolism of the vessel walls. It was given at first hypo-
dermatically or intravenously but the former method was
painful. It was later stated that given by mouth it acted
just as well. The results with the Trunecek serum have not
come up to the expectations that the early favorable reports
promised. The original serum was composed as follows :

244 ARTERIOSCLEROSIS

NaCl, 4.92 gm.; Na 2 S0 4 , 0.44 gm.; Na 2 C0 3 , 0.21 gm.;
K 2 S0 4 , 0.40 gm. ; aqua destil. q. s. ad. 100.0 c.c. Later
this was modified for internal use to the following pre-
scription :

It Natrii chlor 10. gm.

Natrii sulphat 1. gm.

Natrii carbcmat 0.40 gm.

Natrii phosphat 0.30 gm.

Calcii phosphat.

Magnesii phosphat. aa 0.75 gm.

M. Ft. cachets No. XIII.

The contents of every cachet corresponds to 15 c.c. of the
fluid serum or to 150 c.c. of blood serum. The preparation
called antisclerosin consists of the salts contained in the
serum. As to its efficacy, I can not judge, as I have never
felt that it was worth while to use it. Reports of cases in
which it has been tried do not speak very highly of it.

In the general treatment of arteriosclerosis, there is no
one factor of more importance than the regular daily bowel
movement. Attention to this may save the patient much
discomfort and even acute attacks of cardiac embarrass-
ment. The choice of the purgative is immaterial, with this
reservation only, that the mild ones, such as cascara, rhu-
barb, licorice powder and the mineral waters, should be
thoroughly tried before we resort to the more drastic pur-
gatives. Plenolphthalein in 3 to 5 grain doses acts remark-
ably well in some people as a pleasant laxative. Agar-agar
with or without cascara may be useful.

Liquid paraffin under a variety of names is a most useful
and efficacious laxative. As its action is purely mechanical
it may be taken indefinitely without doing harm to the in-
testinal musculature.

The old Lady Webster dinner pill is an excellent tonic
aperient. When the heart is embarrassed and edema of the
legs and effusion into the serous cavities have taken place,
then it becomes necessary to use the drastic purgatives
that cause a number of watery movements. Epsom salts

TKEATMENT 245

given in concentrated form, elaterin gr. 1-12, the compound
cathartic pill, blue mass and scammony, or even croton
oil may be used. Since the observation of a greatly con-
gested intestine from a patient who had been given croton
oil, I have ceased to use this purgative, and I doubt much
whether its use is ever justifiable in these cases.

The management of the ordinary case of arteriosclerosis
resolves itself into a careful hygienic and dietetic regime
with the addition of the iodides, aconite, or the nitrites.
A diet consisting of very little meat, alcohol in moderation
or even absolutely prohibited, and not too much fluid should
be prescribed. Condiments and spices should also be used
sparingly. Cold baths, shower baths, cold and hot sheets
alternating, are of great benefit in assisting the heart to do
its best work by making the large capillary area of the skin
more permeable. It is not true that such baths raise the
blood pressure so markedly. Certain acts, as sneezing, vio-
lent coughing, etc., increase the blood pressure much more
than judicious bathing.

Symptomatic Treatment

The fact that arteriosclerosis really loses much of its own
identity and, in later stages, becomes merged with the symp-
tomatology of the diseases of various organs, as the kidney,
brain, heart, compels us, for completeness 7 sake, to say a
few words about the treatment of these complications.

One of the results of arteriosclerosis of the coronary
arteries, angina pectoris, demands prompt treatment. In
the acute attack, the chief object is to relieve the spasm and
pain. Pearls of amyl nitrite should be inhaled, and mor-
phine sulphate with atropine sulphate given hypodermat-
ically at the very earliest moment. It is senseless to with-
hold morphine. The only possible reason for withholding
it would be uncertainty as to the diagnosis. It is probably
better to err on the safe side, and should the case prove to

246 ARTERIOSCLEROSIS

be one of pseudo angina, in the next attack sterile water
can be given instead of the morphine and atropine.

When a patient is seen in the condition of broken com-
pensation with the much dilated heart, anasarca, dyspnea
and suppression of urine, there is no better practice than
venesection. Especially is this valuable when the tension is
still fairly high and the individual is robust. Following the
abstraction of six to eight ounces of blood (300-500 c.c.)*
the whole picture changes, so that a man who a short while
before was apparently at death 's door, notices his surround-
ings and takes an interest again in life, This should be fol-
lowed up with thorough purgation, and cardiac stimulants
should be ordered. In such cases digitalis is useful, but its
action is never so striking as in cases of this general charac-
ter due to uncompensated valvular disease. It must be re-
membered that in arteriosclerosis the changes in the myo-
cardium must be of a considerable grade for the heart to
give away. Therefore, digitalis can not be expected to act
on a diseased muscle as it acts on a comparatively healthy
muscle. It is only in such cases of broken compensation
that digitalis should ever be used.

Digitalis is not a general vasoconstrictor as used to be
taught. Its action on the kidney is actually a vasodilator
one. And in its action on the heart the digitonin dilates
the coronary arteries, according to Macht, while the digi-
toxin acts on the heart muscle. Overdosing with digitalis
has produced partial heart block in many cases. It is ab-
solutely contraindicated in Stokes-Adams syndrome.

There are, however, some cases, especially those with
transudations, when digitalis may be carefully tried even
though high tension be present. It is sometimes of advan-
tage to combine digitalis with the nitrites although they are
said to be physiologically incompatible.

Still another drug, that is of great value in conditions such
as have been described, is diuretin. This may be given in
capsule or tablets, grs. x. three times daily. There is only

*I have taken as much as 1700 c.c. from a large man. lie recovered and went hack
to work.

TREATMENT 247

one caution to express in the use of this drug. It should not
be given when the kidneys are the seat of chronic inflam-
matory changes; in fact, actual harm may be done by ad-
ministering the drug under such conditions.

The same is true even to a greater extent with theocin.
This is a powerful diuretic. If given by mouth it should be
well diluted as it is most irritating to the stomach. It is
best given intravenously in doses of two and a half to
three grains dissolved in five to six cubic centimeters of
distilled water. One must be reasonably sure that the kid-
neys are not the subject of chronic disease and are func-
tionally, therefore, below par. The intravenous dose should
not be given oftener than once in four days.

For the pain in aneurysm, nothing (except, of course,
morphine) is so valuable as iodide of potassium. Patients
who are suffering agony, when put to bed and given KI
grs. x. three times a day, soon lose all the distressing symp-
toms. This applies particularly to aneurysms of the arch
of the aorta.

When the sclerosis has affected the cerebral arteries to
such an extent that symptoms result, the case is, as a rule,
exceedingly grave. Not much can be done except to relieve
the headaches and keep down the blood pressure, if this is
high, by means of rest in bed, the iodides, aconite, or the
nitrites. The cases of transient monoplegias or hemiplegias
can be much relieved by careful hygienic measures and judi-
cious administration of drugs. Much ingenuity is some-
times required to overcome the idiosyncrasies of patients,
but care and patience will succeed in surmounting all such
difficulties.

The treatment of intermittent claudication is the treat-
ment of arteriosclerosis in general. Sometimes the circula-
tion in the affected leg or legs is much helped by daily warm
foot baths. Light massage might be tried and the galvanic
current mav be used once or twice daily.

248 ARTERIOSCLEROSIS

There are a few distressing symptoms that occur usually
late in the disease, when complications have already oc-
curred, which frequently baffle the therapeutic skill of the
physician. The chief of these insomnia, dyspnea, and
headache may not be late manifestations, but insomnia and
headache are frequently associated with the moderately
advanced stages of arteriosclerosis. At times all the symp-
toms seem to be due to the high tension, the relief of which
causes them to disappear. There are, unfortunately, times
when high tension is not responsible for the headache and
insomnia. Under these circumstances such drugs as trional,
veronal, amylene hydrate, ammonol, etc., may be tried until
one is found which produces sleep. For the headaches,
phenacetin, alone or in combination with caffein and bro-
mide of sodium, may be tried. Acetanilid, cautiously used,
is at times of value. There have been cases of arteriosclero-
sis with low blood pressure, accompanied by severe head-
aches, that have been relieved by ergot. Codeine should be
used with care, and morphine only as a very last resource.

Great care must always be exercised in giving drugs that
depress the circulation, for it is easily conceivable that more
harm than good can come from injudicious drugging.

CHAPTER XIV

ARTERIOSCLEROSIS IN ITS RELATION TO LIFE

INSURANCE

The value of the early recognition of cases of arterioscle-
rosis and hypertension has been spoken of within, but it
needs to be further emphasized. There is perhaps no class
among physicians to whom is afforded a better opportunity
of seeing early cases than the medical examiners of life
insurance companies.

The relationship between a patient and the physician
whom he consults, and the applicant for life insurance and
the examiner are diametrically opposite. In the former
the patient desires to conceal nothing and the physician is
called upon to diagnose and treat disease. In the latter the
applicant, a presumably healthy person, may have much to
conceal and the examiner is there to pass upon the state of
health. The question is this "Is the applicant now in
good health?" It becomes then of vital importance for the
examiner to be able to detect among other abnormal condi-
tions the incipient signs of arteriosclerosis and of hyperten-
sion. Parenthetically it may be stated that arteriosclerosis
and hypertension are not one and the same disease as has
been so frequently insisted upon within; the former may
occur without the latter but the latter can not from its very
nature be present for long without arterial thickening su-
pervening. It is necessary in discussing the question here
to group the two conditions together in order to prevent
needless repetition.

Such a case as the following is common. A successful
business man of forty-four years was brought to me by an
agent in 1905 for examination. The man was six feet tall,
weighed 218 pounds, had a ruddy color and looked to be the

249

250 ARTERIOSCLEROSIS

picture of health. He was not strictly intemperate, he
never became intoxicated, but every day he drank three or
four whiskies and often he had a bottle of wine for dinner
in the evening. When he was examined his pulse was of
good quality and owing to the fleshiness of the wrist it was
difficult to say positively whether the radial artery was
sclerosed or not. In the heart no murmurs were heard, and
it was difficult to be sure that the left ventricle was enlarged.
There was, however, a slight but definite accentuation of the
second sound at the aortic cartilage which might readily
have been overlooked had the patient not been stripped and
a careful examination made with the stethoscope. Upon
taking the blood pressure it was found to be from 170-175
mm. of Hg. The urine specimen examined at the visit was
normal, no casts were found. The applicant was seen at
his home and the blood pressure measured. It was again
the same. He w^as seen a third time and practically the
same systolic blood pressure was found. Under protests
from all the agency staff the man was declined. Two years
later he died of apoplexy. The man was angry at being
refused. Instead of looking the matter squarely in the face
he thrust aside the idea that there was anything the matter
with him. He had never had one ill day in his life, his fore-
bears had lived to ripe old age, and he was sure that he knew
more about himself than the examiner.

Had this applicant showed a sense of reasonableness he
should have been grateful to the doctor for calling his atten-
tion to a condition which surely would sooner or later prove
either fatal itself or lead to some fatal lesion. It was
learned that this man had gone directly to his family physi-
cian who laughed at such nonsense as had been told the
(now) patient by the examiner.

Another illustration of a slightly different type of case is
afforded in the following history.

A man of fifty years of age, five feet ten in height and 164
Ibs. in weight, was brought for examination. In his youth

ARTERIOSCLEROSIS AND LIFE INSURANCE 251

there was a history of a mild attack of scarlet fever. He
was almost a total abstainer, rarely taking liquor in any
form. Physically he appeared to be an excellent risk.
However, on examining the heart it was found that there
was slight hypertrophy with an accentuated second aortic
sound at the base, and the blood pressure was 180 mm. of
Hg. Some sclerosis of the radial arteries was found. One
company had refused him on account of albumin in the
urine. There was none in the first specimen which was
passed while in the office. The specific gravity was 1014.
A morning specimen was obtained and contained a trace of
albumin. Several specimens were then examined. Some
contained albumin, some had no albumin content. The man
was declined; no protests from the agent as albumin had
been found. There was something tangible in that. Had
the applicant been refused on account of his high tension,
sclerosis of the radials, and slightly enlarged heart there
would undoubtedly have been protests. And yet an appli-
cant revealing such a state of the cardiovascular system
without albumin in the urine should unhesitatingly be de-
clined. Attention has been called to hypertension as an
early, and some think an invariable, sign of chronic ne-
phritis. My own experience has confirmed me in the belief
that in hypertension the kidneys are often the seat of
chronic interstitial changes. Careful palpation of the ra-
dial and brachial arteries will in every case reveal more
or less thickening.

There is yet another group of cases which the examiner
sees as healthy subjects, namely those cases of sclerosis of
the peripheral arteries without sclerosis of the aorta and
without high tension. In such cases the radials, brachials,
temporals and other superficial arteries are readily palpa-
ble, sometimes even revealing irregularities along the
course of a vessel. Such cases are not subjects for insur-
ance. The recognition of siK'h a condition is of great impor-
tance to the one who has it and he should be urged to go to

252 ARTERIOSCLEROSIS

his regular physician for thorough examination. Should the
physician ridicule the idea, as has happened to me more
than once when I was actively engaged in insurance work,
the examiner has done his full duty to the company, the
applicant, and himself.

A life insurance examiner has a difficult position to fill.
He has four people to satisfy ; the applicant, the agent, the
medical director and himself. The straight and narrow
path of strict honesty is his only salvation. By being hon-
est with himself he necessarily gives a square deal to the
other three parties.

No applicant who has palpable arteries or hypertension
can be considered a first class risk. It can not be denied
that men with arteriosclerosis live to an advanced age and
may even outlive those who have apparently normal ar-
teries, but the average life expectancy at any age for an
arteriosclerotic is less than that for a normal person. The
apparently healthy applicant who learns for the first time
when examined for life insurance that he has the early or
moderately advanced signs of arterial disease, should thank
the agent and examiner for showing him the danger signals
ahead. The sensible man then orders his life so that he
puts as little strain on his heart, arteries, and kidneys as
possible and may add many years to his life.

It is on account of this very insidiousness of onset that I
have elsewhere urged as a prophylactic measure the exam-
ination every six months of all persons over forty years of
age. I am more and more convinced that it is of vital im-
portance to the health of the public.

As I have remarked, the average man consults his dentist
at least once a year so that no tooth may be so far diseased
that it can not be saved. It is purely a means of preserving
the teeth. Why not do the same with the whole body! Of
what use is it to save the teeth and lose the body! It seems
to me that the great army of life insurance examiners are
in an enviable position in their ability to add years of life

ARTERIOSCLEROSIS AND LIFE INSURANCE 253

to many men and women. I doubt whether they realize
their importance in the campaign for health. I should urge
life insurance companies not to employ recent graduates
unless they have had at least a year's hospital experience.
For the company as well as for the individuals I believe
that there is a prognostic sense which the examiner should
have and this can only be acquired by experience.

I believe that arteriosclerosis and hypertension are in-
creasing for the reasons which have been given in another
chapter. There can be no doubt that when these conditions
are recognized long before symptoms would naturally su-
pervene, men and women would not only live longer but
also die more comfortably and many very likely would be
carried off by some disease having no relationship whatever
to arteriosclerosis. Slight enlargement of the heart down-
ward and to the left, accentuation of the second aortic
sound at the base, a full pulse, arteries which are palpably
thickened, increased blood pressure are signs to which at-
tention must be paid.

When the peripheral arteries are palpable they are not
always sclerosed. The radial artery, the one usually pal-
pated, may lie very close to the bone in a thin person. Un-
der these conditions the artery can be easily felt. It is
better then to palpate for the brachial as it lies beneath the
inner edge of the biceps muscle. Should this artery be felt
then very probably sclerosis is present. Opinion as to
whether or not sclerosis is present, when it is slight, may
differ. It is difficult at times to say definitely. Should
such be the case the applicant should be most carefully
questioned as to his family and past history, the heart
should be carefully outlined by percussion and the blood
pressure should be taken, both the systolic and diastolic
pressures. The urine should be examined with particular
care. I am aware that the average examination for life in-
surance is not made with the care which is bestowed upon a
patient. Yet I see no reason why the same attention to de-

254 ARTERIOSCLEROSIS

tail should not be given in one as in the other. The exami-
nation of the great majority of applicants can be made in a
short time, as there is no question of latent chronic disease.
When the exception turns up he should be given a searching
examination and a full report should be sent to the -Medical
Director. Only in this way will it be possible to weed out
the undesirable risks.

On the surface it does not seem to require any great diag-
nostic acumen to be a life insurance examiner. In the old
days of many of the companies there were no examiners.
The applicant was brought before the president or other
appointed official and he was passed or rejected on his
general appearance. This has changed, and now the med-
ical department with its scores of examiners in the field is
a well organized department.

It seems to me that the examiner should be an exceedingly
able diagnostician and prognosticator. There is no telling
when he may be called upon to pass judgment on a border-
line case. From personal experience I know how difficult
it is to make a decision in some cases. These suspicious
cases after a careful examination had better be passed by
the examiner and a supplementary report sent to the
medical director containing unbiased details. But no ap-
plicant with readily palpable arteries, even though the
blood pressure be normal, should be considered a first class
insurance risk.

The question of the value of the diastolic pressure read-
ing in examinations for life insurance is not yet settled to
the satisfaction of all medical directors. Certain medical
directors with clinical experience behind them, lay great
stress on the increased diastolic pressure and consider a
persistent diastolic of 100 mm. really more significant as
an indication of hypertension than a systolic pressure of
160 mm. Other directors pay little or no attention to the
diastolic reading. Should an applicant show a systolic
above the average normal on several successive readings,

ARTERIOSCLEROSIS AND LIFE INSURANCE 255

he is declined. When one takes into consideration the
psychic effect of knowing that he is being examined for
high blood pressure, it seems unfair to refuse insurance on
such grounds as is constantly done.

Up to the present there are no extensive series of life-
expectancy tables in which hundreds of thousands of cases
are analyzed from the diastolic pressure values. There are
many such tables for the systolic pressures alone. In the
tabulation of such statistics one must not lose sight of the
important fact that the figures are taken by thousands of
men of varying capacity and different degrees of intelli-
gence. Such studies to be of any real value must be taken
from records made at the home offices by capable men. We
shall await these tables with interest. In the meantime we
must be permitted to have the impression that the diastolic
pressure has been much neglected. This has no doubt been
due to the difficulty of measuring it with any degree of ac-
curacy. Now with the auscultatory method and the correct
place to read the diastolic pressure the results of blood
pressure estimations should begin to have some value for
statistical data.

Clinically the diastolic is probably more important than
the systolic. Until proof is brought to the contrary we shall
believe that in life insurance examinations it has the same
importance.

CHAPTER XV

PRACTICAL SUGGESTIONS

The time spent in obtaining a careful history of a case
is time well spent. Qften the diagnosis can be made from
the history alone, the physical examination merely adding
confirmation to the data already obtained.

The younger the patient who has arteriosclerosis, the
more probable is it that syphilis is the etiologic factor.
A denial of infection should have little weight if the history
of possible exposure is present. Miscarriages in a woman
should arouse the suspicion of lues in her husband. The
complement-fixation reaction will often clear up an appar-
ently obscure diagnosis.

There are various ways of examining a patient but there
is only one right way ; the examination should be made on
the bare skin. However skillful one may be in the art of
physical diagnosis, he can gather few accurate data by ex-
amining over the clothes even if he use a phonendoscope.

The immoderate eater is laying up for himself a wealth
of trouble at the time when he can least afford to bear it.
The ounce of advice in time is worth more to him than the
pounds of medicine later.

It is a wise maxim never to drive a horse too far. Apply
that to the human being and the rule holds equally well.

There may be no symptoms in a case of advanced arterio-
sclerosis. Do not on that account neglect to advise a pa-
tient in whom the disease is accidentally discovered.

Many a man owes a debt of gratitude to the life insurance
examiner. He rarely feels grateful.

When a competent ophthalmologist refers a case to a gen-
eral practitioner with the statement that he believes from
the appearance of the fundus of the eye that arterio sclerotic

256

PRACTICAL SUGGESTIONS 257

changes are present over the body, the case should be most
carefully examined. The earliest diagnoses are not infre-
quently made by the ophthalmologist.

It is the part of wisdom never to have such a firmly pre-
conceived idea of the diagnosis that facts observed are
perverted in order to fit into the diagnosis. Let the facts
speak for themselves.

Beware of the snap diagnosis. Even in a case of well-
marked arteriosclerosis when the diagnosis seems to be
written in large letters all over the patient, go through the
routine. Nine times out of ten this may seem needless.
The tenth time it saves your conscience and reputation.
Always consider that you are examining a tenth case.

Gradual loss of weight in a person over fifty years old
should arouse the suspicion of arteriosclerosis.

Do not call the nervous symptoms displayed by a middle-
aged man or woman neurasthenia until you have ruled out
all organic causes, particularly arteriosclerosis.

When palpating the radial artery, always use both hands
according to the method already described. Pay attention
to the superficial or deep situation of the artery.

The examination of one specimen of urine does not give
much information, especially if it should be found to con-
tain no abnormal elements. Fairly accurate data may be
gathered from the mixed night and morning urine; most
accurate data from the twenty-four hour specimen. To be
of any real value there should be frequent examinations oi;
the day's excretion.

In measuring the day 's output a good rule is as follows :
begin to collect urine after the first morning's micturition
and collect all including the first quantity passed the next
morning. It is best to examine the centrifugated urine for
casts even though no albumin be present. It is useless to
look for casts in an alkaline urine.

Casts are not infrequently found in chemically normal
urine from a middle-aged patient. Other things being nor-

258 ARTERIOSCLEROSIS

mal, the finding has no significance. The kidneys must be
carefully tested functionally.

Blood pressure readings should always be taken with the
patient in the same posture at every estimation. At the
first examination it is advisable to take readings from both
brachial arteries. Let the patient sit comfortably and relax
all muscles.

Differentiate as soon as possible between the uncom-
pensated heart caused by valvular disease and that caused
by arteriosclerosis. There is a difference in prognosis.
Both give the same symptoms, and are treated similarly un-
til compensation returns ; thereafter the management of the
two forms is different.

Aortic incompetence that comes on late in life is gener-
ally the result of curling of the free margins of the valves
caused by syphilitic arteriosclerosis. Prognosis is grave
because of the fact that the heart muscle also is the seat of
degenerative changes and compensatory hypertrophy is es-
tablished with difficulty.

When laying down a regime for a patient, consider his
disposition, and individualize the treatment. Eemember
that exercise is an essential feature of the hygiene of the
patient's life but do not forget to be explicit about the
amount and character of the permissible exercise.

In the prophylaxis of arteriosclerosis, a rational mode of
living is the all-important factor. As a rule, the less meat
one eats, the less is the liability of arterial degeneration as
age advances. The exceptions to this rule are many, and
probably depend upon the character of the " vital rubber "
with which the individual begins life.

The diet in well-marked cases of arteriosclerosis should
be carefully selected with regard to its nutritive and non-
irritating character. Animal proteins should be sparingly
used. Milk should have an important place in the dietary.

No drug relieves the pain of uncomplicated aneurysm as
surely as iodide of potassium.

PRACTICAL SUGGESTIONS 259

Iodides frequently upset the stomach. Be cautious in the
use of them. The irritable stomach may turn the scales
against your patient.

Use cardiac stimulants with care and judgment. If all
the valuable ammunition is used up at first, the fight will be
lost.

Use digitalis with especial care. Its chief usefulness is
in steadying the decompensated heart, improving the con-
duction of impulses, and increasing the tone of the cardiac
muscle. It should never be given to patients ivitJi very slow
pulses, the subjects of Stokes-Adams syndrome. Digitalis
has been found to produce partial to complete heart block
when therapeutically administered.

Remember that in the uncompensated heart morphine not
only eases the oppressive dyspnea, but also steadies and
stimulates the heart.

See to it that the patient has a daily movement of the
bowels. In the early stage try the effect of liquid paraffin
or of the mineral waters such as Pluto, or Hunyadi Janos,
or artificial Carlsbad salts (Sprudel salts). These last can
be made as follows : Sodium chloride, i ; sodium bicarbo-
nate, ii ; sodium sulphate, iv. Take two tablespoonsful of
this in a glass of hot water before breakfast. Should these
not succeed, assist the action of the drugs by the use of
enemata. The pill of aloin, strychnine sulphate, and extract
of cascara, with the addition of a small quantity of hyoscy-
amus, is a mild tonic purgative. In cases of constipation
with high tension, there is no drug as valuable as calomel or
one of the other mercurials given occasionally.

Never give Epsom salts unless copious watery stools are
desired to deplete effusion into the serous cavities or into
the subcutaneous tissue.

Chronic constipation increases the gravity of the prog-
nosis.

In case of suppression of urine and anasarca, hot air
packs may be of value. The patient may be wrapped in a

260

ARTERIOSCLEROSIS

hot wet sheet and covered with blankets. I do not believe in
administering pilocarpine to assist the sweating.

Kemember to treat the patient and not the disease. The
careful hygienic and dietetic treatment, combined with the
least amount of drugging, is the best and most rational
method of treatment.

INDEX

Abdominal symptoms, 201
Aconite in treatment, 242
Acquired arteriosclerosis, 159
Adami, effect of syphilis in aorta, 45
Adventitia, 28
Age in arteriosclerosis, 161
Albuminuria, 221

Albutt's classification of arterioscle-
rosis, 186

Alcohol, 166, 228, 235
Anatomy, 25
Angina abdominalis, 201, 216

pectoris, 197, 216

pseudo, 216
Angiosclerosis, 26, 64
Aorta, 27

anatomical lesions in, 33

Aschoff on, 35

normal, 41

syphilis in, 44

thoracic, 29

thoracic and abdominal, arterio-
sclerosis of, 39

velocity of blood in, 66
Aortic incompetence, 61, 258

stenosis, 60
Aortitis, acute, 165
Arcus senilis, 191
Arrhythmia, tonal, 92, 102
Arterial pressure, 85

symptoms, 189
Arteries, 29

examination of, 172, 177

general structure of, 27

large, 30

adventitia of, 30

palpable, 189

pulmonary, arteriosclerosis of, 63
Arteriocapillary fibrosis, 26
Arteriosclerotic endocarditis, 60, 219
Artery, coronary, cross-section of, 36

pulmonary, 209

radial, 29

Aschoff on aorta, 35
Atheroma, simple, 32
Atheromatous abscess, 38
Auricular fibrillation, 133

flutter, 131
Auscultation, 176

Auscultatory blood pressure phenom-
enon, 90

method of taking blood pressure, 83
percussion, 175

Balneotherapy, 233

Basch's blood pressure instrument, 70
Blood, circulation of, 65
velocity of, 65
in animals, 66
in aorta, 66
in capillaries, 66
viscosity of, 68
Blood pressure, 68

auscultatory method of taking,

clinical applications of, 147
diurnal variations of, 102
drugs influencing, 120
estimation of, 179
in cancer, 118
in collapse, 118
in exercise, 105
in head injuries, 148
in hemorrhages, 105, 118, 148
in infectious diseases, 153
in kidney diseases, 155
in meningitis, 118
in obstetrics, 152
in pulmonary tuberculosis, 119
in shock, 105, 148
in surgery, 147
in typhoid fever, 118, 154
in valvular heart disease, 155
increase of, 55
instruments, 70

Brown 's, 74
Cook's, 71

Erlanger's, 72

Faught's, 75, 80

Hill and Barnard's, 70

Hirschf elder's, 73

K. Vierordt's, 70

Marey's, 70

Potain's, 70

Eiva Eocci's, 70

Koger's, 77

Sanborn's, 80

261

262

INDEX

Blood pressure instruments Gont 'd.
Stanton's, 72
technique of, 80
"Tycos," 77
v. Basch's, 70
v. Recklinghausen 's, 76
mechanism of, 55
normal variations of, 88
phenomenon, auscultatory, 90
precautions when estimating, 181
value of, 181

Bowman's capsules, sclerosis of, 62
Brain, changes in, 62
Brown atrophy, 60, 118, 201

Calcification of media, 43, 59
Cancer, blood pressure in, 118
Capillaries, anatomy of, 27, 31
Capillary pulse, 67
Cardiac dullness, 172

irregularities in arteriosclerosis, 131

symptoms, 195
Cerebral symptoms, 203
Circulation of blood, 65

physiology of, 65
Cirrhosis of liver, 64, 216
Classification of arteriosclerosis, 32,

Allbutt's, 186

Collapse, blood pressure in, 118
Congenital arteriosclerosis, 157
Cook's blood pressure instrument, 71
Cor bovinum, 116

Coronary artery, cross section of, 36
Corpus luteum, 241

Definition of arteriosclerosis, 26
Diabetes mellitus, 216
Diagnosis, 210

differential, 215

early, 210

ophthalmic examination in, 214
Diastolic pressure, 69, 83, 85, 94

importance of, 97
Dicrotic pulse, 123
Dietetic treatment, 235
Differential diagnosis, 166, 215
Diffuse arterioclerosis, 32, 37, 38, 57
Digitalis in treatment, 246, 259
Diuretin in treatment, 246
Drug intoxications, 166
Drugs influencing blood pressure, 105,

120
Ductless glands, 171

Dullness, cardiac, 172
Dyspeptic symptoms, 184
Dyspnea, 184

treatment of, 248

Electrocardiogram, 126
Embolism, 59
Endarteritis deformans, 47

obliterans, 46

Endocarditis, arteriosclerotic, 60, 219
Endothelial lining, 27

tubes, 31

Epistaxis, 184, 221
Erlanger's blood pressure instrument,

Erythromelalgia, 192, 208
Estimation of blood pressure, 179
Etiology, 157
Examination of arteries, 172, 177

of heart, 172

of urine, 257
Exercise, blood pressure in, 105

in prophylaxis, 225

in treatment, 230
Experimental arteriosclerosis, 50
Extrasy stole, 138

Faught's blood pressure instrument,

75, 80
Fibrillation, auricular, 133

ventricular, 138
Fibrolysin in treatment, 243
Fingernail palpation, 178
Finger tip palpation, 179
Flutter, auricular, 131
Food poisons in arteriosclerosis, 163

Gibson's law, 154

"H" wave, 126

Habits, personal, 234

Head injuries, blood pressure in, 148

Headache, 184

treatment of, 248
Heart block, 140

boundaries, 172

examination of, 172

hypertrophy of, 60

physical examination of, 172

stimulants, 243, 246, 259

symptoms, 188

INDEX

263

Hemorrhages, blood pressure in, 118
Henle, membrane of, 29
Hill and Barnard's blood pressure in-
strument, 70

Hi rschf elder's blood pressure instru-
ment, 73

His, bundle of, 141, 197
Hygienic treatment, 230
Hyperpietic arteriosclerosis, 186
Hypertension, 60, 106, 169, 185, 249

cause of arteriosclerosis, 159

classification of cases, 112
Hypertrophy of left ventricle, 58
Hypotension, 117

Incompetence, aortic, 61, 258
Indicanuria, 167
Infants, arteriosclerosis in, 158
Infectious diseases in arteriosclerosis,
163

blood pressure in, 153
Insomnia, treatment of, 248
Intermittent claudication, 192, 208

treatment of, 247
Intoxications, chronic drug, 166
Intracranial tension, 105
Involutionary arteriosclerosis, 187
Iodides in treatment, 238, 247, 259

Kidney diseases, blood pressure in, 155
Kidneys, sclerosis of, 61, 170

Life insurance, relation to, 249
Light percussion, 174

touch palpation, 175
Liver, cirrhosis, 64, 216
Local symptoms, 207

Marey's blood pressure instrument, 70
Maximum pressure, 85, 94
Mean pressure, 85
Media, calcification of, 43, 59
Medicinal treatment, 238
Meningitis, blood pressure in, 118
Mental strain, 168
Mesaortitis, 45, 47, 49, 165
Mesentery, cross-section of small ar-
tery in, 56
Milk diet, 237
Minimum pressure, 86, 94

Moenckeberg type of arteriosclerosis,

Morphine in treatment, 243
Mosenthal test meal, 221
Muscular overwork, 169

Nervous symptoms, 191
Nitrites in treatment, 240
Nitroglycerin in treatment, 241
Nodular arteriosclerosis, 32, 37
Normal blood pressure variation, 88

Obstetrics, blood pressure in, 152
Occupation in arterioclerosis, 162
Ocular symptoms, 190
Ophthalmic examination, importance
in early diagnosis, 214, 256
Orthodiagraph, 173
Over-eating, 167, 212, 225, 235.
Over-work, muscular, 169.

"P wave, 129
"P-B" interval, 130
Palpable arteries, 189
Palpation, 174, 180

fingernail, 178

finger tip, 179

light touch, 175
Pathology, 32
Percussion, 174

auscultatory, 175

light, 174

Peripheral symptoms, 207
Personal habits, 234
Phlebosclerosis, 64
Phthalein test, 221
Physical signs, 183
Physiology of the circulation, 65
Potain's blood pressure instrument, 70
Practical suggestions, 256
Pressure, arterial, 85

ausculatory method of determining,
83

diastolic, 83, 94

estimation of, 179

in surgery, 147

maximum, 85, 94

normal variations, 88

pulse, 83, 85, 87, 100

systolic, 82, 85

technique, 80

venous, 120

264

INDEX

Prognosis, 218
Prophylaxis, 224

exercise in, 225
Pseudo angina pectoris, 216
Pulmonary artery, 209
arteriosclerosis of, 63

tuberculosis, blood pressure in, 119
Pulse, 123

capillary, 67

deficit, 135

dicrotic, 123

in arteriosclerosis, 123

pressure, 69, 83, 85, 87, 100

rate, 69

venous, 123

Purgatives in treatment, 244, 259
Pyrosis, 184

"Q E S" complex, 129

Eabbits, lesions produced experimen-
tally in, 50

Eace in arteriosclerosis, 161

Eadial artery, 29

Eadials, sclerosis of, 43

Eaynaud's disease, 192, 207

Eecklinghausen 's blood pressure in-
strument, 76

Eenal disease, 169
symptoms, 199

Eest in treatment, 242

Eiva-Eocci's blood pressure instru-
ment, 70

Eogers' blood pressure instrument, 77

Sanborn's blood pressure instrument,

Scaphoid scapula, 158
Sehwellungsperkussion, 174
Sclerosis of veins, 64
Senile arteriosclerosis, 32, 37, 43, 59
Sex in arteriosclerosis, 161
Shock, blood pressure in, 105, 148
Spinal symptoms, 205
Spirochaeta pallida, 45
Stanton's blood pressure instrument,

Stenosis, aortic, 60
Stokes-Adams syndrome, 197
Stomach, ulcer of, 216
Strain hypertrophy, 47, 54, 55
Surgery, blood pressure in, 147

Symptomatic treatment, 245
Symptoms, 183

abdominal, 201

arterial, 189

cardiac, 195

cerebral, 203

dyspeptic, 184

dyspnea, 184

general, 183

headache, 184

heart, 188

local, 207

nervous, 191

ocular, 190

peripheral, 207

pyrosis, 184

renal, 199

special, 194

spinal, 205

vertigo, 184

visceral, 201
Syphilis, 165

in aorta, 44

Syphilitic arteriosclerosis, 37
Systolic pressure, 69, 82, 85, 94

importance of, 97

"T" wave, 130

Technique of blood pressure instru-
ments, 80

Thayer and Fabyan, 34
Theocin, 247

Thoma on arteriosclerosis, 33
Thoracic aorta, 29
Thyroid extract in treatment, 239
Tobacco, 167, 212, 234
Tonal arrhythmia, 92, 102
Toxic arteriosclerosis, 186
Treatment, 229

aconite in, 242

balneotherapy in, 233

corpus luteum, 241

dietetic, 235

digitalis in, 246, 259

diuretin in, 246

exercise in, 230

fibrolysin in, 243

heart stimulants in, 243

hygienic, 230

iodides in, 238, 247, 259

medicinal, 238

morphine in, 243

nitrites in, 240

nitroglycerin in, 241

of dyspnea, 248

of headache, 248

INDEX

265

Treatment Cont 'd.

of insomnia, 248

of intermittent claudication, 247

personal habits in, 234

purgatives in, 244, 259

rest in, 242

symptomatic, 245

theocin in, 247

thyroid extract in, 239

Trunecek's serum in, 243

venesection in, 242

veratrum viride in, 242
Trunecek's serum in treatment, 243
Tuberculosis, blood pressure in, 119
Tunica intima, 28

media, 28
"Tycos" blood pressure instrument,

Typhoid fever as cause of arterio-
sclerosis, 164
blood pressure in, 118

Ulcer of stomach, 216
Urine, examination of, 257
suppression of, 259

Valvular heart disease, blood pressure

in, 155

Vasa vasorum, 29
Veins, anatomy of, 30

sclerosis of, 64
Velocity of blood in animals, 66

of blood in aorta, 66
Venesection in treatment, 242
Venous pressure, 120

pulse, 123

Ventricle, left, hypertrophy of, 58
Ventricular fibrillation, 138
Veratrum viride in treatment, 242
Vertigo, 184

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