ii'l
I
•ill 'II
Right innominate vein
Left innorhinate vein
Superior vena cava
Innominate* artery
Stump of sup. cava
R. auricular append.
Aorta
Left coronary artery x
Right coronary vessels '
Right marginal artery
Ri^ht ventricle
Left common carotid artery
• Left subclavian artery
Left internal jugular vein
Left pulmonary artery
Inferior pulmo-
nary vein
Left auricular
appendage
Conus anteriorsu*
Interventricular branches
of left coronary vessels
Left ventricle
Fio. 1. — The heart and great vessels, viewed from the front. (After Piersol.)
Left pulmonary artery
Superior left pulmonary vei
Inferior left pulmonary vein
Termination of left coronary
vein
Transverse branch of left
coronary artery
Left ventricle
Superior vena cava
Superior right pulmonary vein
Right pulmonary artery
Inferior right pulmonary vein
Inferior vena cava
Coronary sinus
Right coronary vein
Transverse branch of right
coronary artery
'osterior descending branch of
right coronary artery
Middle cardiac vein
Right ventricle
Fio. 2.— Same, from behind. (After Piersol.)
DISEASES
of the.
HEART AND AORTA
BY
ARTHUR DOUGLASS HIRSCHFELDER, M.D.
ASSOCIATE IN MEDICINE, JOHNS HOPKINS UNIVERSITY
WITH AN INTRODUCTORY NOTE
BY
LEWELLYS F. BARKER, M.D., LL.D.
PROFESSOR OP MEDICINE, JOHNS HOPKINS UNIVERSITY
329 ILLUSTRATIONS BY THE AUTHOR
PHILADELPHIA & LONDON
J. B. LIPPINCOTT COMPANY
COPYRIGHT, 1910
BY J. B. LIPPINCOTT COMPANY
Th* W nted ^ J' B' LiPPinc°*t Company
Washington Square Press, Philadelphia^. S.
TO
MY FATHER
<&aftlanfc
Professor of Clinical Medicine, I. eland Stanford Junior University
AND TO
£ctoellp£ jf, 25ather, ;|ttJB[>M H31JBD,
Professor of Medicine, Johns Hopkins University
CHIEFS OF THE CLINICS IN WHICH THE WORK WAS DONEJ WHO
HAVE TAUGHT ME BY PRECEPT AND EXAMPLE HOW
SCIENCE, ART, AND HUMANITY SHOULD
BE WOVEN INTO PRACTICE
OF MEDICINE
THIS BOOK IS AFFECTIONATELY DEDICATED
INTRODUCTORY NOTE
THE researches in the great field of inner medicine have so multiplied
in recent years that it has become highly desirable that we should have
from time to time, in addition to the summaries of progress contained
in the general text-books on practice, monographs which picture more
completely the status of our knowledge in the several special divisions
of the subject. In diseases of the circulatory system new methods of
study have led to the discovery of many new facts, and a great many
workers have been attracted during the last twenty years to this domain
of cardiovascular inquiry.
In the medical clinic at the Johns Hopkins Hospital, Dr. Hirsch-
felder has during the past few years occupied himself especially with
such studies. The present volume is an attempt to epitomize the actual
condition of the subject at the present time, as viewed from the stand-
point of an active investigator of extensive first-hand experience who
has also a wide acquaintance with the literature of the physiology and
pathology of the circulatory apparatus.
The clearness and brevity of the presentation and the excellent
arrangement of the material will, I am sure, appeal to students and
practitioners of medicine. It is no easy matter adequately to combine
the most recent results of anatomical, physiological, pathological, and
clinical studies in a form which will satisfy the critical demands of the
scientific investigator and at the same time be useful as a guide to
the every-day practitioner. Especial attention has been paid in the
volume to the practical facts of diagnosis and treatment; in the more
theoretical portions there will be found evidence of careful, critical
sifting, and an appreciation of the distinction between what is essential
and what non-essential for the more general reader.
The bibliographic references make no attempt at completeness, but
have been chosen with the idea in mind of permitting those who desire
to do so to consult the most important, and especially the more recent,
treatises, monographs, and original articles which deal with the various
matters discussed.
A notable feature of Dr. Hirschfelder's book is the liberality of illus-
trations; the majority of the figures are made from original drawings
and tracings and are in pleasing contrast with the time-worn figures
which pass from compilation to compilation.
LEWELLYS F. BARKER.
BALTIMORE, May 12, 1910.
PREFACE
IN the preparation of this book it has been the writer's aim to present
side by side the phenomena observed at the bedside and the facts learned
in the laboratory in order to show how each supplements the other in
teaching us how to observe the patient and to direct the treatment. Many
of the results obtained in the laboratory have not yet attained practical
importance because they have been scattered through the literature and
have not reached the eye of the clinician; but wherever the clinicians have
looked to the laboratory or laboratory workers have looked to the clinic
for verification or application of their theories the great pillars of progress
have been raised. In accordance with this idea the clinical presentation
in each chapter is preceded by an introductory section dealing with the
experimental pathology and more fundamental principles of the subject,
which has been used as a basis for frequent reference in the clinical dis-
cussions.
The trend of clinical observation during the past two decades has been
toward more accurate study of disturbances of function and toward the
introduction of mechanical methods for their observation, methods of
precision which tend to supplement or supplant the older and simpler
methods of physical diagnosis. Chief among these may be mentioned the
study of blood-pressure, the graphic studies upon alterations in cardiac
rhythm by means of the venous pulse, the outlining of the heart and vessels
by means of the X-ray, and the phonographic recording of the heart sounds.
Each of these subjects has been reviewed with special reference to the
general principles upon which the method is based, in order to point out
its applicability, its limitations, the character of information which it has
yielded in clinical conditions, the conditions under which the same informa-
tion may be gained by simpler methods, the conditions under which its
employment is essential and those under which it is superfluous.
The failure of the heart has been traced through its varying stages
from the simple fatigue of the normal heart in exercise, through the stage
of primary overstrain, to that of broken compensation, especial attention
being devoted to the states of broken pulmonary compensation arising
from failure of the left ventricle and of broken systemic compensation
from failure of the right.
vii
viii PREFACE.
The pathogenesis of cardiac symptoms is fully discussed, with their
pathological physiology, occurrence, and the symptomatic treatment for
their relief.
The general methods of treatment in cardiac diseases, dietetic, phar-
macological, gymnastic, hydrotherapeutic, and electrical, have been treated
both as empirical procedures and as experimental methods to correct
definite disturbances in the physiology of the circulation, especially changes
in cardiac force, cardiac tonicity, and peripheral resistance.
The chapters upon the individual organic lesions include discussions
of pathological anatomy, pathogenesis, pathological physiology, as well
as of symptomatology, course, notes of typical cases, diagnosis, treatment,
and prognosis. Considerable attention is also paid to functional disturb-
ances (valvular insufficiencies, etc.) which may bring about conditions
similar to those resulting from organic changes or may accompany the
latter. The Adams-Stokes syndrome seems so definitely associated with
lesions of the auriculoventricular muscle bundles as to justify its classifi-
cation among conditions due to organic lesions.
The congenital heart lesions are viewed as disturbances in embryologic
development in which primary malformations or states in fetal life have
diverted the blood current, modifying the further course of development
and producing concomitant secondary malformations. The effect of these
lesions upon the adult circulation and their relation to cardiac overstrain
in producing the syndrome of the morbus cceruleus are discussed, as well
as the signs, diagnosis, prognosis, and treatment.
Short chapters are devoted to the subjects of pregnancy in heart
disease and the effects of trauma and wounds of the heart.
Considerable space is given to the purely functional disturbances of
cardiac action, especially to the physiological mechanisms by which many.
of them result from disturbances in distant organs as well as to the improve-
ments resulting when these disturbances are corrected.
A great deal of care has been bestowed by the writer in the prepara-
tion of the illustrations, especially upon the cardiosphygmographic trac-
ings, the diagrammatic representations of clinical conditions and of effects
upon the blood flow in different parts of the circulation as well as in differ-
ent stages of the disease. When necessary, figures have been borrowed
from other sources, to whom due credit has been given.
Since the aim of the book is not only to present the principal facts
but to aid the reader in following out lines in which he is especially inter-
ested, an adequate bibliography has been added to each chapter, embrac-
ing the articles referred to in the text.
It is a pleasant duty for the writer, in conclusion, to express his thanks
to Professors Barker and Thayer for the privilege of using the clinical
PREFACE. ix
material and records of the Johns Hopkins Hospital, to Professor T. B.
Futcher for that of the Johns Hopkins Dispensary, and to his father, Pro-
fessor J. O. Hirschfelder, for the cases at the City and County Hospital
of San Francisco; to Professor F. P. Mall and Drs. Knower, Retzer, and
Evans in matters of anatomy and embryology; to Professors W. H. Howell,
J. Loeb, and Dr. D. R. Hooker in physiology; to Professors W. S. Hal-
sted, T. S. Cullen, and J. M. Slemons in matters of surgery, gynaecology,
and obstetrics; to Professors W. G. MacCallum and W. Ophiils, as well
as to Major F. F. Russell, Dr. Lamb, and Dr. Gray, of the Army Medical
Museum, for the use of pathological material; to Professor C. M. Cooper
for the collection of radiographs; to Dr. Chas. S. Bond for his untiring
labors in the preparation of photomicrographs; to Professor W. Einthoven
of Leyden for the use of electrocardiograms; to Professor Max Broedel
for his kind instruction and suggestions in matters of illustration; to Dr.
Caroline B. Towles for her assistance in reading of proof as well as for
many helpful suggestions; and to Miss Alberta E. Bush for her care in the
technical matters pertaining to the manuscript and index.
CONTENTS
PART I.
GENERAL CONSIDERATIONS AND METHODS OF DIAGNOSIS.
PAGE
I. PHYSIOLOGICAL CONSIDERATIONS 1
II. BLOOD-PRESSURE AND BLOOD VISCOSITY 18
III. THE ARTERIAL PULSE 41
IV. THE VENOUS PULSE AND ELECTROCARDIOGRAM IN HEALTH AND DISEASE . . 49
V, X-RAY EXAMINATION 82
VI. PHYSICAL EXAMINATION 88
PART II.
DISEASED CONDITIONS DUE TO DIFFUSE PATHOLOGICAL PROCESSES.
I. PRIMARY CARDIAC OVERSTRAIN 121
II. PATHOLOGICAL PHYSIOLOGY OF EXERCISE, CARDIAC OVERSTRAIN, HEART
FAILURE, AND BROKEN COMPENSATION 129
III. SYMPTOMS OF CARDIAC DISEASE 147
IV. GENERAL PRINCIPLES OF TREATMENT OF FAILURE OF THE HEART 163
V. THE EFFECTS OF DRUGS IN CARDIAC DISEASE 172
VI. GYMNASTICS AND HYDROTHERAPY 193
VII. HYPERTROPHY AND ATROPHY^ 203
VIII. FATTY DEPOSITS IN AND ABOUT THE HEART , ' 214
IX. AFFECTIONS OF THE MYOCARDIUM 224
X. ARTERIOSCLEROSIS 249
XI. VASOMOTOR CRISES, ETC., AND THH ANGIONEUROTIC LESIONS 270
XII. SCLEROSIS OF THE CORONARY ARTERIES, AND ANGINA PECTORIS 280
PART III.
DISEASED CONDITIONS DUE TO LOCALIZED LESIONS.
I. ENDOCARDITIS 299
II. MITRAL INSUFFICIENCY 321
III. MITRAL STENOSIS 341
IV. AORTIC INSUFFICIENCY •. 360
V. AORTIC STENOSIS 381
VI. PULMONARY INSUFFICIENCY 390
xi
xii CONTENTS.
PAGE
VII. TBICUSPID INSUFFICIENCY 398
VIII. TRICUSPID STENOSIS 406
IX. PREGNANCY AND LABOR IN CASES OF HEART DISEASE 413
X. CONGENITAL HEART DISEASE 421
XI. HEART-BLOCK AND ADAMS-STOKES SYNDROME 460
XII. PERICARDITIS 480
XIII. WOUNDS OF THE HEART AND CARDIAC TRAUMA 513
XIV. ANEURISM 521
PART IV.
FUNCTIONAL DISEASES WITHOUT ANATOMICAL LESION.
I. PAROXYSMAL TACHYCARDIA 560
II. THYROID HEART 574
III. MISCELLANEOUS DISTURBANCES OF CARDIAC FUNCTION — THE SO-CALLED
" CARDIAC NEUROSES " AND " CARDIAC NEURASTHENIA " . . ., 593
LIST OF ILLUSTRATIONS
TIG. PAGE
1. The heart and great vessels, viewed from the front frontispiece
2. The heart and great vessels, from behind frontispiece
3. Relations of the heart and great vessels, viewed from the front xxiv
4. The heart and thoracic viscera, viewed from behind xxiv
5. Sagittal section of the thorax, viewed from the right xxiv
6. Heart muscle-fibres 1
7. Section through the endocardium, showing section of the muscle-fibres 2
8. Apparatus for perfusing the mammalian heart 3
9. The auricular end of the human heart, viewed from the right 5
10. The sinus region of the heart, the veno-auricular or venosinal bands of striated
muscle, and the auriculo (at rio) ventricular or sinoventricular muscle bundle ... 6
11. Arrangement of ventricular muscle-fibres 8
12. Apparatus for registering the volume of the ventricles 9
13. Volume curves of the ventricles at different heart rates 9
14. Methods for demonstrating the movements of the heart valves 10
15. Volume curves showing the effect of variations in venous pressure and in tonicity
upon the rate at which the ventricles are filled during diastole 12
16. Volume curve showing the effect of low venous pressure or of high tonicity upon
the amount of blood entering the ventricles 12
17. Diagram illustrating the changes in volume of the ventricles in systole and diastole
associated with variations in tonicity and systolic output 12
18. Origin and course of the cardiac nerves, and cutaneous distribution of the corre-
sponding schematic branches 14
19. Curve of intra ventricular and aortic pressures 18
20. Riva-Rocci blood-pressure apparatus as modified by Stanton 20
21. Correct method of feeling the pulse in Strasburger's determination of minimal
pressure 21
22. Erlanger blood-pressure apparatus with Hirschfelder polygraph attachment .... 21
23. Diagram showing arrangement of Erlanger apparatus 22
24. Curve taken with the Erlanger apparatus, showing points of maximal and minimal
pressures 22
25. V. Recklinghausen apparatus for determining the maximal and minimal blood-
pressure in man 22
26. Diagram showing the maximal and minimal pressures in various parts of the
circulatory system 24
27. Diagram showing effects of vasoconstriction, vasodilation, increased and decreased
force of ventricular contraction upon the maximal and minimal blood-pressures
and upon the form of the pulse 25
28. Mosso plethysmograph 26
29. Diagram showing the curve of blood-pressure during asphyxia
30. Diagram showing typical blood-pressures in various diseases 29
31. Hooker and Eyster's modification of V. Recklinghausen's method of determining
the venous pressure in man 33
32. Determann's apparatus for determining the viscosity of the blood 38
33. Brachial pulse-curves taken with the Erlanger blood-pressure apparatus from the
arms of two patients 42
xiii
xiv LIST OF ILLUSTRATIONS.
34. Absolute sphygmograms, all of which correspond to the radial tracing above .... 43
:5.">. Significance of the pulse-curve 44
36. Diagram showing the time relations of ventricular volume and pressure curves to
pulse tracings from the aorta, carotid and radial arteries 44
37. Three types of arterial pulse-curve corresponding to the same pulse-pressure and
same pulse-rate 45
38. Effect of inhalation of amyl nitrite upon the pulse form 45
39. Mercury manometer tracing from the carotid artery of a dog, showing rhythmic
variations in blood-pressure and rhythmic increase in dicrotism . . 46
40. Diagram showing various forms of pulse-curve encountered clinically 46
41. Sites for recording the jugular and carotid pulsations 51
42. Apparatus for recording the respiration 52
43. V. Jaquet's cardiosphygmograph 52
44. Normal venous tracings 53
45. Diagram representing the various events in a cardiac cycle 53
46. Venous tracing showing absence of the c wave in a case of heart failure 54
47. Venous tracing showing auricular paralysis (absence of a wave) with large (x)
depression 54
48. Venous tracing from a very slow heart, with loud third heart sound, showing the
presence of the h wave 56
49. Tracing from the same person one hour later, after giving atropine and quickening
the pulse 56
50. Showing a wave w occurring shortly before the a wave 56
51. Positive or ventricular type of venous pulse in tricuspid insufficiency, showing
absence of the a wave 57
52. Positive or ventricular type of venous pulse in tricuspid insufficiency, showing
absence of the a wave 57
53. Method of taking tracing from the oesophagus to show the contractions of the left
auricle i»g
54. (Esophageal and carotid tracings from a normal man 58
55. Simplest form of apparatus for recording the electrocardiogram and cardiogram
simultaneously 59
56. Patient with both hands in salt-solution jars ready for taking electrocardiogram . . 59
57. Course of the electrical variations due to the heart-beat in man 59
58. Normal electrocardiogram showing the time relations to the venous and carotid
pulse-waves ^g
59. Normal electrocardiogram 59
60. Diagram representing various types of irregular pulse 63
61. Respiratory arrhythmia ^4
62. Venous tracings in heart-block. Partial heart-block (3 : 1 rhythm) during pres-
sure on the vagus, in a case of Adams-Stokes disease 66
63. Venous tracings in heart-block. Complete heart-block in a case of Adams-Stokes
disease
64. Occasional absence of apex impulse during inspiration simulating interventricular
heart-block __
67
65. Alternating pulse in a case of paroxysmal tachycardia 68
66. Response of frog's ventricle to abnormal stimuli «c
racing from jugular vein and brachial artery in man, showing ventricular
extrasystoles
racings from the jugular vein and brachial artery of a patient with trigeminal
pulse
AC
67. Tracing from jugular vein and brachial artery in man, showing ventricular
extrasystoles
68. Tracings from the jugular vein and brachial artery of
69. Diagrammatic reproduction of the electrocardiogram obtained' in the'dog as the
result of extrasystoles
70. Electrocardiogram of a patient with mitral stenosis, showing extrasystoles . . 70
LIST OF ILLUSTRATIONS. xv
71. Volume curve of the ventricles, showing the dilatation which followed the entrance
of an air-bubble into the right auricle 71
72. Extrasystoles with shortened conduction time, supposed to arise in the auriculo-
ventricular bundle 73
73. Variations in conduction time in a case of mitral stenosis 73
74. Tracing showing absolute arrhythmia with weak ineffectual systoles 74
75. Diagram showing the alterations of rhythm which may cause a pulsus bigeminus . . 74
76. Absolute permanent irregularity with a wave preserved in a case of mitral
stenosis 75
77. Perpetually irregular pulse with absence of a wave 76
78. Electrocardiogram from a case of perpetual absolute arrhythmia showing extra-
systole 77
79. Effect of arrhythmia on the circulation, blood-pressure, and volume of the
ventricles 77
80. Radiograph of normal chest 83
81. X-ray shadows in different axes of the body 84
82. A simple form of orthodiagraph 85
83. Diagram showing the.use of the orthodiagraph 85
84. Orthodiagraphic outline of normal heart, showing Moritz's conjugates 85
85. Movements of the heart leading to the protrusions and retraction during systole . . 89
86. Rubber funnel for cardiographic tracings 90
87. Cardiograms obtained over right and left ventricles 90
88. Various forms of apex tracings 91
89. Areas of pulsation and retraction 92
90. Eddies producing thrills as illustrated by a stream of water 92
91. Goldscheider's orthopercussion 93
92. Percussion with the orthoplessimeter 94
93. Diagram to show the cause of unavoidable error in percussion of the cardiac
outlines 95
94. Areas of cardiac dulness and flatness in a normal man 95
95. Cardiac outlines in a child of nine years 96
96. Diagrams illustrating the movements of the normal heart on change of posture
from side to side, and in the various phases of respiration 97
97. Graphic records of the heart sounds 98
98. Diagram for representing the heart sounds in clinical notes 99
99. Choice of stethoscope bells : 101
100. The " valvular areas " 102
101. The propagation of the heart sounds from valves to chest wall 103
102. Graphic records of the fetal heart sounds 104
103. Diagram illustrating the split sounds and gallop rhythms and their phonetic
equivalents 105
104. Graphic record of a split pulmonic second sound 106
105. Graphic record of the third heart sound 107
106. Jugular and carotid tracings from a normal individual with a well-marked third
heart sound 108
107. Forces supposed to be at work in the production of the third heart sound 108
108. Similarity between the .production of voice sounds and the production of murmurs 110
109. Distribution of the accidental murmur 114
110. Graphic record of an accidental murmur : . . . . 115
111. Diagram showing the relation of the more common simple murmurs to events of
the cardiac cycle 116
112. Cardiac dulness in v. Leyden's case upon his three successive admissions 125
113. Alterations of blood-pressure due to rapid lifting of light weights with the feet. . 130
114. Effect on patient with badly broken eompensation of walking on a level 131
xvi LIST OF ILLUSTRATIONS.
115. Effect of prolonged exercise upon the blood-pressure of men in various degrees of
muscular strength
116. Rise of blood-pressure during Valsalva's experiment and during exercise
11?! Variations in size of the heart of a long-distance bicycle rider, as the result of a
very long race •
118. Effect of strain upon the dog's heart whose tonicity is good
119. Volume curve of a dog whose cardiac tonicity is low
120. Effect upon the volume of the dog's heart produced by clamping the descending
thoracic aorta 137
121. Diagram showing changes in the circulation: I, normal; II, broken pulmonary
compensation; III, broken systemic compensation; IV, both compensations
fail; stases in lungs and veins 139
122. The two types of Cheyne-Stokes respiration in their relations to the blood-pressure
curves 152
12.3. Legs of a patient with extreme oedema and tremendous ulcers 154
124. Curschmann's modification of the Southey tubes for draining oedema of the legs . . 155
125. Electrical record of afferent impulses travelling up the vagi 157
126. Insertion of the knife in venesection 166
127. Effect of venesection on the cardiac outline, showing diminution in size of right
heart 167
128. Typical effect of venesection upon the circulation 167
129. Tracing showing the action of digitalis upon the dog's blood-pressure. . . 175
130. Variations in blood-pressure in a patient under the influence of digitalis and
nitroglycerin 176
131. Effect of digitalis on cardiac tonicity in the dog 177
132. Curve showing the effect of strychnine upon cardiac tonicity 182
133. Effects of drugs of the nitrite series upon the blood-pressure in man 187
134. Schott resisted movements 196
135. Orthodiagraphic outline of a patient with dilated heart, showing the effect of
Schott movements 197
136. Hypertrophic, normal, and atrophic hearts 203
137. Photomicrographs of atrophic and hypertrophic heart muscle 204
138. Heart of normal dog and of dog which has run for three months on a treadmill . . 206
139. Areas of pulsation and retraction hypertrophy of the right and left ventricles .... 209
140. Diagram showing power of normal and hypertrophied (athlete's) heart at rest and
during exercise, compared with that of a diseased heart 211
141. Distribution of fat in and about the heart 214
142. Photomicrographs of fat deposits in the heart 215
143. An excessive deposit of epicardial fat 216
144. Infiltration along the course of the blood-vessels in subacute myocarditis; blood-
vessels injected 225
145. Septic myocarditis with multiple abscesses in the heart wall 226
146. Photomicrograph showing an abscess in the heart muscle 227
147. Orthodiagraphic outlines of the heart of a child during the course of a severe
diphtheria 230
148. Specimen showing a cardiac aneurism covered with pericardial adhesions 234
149. Chronic myocarditis (cardiosclerosis) 234
150. Specimens showing chronic myocarditis 235
151. Hypertrophy of some muscle bundles in the auricle with atrophy (transparency)
of other areas 236
152. Curve of blood-pressure in a case of chronic myocarditis; high blood-pressure per-
sisting until shortly before death 237
153. Various types of arteriosclerotic lesions. (Schematic.) 251
154. Cross section of a radial artery showing arteriosclerotic changes in the medja 252
LIST OF ILLUSTRATIONS. xvii
155. Arteriosclerosis of the descending aorta, showing atheromatous plaques 253
156. Atheromatous plaque, showing the changes in the intima 254
157. Tortuous radial artery 260
158. Retinal changes in arteriosclerosis 260
159. Effect of arteriosclerosis upon the circulation 261
160. Blood-pressure chart of case of typical vasomotor crises 271
161. Blood-pressure chart showing a vascular crisis of the cerebral type 272
162. Diagram to illustrate the elimination of CO2 by the blood in normal and sclerotic
arteries 273
163. Thromboangitis obliterans and endarteritis obliterans 276
164. Hands and feet of a patient with Raynaud's disease, showing gangrenous ulcers
and the stumps of amputated toes 277
165. Effect of ligation of a large coronary artery upon the blood-pressure 280
166. Sclerosis of a coronary artery, producing an area of infarction near the apex .... 282
167. Distribution of pain in attacks of angina pectoris 286
16S. Distribution of attacks of pain and sensory disturbances in a case of angina
pectoris 287
169. Blood-pressure curve showing crises of hypertension during attacks of angina
pectoris 288
170. Fibrinous deposit upon an aortic cusp one hour after mechanically injuring the
valve 299
171. Mitral endocarditis showing large vegetations 300
172. Injection of chronically inflamed valves 300
173. Structure of the normal auriculoventricular valve 301
174. Photomicrograph of a specimen showing acute and subacute endocarditic lesions
upon the mitral valve 302
175. Portals of infection in endocarditis 303
176. Temperature curve from a case of malignant endocarditis 305
177. Temperature curve from a case of simple acute endocarditis 305
178. Diagram showing relative frequency of the most important valvular lesions at
various ages 312
179. Diagram showing the relative frequency of the various valvular lesions in cases of
valvular heart disease 312
180. Regurgitant streams in organic and functional mitral insufficiencies 322
181. Diagram showing the volume and pressure curves under these conditions 324
182. Curve of intra ventricular pressure in mitral insufficiency produced on a mechanical
model 325
183. Diagram showing the effects of mitral insufficiency upon the circulation 326
184. Distribution of the murmur in mitral insufficiency 329
185. Cross section of the body showing how the murmur reaches the chest wall 330
186. Radiograph of a patient with mitral insufficiency, showing horizontal enlarge-
ment of the heart to the left 330
187. Diagram of Fig. 186, showing the directions in which cardiac enlargement has
taken place 331
188. Graphic records of the heart sounds, showing the systolic murmur 331
189. Human heart, showing mitral and tricuspid stenosis; viewed from above; the
auricles have been cut through 341
190. Diagram showing the changes in the circulation due to mitral stenosis 343
191. Volume of the ventricles in experimental mitral stenosis 344
192. The variations in the volume curve of the ventricles in increasing degrees of mitral
stenosis 344
193. Direction of the stream entering the left ventricle through the stenotic mitral
orifice 346
194. Cardiac outline and distribution of the presystolic rumble in mitral stenosis 347
B
XV111
LIST OF ILLUSTRATIONS.
195. Radiograph from a case of mitral stenosis, showing increase of the shadow due to
the dilated left auricle
196. Diagram representing the shadows shown in Fig. 195
197. Graphic record of carotid pulse and heart sounds in mitral stenosis
198. Diagram showing the relations of the various sounds heard in uncomplicated
mitral stenosis to events in the filling and emptying of the ventricle 349
199. Venous pulse of a patient with mitral stenosis during an attack of acute heart
failure 35°
200. Permanent arrhythmia in a case of mitral stenosis, showing persistence of the
auricular contractions (a wave) upon the venous pulse 354
201. Specimen showing vegetations upon the aortic valves 360
202. The various forms of lesion producing aortic insufficiency 361
203. Effect of aortic insufficiency in the mechanical model 362
204. Diagram of the circulation in aortic insufficiency 363
205. Diagram showing how the high cardiac tonicity hastens the equilibrium between
aortic pressure, intra ventricular pressure, and tonicity, and thus diminishes
the amount of blood regurgitating 364
206. Effect of rupturing an aortic valve in a dog, showing a transitory dilatation
followed by a permanent diminution in size 364
207. Area of cardiac dulness and distribution of the cardiac sounds and murmurs in
aortic insufficiency 368
208. Radiograph of a case of aortic insufficiency, showing elongation of the long axis of
the heart 368
209. Diagram of Fig. 208, showing the hypertrophy of the left ventricle 368
210. Direction of the primary regurgitant streams in aortic insufficiency 370-
211. Relation of murmurs in aortic insufficiency to the cardiac cycle 371
212. Functional mitral stenosis in aortic insufficiency as demonstrated on the excised
heart by Baumgarten's method 371
213. Variations in the form of the pulse-wave encountered clinically in aortic insuffi-
ciency 372
214. Tracings from a dog with experimental aortic insufficiency, showing the con-
version of a collapsing into an anacrotic pulse by clamping the descending aorta 373
215. Radial pulse tracings showing extrasystoles, probably of ventricular origin 374
216. Specimen showing aortic stenosis. Viewed from above. 381
217. Forms of stenotic aortic orifices 381
218. Carotid pulse and intraventricular pressure in experimental aortic stenosis 382
219. Diagram of the circulation showing the effect of aortic stenosis 383
220. Diagram showing the cardiac outline and distribution of the murmur in aortic
stenosis 334
221. Murmur of aortic stenosis 335.
222. Diagram showing the pulsus tardus and the anacrotic type 386-
223. Pulse tracings from cases of aortic stenosis 386
224. Diagram of the circulation in pulmonary insufficiency 391
225. Distribution of the murmur in pulmonary insufficiency 392*
226. The outline of a normal heart superposed upon that of a dilated heart, showing the
enlargement of the tricuspid orifice 397
227. Diagram showing the changes in the circulation in tricuspid insufficiency 398
i. Venous pulse of patients with tricuspid insufficiency (positive venous pulse) 399
229. Venous pulse of another patient 399,
230. Distribution of the murmur and cardiac outline in tricuspid insufficiency 401
231. Cross section of the body, showing the paths of propagation of the murmur of
tricuspid insufficiency 40j
232. Tracings of liver pulsation ' ' ' ' ' 402
233. Systolic pulsation of the liver of patient W. H 493,
LIST OF ILLUSTRATIONS. xix
234. Diagram showing the changes in the circulation in tricuspid stenosis 408
235. Cardiac outline and distribution of the presystolic rumble and snapping first
sound in tricuspid stenosis 409
236. Very early stage in the development of the human circulatory system 421
237. Human embryo 4 mm. long 422
238. Heart of an embryo 4 mm. long slightly older than that shown in Fig. 237, show-
ing the earliest stages in the formation of two auricular and two ventricular
pouches 423
239. A diagram showing the interior of this heart 423
240. Development of the arterial system from out of the primitive aortic arches 423
241. Heart of slightly older embryo, showing separation of aortic and pulmonary
channels in truncus arteriosus 424
242. Still later stage, showing the complete division of the truncus arteriosus into
pulmonary artery and aorta 425
243. Auricular end of the same heart 425
244. Development of the pericardial cavity 426
245. The circulation in the foetus just before birth 428
246. Pulmonary stenosis due to fusion of the cusps 431
247. Pulmonary stenosis due to a lesion of the infundibulum 431
248. Complete pulmonary atresia 431
249. Schema illustrating the genesis of pulmonary stenosis 432
250. Currents and lines of force in the embryonic heart which result from pulmonary
stenosis and tend to produce patency of the septa and of the ductus
arteriosus 434
251. Three-chambered heart (cor biatriatum triloculare) produced by complete
atresia of the pulmonary and tricuspid orifices 435
252. Diagram of the circulation in pulmonary stenosis and atresia 436
253. Dilatation and irregularity of the retinal vessels 439
254. Clubbed fingers 439
255. Distribution of the pulmonary systolic murmur of pulmonary stenosis 440
256. Direction of blood-streams and propagation of murmurs accompanying defect in
the interventricular septum, pulmonary stenosis, and open ductus arteriosus. . 440
257. Distribution and character of the murmur due to a patent interventricular
septum (Roger's murmur) 444
258. Open foramen ovale 446
259. Diagram showing a cross section of the same 446
260. Openings between strands of muscle in the interauricular septum 447
261. Radiograph of a thirteen year old boy with patent ductus arteriosus and aneuris-
mal dilatation of the ductus and pulmonary artery 451
262. Stenosis of the isthmus of the aorta above the ductus arteriosus, type of the
new-born f 453
263. Stenosis below the ductus arteriosus, adult type 454
264. Transposition of the viscera in embryo and adult 456
265. Transposition of the valves 457
266. Pulmonary artery with four cusps 457
267. Tracing of the apex beat in a case of Adams-Stokes disease 461
268. Partial heart-block (3 : 1 rhythm) produced by pressure upon the vagus in a
patient with disturbed conductivity who was also subject to attacks of the
Adams-Stokes syndrome , 462
269. The right branch of the auriculoventricular bundle in the dog's heart 463
270. Tracings from the carotid artery and the jugular vein of a patient with Adams-
Stokes disease 464
271. The Erlanger heart-block clamp compressing the auriculoventricular bundle 465
272. Effect of gradually tightening the clamp 465
xx LIST OF ILLUSTRATIONS.
273. Tracing from jugular vein and carotid artery in a case of complete heart-block
after the syncopal attacks had subsided *
•274 Diagram representing the conditions found in the tracing Fig. 273 4
375 Heart of a patient showing calcifications which produced Adams-Stokes disease . . 4
276. Diagram showing the two types of ventricular stoppage producing the Adams-
Stokes syndrome
277. Section of a luetic infiltration of the auriculoventricular bundle 4
278. Acute fibrinous pericarditis 482
279. Tuberculous pericarditis (cor villosum) 482
280. Diagram showing the relations of the pericardial and pleural frictions to the
cardiac and respiratory movements 4
281. The circulation in cases with pericardial effusion 488
282. Area of cardiac dulness from pericardial effusion 489
283. Positions of the heart in pericarditis with effusion 49.
284. Radiograph of a patient with pericardial effusion 492
285. Sites for paracentesis pericardii and pericardiotomy 496
286. Specimen showing the two layers of pericardium united in some parts by long
strands and in others by short bands of dense adhesions 500
287. Sections showing adherent pericardium 501
288. Anterior and posterior pericardial adhesions. (Semi-schematic) 502
289. Cardiac outline in adherent pericardium 505
290. Adhesions causing inspiratory and expiratory dropping of beats (Riegel's pulse
and the pulsus paradoxus) 506
291. Radiograph of a case of adherent pericardium. . . : 507
292. Case of pericarditic pseudocirrhosis 509
293. Wounds of the left ventricle 514
294. Exposure of the heart for suturing a wound . 516
295. Specimen of a large aneurism 521
296. Aneurism arising just above a sinus of Valsalva 524
297. Aneurism of the ascending arch and innominate artery 524
298. Aneurism of the transverse portion of the aortic arch penetrating through the
sternum 524
299. Aneurism of the descending aorta eroding the vertebra 524
300. Sections through the wall of an aneurism 525
301. Composite figure showing the relations of various aneurisms to surrounding
structures 528
302. Tracings of the outlines of an aneurism of the innominate artery, showing its
growth and the formation of secondary prominences upon its surface 529
303. Method of inspecting for pulsations 532
304. Effect upon the circulation of interposing an inelastic and an elastic bulb along
the course of an artery in a model of the circulation 534
305. Effect of aneurisms at various sites upon the blood-pressure, rate of transmission,
and the form of the pulse-wave 535
306. Radial pulse tracings from the right and left radial arteries of a patient with
aneurism of the first part of the arch of the aorta 535
307. Radiograph of a patient with a large aneurism of the ascending aorta and the
arch, viewed from behind 535
308. Radiograph of a patient with diffuse dilatation of the arch of the aorta 537
309. Diagram of the radiograph shown in Fig. 308 537
310. Cardiac dulness in cases of aneurism 540
311. Area of cardiac dulness in a patient with dilated arch of the aorta 543
312. Tumor and pulsation in a case of aneurism of the abdominal aorta 545
313. Tortuous subclavian artery, simulating a small aneurism 546
314. Dissecting aneurisms 547
LIST OF ILLUSTRATIONS. xxi
315. Diagram showing the various methods for the operative treatment of aneurism . . 553
316. Specimen of wired abdominal aneurism, showing an island of clot within the coils
of wire surrounded by a free blood channel 554
317. Venous pulse in a case of paroxysmal tachycardia 561
318. Diagram showing the various types of tachycardia 562
319. Experimental paroxysm of tachycardia produced by faradization of the dog's
auricle 563
320. Diagram showing the effect of a paroxysm of tachycardia upon the circulation .... 565
321. Photograph of a patient with Basedow's disease 579
322. Photograph of a portion of the thyroid gland removed from the patient shown
in Fig. 321 577
323. Drawing of a histological specimen from the same thyroid 578
324. Diagram showing the relation of the various anatomical structures concerned in
the production of the ocular and cardiac manifestations of Basedow's disease . . 584
325. Respiratory arrhythmia in a young cigarette smoker 594
326. Cross section of the thorax of a flat-chested individual, showing the systolic
heaving of the chest wall and the forces bringing it about 596
327. Low, normal, and high hearts. (Semi-schematic.) 598
328. Radiograph of a patient with dropping heart (bathycardia) 599
329. Photograph of a patient with enteroptosis 602
SYNONYMOUS ANATOMICAL TERMS.
Old Terminology.
Basle Anatomical Nomenclature
(BNA) '.
Latin.
Auriculoventricular groove . . . Coronary sulcus
Interventricular septum Septum of ventricles
Muscular septum
Membranous septum
Auricle
Auricular appendix
Interauricular septum
Columnse carneae
Annulus ovalis . .
Intervenous tubercle of Lower
Eustachian valve .
0
Valve of Thebesius; coronary
valve
Foramina Thebesii . . . 9
% e*
Tricuspid valve (right auri-
culoventricular valve)
Infundibular cusp
Marginal cusp
Septal cusp
Left auriculo ventricular valve
Corpora Arantii
Ductus arteriosus (Botalli) . . .
Auriculoventricular bundle
(Kent, His)
Forechamber .
Auricle .
Septum of atria
Fleshy cords
Edge of oval fossa.
Valve of inferior vena cava. .
Value of coronary sinus
Foramina of the smallest
veins
Tricuspid valve
Anterior cusp
Posterior cusp
Medial cusp
Bicuspid or mitral valve . . .
Nodules of the semilunar
valves
Arterial duct
Atrioventricular bundle (His)
Sulcus coronarius.
Septum ventriculorum.
Septum musculare.
Septum membranaceum.
Atrium.
Auricula.
Septum atriorum.
Trabeculae carneae.
Limbus fossae ovalis (Vieus-
senii) .
Tuberculum intervenosum
(Loweri) .
Valvula venae cavae (infe-
rioris, Eustachii).
Valvula sinus coronarii (The-
besii) .
Foramina venarum minim-
arum (Thebesii).
Valvula tricuspidalis.
Cuspis anterior.
Cuspis posterior.
Cuspis medialis.
Valvula bicuspidalis (mi-
tralis).
Noduli valvularum semilu-
narium. *
Ductus arteriosus (Botalli).
Fasciculus atrioventricu-
laris.
1 Quoted from Barker, L. F., Anatomical Terminology, with special reference to the
BNA, Phila., 1907.
The Basle Anatomical Nomenclature (BNA) is the terminology adopted by an inter-
national convention of anatomists at Basle in 1895, for the purpose of securing uniformity
of terminology. As it has not yet supplanted the old terminology in clinical usage,
the hitter is adhered to in this book, though the BNA terms are frequently given in
parentheses.
xxiii
FIG. 3. — Relations of the heart and great vessels, viewed from the front. SVC, superior vena
cava; R A, right auricle (atrium) ; L V, left ventricle; R V, right ventricle ; P A, pulmonary artery;
PL, pleura.
FIG. 4. — The heart and thoracic viscera viewed
from behind. The lungs have been cut away. L A,
left auricle ; L V, left ventricle.
FIG. 5.— Sagittal section of the thorax viewed
from the right. AZ., great azygos vein ; POST.
MEDIAST., posterior mediastinum; ANTER.
MEDIAST., anterior mediastinum; R A, right
auricle ; PHREN, right phrenic nerve.
DISEASES
OF THE
HEART AND AORTA
PART I.
GENERAL CONSIDERATIONS AND METHODS OF DIAGNOSIS.
I.
PHYSIOLOGICAL CONSIDERATIONS.
PROPERTIES OF 'HEART MUSCLE.
THE heart is composed of striated muscle-fibres which differ anatomi-
cally from the skeletal muscles in being almost devoid of connective-tissue
sheaths and from most of the skeletal muscles 1 in the fact that they anas-
tomose freely with one another, forming a continuous meshwork of muscle
Fia. 6.— Heart muscle-fibres^ 375. (After Piersol.)
tissue (Figs. 6 and 7). Physiologically fceart muscle differs from skeletal
muscle, for (1) it is continually undergoing rhythmic contractions, and
(2), as Bowditch has shown, every contraction is maximal.
A great deal of perspicuity has been added, especially to the clinical
study of the cardiac function, by discriminating between influences which
affect the cardinal properties of the cardiac muscle (Engelmann). One
recognizes those which affect (1) rhythmicity (chronotropic in-
1 The tongue of the frog and some other forms of muscle somewhat resemble heart
muscle in structure.
1
2 DISEASES OF THE HEART AND AORTA.
fluences); (2) irritability (bathmotropic); (3) conductivity
(dromotropic); (4) contractility (inotropic), as well as (5)
t on i city (Mackenzie). . .
Influences improving these properties are designated as positive,
those which depress them as negative.
Endotheliutn
Subendothelial • 'JX^g^^C1
stratum £&-£irjg^5*A
Layer rich in
elastica
Deepest layer
Heart muscle •
Blood-vessel
FIG. 7. — Section through the endocardium showing cross-section of the muscle-fibres. (After Piersol.)
ORIGIN OF THE HEART-BEAT.
Role of the Salts. — Merunowicz, under Ludwig's direction, demon-
strated that the rhythmicity of the heart depended not only upon its
intrinsic characteristics but particularly upon the action of the inorganic
salts present in the blood serum. Ringer (1882), and later Howell, showed
that the antagonistic actions of potassium and calcium salts were the
factors chiefly concerned in determining the rhythm of the heart, while
Loeb and his pupil, Lingle, showed that without the sodium salts it
would not beat at all. Accordingly, as Loeb and Howell agree, the heart-
beat can be maintained only when these three salts or their ions are
present in certain definite proportions, or in what Loeb has termed ' ' a
balanced solution." However, while Ringer and Howell
believe that the calcium liberates the motive power of
the cardiac contraction, Loeb and his pupils believe
that this is done by the sodium and that the calcium and
potassium merely keep the sodium from liberating too much.
Their mode of action has been explained by Loeb in 1899 in the
following words:
" The salts or electrolytes in general do not exist in living tissues as such exclusively,
but are partly in combination with proteids (or fatty acids). The salts or electrolytes do
not enter into this combination as a whole, but through their ions. The great impor-
tance of these ion-proteid combinations (or soaps) lies in the fact that by substitution of
one ion for another, the physical properties of the proteid change (e.g., their surface ten-
sion, their power to absorb water or their viscosity or state of matter). We thus possess
in these ion-proteid or soap compounds essential constituents of living matter, which can
be modified at desire, and hence enable us to vary and control the life phenomena themselves.
"Life phenomena, and especially irritability, depend upon
the presence in the tissues of a number of the various metal pro-
teids, or soaps (Na, Ca, K, and Mg) in definite proportions.
Solutions of Na-salts produce rhythmical contractions only if the muscle cells contain
PHYSIOLOGICAL CONSIDERATIONS.
Ca-ions in sufficient numbers. As soon as there is a lack of Ca-ions in the tissues the Na-
ions are no longer able to cause rhythmical contractions. On the other hand, if we add
Ca-salts in sufficient quantity to the NaCl solution, it will no longer cause rhythmical con-
tractions in the fresh muscle of the frog. . . . It is hardly necessary to mention that
this suggested the possibility that muscular contraction in general is due to a substitution
of Na for Ca, or vice versa, in certain compounds (proteins or soaps) in the muscle."
The hypothesis that the main physiological antagonism lies between
K and Ca is stated by Howell in the following words:
" The well-nourished heart contains a large supply of energy-yielding material which
is in a stable form, so that it neither dissociates spontaneously nor can be made to do so
by the action of external stimuli. It is possible that this stable, non-dissociable form con-
sists of a combination between it and the potassium or the potassium salts, and that
therein lies the functional importance of the potassium contained in the tissue. This
compound reacts with the calcium or with the calcium and sodium salts and a portion of
the potassium is replaced; and a compound is formed which is unstable. At the end of
the diastolic period this compound reaches a condition of instability such that it disso-
ciates spontaneously, giving rise to the chain of events that culminates in the normal
systole. Before spontaneous dissociation occurs it may be hastened by an external stimu-
lus, as we know is the case when a mechanical or electrical shock is applied to the heart at
any time after diastole begins."
Any single ion or salt is poisonous by itself, but in the presence of
certain others may be beneficial. This very interesting question of "bal-
anced ion solutions" has been extensively investigated by Loeb and
his pupils, not only upon heart but upon skeletal muscle and upon lower
medusae, molluscs, and fishes.
Even the mammalian heart can be readily revived and
kept beating outside the body if perfused with a solution containing these
substances together with sodium bicarbonate (Howell) and saturated with
oxygen (Locke's solution, — NaCl 0.9 per cent, -f CaCl2 0.024 per cent. +
KC1 0.42 + NaHCO3 0.01 to 0.03 +
dextrose 0. 1 per cent.) . It is necessary
to maintain the blood-pressure at 50-
100 mm. Hg, and also the tempera-
ture 36° to 37°. Kuliabko and others
have revived excised human hearts
many hours after death. Fibrillary
contractions occasionally set in, but
may be stopped by perfusing with
KC1 1.0 per cent, for a few minutes
instead of Locke's solution. The
heart then comes to a stand-still
and resumes beating under Locke's
solution.
FIG. 8. — Apparatus for perfusing the mamma-
lian heart. A, auricle; V, ventricle; TAMB.,
tambour; TH., thermometer; MAN., manometer;
GASCH, gas check; Ot, tank of oxygen.
The study of the excised heart has been very useful both in testing
the effect of drugs and in simulating conditions of disease; but the condi-
tions of circulation are not exactly comparable to those within the animal,
and the results should always be carefully checked upon the intact animal
before assuming them to be normal or drawing any conclusions as to
pharmacological action.
Myogenic and Neurogenic Theories. — Whether the salts or ions which
maintain the rhythmicity of the heart-beat do so by acting directly upon
4 DISEASES OF THE HEART AND AORTA.
the muscle tissue (myo genie), or whether the stimuli are first generated
in nerve tissue (neurogenic) and then transmitted to the muscle, is a
question which has been disputed for centuries. And though the pendulum
has repeatedly swung from one opinion to the other, this question cannot
at present be answered. It is quite certain that all the extrinsic cardiac
nerves can be removed without stopping the rhythmic contractions, and
that the ganglion cells may be stimulated without materially affecting the
rhythm (Gaskell). But the meshwork of muscle-fibres in the heart is so
permeated by a meshwork of fine nerve-fibres that it has been impossible
to determine whether the impulse arises in the muscle-cells or in the nerve
endings upon their surfaces. Wm. His, Jr., has indeed shown that the
heart of the chick embryo beats before nerve-fibres have entered it at all,
but the possibility still remains that after once entering the heart the
nerves may take the initiation of contraction away from the adult heart-
muscle. Moreover, the recent experiments of Carlson and of Magnus in
allied fields give considerable evidence that such may be the case; so that,
in spite of its importance for both the physiology and the pathology of the
heart, neither the myogenic nor the neurogenic theory of the heart-beat
has been finally proved.
Maximal Contractions and Irritability. — As Bowditch has shown, the
heart liberates all its available energy at each contraction, which resembles
in this way the explosion of gunpowder or the liberation of a spring by a
trigger. Like the power of the spring, the strength of the cardiac contrac-
tion depends upon the energy stored up. This energy seems to depend
upon the regeneration of the contractile substance mentioned above by
Howell. When the next contraction, normal or abnormal (extrasystole),
occurs soon after the last (early in diastole), the contraction is weaker than
the preceding, since it liberates less energy, but the contractile substance
is again completely destroyed and requires another pause (compensatory
pause, see page 69) to regenerate it. When it occurs late, the contrac-
tion is of almost or quite original strength, and the stored-up energy is again
liberated completely. Moreover, Erlanger has shown that the irritability of
the heart increases progressively as diastole is prolonged and as the muscle
becomes overloaded with the energy-producing substance.
ORIGIN AND COURSE OF THE CARDIAC IMPULSE.
The Sinus as "Pace-maker" of the Heart.— In the frog, where the
cardiac impulse travels slowly, it is very easy to see that it arises at the
sinus venosus, which executes a contraction. This is followed by contrac-
tion of the auricle, the latter after an appreciable interval by a visible con-
traction of the small ring of muscle about the auriculoventricular ring
(Bond), and this in turn by contraction of the ventricles.
It is probable that the sinus initiates the cardiac rhythm, because it
is the chamber which, when isolated, beats at the fastest rhythm in the
blood-serum, and hence it becomes what Erlanger terms "the pace-maker
of the heart." ] Indeed, if the impulse from the sinus is blocked by crushing
' Under pathological conditions and especially in the excised heart the ventricle may
e more irritable and may become the pace-maker (reversed rhythm).
PHYSIOLOGICAL CONSIDERATIONS.
or by cooling the sino-auricular border, the impulses no longer reach the
auricles, which must then contract by their own slower rhythm or not beat
at all (sinu-auricular heart-block).
Anatomy of the Sinus Region in Mammals. — In man and other mam-
mals the sinus no longer exists as a separate chamber, though in the early
embryo (Fig. 243, page 425) its homologue, the sinus reuniens, is separated
off from the rest of the auricular cavity by the Eustachian valve. This
sinus chamber receives the two venae cavze and the coronary sinus. In
the course of development the growth of the sinus region does not keep
pace with that of the auricle, and it becomes swallowed up in the latter,
so that in the adult the sinus corresponds roughly
to the area bounded by the mouths of the two venae
cavae, the coronary sinus, and the interauricular
septum.
Systemic aorta
Pulmonary aorta or artery
Right auricular appendage
Right ventricle, conus
arteriosus
Right a u -
riculo-
ventricu-
lar valve
Sup. pulm
vein
Inf. pulm.
vein
Fossaovalis
surrounded
by annulus
Inferior
vena cava
Orifice of coronary sinus, guarded by Thebesian valve
Eustachian valve Depression receiving Thebesian veins
FIG. 9. — The auricular end of the human heart viewed from the right. (After Piersol.)
Comparatively little is known concerning the structure of this impor-
tant region. The most careful studies (Keith, Retzer, Schonberg) are con-
cerned more with the structure of the veno-auricular junction or the sino-
ventricular connections than with the structure of the sinus as a whole,
or the sinu-auricular border which is included within the body of the
right auricle.
The Veno-auricular Junction. — Schonberg studied the veno-auricular junction in a
large number of normal and abnormal human hearts by means of serial sections, each series
being composed of 300 to 800 sections. At a level 10 to 15 mm. above the entrance of the
superior vena cava into the auricle (atrium) he found the usual structure of vein wall.
Below this level the media is found to contain groups of striated muscle-fibres separated
from one another by fat and connective tissue. These striated muscle-fibres arise in the
6 DISEASES OF THE HEART AND AORTA.
vicinity of non-striated fibres but are never continuous with than Bundles of these
fib el (to 1 mm. in diameter run transversely across the vein toward the auricle, gradual y
converging into larger bundles, which are separated from one another by a tissue rich in
^mphgand blood-vessels. In the angle (sulcus) formed between the auricle (atrium 'and
v^cava these bands of striated muscle become much thinner and contain numerous
tortuous fibres resembling Purkinje fibres. In this region there is a considerab le deposit of
fat lymphoid and connective tissue, forming a more or less definite border-line. The
muscle-fibres of the auricle (atrium) are inserted in the connective tissue here^ The
connection between the musculature of the ve na cava and that
of the auricle is made by the numerous small bundles of striated
muscle-fibres lying just beneath the endocardium, which pass across this junc-
tion and end in the fibres of auricular muscle. "In the macroscopic prepa-
rations it is almost always readily seen that the sulcus is
bridged at its posterior lateral third by a muscle-bundle which
ascends upwards and backwards from the auricle (atrium) to the
superior vena cava, where it is strengthened by fibres from the
FIG. 10. — The sinus region of the heart, the venorauricular or veno-sinal bands of striated muscle
and the auriculo(atrio)ventricular or sinu-ventricular muscle bundle. (Schematic, constructed from the
findings of Keith, Schonberg, and Retzer.) A. Seen from the right side. The dotted area represents
the sinus region ; the striae represent the veno-auricular muscle strands. V.C.S., superior vena cava;
V.C.I., inferior vena cava; SC, coronary sinus; A V B., auriculo(atrio)ventricular muscle bundle
(His bundle); TRIG, tricuspid valve; PAP, papillary muscle. B. The same region seen from the front.
MIT, mitral valve; A O, aorta.
circular musculature of the lower part of the vein. This bundle
is also well seen microscopically, but numerous other smaller muscle bundles are seen as
well. It corresponds quite well with that described by Keith and Flack, and Wenckebach.
Schonberg found that the region of the sulcus is particularly rich in nerve-fibres,
ganglion cells, blood-vessels, and lymphoid tissue, and is therefore particularly liable to
pathological infiltrations and cicatrizations.
It is worthy of note that the sulcus noted by Schonberg does not repre-
sent the sinu-auricular junction but the veno-sinal junction. The strands
of striated muscle which he describes are derived from the sinus. The sinu-
auricular (sinu-atrial) junction on the other hand is actually situated within
the body of the auricle (atrium) . '
Role of the Sinus in Mammals. — There is a considerable amount of
physiological as well as anatomical evidence that in the adult mammal
as well as in the amphibian this is the region in which the cardiac
impulse arises.
PHYSIOLOGICAL CONSIDERATIONS. 7
MacWilliam in 1888 was able to show that this intervenous
area was the only region at which the application of heat
quickened andcold slowed the heart rate. Adam and the writer
were able to confirm this observation. H. E. Hering has shown that this area is
often the last to cease contraction in dying mammalian and human hearts, though this is
not always the case (Hirschfelder and Eyster). Langendorff and Lehmann and also Leon
Fredericq showed that even in the excised heart portions of the auricles cut off from this
area ceased to beat or beat at a slow rhythm, while those which remained attached to the
sinus region beat at about the original rate. Erlanger and Blackmann were able to produce
halving of the heart rate (sinu-auricular block?) by torsion of this area in the excised heart,
but like Hirschfelder and Eyster were unable to produce it by clamping experiments
upon the heart in situ. The most conclusive experiments are those of Lohmann who
poisoned the cells in this area by direct application of cotton soaked in formalin, and
found that the heart at once slowed, auricles no longer followed ventricles, and the auricles
and ventricles beat simultaneously (nodal rhythm, see page 76).
Course of the Impulse after Leaving the Sinus. — From the sinus
region the cardiac impulse travels to the walls of the auricles and gives
rise to the auricular contraction. It is also propagated downward toward
the ventricles, which it reaches about one-fifth of a second later.
It is a mooted point at present whether the path from sinus to ventricle is through
auricular tissue or whether there is a direct sino-ventricular pathway, as believed by
Retzer, who thinks that the auricle is off on a side path and contracts first merely
because it is nearer to the sinus than is the ventricle. However, Bond's observations
on the frog, showing that the auricle contracts a considerable time before the mus-
culature of the auriculoventricular ring, indicates that the impulse passes from the
former to the latter.
Kent, His, Retzer, Braeunig, Keith, and Tawara have shown that the
cardiac impulse is propagated from auricles to ventricles through the system
of Purkinje fibres, which forms a ^ whose shaft arises in the right auricle
at or near the sinus, runs in the membranous septum (auriculoventricular
bundle) downward to the muscle septum, where it divides into two branches
which straddle the muscular septum and then pass to the right and left
ventricles. W,ithin these chambers the branches divide into numerous
ramifications which lie just beneath the endocardium and pass downward
as a meshwork of light-colored translucent strands to the papillary muscles
and walls of the ventricles. Occasionally instead of following the walls
they cross the ventricular cavity to the papillary muscle as isolated strands
(moderator bands, T. W. King, Tawara) . In this bundle also the
presence of numerous nerve-fibres (Tawara) and of ganglion cells (Gordon
Wilson) renders it doubtful whether the impulse travels through nerve or
muscle. The slow time of transmission is a little in favor of the latter.
COORDINATION OF THE CARDIAC CHAMBERS.
Under all circumstances (except those mentioned on page 67) the
contractions of both auricles and of both ventricles are absolutely synchro-
nous. Barker and Hirschfelder have shown that simultaneous contractions
of the two ventricles continue after the branch of the conduction system
to one (the left ventricle) has been cut, and hence the coordination does
not depend upon the auriculoventricular conduction system but upon the
ventricular musculature.
8
DISEASES OF THE HEART AND AORTA.
Anatomy of the Ventricular Muscle.— This is not surprising, since, as
Ludwig, Krehl, and J. B. MacCallum have shown, each strand of muscle-
fibres passes from ventricle to ventricle. These muscle-fibres are arranged
in three distinct layers so placed that they are wound up like a scroll, the
most superficial layer of the left ventricle penetrating to become the deepest
layer of the right (Fig. 11, I, II, III). Besides these MacCallum has de-
scribed a fourth band of muscle, independent of the latter, which sur-
rounds both the aortic and mitral orifices in a single ring of muscle (mitro-
aortic ring), across which a septum of connective tissue separates the
aortic orifice from the mitral ring (Fig. 11, V). This band is more or less
homologous to the bulbus arteriosus of the lower vertebrates, and plays
a most important role in preventing leaks at the valvular orifices.
EMPTYING AND FILLING OF THE HEART, AND MOVEMENTS
OF THE VALVES.
The Presphygmic Period.-The instant before the beginning of ven-
ricular systole the mitral and tricuspid valves are open, while the aortic
it at on " V±eS are ClOSed' When the ^ricular contraction begins^
t at once ra,ses the pressure within the ventricles above that in the auricles
causing the mitral and tricuspid valves to close with a snap There I thus
a short interval, the presphygmic (.07-.09 sec.), at the very beginning of
eSn auT ^t "I ^ ^ "* ^ and -oveLnt" of blood
the ven?ricL n ^^ This Period ^sts until the pressure within
pressure)' after
PHYSIOLOGICAL CONSIDERATIONS.
9
FIG. 12. — Apparatus for registering the volume of
the ventricles. CARDIOM., cardiometer.
Method of Recording the Volume Curve. — Yandell Henderson has recorded the
emptying and filling of the ventricles by means of a specially constructed cardiac plethys-
mograph or cardiometer like that of Tigerstedt and Johannson. Henderson's cardiometer
was made from an ordinary rubber ball, out of which a large window was cut and then
closed hermetically by cementing on a cur-
tain of rubber dam. In the centre of the
rubber dam a hole was cut just large enough
for it to fit air-tight in the auriculoventricular
groove. The heart was then pushed in
through the hole until the dam slipped into
the groove. The changes of pressure within
the air space surrounding the heart were cotr-
municated to a recording tambour through
a glass tube cemented in the opposite surface
of the ball (Fig. 12). Dr. Cameron and the
writer have found it most convenient to have
the recording tambour inverted, so that upstrokes record systole and down-
strokes diastole, while a general rise in the curve indicates
diminution in volume, and a general fall indicates dilatation.
Outflow during Systole. — By this means Henderson has found that
during systole the ventricles do not empty themselves with a rush at the
beginning of systole, but that the outflow continues quite uniform through-
out at least nine-tenths of the latter period (outlasting the rise of the arterial
pulse-wave) and begins to slow only toward the very end (slight rounding
of the crest of the curve). At the cessation of outflow there is an instant
during which the ventricular pressure is falling, in which no inflow takes
place, but this is only one or two hundredths of a second and is difficult to
estimate accurately. This instant corresponds to the dicrotic notch upon
the aortic pulse-wave.
Filling of the Ventricles. — The ventricles then begin to fill at a rapid
and uniform rate until they are almost completely distended. If the
pulse-rate is rapid, the next systole takes place before the filling is as com-
plete as possible, and cutting short the filling diminishes the volume of the
heart; not only the total volume, but the amount of blood discharged at
each systole (Fig. 13).
AORTA
VOLUME
OF VENTRICLES
S
SLOW NORMAL
RAPID
FIG. 13. — Volume curves of the ventricles at different heart rate?. (Modified from Henderson.)
The dotted line shows how the curve of the typical cycle may be superposed upon the curve corresponding
to a different rate. A, quota of blood forced in by auricular systole.
Diastole and Diastasis. — If, on the other hand, the heart rate is slow
(Fig. 13), as after stimulation of the vagus, the influx begins at the same
rate as before and continues uniformly for about two-fifths of a second
(steep ascent of the curve) until the ventricles are distended, after which
scarcely any blood flows into the ventricles no matter how long the interval
10 DISEASES OF THE HEART AND AORTA.
to the next beat. The diastolic period is thus divided into two parts : (1) the
phase of diastole proper during which filling of the ventricles
takes place; (2) the phase of d i a s t a s i s in which little or no f
occurs The slower the heart the greater is the disatolic filling and the
longer' its duration. The greatest amountof output in
unit time occurs at a rate which just allows the phase
of diastolic filling to be complete but in which the next
beat occurs before diastasis sets in. Any rate above or below this brings
about some slowing of the circulation.
Position of the Valves in Diastole.— Baumgarten (1843) has been able to demonstrate
upon the excised heart that the cusps of the mitral and tricuspid valves are floated together
by the influx of blood and the valves close spontaneously when the inflow ceases. Ine
writer has been able to show that the occurrence of diastasis is not necessarily caused by
the valves being closed, but by the fact that the heart fills for a time before the walls are
FIG. 14. — Methods for demonstrating the movements of the heart valves.
Baumgarten 's method.
A, Gad's method; B,
put upon a stretch, and then the passive elasticity of the walls prevents further filling.
If the venous pressure is materially increased, further increase in volume then takes
place. The closure of the valves in early diastole depends chiefly
upon the suddenness both of the filling and of its cessation.
A very pretty and instructive demonstration of the opening and closing of the heart
valves has been devised by J. Gad by an experiment shown in Fig. 14, A, which can be very
nicely performed upon a sheep's heart as bought at a butcher's shop%
The left auricle is cut away and the bowl of a large thistle tube tied in the place by
a circular ligature. A large glass tube is thrust through the aorta into the ventricle and
ligatured in" place. Both the thistle tube and the aortic cannula are connected with fun-
nels by means of rubber tubes, and the chambers of the heart may be then completely
filled with water. The opening and closing of the valves may be brought about by raising
and lowering one or the other of the funnels, and may be watched through the wall of the
bulb. Insufficiency of the valve may be produced by cutting or stretching one of the
chordse tendineae, but after the experiment has been repeated a few times upon the same
heart a certain amount of insufficiency usually sets in spontaneously. The sounds pro-
duced by the valves and blood stream independently of the contraction can be well studied
by placing the stethoscope upon such a heart, provided all the air has been removed from
the cardiac chambers. In a similar manner the phenomena can be observed in the right
PHYSIOLOGICAL CONSIDERATIONS. 11
heart. The closure of the aortic or pulmonic valves can also be demonstrated by drawing
the glass tube out of the ventricle up into the vessel, tying it there close to the valves, and
cutting off the walls of the vessel above the ligature.
Still simpler is the older method of Baumgarten (1843) of cutting away the auricles
to expose the valves and then pouring in water from a beaker (Fig. 14, B).
RELAXATION OF THE HEART, AND TONICITY OF THE CARDIAC MUSCLE.
It has been supposed by some writers that the diastolic dilatation of
the heart is brought about by some active muscular contraction, since the
pressure within both ventricles becomes negative, even to the extent of
— 55 mm. Hg. This negative pressure is of only momentary duration, and
may be compared to that occurring within a rubber ball when squeezed
and let go. The walls of the heart are sufficiently rigid and are sufficiently
provided with elastic fibres to resume their shape like a rubber ball, and,
on the other hand, the pressure in the coronary arteries tends to hold them
distended as though by a wire frame.1
The heart muscle is quiescent and the heart walls are relaxed during
the entire period of diastole, so that neither the most delicate recording
levers nor the most sensitive galvanometers reveal the slightest signs of
contraction. Nevertheless, as will be seen, the degree of this diastolic relax-
ation of the walls varies considerably under different circumstances depend-
ent upon the tonicity of the heart muscle. This is shown by variations
in the length of strips of cardiac muscle under a constant load, as well as
by variations in the cardiac volume.
Tonicity. — T onicity may be defined as the resistance
of the heart muscle to stretching in diastole; or, less
accurately, as its diastolic rigidity.
The force which stretches the heart walls in diastole is the pressure at
which the blood enters the heart from the great veins, namely the venous
pressure, so that with a high venous pressure (unless antagonized by a high
tonicity) they will be stretched considerably (dilatation), while with a low
venous pressure comparatively little blood will enter and the heart will
remain small. In all cases filling will continue until an
equilibrium is reached between the venous pressure
and the cardiac tonicity, unless the heart rate is so rapid that
the filling is interrupted by the next systole. A high tonicity will, how-
ever, antagonize a high venous pressure and prevent overfilling.
Moreover, Howell and Donaldson have shown that the systolic output
of the heart depends to a great extent upon the amount entering the latter
from the great veins, and hence, upon the venous pressure. If the venous
pressure falls below a certain level, the heart fills incompletely, and the ven-
tricles are unable to pump enough blood into the arteries to maintain the
blood-pressure at the usual level.
The rate of filling of the heart is accelerated (curve of filling steeper)
(Fig. 15) when either the venous pressure is high or the tonicity is
low; the filling is slowed (curve more oblique) when either the tonicity is
1 For a detailed account of the various theories of the cardiac relaxation, with full
bibliography, consult E. Ebstein, Die Diastole des Herzens, Ergebnisse der Physiol.,
Wiesb., 1904, iii 2 Abth.
12
DISEASES OF THE HEART AND AORTA.
high or the venous pressure is low. So that, as regards filling of the heart,
a high tonicity is equivalent to a low venous pressure, and conversely, a
low tonicity is equivalent to a high venous pressure (Fig. 16).
Influences which affect tonicity may be studied objectively in isolated
strips of cardiac muscle by means of their shortening or lengthening, or
upon the intact heart by changes
in the volume curve.
FIG. 15. — Volume curves showing the effect
of variations in venous pressure ( V P) and in ton-
icity (T) upon the rate at which the ventricles are
filled during diastole.
V P 5 CM.
FIG. 16. — Volume curves showing the effect of
low venous pressure or of high tonicity upon the
amount of blood entering the ventricles. (Modified
from Y. Henderson.) A fall in the venous pressure
is equivalent to an increased tonicity. CM, centi-
metres of HzO pressure.
The total volume of the heart at any given instant may be regarded
as follows:
Volume of heart = voluma of heart walls + volume of blood within cardiac chambers.
Volume of walls = volume of muscle + coronary blood + lymph. (The two latter
factors vary somewhat, though relatively slightly, the lymph
increasing considerably in cardiac stasis.)
Volume of blood within chambers = output at each systole + blood remaining at end
of systole (residual blood).
Residual Blood. — The residual blood undergoes gre'at
variations. In dilated hearts it may attain to several times the
amount of the systolic output (cf. Fig. 17), while in small hearts it may
be only a fraction of the latter. The systolic output, on the other hand,
may undergo equally large variations.
FIG. 17. — Diagram to illustrate the changes in volume of the ventricles in systole and diastole
associated with variations in tonicity (T) and systolic output (S. O.). N, NORM., normal; +, increased;
— , diminished. Length of heavy black line indicates degree of tonicity.
The changes in tonicity may be measured by the volume of the heart
at the end of diastole, i.e. when the filling is most complete, a large diastolic
volume representing low tonicity (when venous pressure and pulse-rate are
constant), a small volume indicating a high tonicity.
Nature of Changes in Tonicity. — Porter has found that a strip of heart
muscle can be made to remain elongated (diminished tone), or can then be
made to remain shortened when not receiving any stimuli whatever (in-
creased tone^l. Several degrees of this permanent shortening can be super-
PHYSIOLOGICAL CONSIDERATIONS. 13
posed on one another with great similarity to the tetanus of skeletal muscle
("tetanus of tone," Porter). Barcroft and Dixon have shown that the
muscle when in tone gives off more CO2 than when at rest, further support-
ing this view of the role of increase and decrease in tone.
Factors producing Changes in Tonus. — F. B. Hoffmann has demon-
strated that there are two separate sets of fibres in the frog's vagus. One set
influences the heart rate only (chronotropic effect), the other increases the
size and force of contraction (augmentor effect) and also increases the
cardiac tonus but does not affect the rate at all. This group of fibres is
found only in the interauricular and interventricular septum (septal nerves)
in the frog. In other animals the two groups of fibres pass side by side and
cannot be dissociated, though it is frequent in weak stimulation of the vagus
to find one effect occurring without the other.
P. D. Cameron, in the writer's laboratory, has found that in dogs the
intravenous administration of digitalis, strophanthus, nitroglycerin, and
calcium salts increases cardiac tonicity. The effect of small (therapeutic)
doses of these drugs is exerted almost entirely upon the tonic fibres in the
vagus, and fails to appear if the vagi have been cut or paralyzed with atro-
pine. Larger doses, however, exert similar effects by direct action on the
heart muscle. Atropine itself illustrates these effects by causing a primary
depression of tonus as the vagi become paralyzed, which is followed by an
increase in tonicity from direct action on the heart muscle. Potassium
salts, asphyxia, formic acid, adrenalin depress tonicity. Aconite in thera-
peutic doses affects rate more than tonus in the dog.
Since the exact volume of the heart cannot be determined clinically,
the area of the cardiac shadow in diastole furnishes the best index of the
tonus, especially when combined with study of the venous pressure. Com-
paratively little investigation has been carried on in this field. Moritz and
Dietlen have shown that exercise usually increases tonus in healthy per-
sons. The study of tonus has also proved of value in the study of exercise
and in the controlling of hydrotherapy and drug treatments, as well as in
the study of myocardial insufficiency.
ACTION OF THE CARDIAC NERVES.
The heart rate is determined by action of the vagus and accelerator
nerves, and particularly by the tonic activity of the centres near the calamus
scriptorius of the medulla: the former nerve slows the heart (inhibitory
effect) , lowers the blood-pressure (depressor effect) , and diminishes
the conductivity (negatively dromotropic effect) from auricle
(atrium) to ventricle; the latter quickens the heart (accelerator
effect), increases the force of the contraction and cardiac tonus
(augmentor), and improves conductivity (Bayliss and Starling). In
some cases stimulation 'of the accelerators may revive a heart that has
ceased to beat (Hering).
Both vagi and accelerators are normally in tonic
activity. Reflex quickening of the pulse-rate, as from emotion, pain,
sensation, and other reflex causes (Reid Hunt), and moderate exercise
(Hering and Bowen), is due partly to diminution of tonic activity of the
14 DISEASES OF THE HEART AND AORTA.
vasi partly to direct stimulation of the accelerators (Hooker); while the
acceleration after violent exercise is due to stimulate of the Accelerators
(Herin- Bowen). Acceleration upon mild exercis3 can also be obtained
n patients whose vagi are made inactive by 0.5 to 1.0 mg. (TJT to A gr.)
atropinc (Hirschfelder). On the other hand, exercise caused no accelera-
tion but a slight slowing of the pulse in a dog from which Fnedenthal had
removed all the cardiac nerves.
FIG. 18. — Origin and course of the cardiac nerves, and cutaneous distribution of the corresponding
branches. (Schematic; modified from Douglas Powell and Gibson.) MOT SENS, nuclei of the efferent
(motor) and afferent (sensory) fibres of the vagus; C 1,2,3,4, 5, 6, 7, 8, and T 1, 2, 3, 4, 5, 6, 7, 8,
cervical and thoracic (dorsal) spinal nerves and their cutaneous distribution; SCO, MCG, ICG, superior,
middle, and inferior cervical ganglia; REC LAR, recurrent laryngeal nerve; C PL, cardiac plexus.
The mode of action of the cardiac nerves has been shrouded in mystery, especially
that of the inhibition by the vagus. Howell and Duke in a most brilliant series of researches
have shown that potassium is given off from the heart muscle and
can be found in increased quantity in the perfusion liquid after
the vagus has been stimulated. Controls without vagus stimulation show
no such increase. It would therefore appear that vagus inhibition is a true
potassium effect, a fact further borne out by the close analogy between
the action of this element and stimulation of the vagus, as well as by the marked increase
in the action of the vagus after the administration of large quantities of potassium or
after increase of potassium in the blood.
These observers were unable to demonstrate any effect of the accelerators upon the
liberation of calcium, potassium, or nitrogen.
PHYSIOLOGICAL CONSIDERATIONS. 15
BIBLIOGRAPHY.
PHYSIOLOGY.
Bowditch, H. P.: Ueber die Eigenthumlichkeiten der Reizbarkeit, welche die Muskel-
fasern des Herzens zeigen, Ber. d. math. phys. Cl. d. k. sachs Gesellsch. d. Wissensch.,
Leipzig, 1871.
Engelmann, Th. W.: Ueber den Ursprung der Herzbewegungen, Arch. f. d. ges. Physiol.,
Bonn, 1897, Ixv, 109.
Mackenzie, James: A Preliminary Inquiry into the Tonicity of the Muscle-fibres of the
Heart, Brit. M. J., London, 1905, ii, 1689.
Merunowicz. Quoted from Schaefer's Physiology.
Ringer, S.: Concerning the Influence Exerted by Each of the Constituents of the Blood
on the Contractions of the Ventricle, J. Physiol., Cambridge, 1882, iii, 380. A Further
Contribution Regarding the Influence of the Different Constituents of the Blood on
the Contraction of the Heart, J. Physiol., Cambr., 1884, iv, 29. A Third Contribution
Regarding the Influence of the Inorganic Constituents of the Blood on Ventricular
Contraction, ibid., p. 222.
Howell, W. H.: On the Relation of the Blood to the Automaticity and Sequence of the
Heart-beat, Am. J. Physiol., Bost., 1898, ii, 47.
Greene, C. W.: On the Relation of the Inorganic Salts of Blood to the Automatic Activity
of a Strip of Ventricular Muscle, ibid., p. 82.
Howell, W. H.: The Cause of the Heart-beat, J. Am. M. Assoc., Chicago, 1906, xlvi, Nos.
22 and 23.
Loeb, J.: Ueber lonen welche rhythmische Zuckungen des Skelettmuskels hervorrufen,
Beitrage zur Physiologic (Festschr. f. A. Fick), Braunschweig, 1899, p. 101. The
Dynamics of Living Matter, N. York, Columbia Univ. Press, 1906, for complete dis-
cussion of work upon the comparative physiology of salt action.
Lingle, D. J.: The Action of Certain Ions on Ventricular Muscle, Am. J. Physiol., Bost.,
1900, iv, 265.
Moore, A.: The Effect of Ions on the Contractions of the Lymph Hearts of the Frog, Am.
J. Physiol., Bost., 1901, v, 87.
I/>eb, J., 1. c.
Locke, F. S.: Die Wirkung der Metalle des Blutplasmas und verschiedener Zucker auf
das isolirte Saugethierherz., Centralbl. f. Physiol., Leipz. u. Wien., 1901, xiv, 670.
Langendorff, O.: Untersuchung am uberlebenden Saugethierherzen, Arch. f. d. ges. Phy-
siol., Bonn, 1895, Ixi, 291.
Rusch, H.: Experimentelle Studien iiber die Ernahrung des isolirten Saugethierherzens,
ibid., 1898, Ixxiii, 535.
Kuliabko, A.: Wiederbelebung des menschlichen Herzens, Centralbl. f. Physiol., Leipz.
und Wien, 1902, xvi, 330.
d'Hallion, M.: Reviviscense d'un coeur d'enfant 36 heures apres la mort, J. d. sc. mdd. de
Lille, 1903, ii, 481.
Deneke, Th., and Adam, H.: Beobachtungen am isolirten iiber lebenden menschlichen
Herzen, Ztschr. f. exper. Path. u. Therap., Berl., 1906, ii, 491.
Gaskell, W. H.: On the Rhythm of the Heart of the Frog and the Nature of the Action
of the Vagus Nerve, Phil. Trans. Roy. Soc., London, 1882, p. 993. On the Innerva-
tion of the Heart, with Especial Reference to the Heart of the Tortoise, J. Physiol.,
Cambridge, 1884, iv, 43. The Contraction of Cardiac Muscle, Schafer's Text-book of
Physiol., Edinb. and Lond., 1900, ii, 169.
His, W., Jun.: Die Thatigkeit des embryonalen Herzens und deren Bedeutung fur die
Lehre von der Herzbewegung beim Erwachsenen, Arb. a. d. med. Klin, zu Leipz.,
1893, 14.
Bond, G. M. — Unpublished experiments.
Erlanger, J.: Irregularities of the Heart resulting from Disturbed Conductivity, Am. J.
M. Sc., Phila., 1908, n. s. cxxxv, 797.
Keith, A., and Flack, M. W.: The Auriculoventricular Bundle of the Human Heart, Lan-
cet, Lond., 190f>, ii, :;.V.).
Keith, A. : An Account of the Structures Concerned in the Production of the Jugular Pulse,
J. Anat. and Physiol., Lond., 1908, xlii, 1.
16 DISEASES OF THE HEART AND AORTA.
Retzer, R.: Some Results of Recent Investigations on the Mammalian Heart, Anat. Rec.,
Phila., 1908, ii, 149.
Schonberg, S.: Ueber Veranderungen im Sinusgebiet des Herzens bei chronischer Arrhyth-
mic, Frankf. Ztschr. f. Path., Wiesb., 1908, 'ii, 153.
De Witt, L. M. : Observations on the Sino-ventricular Connecting System of the Mammalian
Heart, Anat. Rec., Phila., 1909, iii, 475.
McWilliam, J. A.: On the Rhythm of the Mammalian Heart, J. Physiol., Camb., 1888,
ix, 167.
Adam, H. : Experimented Untersuchungen ueber den Ausgangspunkt der automatischen
Herzreize beim Warmbluter, Arch. f. d. ges. Physiol., Bonn, 1906, cxi, 607.
Hering, H. E.: Ueberleitungsstorungen am Saugethierherzen mit zeitweiligem Vor-
hofssystolenausfall, Ztschr. f. exper. Path. u. Therap., Berl., 1906, iii, 511; and
Ueber die Automatic des Saugethierherzens, Arch. f. d. ges. Physiol., Bonn, 1907,
cxvi, 143.
Hirschfelder, A. D.,and Eyster, J. A. E.: Extrasystoles in the Mammalian Heart, Am. J.
Physiol., Bost., 1907, xviii, 222.
Langendorf, O., and Lehmann, C.: Der Versuch von Stannius am Warmbliiterherzen, Arch,
f. d. ges. Physiol., Bonn, 1906, cxii, 352.
Fredericq, L.: La pulsation du coeur du chien est une onde de contraction qui debute dans
1'oreillette droite, etc., Arch, internat. de physiol., Liege, 1906, iv, 57.
Lohmann, A.: Ueber die Funktion der Bruckenfasern, an Stelle der grossen Venen die
Fiihrung der Herztatigkeit beim Saugetiere zu iibernehmen, Arch. f. d. ges. Physiol.,
Bonn, 1908, cxxiii, 628.
Kent, His, Retzer, Braunig, Tawara. See Part III, Chapter XI.
King, T. W. See Part III, Chapter VII.
Wilson, J. G.: The Nerves of the At rio ventricular Bundle, Proc. Roy. Soc., Lond., 1909,
ser. B, vol. Ixxxi, 151.
Ludwig, C.: Ueber den Bau und die Bewegungen der Herzventrikel, Ztschr. f. rat. Med.,
Heidelb., 1849, vii, 189. ]
Krehl, L.: Beitrage zur Kenntniss der Fullung und Entleerung des Herzens, Ahbandl.
d. Kgl. sachs. Gesellsch. d. Wissensch., Math.-phys. Kl., Leipz., 1891, xvii, 341.
MacCallum, J. B.: On the Muscular Architecture and Growth of the Ventricles of the Heart,
Contrib. Sc. Med. dedic. to W. H. Welch, Baltimore, 1900, 307.
Baumgarten, A.: Ueber den Mechanismus durch welchen die venosen Herzklappen gesch-
lossen werden, Arch. f. Anat., Physiol. u. wissensch. Med., Berl., 1843, 463.
Howell, W. H., and Donaldson, F.: Experiments upon the Heart of the Dog, Phil. Tr. Roy.
Soc., Lond., 1884, Part I, 139.
Henderson, Y. (with the collaboration of M. McR. Scarborough and F. P. Chilling-
worth) : The Volume Curve of the Ventricles of the Mammalian Heart and the Signifi-
cance of this Curve in Respect to the Mechanics of the Heart-beat and the Filling of
the Ventricles, Am. J. Physiol., Bost., 1906, xvi, 325.
Gad, J.: Klappenspiel im Ochsenherzen, Arch. f. Physiol., Leipzig, 1886, p. 380.
Hooker, D. R.: May Reflex Cardiac Acceleration Occur Independently of the Cardie-inhib-
itory Center? Am. J. Physiol., Bost., 1908, xix, 417.
Stewart, H. A.: A Clinical and Experimental Study of the Blood-pressure and Pulse in
Aortic Insufficiency, Thesis, Edinb., 1907; also Arch. Int. Med., Chicago, 1908, i.
Porter, W. T.: Observations on the Tonus of Heart Muscle, Am. J. Physiol., Bost., 1906,
Barcroft, J., and Dixon, W. E.: The Gaseous Metabolism of the Mammalian Heart J
Physiol., Cambr., 1907, xxxv, 182.
Hofmann, Fr.: Ueber die Function der Scheidewandnerven des Froschherzen Arch f d
ges. Physiol., Bonn, 1895, Ix, 139.
Cameron, P. D.: Physiological and Pharmacological Studies upon the Tonicity of the
Mammalian Heart, Thesis, Edinb., 1908.
Bayliss, W. M., and Starling, E. H.: On Some Points in the Innervation of the Mammalian
Heart, J. Physiol., Camb., 1892, xiii, 407.
Hunt, Reid: Direct and Reflex Acceleration of the Mammalian Heart, with Some Obser-
,tions upon the Relations of the Inhibitory and Accelerator Nerves, Am. J. Physiol.
Bost., 1899, ii, 395.
PHYSIOLOGICAL CONSIDERATIONS. 17
Hering, H. E. : Ueber die Beziehungen der extracardialen Herznerven zur Steigerung der
Herzschalgzahl bei Muskeltatigkeit, Arch. f. d. ges. Physiol., Bonn, 1895, Ix, 429.
Bowen, W. P.: A Study of the Pulse-rate in Man as Modified by Muscular Work, Contrib.
to Med. Research (Vaughan), Ann Arbor, 1903, p. 462.
Hirschfelder, A. D.: Observations upon Paroxysmal Tachycardia, Johns Hopkins Hosp.
Bull., Bait., 1906, xvii, 337.
Friedenthal, H.: Ueber die Entfernung der extracardialen Herznerven bei Saugethieren.,
Arch. f. Physiol., Leipz., 1902, p. 135.
Howell, W. H., and Duke, W. W.: The Effect of Vagus Inhibition on the Output of Potas-
sium from the Heart, Am. J. Physiol., Bost., 1908, xxi, 51. Note upon the Effect
of Stimulation of the Accelerator Nerve upon the Calcium, Potassium, and Nitrogen
Metabolism of the Isolated Heart, ibid., 1908-1909, xxiii, 174.
II.
BLOOD-PRESSURE AND BLOOD VISCOSITY.
THE BLOOD-PRESSURE IN HEALTH AND DISEASE.
Definition.— The blood-pressure, or " arterial tension," is the pressure
which the blood is exerting upon the walls of the vessel in which it is to
be measured (lateral pressure), or upon the column of blood ahead of it
in the direction in which it is flowing (end pressure).
The end pressure is equal to lateral pressure + velocity head, but as a rule differs
by only a few millimetres from the lateral pressure. The end pressure in the branch of a
vessel is equal to the lateral pressure in the vessel from which it branches.
FIG. 19. — Curve of intraventricular and aortic pressures. (After Huerthle.) A , aortic pressure ;
V, intraventricular pressure; D, curve, taken with a differential manometer, showing the differences of
pressure between left ventricle and aorta.
Pressure within the Left Ventricle. — It is evident that in a system of
elastic tubes like the arteries, the pressure of the blood in any segment of
artery is brought about by the tendency of the inflow (from the heart) to
remain in excess of the outflow through the capillaries. The inflow to the
arteries is maintained by the pumping action of the heart, that is, by the
intraventricular pressure during systole. As shown by Huerthle and Porter
the pressure within the ventricle remains tolerably constant throughout
systole and takes the form of a plateau more or less independent of the pulse
curve in the aorta (Fig. 19), though the floor of the plateau slopes down-
ward with peripheral dilatation and upward with constriction.
If the systole is too weak to open the aortic valves, and the heart
contracts without change in volume (iso metrically) , the curve does not
remain a plateau, but has a rounded apex like that of the isometric con-
traction of skeletal muscle. The pressure within the ventricle when the
18 *
BLOOD-PRESSURE AXD BLOOD VISCOSITY. 19
aortic valves are open is slightly in excess of that within the aorta, that
is, very little above the maximal pressure as measured in the latter, and it
remains at this height until the end of systole, when the aortic valves close.
Huerthle and others have shown that the intraventricular pressure is not always
constant throughout systole, but that when the peripheral resistance is very low it falls
toward the end of systole, while if the peripheral resistance is very high it rises toward the
end of systole.
The Maximal, Minimal, and Pulse Pressures. — Accordingly, when the
aortic valves open (.07 to .09 second) after the beginning of ventricular
systole (see Fig. 45, page 53), the pressure in the aorta soon rises to its
maximum, and from that time until the beginning of the next systole
it diminishes more or less gradually as the excess of blood flows out from the
arterial tree through the capillaries and into the veins. The minimal
pressure is reached just before the beginning of the next systole. The
pulse-pressure is the difference between the maxi-
mal and minimal pressures.
Characteristics of the Pulse. — It is evident that the maintenance of
the circulation depends upon the head of pressure in the arteries, and
accordingly much attention was paid by the older clinicians to the "arterial
tension " and the " quality of the pulse, " which they thought were mani-
festations of it. The arterial tension was judged by the force necessary
to obliterate the pulse at the wrist when the fingers are pressed upon the
radial artery.
A still more accurate method of feeling the pulse is to empty the artery for a few
centimetres by "milking" out the blood with two ringers of one hand, while obliterating
the artery above the wrist with the ringers of the other hand. The pressure of the latter is
then gradually diminished until the return of the pulse is felt, this point marking the m a x i-
m a I or systolic pressure. By careful training of the sensations and comparing the observa-
tion with the results of a good sphygmomanometric determination made at the same time,
a great degree of skill in judging pressures may be attained; one of the writer's teachers,
who has cultivated this perception to a remarkable degree, voices the general experience
in saying, " I can estimate the blood -pressure with the fingers alone quite accurately in
about eight cases out of ten, but those in which it is of real importance are always the
other two. "
The minimal pressure may also be judged, but even less accurately, by estimating
the amount of pressure at which the size of the pulse just begins to decrease as one raises
the pressure in the artery.
Determination of Maximal Blood-pressure. — Instruments for determin-
ing the blood-pressure date from 1855, when K. Vierordt determined the
weight that could be placed over the radial artery before the pulse was
obliterated.
Marey (1876) devised the first useful apparatus for estimating the blood-pressure in
man. He placed the hand in a plethysmograph connected with a bottle for raising the
pressure and a sphygmoscope tambour for recording the size of the pulse-waves. He states
(1878) that the maximal pressure may be determined as the point where the pulsation
disappears, the minimal as the point where the oscillations are largest. It is worthy of
note that Marey was twenty-five years in advance of the times, and that his methods
and conclusions are almost exactly those of the best modern methods (Erlanger and v.
Recklinghausen). Unfortunately, the work of Marey was little known, and the first
apparatus to attain general use was that of v. Basch (1887). Unlike Marey, v. Basch
studied only the maximal pressures, but much good pioneer work was done with this
20
DISEASES OF THE HEART AND AORTA.
It
use
78 mm. Hg (Tigerstedt).
Riva-Rocci (1896) and L. Hill and H. Barnard (1897) introduced the
of a rubber bag about the upper arm, surrounded by a non-elastic cuff
uk (Riva-Rocci) or of leather (Hill and Barnard) instead of the small
bag that Potain pressed upon the artery, and they
compressed the artery with pressure from an air-
pump or Davidson syringe, feeling the return of the
pulse at the wrist as the air was allowed to escape
and reading off the pressure corresponding. These
are the methods now in most general use, the only
modification being that the rubber bag must not be
less than 12 cm. in diameter instead of 5 cm, as used
by Riva-Rocci; for v. Recklinghausen has shown that
with narrow cuffs a great deal of pressure is lost in
squeezing the tissues, and hence the readings obtained
with them are too high, but this is now remedied by
using the broad cuff. Riva-Rocci' s method was used
only for determining the maximal pressure.
However, Marey (I.e.) had shown
that the maximal pulse-wave was ob-
tained when the pres-
sure about an organ
was equal to the pres-
sure within the artery
supplying it (i.e., the
minimal pressure — Ho well
and Brush) , and this observa-
tion furnished a basis for such
determinations in mar.
Determination of Mini-
mal Blood = pressure. — Nu-
merous methods for determining the minimal blood-pressure have
been devised, especially those of Hill and Barnard, and Mosso, but those
which are useful and reliable in practice date from 1901, when Masing
began to determine minimal pressure by the point at which the radial
pulse seemed to become largest. About the same time Janeway esti-
mated the minimal pressure at the point where the
oscillations of the mercury column in the manom-
eter seemed greatest. This is a satisfactory method in most
cases, but the judgment by the eye is sometimes difficult and in small
pulses may be impossible.
In 1904 Strasburger revived Masing's method, as did also Sahli, wlio recorded
the maximal pulse- wave with a sphygmograph at the wrist. The latter method is
very cumbersome. For practical purposes the method of Masing and Strasburger
Fio. 20. — Riva-Rocci blood-pressure apparatus as modified
by Stanton. (Kindness of the A. H. Thomas Co.)
BLOOD-PRESSURE AND BLOOD VISCOSITY.
21
FIG. 21. — Correct method
of feeling the pulse in Stras-
burger's determination of mini-
mal pressure.
is fairly satisfactory, piovided a few precautions are taken. First, it is necessary
to exert an absolutely uniform pressure with the fingers upon the radial artery
throughout the determination. Ordinarily this is very difficult ; but if the
artery is palpated with the ball of the
finger instead of the finger-tips, while
the finger-tips rest against the radius,
as shown in the figure (Fig. 21), any changes of pres-
sure by the fingers are exerted against the bone and
not against the artery, and a very uniform pressure
is exerted upon the latter. Secondly, it is necessary
to raise and then gradually let out the pressure from the
bag while feeling the pulse in this way, in order to
acquaint oneself with the changes of pulse to be expected.
Thirdly, it is necessary to repeat the determination
four to six times in order to eliminate the great discrep-
ancies that creep in when single readings are made.
All the non-concordant readings should be disregarded.
In this way fairly accurate determinations of minimal pressure may be obtained
(within 5 mm. of those obtained by Erlanger's apparatus).
Erlanger's Sphygmomanometer. — The most accurate and sat-
isfactory, if somewhat bulky, sphygmomanometcr is that of Erlanger
with which graphic records of both maximal and minimal pressures may
be obtained (Fig. 22). Erlanger's apparatus differs from the Riva-Rocci
with Recklinghausen cuff only in
the fact that by means of a T-tube
the cuff is connected also with a
rubber pressure-bag in a glass case.
The oscillations of pressure in the
cuff are thus communicated to the
pressure bag, and the oscillations
of this bag are communicated to
the air in the glass case around it,
and are recorded by the movements
of a Marey tambour upon the smoked
paper on a small drum. He is also
able to let the pressure flow out
very slowly by a series of capillary
outlets of different bores. A com-
plicated stop-cock allows any of
these to be used at will.
In using the Erlanger apparatus, one
turns the stop-cock to the point marked
"In," then raises the pressure in the bag
to well above the maximum arterial pres-
sure, and turns the stop-cock to the point
marked 1 or 2, which corresponds to capil-
lary outlets of different sizes. The pressure
in the bag falls gradually, and soon small
oscillations of the lever are seen, due to the impact of the compressed artery upon the upper
margin of the bag. A sudden increase in the size of these wavelets soon takes place and marks
the maximal pressure, which is read off on the manometer; it is just a trifle below the maxi-
mal pressure that the first pulse- wave passes completely through under the cuff and causes
the larger wave, upon which also a small shoulder is usually seen. Below this point the oscil-
lations continue to increase in size and then begin to decrease, the manometer being watched
Fio. 22. — Erlanger blood -pressure apparatus
\vith 1 1 irschfelder polygraph attachment. (Kind-
ness of Schneider Bros.)
DISEASES OF THE HEART AND AORTA.
22
a,, the Whi,e. The point at Which
minimal pressure.
In order to keep these records per-
manent Fontaine marks off on the drum
the points which correspond to each fall
of 5 or 10 mm. Hg in the manometer.
These marks are made by means of one
FIG. 23. — Diagram showing arrangement of
Erlanger apparatus. (After Howell.)
FIG. 24. — Curve taken with the Erlanger
blood-pressure apparatus, showing the points of
maximal and minimal pressures.
of the tambours upon the . polygraph (Hirschfelder) attachment which is caused to
vibrate by squeezing a small pipette inserted into the long rubber tube.
This apparatus has been carefully tested, both upon animals and upon mechanical
models, and has been shown to give accurate results. Of course it cannot be used unless
the muscles of the arm are at rest, but neither can any other sphygmomanometer, without
introducing a large error. The readings ob-
tained in determining both maximal and mini-
mal pressures in arteriosclerotics are too high,
but this error is also universal and at present
unavoidable. At times the systolic increase
in size is not sudden, but this can usually be
remedied by pressing the lever a little more
tightly than before against the drum. Occa-
sionally a larger or smaller capillary outlet
is required and these may be readjusted.
The readings obtained by Erlanger's method
are, as a rule, about 5 mm. higher for the
maximal (systolic) pressure than by the
broad cuff Riva-Rocci, and for the minimal
(diastolic) within about 5 to 10 mm. of the
readings by the method of Masing and
Strasburger as modified by the writer (Hirsch-
felder, also Brush). Erlanger's method
gives results sufficiently unequivocal to
form the basis for a research, although the other method is often quite satisfactory.
V. Recklinghausen's Sphygmotonometer. — Numerous other sphygmomanometers
have been devised of late, notably the sphygmoscope of. Pal for visual deter-
mination of pressure by the movement of a drop of colored liquid, and the visual
(tonometer) and graphic (tonograph) methods of v. Recklinghausen, upon the same
principle as Erlanger's, but they do not possess any special advantages in their respective
spheres of usefulness over the methods given above.
FIG. - 25. — V. Recklinghausen apparatus.
(After v. Recklinghausen, Arch. /. exper. Path. u.
Pharmacol., Iv.)
BLOOD-PRESSURE AND BLOOD VISCOSITY. 23
Auscultatory Method for Determination of the Blood-Pressures. — A very ingenious
method for determining the maximal and minimal blood-pressures was devised by
Korotkoff in 1905. If the pressure in a rubber cuff upon the upper arm is allowed to
fall gradually from a point above the maximal arterial pressure, while the observer listens
with a stethoscope pressed upon the brachial artery at a point about two centimeters
below the lower border of the cuff, no sound will be heard until as soon as the pressure
in the cuff falls below the maximal arterial pressure. As the minimal arterial pressure
is approached, the second sound also becomes louder, reaches its maximum at the
minimal arterial pressure (where there is the greatest alternate expansion and con-
traction of the artery), and disappears rapidly when the pressure in the cuff is a trifle
below the minimal (diastolic) pressure. Indeed, Fellner has found this method accurate
to within 5-10 mm. Hg of the readings with the v. Recklinghausen apparatus. Miss Allen
and Mr. Engle, in the study of the blood-pressures of 35 patients in the Johns Hopkins
Hospital, found that the readings by this method never differed more than 2-5 mm. from
control determinations made at the same time with the Erlanger apparatus, though they
took the minimal pressure at the point at which the second sound absolutely disappeared.
The method seems therefore to be one of considerable accuracy, though in persons
with very small vessels it may be difficult or impossible to use.
Pocket Form of Blood-Pressure Apparatus. — The exigencies of the busy practitioner
demand an apparatus to occupy small space and yet give results of reasonable accuracy.
To this end Potain made use of a small dial upon which the pressure was shown by the
compression of a spring calibrated in centimetres of mercury. More recently a number
of such forms have been devised in which the pressure chamber is connected with the
usual Riva-Roci-Recklinghausen cuff. The Tycos apparatus represents one of the most
compact of these. It is practically a miniature v. Recklinghausen sphygmotonometer,
packed so small that it may be carried in the pocket with ease. The readings are made
by the same method as upon the v. Recklinghausen, but the excursions are much smaller,
a fact which often interferes with the determination of minimal pressure. Nevertheless,
Messrs. Engle and Dandy, in the Johns Hopkins Medical Clinic, have found that determi-
nations with this apparatus usually approach within 5-10 mm. of the determinations
with the Erlanger apparatus. This error is usually due to the fact that the maximal
pressure is determined by digital palpation, in which there is an inherent error of about
this amount, regardless of the form of apparatus used. The determinations of minimal
pressure usually fell within 5 mm. of those made with the Erlanger.
When the readings were made by the auscultatory method it was possible to reach
absolute accuracy in many cases with this pocket form of apparatus. Like all spring
pressure gauges, this spring is liable to wear out in time, so that it should be controlled
every few months by comparison with a mercury manometer at various points through-
out the range of pressure.
Gibson's Sphygmomanometer. — Still more recently Gibson and Sahli have devised
an apparatus similar to Erlanger's but recording the oscillations of the mercury manome-
ters directly by a float instead of by the Marey tambour. These instruments give results
fairly concordant with the Erlanger and have the advantage of recording the corresponding
pressure directly in absolute figures.
Normal Blood-pressures. — For young persons (19 to 25 years old) in the reclining
posture the average blood-pressure according to Erlanger is maximal 110 mm., minimal
65 mm., pulse-pressure 45 mm. In general the limits in normal individuals at rest are
maximal 110 to 135 mm., minimal 60 to 90 mm., pulse-pressure 30 to 45 mm. In the
experience of the writer a maximal pressure of 115 to 120 mm., with a minimal of 75 to
85 mm., pulse-pressure 30 to 40, is more common.
MECHANISM OF THE CIRCULATION.
Pressure in Different Parts of the Vascular System.- — Dawson has shown
that the mean pressure is very constant throughout the arterial system,
while the maximal pressure falls greatly as one approaches the periphery.
The minimal pressure is also quite constant. As one approaches the periph-
ery the maximal pressure falls quite rapidly to meet the minimal, and in
the smallest arteries they are practically equal. Hence the pressure
24
DISEASES OF THE HEART AND AORTA.
these arterioles does not differ greatly from
minimi?! pressure in the aorta although it is certam y
a few millimetres less. The minimal arterial blood-pre
ure therefore represents the peripheral resistance
(vasomotor changes), while the maximal pre SB?." aPP;"^
mates the in t r a ve nt ri cul ar pressure. Marey (I.e.) has
shown that this approximation is closest when peripheral resistance is
high. Accordingly the pulse-pressure, or difference between the two
represents the head of pressure tending to drive the blood from the heart
through the aorta and large arteries onward into the peripheral arterioles.
The fall in pressure may be compared to a cascade
whose first descent is from heart to arterioles,
whose second from arterioles to capillaries, and whose
third is from the capillaries back to the heart. The
actual head of pressure at any point in the arteries is never equal to
the total head (maximal pressure) which would be active if the fall
were uninterrupted by interposed resistance, but is more nearly equal
to the pulse-pressure.
FACTORS DETERMINING MAXIMAL AND MINIMAL PRESSURE.
The fall in blood-pressure during diastole continues until the next
systole takes place. If the pulse-rate is rapid the diastole is short and the
blood-pressure has not time to fall much; hence, other things being equal,
minimal pressure rises and pulse-pressure falls as
pulse-rate increases.
FIG. 26. — Diagram showing the maximal and minimal pressures in various parts of the circulatory system.
Erlanger and Hooker have claimed that under ordinary conditions the product of
pulse-pressure multiplied by pulse-rate is tolerably constant,
and represents roughly the velocity of blood flow, although Y. Henderson, the writer,
and others have proved that this is very inaccurate and may involve an error of more than
BLOOD-PRESSURE AND BLOOD VISCOSITY.
25
50 per cent. The curves of Dawson and Gorham, who claim that the pulse-pressure is a
"reliable index" of the systolic output (per beat) of the ventricles, indicate that these
writers referred to qualitative rather than quantitative changes. Henderson has shown,
however, that within a certain range of pulse-rate the ventricular output per beat varies
inversely as the pulse-rate. Within this, the usual, range the velocity of blood flow is
greatest. At rates below it time is lost during the periods of diastasis; above it the suc-
cessive systoles encroach upon the period of ventricular filling and cut short the inflow.
Within the limits indicated by Henderson, Erlanger and Hooker's index of velocity may
often be correct, especially when there are no extreme vasomotor changes.
FIG. 27. — Diagram showing effects of vasoconstriction, vasodilation, increased and decreased force
of ventricular contraction upon the maximal and minimal blood-pressures and upon the form of the pulse.
SYS, systole; DIAS, diastole; ART, large arteries; AOL, arterioles; CAP, capillaries.
•
If the peripheral vessels dilate, more blood can flow through in the same time, and
hence when the pulse-rate is constant, vasodilation brings about fall in
minimal pressure, rise in pulse-pressure; vasoconstriction
brings about rise in minimal pressure, fall in pulse-pressure,
but a change in maximal pressure following the change in minimal usually occurs reflexly.
Figure 26 shows the various relations of maximal, minimal, and pulse-pressures to the
state of the intraventricular pressure.
Erlanger and Hooker give the following table to indicate the conditions present in
the circulatory system; but owing to the inaccuracy of the calculations this furnishes use-
ful information only when the changes are extremely marked.
Minimal (mean)
blood-pressure.
Pulse-pressure X pulse-
rate velocity.
Energy of heart.
Peripheral resistance.
f
Increased
Diminished
Constant <
Diminished
Diminished
Increased
(
Unchanged
Increased
Increased
Increased . . .
Increased
Unchanged
Diminished
Unchanged
Increased
Unchanged
Diminished
Diminished
Increased
Unchanged
Diminished
Increased
Unchanged
Changes in the peripheral vessels can be recorded by placing the patient's hand in a
plethysmograph (Fig. 28) which is sealed hermetically about the forearm by means of a
rubber cuff. The free space in the plethysmograph is filled with water, which runs in or
siphons out of a tube leading to a movable test-tube. Changes in volume of the arm are
recprded by upward or downward movements of the test-tube.
26 DISEASES OF THE HEART AND AORTA.
Work of the Heart.— Since the intra ventricular pressure is almost con-
stant throughout systole, it is evident that the work done by the heart is
tolerably constant throughout this period; and since no work is done during
diastole it is evident that the work of the heart per minute may be esti
mated, at least roughly, by the product of intraventricular pressure :
tion of systole X pulse-rate.1
Fio. 28.— Mosso plethysmograph. (After Howell.) a, cylinder of plethysmograph; /, water in
recording test-tube, which moves by extension of spring a (spring s is arranged of a strength that keeps
water in I at a constant level); p, point recording the excursions of test-tube L
The value of blood-pressure determinations as an index of the func-
tional power of the heart will be discussed on page 142 in relation to exercise
and cardiac overstrain.
VARIATIONS IN BLOOD-PRESSURE UNDER PHYSIOLOGICAL
CONDITIONS.
1. Change of position. Erlanger and Hooker have shown that the minimal
pressure usually rises considerably and the pulse-pressure always decreases
upon standing after having lain down. The pulse-rate increases accordingly. They have
shown that these effects are entirely due to the rule of gravity.
2. After meals the maximal pressure and pulse-pressure are
increased, also the pulse-rate, and the minimal pressure* may be increased but to a
less extent. The circulation is accelerated.
3. After exercise the effect is the same as after meals, only more marked. When
exercise is continued to the point of fatigue the pressures fall, the pulse-rate falls also, and
the circulation is slowed (Schott, Masing, Cabot, Bowen). (See page 131.)
1 For more complicated and perhaps more accurate formulae cf. Tigerstedt (1. c.).
Pulse-pressure
10 Maximal (systolic) pressure °r Blood-Pressure coefficient is used more or
less as an index of circulatory conditions. Its significance may be given as follows:
P. P. X P. Rate = Velocity )
Syst. P. X P. Rate = Work \ =Efficiency of heart as a pump. In a normal indi-
vidual this coefficient is 25 per cent, to 35 per cent.
BLOOD-PRESSURE AND BLOOD VISCOSITY.
27
4. Upon sensory stimulation the vasomotor centre in the medulla usu-
ally responds by constricting the peripheral vessels, and the pressure, especially the mini-
mal pressure, rises. The pulse-rate usually quickens also. There are great variations
in the response of different healthy individuals to pain sensations. Dr. A. Berg, under the
writer's direction, has tested the effect of pinching the ear upon the blood-pressure of healthy
individuals, and has found in some persons a rise of blood-pressure amounting
to 10 to 20 mm. Hg, in others no effect, in others a fall of about 10 mm. Too intense
stimuli produce shock. Mental exertion has a similar effect — a definite vasocon-
s t r i c t i o n setting in, which is shown by the shrinkage of the arm in a plethysmograph.
5. In sleep the opposite effects are seen : there is a general vasodilation
and a fall in minimal blood-pressure (Howell, Brush, and Fayerweather) .
There is probably also a slight fall in maximal pressure.
VARIATIONS IX BLOOD-PRESSURE UXDER PATHOLOGICAL
CONDITIONS.
ASPHYXIA AND THE EFFECT OF EXCESS OF CO2.
When the heart fails the circulation is slowed, and the blood becomes
incompletely aerated and overloaded with CO2 (f. Bohr). These condi-
tions closely simulate the conditions present in asphyxia (Traube), or after
breathing an atmosphere overladen with CO2 (Klug has shown that the
effect of these is quite similar).
Experimental Asphyxia. — The <Q £± g-2 £<
conditions as observed in experi-
mental asphyxia somewhat fore-
shadow those due to accumulation
of CO2 from heart failure. The
blood-pressure changes in asphyxia
have been most carefully studied
by Konow and Stenbeck in Tiger-
stedt's laboratory, who found as-
0 uj 2 O
sz gs
11 &
os
^ ^
8?
!§
\
PR
phyxiation in rabbits resulting in
the following series of events:
1. At the beginning of asphyxia the
vasomotor and cardiac centres
in the medulla are stimulated,
as is also the inhibitory centre. Blood-
pressure rises and the pulse is
slowed. (Cameron has shown that, on
the other hand, the tonicity of the
heart muscle promptly decreases
with the first stage of asphyxia and re-
mains diminished throughout.)
2. As asphyxia continues, the effect
of slowing of the pulse exceeds that of
the rise of pressure and the blood-
pressure falls.
3. This condition slows the circula-
tion still more, CO2 accumulates in the blood, bathing the vasomotor centre, the latter
stimulates the arterioles to still further constriction, the vagus can no longer overcome
these effects, and in spite of its continued action the pulse quickens and blood-
pressure again rises.
4. The activity of the vasomotor centre diminishes while the vagus centre remains
at maximal activity, and the pulse-rate again slows and blood-pres-
sure again falls.
Rp
A
FIG. 29. — Diagram showing the curve of blood-
pressure during asphyxia. (Schematic, illustrating
the results of Konow and Stenbeck.) N, normal ;
BP, blood -pressure ; PR, pulse-rate.
28 DISEASES OF THE HEART AND AORTA.
5 The vagus centre fatigues, the accessory vasomotor centres in the spinal cord
are again stimulated, and blood-pressure and pulse-rate again rise.
6 Conductivity of the heart diminishes, occasional beats are dropped by the ven-
tricle, blood-pressure and pulse-rate fall, and the animal dies at this
stage unless respiration is promptly restored.
Occasionally in asphyxia periodic changes in rhythm of the heart occur, such as have
been described by Luciani in frogs and by Langendorff in cats. These irregularities occur
when the vagi are sectioned as well as when they are active; this also occurs when the animal
is made to breathe an excess of CO2 (Klug). When, however, the vagi are inactive (cut),
the rise of blood-pressure in asphyxia is continuous from the onset until the vasomotor
centres fail (i.e., in the fourth stage). When the cervical nerves have been cut and the
vagi are active, there is an immediate fall in both blood-pressure and pulse-rate; the rise
in blood-pressure sets in much later when the accessory vasomotor centres in the spinal
cord are stimulated, or the animal may die if these fail to respond.
BLOOD-PRESSURE IN VARIOUS DISEASES.
Importance of Determining the Mechanism Producing the Change.—
Variations in blood-pressure occur not only in conditions of health but still
more under pathological conditions. As will be seen, the mechanism which
brings these changes about is not always a simple one, and the causal factor
may not be affected by merely resorting to therapeutic methods which
lower a high blood-pressure or raise a low one. It is therefore necessary
for the clinician to investigate, as far as possible the condition of the vaso-
motor nerves, the strength of the heart-beat, to determine also whether the
blood is properly aerated, and learn whether the kidneys are performing
their function properly, before proceeding to symptomatic treatment of
high or low blood-pressure when the cause is in any way obscure.
DISEASES WITH HIGH BLOOD-PRESSURE (HYPERTENSION).
The following represent the typical blood-pressure findings in various
diseases. In exceptional cases more extreme variations are seen:
1. Nephritis, especially the chronic forms (maximal pressure 160 to 220, minimal
120 to 160, pulse-rate 50 to 80). High blood-pressure is common in both parenchymatous
and interstitial cases. Passler and Heineke found that in animals from which almost all the
kidney substance had been removed, blood-pressure rose pari passu with the occurrence of
signs of renal insufficiency in the metabolism.
Excellent reviews of this subject have recently been published by
T. C. Janeway and by Pearce. There seems to be a striking parallelism
between continuous high blood-pressure and oversecretion of the adrenals,
usually leading to an hypertrophy of the latter (see 'page 208).
In acute nephritis the blood-pressure may not arise, but Buttermann reports
a case of scarlatinal nephritis where a rise of 50 mm. heralded the onset of the nephritis.
Here it is of diagnostic and prognostic importance.
In uraemia blood-pressure rises at the beginning of the attack, but may grad-
ally fall a few days before a fatal termination (Laqueur). Gradual fall in blood-pressure
Iso accompanies amelioration. Engel finds that there is no rise in the mildest cases of
nephritis, but that the rise of pressure runs parallel to the severity of the disease until the
terminal fall sets in from cardiac weakness.
I Arteriosclerosis.— Increased blood-pressure (maximal 150 to 170, minimal 110
e 60 or over) is the rule in arteriosclerosis, though there are occasional excep-
lons where the maximal pressure does not exceed or even reach 110 mm. (Israel). (See
also chapter on Arteriosclerosis.)
BLOOD-PRESSURE AND BLOOD VISCOSITY.
29
3. Lead Poisoning (plumbism). — Acute and chronic forms are usually associated with
high blood- pressure, as in arteriosclerosis.
4. Chronic Hypertrophy of the Heart from other causes, as in athletes, or as the
result of smoking in excess, of compensated heart lesions, etc. (maximal pressure 140 to 160,
minimal 90 to 110 mm., pulse-rate normal or increased).
5. Aortic Insufficiency is often but not always associated with high maximal pres-
sure (maximal pressure 170 to 220 mm. Hg, minimal 60 to 140, pulse-rate usually increased,
being even as high as 120). This is usually associated with arteriosclerosis. In young indi-
HYPE.RTEN5ION I NORMAL HYPOTENSION
FIG. 30. — Diagram showing typical blood-pressures in various diseases. Solid black, minimal pressure;
striped shading, pulse-pressure; dot, pulse-rate.
viduals, as in experimental aortic insufficiency in animals, the maximal pressure is usually
little changed, the minimal pressure lowered (maximal 120 to 130, minimal 50 to 60, pulse-
rate normal or increased).
6. Conditions associated with increased pressure in the cranial cavity
(meningitis, apoplexy, cerebral thrombosis, fracture of the
skull, intracranial hemorrhage, rapidly growing brain tumors,
some cases of uraemia, Jacksonian epilepsy). Maximal blood-pressure
may rise to 300 or 400 mm. Hg, minimal pressure to 160 or over, pulse-rate slow, 60 or
under. Gushing has shown that when the intracranial pressure is raised above the blood-
pressure, the anaemia of the vasomotor centre brings about a tremendous vasoconstriction
and action of the augmentor fibres in increasing the strength of the heart-beat. The blood-
pressure rises in successive stages (Traube-Hering waves) until the mean pressure exceeds
the intracranial pressure. The rise of blood-pressure expresses the
need of the brain for blood; to counteract the vasoconstriction
30 DISEASES OF THE HEART AND AORTA.
with nitrites or other vasoconstrictors or by venesection only
increases the task of the heart. The only medical treatment which aids it
at all is administration of atropine to paralyze the vagi, quicken the heart, and permit the
pressure to rise more readily. Lumbar puncture helps somewhat by removing the excess of
intracranial fluid. If this does not suffice, Gushing advises surgical interference m many
cases —a flap of the skull being lifted temporarily in order to relieve the intracranial tension
and to allow the blood-pressure to fall. This procedure is almost devoid of danger in the
hands of a surgeon whose asepsis is perfect, but very dangerous if it is imperfect, and this
point alone will often decide the advisability or inadvisability of the operation.
7. Attacks of Idiopathic Epilepsy are associated with very high blood-pressure
and slow pulse. The blood-pressure falls within a few minutes after the fit, which assists to
differentiate it from uraemia (Pilcz).
8. Vascular Crises.— Pal has described an important group of cases associated with
crises of high blood-pressure due to vasoconstriction. Among these he classes uraemia,
certain cases of arteriosclerosis, especially with abdominal and cardiac symptoms,, and
especially the tabetic visceral crises with intense pain. He has shown that these as well as
attacks of lightning pains are associated with marked vasoconstriction and rise in blood-pres-
sure, and states that they are even relieved by the administration of nitroglycerin. He also
classes angina pectoris, intermittent claudication, and Raynaud's disease under this head.
9. Attacks of Angina Pectoris.
10. Some Cases of Adams-Stokes Diseases between Attacks. — Gibson repor ts a
case with maximal pressure 270, minimal pressure 70, pulse-rate 27. The pressure may,
however, never rise materially. During the attacks it always falls almost to zero (see
page 460).
11. Exophthalmic Goitre (Graves's or Basedow's disease) is often accompanied by
hypertrophy of the heart with increased maximal, 140 to 160 mm., minimal 90 to 110
mm., and pulse-pressure 30 to 50 mm., pulse-rate accelerated to 120 and over. In
some cases of Graves's disease the pressure remains low (maximal 120, minimal 90).
12. The End of Pregnancy, the onset of laborr and the puerperium are accom-
panied by a slight (10-15 mm.) rise of maximal pressure with little change in minimal
pressure (Slemons and Goldsborough; see Part III, Chapter IX).
13. Chronic Primary Polycythaemia. — The increased number of red corpuscles
increases the viscosity of the blood, and thereby the work of the heart, besides arterioscle-
rosis is usually associated. On the other hand, as shown by W. Erb, Jr., increase in blood-
pressure causes liquid to leave the vessels and thereby increases the viscosity of the blood
further — introducing a vicious cycle.
14. Cyanosis in Heart Failure with Broken Compensation, which occurs at some
stage in almost all failing hearts. The blood becomes overloaded with CO2, and vasocon-
striction plus augmentation results as in asphyxia (see page 237). Usually the pulse is
quickened, probably from fatigue of the vagus centre. This condition is of great clinical
importance, since the high blood-pressure increases the work of the heart and accelerates its
failure. Venesection, nitrites, digitalis, anything which accelerates the velocity of blood
flow through the lungs, brings about improvement and lowering of the blood-pressure.
PATHOLOGICAL CONDITIONS ASSOCIATED WITH LOW BLOOD-PRESSURE
(HYPOTENSION).
Although the occurrence of low blood-pressure is usually associated
in the mind with the idea of a diseased heart, such is, as a rule, not the
case. In fact, in most chronic diseases of the heart the maximal pressure
is increased rather than decreased, as has been shown above. In one case
of aortic insufficiency, for example, the writer found a maximal pressure
of 150 and a minimal pressure of 110 two minutes before death, in spite
of intense heart failure.
A low blood-pressure is more commonly an index of fail-
ure of the vasomotor centre than of the heart, and occurs in condi-
tions where the strength of the heart is uninjured (Romberg and Passler, Hasenfeld and
Fenevessy, Crile).
BLOOD-PRESSURE AND BLOOD VISCOSITY. 31
Conditions in which low blood-pressure is found are:
1. Acute infectious diseases, except meningitis (where the blood-pressure is high
from increased intracranial tension). Romberg and Passler have shown that bacterial
poisons diminish the tonic activity of the vasomotor centre, and may even paralyze it.
The strength of the heart is shown to be undiminished if the vasodilation is counteracted by
adrenalin, compression of the abdominal aorta, etc. The blood-pressure falls because the
arterioles are dilated and the outflow from the arteries is too rapid (maximal pressure 90 to
110, minimal pressure 50 to 90, pulse-rate increased, see table, page 29).
The lowest blood-pressure is in typhoid fever (Barach) and peritonitis,
where the dilatation of abdominal vessels from the local inflammation add their effect to
that of the cutaneous vasodilation. In typhoid fever the writer has seen maximal pressures
as low as 65 mm. Hg (Riva-Rocci), although maximal 100 to 120 with minimal 60 to 90 is
more common. Crile and Briggs have described rises in blood-pressure at the onset of per-
foration due to splanchnic stimulation, but the writer has had two cases (one of which
is mentioned by Briggs) in which inactivity of the vasomotor centre prevented this rise
from occurring.
In pneumonia the blood-pressure may not be changed much (maximal 110 to
130, minimal 90, pulse-rate 120); it may rise as mild asphyxia sets in, or it may fall very
low from vasomotor paralysis.
In diphtheria, scarlet fever, measles, acute rheumatism, and
and in fact in all other acute infectious diseases, the maximal pressure usually falls below
100 during the height of the fever (Weigert).
2. Phthisis. — In this disease all ranges of blood-pressure may be found. John,
Naumann, Burckhardt, and Stanton have found uniformly low pressures, 90 to 100 mm.
with the Gaertner and Riva-Rocci apparatus, but this may arise from the pallor of the skin.
Janeway found that variations of maximal pressure between 80 and 120 mm. Hg are
common in the same patient, and the writer's experience bears this out. The pulse-rate is
usually rapid, 80 to 100 per minute. Peters finds that there is usually a rise of blood-pres-
sure when improvement sets in, and a fall when the case is getting worse.
3. Shock. — Crile has shown that in surgical shock from injury or pain there is loss
of tonic activity of the vasomotor centre exactly as in acute infectious diseases. Syncope
from emotional excitement, etc., is of similar origin. Crile counteracts the vasomotor
paralysis by putting a double-walled rubber suit upon the patient and inflating the cham-
ber between the walls until the pressure compensates for the loss of vascular tone.
Henderson, while confirming Crile's observations as regards the paresis of the vaso-
motor centre, believes that this is not the primary phenomenon. He calls attention to the
similarity between the phenomena of shock and those of mountain sickness, which Mosso
has shown to be due to a low CO2 content of the blood (acapnia) ; Henderson believes that
the mechanism of the two conditions is similar and is able to substantiate his claim by
producing shock experimentally under all conditions in which CO2 is made to escape
rapidly from the blood, either through rapid aeration of the lungs or through exposure
of the intestines and mesentery to a current of warm moist air. He has shown further
that CO2 is the hormone which preserves the tonic contraction of the walls of the veins.
Bancroft has also shown that these are under nervous control as well as the arteries and
that their nerves arise in the same regions as do the vasomotor nerves to the latter.
According to Henderson the sequence of events in shock is as follows:
(1) Pain or emotion; (2) hyperpnosa; (3) overaeration of the blood (lowering of the
CO2 content, acapnia), dilatation of the veins and accumulation of blood in the latter,
lowering of the venous pressure (and hence diminished entry of blood into the heart);
(4) fall in arterial pressure, accompanied by loss of arterial tone (vasodilatation) ; (5)
cerebral anaemia.
There is an accumulation of blood in the veins with depletion of the arteries (an
arterial anaemia).
In fevers the high temperature gives rise to a slight polypnoea and also favors
the evaporation of CO2 from the lungs. Henderson believes that these factors cooperate
with the toxins in producing the vasomotor pareses of infectious diseases.
It will be seen that in many of the functional cardiac diseases accumulation of blood
in the veins with depletion of the arteries is the most striking disturbance in the circula-
tion, and plays an important role in producing the clinical picture.
32 DISEASES OF THE HEART AND AORTA.
Whether an occasional whiff of CO2 or merely occasionally holding the breath will
relieve the acapnia and restore the vascular tone in such cases remains to be proved.
4. Collapse from various poisons, carbolic and salicylic acid, arsenic, phosphorus,
drugs of the antipyretic series, etc., is due to the same cause— failure of the vasocon-
strictor centre,— and likewise is accompanied by low blood-pressure.
5. After extensive hemorrhage a fall of blood-pressure sets in (except after vene-
section in some cases where a failing heart is relieved), owing to lack of blood to fill out
the arteries. This is usually relieved by subcutaneous or intravenous NaCl infusion, or
even by direct arterial transfusion (Crile).
6. In diarrhoea, dysentery, cholera, or after profuse vomiting, as from cancer
of the stomach, intestinal obstruction, peritonitis, etc., when large amounts of fluid have
left the body, the arteries may also be depleted of fluid and a very lov/ blood-pressure
result. This is also relieved by infusion.
7. In pleurisy, especially pleurisy with effusion, blood-pressure is uniformly low.
8. Pericarditis is accompanied by low blood-pressure (maximum 100 to 120,
minimum 70 to 90, pulse-rate increased) unless complicated by hypertrophy of the heart
or some other factors.
9. Acute cardiac diseases of all types, which have not been preceded by chronic
processes and are not associated with marked cyanosis. Here the above-mentioned toxic
action on the vasomotor centre is usually present if the endocarditis is of the infectious
variety, and besides there is some weakening of the heart. The quickened pulse-rate
prevents CO2 from accumulating in the blood and the asphyxial rise in pressure does not
occur. K. Weigert reports all ranges of pressure between 95 and 140 mm. Hg.
10. In chronic mitral stenosis the maximal and minimal pressures are usually
normal or a little below normal, when the left ventricle does not hypertrophy; but this
may vary considerably.
11. Chronic wasting diseases, cancer, chronic phthisis, anaemias, etc., are associated
with brown atrophy of the heart muscle (see page 211), with weakened heart action,
hence with lowered blood-pressure (10 to 20 mm. lower than normal, pulse-rate usually
increased) .
BLOOD-PRESSURE IN THE VEINS.
Various methods have been devised for the determination of the venous
blood-pressure in man, the first being introduced by v. Basch and being
but a slight variation of his arterial sphygmomanometer.
A very similar apparatus has been constructed recently by Sewall, but this gives
rather unsatisfactory results in practice. V. Frey and later Gaertner also determined
the pressure by considering it equal to the height above the angle of Ludwig at which
the veins of the hand could be seen to collapse. This method is not quite as good as the
former. A considerable advance was made by v. Recklinghausen, who compressed the
vein by inflating a small rubber capsule provided with a glass window in the top and a
rubber-dam floor having a hole in its centre. This dam was coated with glycerin so as to
insure perfect contact. It is then placed over a vein, preferably upon the back of the hand
or wrist, and the system blown up until the vein can be seen to disappear, at which point
the pressure is read off upon a water manometer. Eyster and Hooker have modified this
chamber by constructing one of aluminum with the entire top of glass and the two ends
concave so as to avoid pressure upon the veins, and their apparatus seems to give results
concordant within 1 cm. H2O. They find that the normal venous pressure at the sterno-
xiphoid articulation is 5-10 cm. H2O.1 It is increased by exercise and in cardiac cases
with broken compensation, when it may rise to 27 cm. or over. When the veins are not
sufficiently distended at that level the hand may be lowered a known distance, the
pressure read; and the distance lowered subtracted from the amount of the reading will
represent the venous pressure. In cases where phlebosclerosis is present no satisfactory
determinations could be made.
1 These figures agree well with direct manometric determinations recently made in
man by Moritz and v. Tabora (Verhandl. d. Kong. f. innere Med., 1909, xxvi, 378).
BLOOD-PRESSURE AND BLOOD VISCOSITY.
33
The pressure in the capillaries of vascular areas, especially of the lips, m&y
be determined in the same way, using the point of blanching as the criterion.
The study of the venous pres-
sure is of undoubted importance
as an index of accumulation of
the blood in the systemic circu-
lation and thus as an index of
heart failure. Moreover, it is the
most important physiological
factor bringing about variations
in the volume of the heart; a high
venous pressure causing dilata-
tion, a low venous pressure causing
diminution in volume (insufficient
filling) . This may prove to be an
important factor in bringing about
certain conditions in which there
is "arterial anaemia" (shock, car-
diac neurosis, etc.).
THE PULMONARY CIRCULATION-
Before birth the resistance in
the vessels of the collapsed lung is
greater than that in the systemic
arteries, and hence blood passes
from the pulmonary artery to
the aorta through the ductus
arteriosus (Botalli).
FIG. 31. — Hooker and Eyster's modification of
v. Recklinghausen's method of determining the venous
pressure in man.
As the blood -pressure in young
infants is 80 mm. Hg (Trumpp), it must
be assumed that the pulmonary pressure
is somewhat greater than this. When the area of lung capillaries widens with the first
inspiration, the resistance in the pulmonary vessels decreases very markedly. This
decrease continues during the period of infancy until the lung is fully expanded.
According to a number of observers (Beutner, Lichtheim, Openchowski, Bradford and
Dean, Plumier), the mean pressure in the pulmonary artery of rabbits, cats, and dogs
varies from 6 to 35 mm. Hg. It may be said to be approximately one-third
that of the aorta but subject to considerable variations. Tigerstedt has found
that in rabbits with 142 mm. pressure in the aorta the pressure within the right ventricle
is much greater than this.
The pulse-pressure in the pulmonary artery is much smaller than that
in the aorta, probably about 6-12.5 mm. Hg in small animals, and in
man not far from these figures.
Work of the Right Heart. — The pressure within the pulmonary artery
and hence the work of the right heart varies within wide limits under
experimental conditions.
These variations are in part passive, due to passive stasis of blood
within the pulmonary vessels, and in part may be the result of vaso-
motor changes in the pulmonary vessels.
3
34 DISEASES OF THE HEART AND AORTA.
The conditions in which the changes in pulmonary pressure arise
passively from changes in the left ventricle are the most common and are
clinically the most important.
Increased mean pulmonary pressure may arise:
1. When an increased amount of blood enters the right heart from the veins and is
expelled into the pulmonary artery.
2. The pulmonary blood-pressure also undergoes rhythmic variations, falling during
inspiration as a result of suction (as shown by de Jager) and rising during expiration.
3. When the left ventricle fails to pump an equal amount onward into the aorta,
causing blood to accumulate in the pulmonary capillaries until these are overfilled and
aid in increasing the resistance in this circuit. (The left ventricle acts upon the pul-
monary circulation as a suction pump.)
4. Probably from constriction of the pulmonary arteries under the influence of
vasomotor nerves.
Pulmonary Vasomotor Nerves. — The existence of vasomotor nerves in
the pulmonary artery, first suggested by Brown-Sequard (1870 to 1873) and
later by Badoud, has been much disputed, but seems now to be proved.
Francois-Franck has shown that stimulation of the lower cervical and upper five
thoracic ganglia in the dog uniformly caused a rise of blood-pressure in the pulmonary
artery, a fall of pressure in the left auricle, and an increase in the volume of the lungs,
probably due to accumulation of blood on the arterial side of the capillaries. This rise in
pulmonary pressure bore no constant relation to the pressure in the femoral artery, which
sometimes rose and sometimes fell. This evidence strongly favors the existence of vasocon-
strictor fibres. Francois-Franck showed further that these same changes in pulmonary
arterial pressure, left auricular pressure, and lung volume occurred reflexly when the central
end of the femoral nerve or a proximal branch of the solar plexus was stimulated. This
reflex, as he. shows in a subsequent paper, may have important bearings in the production
of certain cardiac symptoms and in influencing the course of cardiac diseases.
Action of Drugs on the Pulmonary Circulation. — Frangois-Franck's re-
searches are very convincing. They have been confirmed by H. C. Wood, Jr.,
and others, and are accepted by as keen a critic as Tigerstedt; but Wood, Jr.,
and also Petitjean have found that all drugs exert a much less
marked effect on the pulmonary circulation than on the
systemic. It must be admitted that acceptance is not universal. The
clinical importance of the problem renders it a matter of universal interest.
It may be considered proved by Francois-Franck's work that sensory
stimuli, stimulation of the sympathetic nerves, asphyxia, etc., may cause
the pulmonary arterial pressure to rise to about double its original height,
and hence in chronic conditions may play an important ratio in bringing
about hypertrophy of the right ventricle. Moreover, changes of pressure
which are relatively small when applied to the left ventricle assume much
greater proportions when applied to the weaker right ventricle, and appar-
ently slight changes in the strength of this chamber may then be impor-
tant factors in the mechanism of the circulation.
Tonicity of the Right Ventricle.— More important than the changes in
pressure in the pulmonary artery are the changes in tonus of the right
ventricle. Owing to the thinness of the wall, changes in tonicity affect
this chamber much more readily than they do the left; overstretching of
the fibres sets in more readily, and weakening of the right ventricle results
more readily. These changes may have no direct relation to the changes
in pulmonary arterial pressure.
BLOOD-PRESSURE AND BLOOD VISCOSITY. 35
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Pilcz, A.: Ueber einige Ergebnisse von Blutdruckmessungen bei Geisteskranken, Wien.
klin. Wochenschr., Wien, 1900, xiii, 276.
Pal, J.: Die Gefasskrisen, Leipz., 1905.
BLOOD-PRESSURE AND BLOOD VISCOSITY. 37
Gibson, G. A.: Heart-block, Brit. M. J., Lond., 1906, ii, 1113.
Siemens, J. M., and Goldsborough, F. C. See chapter on Pregnancy.
Hasenfeld, A., and Fenevessy, B.: Ueber die Leistungsfahigkeit des fettig entarteten
Herzens, Berl. klin. Wchnschr., 1899, xxxvi, 80, 125, 150.
Crile, G.: The Blood-pressure in Surgery, Phila., 1903.
Henderson, Y. (with the collaboration of M. McR. Scarborough, F. P. Chillingworth, and
J. R. Coffey) : Acapnia and Shock. I, Carbon Dioxide as a Factor in the Regulation
of the Heart-rate, Am. Journ. Physiol., Bost., 1908, xxi, 126; Part II, ibid., 1909,
xxiii, 345, and Part III, ibid., 1909, xxiv, 66.
Mosso, A.: Sui rapporti della respirazione abdominal e toracica., Arch, per la sci. med.,
1878, Fisiologia dell'uomo sulla Alpi, 2d ed., 1888.
Mosso, A. : La respiration pe"riodique (phenomene de Cheyne-Stokes) telle qu'elle se
produit chez I'homme sur les Alpes par 1'effet de 1'acapnie, Arch. ital. de biol., Turin,
1905, xliii, 81. Differences individuelles dans la resistance £ la pression partie le de
1'oxygene, ibid., 1905, Ixiii, 197. Demonstration des centres respiratoires spinaux
au moyen de 1'acapnie, ibid., 1905, Ixiii, 216.
Barach, J. H.: Blood-pressure Studies in Typhoid, N. York M. J., 1907, Ixxvi, 348.
Crile, G.: Diagnostic Value of Blood-pressure Determinations in the Diagnosis of Typhoid
Perforation, Jour. Am. M. Assoc., Chicago, 1903, xl, 1292.
Briggs, J. W., and Cook, H. W.: Clinical Observations on Blood-pressure, Johns Hopkins
Hosp. Bull., Bait., 1903, xi, 451.
Weigert, K.: Ueber das Verhalten des arteriellen Blutdrucks bei den akuten Infections-
krankheiten, Samml. klin. Vortrage, Leipz., 1907, Inn. Med., No. 138.
John, M.: Ueber den arteriellen Blutdruck bei Phthisiker, Ztschr. f. diat. u. physik. Therap.,
Leipz., 1901, v, 275.
Naumann: Blutdruckmessungen an Lungenkranken, Ztschr. f. Tuberkulose u. Heilstat-
tenw., Leipz., 1904, v, 118.
Stanton, W. B.: The Blood-pressure in Tuberculosis, Internat. Clin., Phila., 1907, 17th
Ser., 60.
Peters, L. S.: Blood-pressure in 100 Cases of Tuberculosis at High Altitudes, Arch. Int.
Med., Chicago, 1908, ii, 42.
Crile, G., and Dolley, D. H.: A Method of Treatment of Hemorrhage, Jour. Am. M. Assoc.,
Chicago, 1906, xlvii, 189.
V. Recklinghausen, H.: Unblutige Blutdruckmessung, Arch. f. exper. Path. u. Pharmakol.,
Leipz., 1906, Iv.
Hooker, D. R., and Eyster, J. A. E.: An Instrument for the Determination of Venous Pres-
sure in Man, Johns Hopkins Hosp. Bull., Bait., 1908, xix, 274.
PULMONARY CIRCULATION.
Trumpp, J.: Blutdruckmessungen an gesunden und kranken Sauglingen, Jahrb. f. Kinder-
heilk., Berl., 1906, Ixiii, 43.
Beutner, Lichtheim, Openchowski, Bradford and Dean, Plumier, quoted from Tigerstedt,
R.: Der kleine Kreislauf, Ergeb. d. Physiologic, Wiesb., 1903, ii, 528 (in which a com-
plete summary of the literature to that date is to be found, with an excellent resume
of the facts).
De Jager, S.: Ueber den Blutstrom in den Lungen, Arch. f. d. ges. Physiol., Bonn, 1879,
xxi, 426.
Francois-Franck, Ch. A.: Nouvelles recherches sur 1'action vaso-constrictive pulmonaire
du grand sympathique, Arch, de physiol. nor. et path., Par., 1895, 5 Se>., vii, 744, 816.
Etude critique et experimental de la vasoconstriction pulmonaire re"flexe, ibid., 1896,
5 Se>., viii, 178, 193.
Wood, H. C., Jr.: A Physiological Study of the Pulmonary Circulation, Am. Jour. Physiol.,
Bost., 1902, vi, 283.
Petitjean, G.: Action de quelques medicaments vasomoteurs (nitrite d'amyle, adrenaline,
ergot de seigle) sur la circulation pulmonaire, J. de physiol. et de path, gen., Par.,
1908, x, 403.
38
DISEASES OF THE HEART AND AORTA.
VISCOSITY OF THE BLOOD.
One of the most important factors in determining the work of the heart
and the nutriment of the tissues is the viscosity of the blood, — that is, the
friction which its molecules exert upon each other and upon the walls of
the blood-vessels.
Poisseuille and later Arrhenius introduced a method for determining viscosity quan-
titatively for indifferent fluids by observing the time taken for a given volume of fluid to
flow vertically down a given length of capillary tube. The time taken by water to flow
under the same conditions was used as the unit. Poisseuille found
Quantity of blood flowing in given time = viscosity coefficient X (diameter of
capillary)4 X height of pressure : length of tube for distance of flow.
Huerthle found that Poisseuille's law also held for pulsating fluids and measured the
viscosity of the blood in the living animal by comparing the outflow of blood from a capil-
lary tube introduced into the aorta to the outflow of water under the same conditions.
Viscosity coefficient (water) = 4700
Dog's blood = 1045
Water 4700
Coefficient of viscosity.
Dog's blood 1045
= 4.5
Apparatus for Clinical Determination of Viscosity. — Various forms of
apparatus have been devised for determining the viscosity clinically, most
of them depending upon the time taken for a column of blood in a given
capillary to traverse a given distance
or to flow out of a given orifice when
subjected to the pressure exerted by
a constant column of water.
_.!fe CL
WATERJACKETl
FIG. 32. — Determann's apparatus for determining the viscosity of the blood. (After Brugsch and
Schittenhelm.) A. Apparatus at rest on its stand, pivoted on the thermometer and the handle as an axis.
Jn the blood-receiving tube within the water-jacket ae = df, ab = cd. B. Method of application. (After
Brugsch and Schittenhelm.)
Such apparatus has been described by Huerthle, Burton-Opitz, Hirsch and Beck,
Determann. Hess and also McCaskey have devised very simple forms of apparatus in
which suction from a rubber bulb is used instead of positive pressure. C. R. Austrian in the
Johns Hopkins Medical Clinic has found that the Hess apparatus gives results with normal
blood which tally well with the blood count, and which therefore seem quite satisfactory.
Determann's newer apparatus (Fig. 32) , however, combines clinical
convenience with accuracy and is probably the most satisfactory now in use. It con-
sists of a capillary tube surrounded by a small condenser-jacket of glass containing water
at 38°. The jacket bears two side arms which rest in the forks of two uprights so that the
BLOOD-PRESSURE AND BLOOD VISCOSITY. 39
jackets always assume a vertical position. The apparatus is taken up as a whole and the
blood sucked up to a mark on the capillary. The apparatus is then placed back on the
forks, and the time taken for the blood to flow out until it reaches a second (lower) mark
is noted. (This should require 30-40 seconds.) A similar determination is made with water
(6-8 seconds).
In order to keep the blood from clotting, a little hirudin may be placed upon the
ear before stabbing it. This does not alter the viscosity as do adding sodium oxalate,
laking, and defibrination ; and keeps the blood from clotting for 20-30 minutes.
Determann obtains a few drops of blood quickly by having the patient exert a forced
expiration with the glottis closed (Valsalva's experiment).
Factors Influencing Viscosity. — Heubner, Determann, and others have
found that the chief factor in determining the viscosity is the viscosity of
the red corpuscles, to which about two-thirds of the viscosity of the blood is
due. Indeed in many cases these observers, and also Austrian, have found
that the blood-count and the viscosity furnish accurate controls of one
another, — though there are exceptions under pathological conditions
(leukaemia, etc.). There is little if any difference between the viscosity of
the normal blood in the arteries, capillaries, and veins. But in venous
stasis the viscosity increases tremendously.
In a polycythaemica with 11,000,000 red corpuscles the vis-
cosity may be three or more times the normal (Stern) .
On the other hand, in anaemias, fever, the hydraemia
which is associated with anasarca in broken compensation or exudates the
viscosity is uniformly greatly diminished.
Burton-Opitz found that diet exerted a considerable effect, meat
raising the viscosity, carbohydrates and fats lowering it.
He also found that hot baths lowered viscosity while cold baths increased
it. Hot-air baths seem to have little effect.
In compensated heart disease the water content of the blood does not
change (Askanazy), nor does the viscosity, but the water is increased and
the viscosity diminished (3.74 to 4.21) when compensation is broken (Deter-
mann). In bronchitis and diabetes it is high (5.5).
Determann cannot confirm the findings of Otfried Miiller and Inada
that potassium iodide lowers viscosity; and indeed the changes which they
obtained were less than 1.0 per cent., well within the limits of experimental
error. Their paper, as well as those of Hirsch and Beck, illustrates the
tendency of workers in the field to draw too definite conclusions from too
small variations.
BIBLIOGRAPHY.
VISCOSITY.
Poisseuille: An de chim. et de phys., Par., 1847, 3 se"r., i, 21 (quoted from Hirsch and Beck).
Arrhenius, S.: Innere Reibung wasseriger Losungen, Ztschr. f. physik. Chem., Leipz., 1887,
i, 289.
Huerthle, K: Widerstand der Blutbahn, Deutsch. med. Wochenschr., Leipz., 1897, 809.
Ueber eine Methode zur Bestimmung der Viskositat des lebenden Blutes und ihre
Ergebnisse, Arch. f. d. ges. Physiol., Bonn, 1900, Ixxxii, 415.
Burton-Opitz, R.: Ueber die Veranderung der Viskositat des Blutes unter dem Einfluss
verschiedenes Ernahrung und experimenteller Eingriffe, Arch. f. d. ges. Physiol.,
Bonn, 1900, Ixxxii, 447. Vergleich der Viskositat des normalen mit der des Oxalat-
blutes und des defibrinirten Blutes und des Blutserums bei verschiedener Tempera-
ture, ibid., 1900, Ixxxii, 464. Weitere studien ueber die Viskositat des Blutes, ibid.,
40 DISEASES OF THE HEART AND AORTA.
1906, cxii, 189; also Am. Med., 1900, vii, 111. The Effect of Changes in Tempera-
ture upon the Viscosity of the Living Blood, J. Exper. Med., N. York, 1906, viii, 59.
The Effect of Intravenous Injections of Solutions of Dextrose upon the Viscosity of
the Blood, ibid., viii, 240.
Hirsch, C., and Beck, C.: Studien zur Lehre von der Viscositat (innere Reibung) des
lebenden menschlichen Blutes, Deutsch. Arch. f. klin. Med., Leipz., 1900, Ixix, 503;
and 1902, Ixxii, 560.
Determann: Klinische Untersuchungen ueber die Viskositat des menschlichen Blutes,
Ztschr. f. klin. Med., Berl., 1906, lix, 283. Discussion upon this paper in the Zentralbl.
f. inn. Med., 1906, xxvii, 519. Die Beinflussung der Viskositat des menschlichen
Blutes durch Kaltereize Warmeentziehung, Warmezufuhr, und Warmestauung, Berl.
klin. Wochnschr., 1907, xliv, 687, 723.'
Hess, W. : Ein neuer Apparat zur Bestimmung der Viscositat des Blutes, Cor.-Bl. f . schweiz
Aerzte, Basel, 1907, xxxvii, 73.
McCaskey, G. W.: The Viscosity of the Blood; Its Value in Clinical Medicine, J. Am. M.
Assoc., Chicago, 1908, li, 1653.
Determann: Ein einfaches, stets gebrauchfertiges Blutviskosimeter, Muenchen med.
Wochnschr., 1907, liv, 1130.
Heubner, W.: Die Viskositat des Blutes, Arch. f. exper. PathoL u. Pharmakol., Leipz.,
1905, liii, 280.
Stern: Discussion of Determann's paper.
Askanasy, S. : Ueber den Wassergehalt des Blutes und des Blutserums bei Kreislaufstorung,
u. s. w., Deutsch. Arch. f. klin. Med., Leipz., 1897, lix, 385.
III.
THE ARTERIAL PULSE.
Historical. — Observation of the arterial pulse began almost synchronously with the
accurate observation of disease in general. Hippocrates (B. C. 500) noted the marked
pulsation (ofvypd? ) of the arteries in certain diseases, but did not associate it with the beat
of the heart. Herophilus (B. C. 300) observed the relative synchronism of these two events
and speaks of the quiet pulse in health (ojvyftdf) in contrast to the marked pulsation in
disease (the iratyde of Hippocrates). Eristratus (B. C. 280) showed that the arteries near
the heart beat before the arteries more distant from it. Aristotle and later Archigenes
(first century after the Christian era) made numerous observations upon the pulse in various
diseases, and the latter described and gave the name to the d i c r o t i c type in cases
of fever, although he still believed that the arteries were filled with air. Galen (A. D. 131
20*2) demonstrated that the arteries were filled with blood and studied the influence of sex,
age, climate, sleep, hot and cold baths upon the rhythm of the pulse.
The old Chinese physicians also described the pulse and even made drawings to
illustrate their sensory impressions — a practice which did not begin in Europe until the
time of Henri Fouquet in 1767. After Harvey's demonstration of the circulation of the
blood (1628), the study of the pulse was resumed with renewed vigor and has continued
to the present day.
Examination of the Pulse. — The characteristics of the pulse-wave are,
as a rule, determined upon the radial artery, in which the arterial tension
may be estimated as described on page 19, the wall of the artery being also
rolled under the finger while the artery is empty, and thus the presence or
absence of arteriosclerosis noted. The walls of a normal artery are barely,
if at all, palpable; an atheromatous artery may feel like the trachea of a
small animal (goose-neck); a diffusely sclerotic artery feels like a piece of
thick-walled rubber tube.
It is important to note the palpability of several arteries, since one
of them may escape a sclerotic process. All the blood must have been
pressed out of their lumina and of the vense comites that accompany them
before palpation is begun, or else normal arteries may appear to be
sclerotic. The pressure is then relieved, and the tips of two or three fingers
are pressed upon the artery until the pulse appears maximal (at about
the minimal pressure), when the following characteristics are noted: (1)
whether the artery (hence the pulse) feels large and dilated (pulsus mag-
nus) or small and constricted (pulsus parvus); (2) whether the
pulse is hard (pulsus durus) or soft (pulsus moll is), — i.e., whether
the minimal pressure is low or high; (3) whether the onset of the wave is
sudden (p u Isu s celer) or gradual (p u Is u s tardus); (4) whether
the wave is sustained (anacrotic) or subsides suddenly under the
finger (collapsing, water-hammer, or Corrigan pulse) ; (5) the
rate of the heart per minute (counted continuously during at least a half
minute) ; (6) whether the rhythm is regular (pulsus regularis)or
irregular (pulsus irregularis).
Clinical Sphygmographs. — An instrument (sphygmograph) to
record the pulse-wave graphically was first devised by K. Vierordt (1855),
41
42 DISEASES OF THE HEART AND AORTA.
«
but it was not until 1860 that E. J. Marey devised a thoroughly practi-
cal and accurate form, almost devoid of error, which is still in use.
Marey's sphygmograph consists of a button (pelotte) pressed against the skin over
the artery by means of a spring so as to receive the pulsations from the artery. It is held
in place by a leather cuff, and it is most important that the pelotte remain exactly over and
not to one side of the artery. The pelotte is surmounted by a vertical rod or screw which
articulates by a movable joint with a long writing lever. The writing lever records the
magnified pulse movements upon a surface of smoked paper held in vertical position by a
brass upright and driven by a small piece of clock-work.
A more compact and convenient form of sphygmograph is that of Dudgeon, in which
the straight lever is supplanted by a double-jointed one which writes on a horizontal instead
of a vertical strip of smoked paper. The tension of the spring pressing down the pelotte
is roughly adjustable, which allows some variation in the pressure over the artery.
V. J a q u e t has improved Dudgeon's apparatus by adding to it a small time marker
recording fifths of a second. •
Another excellent form of sphygmograph is that devised by Roy and Adami, which,
by means of a delicate adjustment, enables the observer to obtain a pulse record at
exactly diastolic pressure. Unfortunately, it has never been placed on. the market, and
A hence has not been subjected to the test of
general use, but any one who is interested
in sphygmographs should certainly familiar-
ize himself with their observations.
FIG. 33.— Braehial pulse-curves taken with the Erlanger blood-pressure apparatus from the arms
of two patients, merely varying the pressure in the cuff. The figures indicate the pressures at which the
curves are taken, those underlined indicating maximal and minimal pressures respectively.
Errors in Sphygmography.— In spite of the existence of these fairly
satisfactory sphygmographs and of their wide use, discrepancies between
the clinical observations and the tracings obtained are so great that Cabot
refers to the sphygmograph as " an interesting little toy." The reason that
it is not of value must be either that the apparatus itself is subject to
inherent errors, or that, as Mackenzie states, " it was expected to give in-
formation of a kind that it was incapable of supplying." Unfortunately,
both are the case.
Athanasiu, in investigating the accuracy of graphic recording devices, found that all
sphygmographs which magnified the movement more than twenty times introduced a
large inherent error, that of all the forms in use Marey's introduced the least error, while
the Dudgeon apparatus and the Jaquet magnified it 130 times, introducing tremendous
distortion from flinging large pulsations.
On the other hand, the writer, D. Gerhardt, and Stewart have been able to show
that not only the size but also the entire type of the pulse-curve obtained depends upon
the pressure exerted upon the artery and other similar factors; the true form of the pulse-
wave being obtained only when the pressure exerted by the sphygmograph is exactly equal
THE ARTERIAL PULSE.
43
to the pressure within the artery. Fortunately, this is the point at which the pulse excur-
sion is maximal, and as all observers strive for the largest excursion, it is probable that
most sphygmographic records are taken at about this pressure. The ideal apparatus is
the one in which it is not merely probable but certain, and
hence that of Roy and Adami is the only one which abso-
lutely fulfils the requirements.
The Absolute Sphygmogram. — A very con-
venient and instructive method of recording pulse
tracings has been introduced by Sahli. Sahli
transfers the pulse -curve to coordinate paper
upon which the ordinates represent millimetres
of mercury and the abscissae represent fractions
of a second. The lowest point of the pulse-curve
he marks at the level corresponding to the mini-
mal blood-pressure, determined at the time with
the sphygmomanometer; the highest point at the
level corresponding to the maximal pressure; and
maps out besides this the other main points of
the pulse-curve (predicrotic fall and wave, dicrotic
notch, summit of dicrotic wave, etc.) at heights
and distances proportional to their occurrence upon
the sphygmogram, but translated to this new
scale of pressure and time. This curve he terms
the absolute sphygmogram.
The absolute sphygmogram can also be read off from
the ordinary jsphygmogram by using the lowest point on
the tracing as the ordinate of minimal pressure and as a
the pressure at other points, and calculating these from the
Ordinate of point : Total height of pulse-wave =
Pressure at that instant (above minimal arterial pressure) : Pulse-pressure.
Discrepancies between Feeling and Recording the Pulse.— Not all the
discrepancies between sensory impression and sphygmogram are the fault
of the instrument. In the first place, there is no absolute uniformity in
the minds of physicians as the standard to be applied to the individual
pulse. Thus, the writer has seen one eminent clinician dictate a note,
" pulse not collapsing," and another a few minutes later state that the
same "pulse is collapsing in quality." The pulse had not changed, but
the subjective criteria of the two men were slightly different.
Again, between pulse palpation and sphygmogram there is a difference. It is very
difficult, almost impossible, to determine just how long a pulse is sustained and how quickly
it falls, since these judgments are based upon a sequence of events lasting for an interval
of about one-tenth of a second, and changes both in time and in pressure must be con-
sidered without the presence of any simultaneous standard for comparison. Psychologic-
ally, such comparisons must be very fallible. Practically they are not as fallible as they
appear, for the judgment is based not upon form or duration, unless the abnormalities are
marked, as much as upon changes of pressure. What one really appreciates most in feel-
ing the pulse is the amount of minimal pressure ("hardness" of the pulse) and the amount
of the pulse-pressure (size of pulse), and only to a lesser extent the duration of the pulse-
wave. Hence, the sensation due to a high pulse-pressure with a moderate diastolic
pressure is often mistaken for that due to a collapsing pulse, though the form of the pulse-
FIG. 34. — Absolute
sphygmograms, all of which
correspond to the radial trac-
ing above. The figures to the
left indicate pressures in
mm. Hg.
base line for determining
proportion
44
DISEASES OF THE HEART AND AORTA.
SYSTOLE
FIG. 35. — Significance of the pulse-curve.
/, inflow into the artery from heart; O, outflow
from the artery toward the periphery.
wave may show that it is quite well sustained. In comparing the pulse sensation with the
sphygmogram, one is therefore comparing two somewhat different standards, and this
inherent difference must be taken into account.
Significance of the Pulse=curve. — Assuming, however, that one has ob-
tained a correct tracing from the artery, what deductions are allowable ? It
is evident that the artery expands somewhat under an increase in pressure
(causing a rise in the pulse-wave) and
contracts when pressure decreases
(causing a fall in the pulse-wave).
Further, the pressure in the artery in-
creases or decreases, depending upon
whether more blood enters it than can
leave it at that instant (Fig. 35, I>O)
or whether the reverse is the case
(I<O). When the inflow exactly
equals the outflow (I = O), no change
of pressure occurs and a plateau
results. The pulse tracing is merely the record of these events — the
record of the ratio that the inflow into the artery from the heart bears
to the outflow toward the periphery at each instant of the cardiac cycle.
The normal pulse-wave has the
following forms: an upstroke more
or less steep (percussion wave;, a
rather acute summit, and sudden fall
(predicrotic) followed by a very small
rebounding wave (predicrotic wave),
then another more gradual fall termi-
nating in a small notch (dicrotic notch)
which marks the end of systole
(Marey, Huerthle), then a gradual fall
during diastole. In the aorta the fall
in waves is not as steep as in the
radial artery, which indicates that
the former reflects the conditions
near the heart, the latter shows the
conditions at the periphery (Marey)
Relation of Pulse Form to Peri=
pheral Resistance. — There are three
general types of pulse (Marey, Hirsch-
felder) which may occur without any
heart lesion whatever, and even in the same individual at the same maxi-
mal and minimal pressures, though usually the maximal and minimal pres-
sures vary with these conditions. (Fig. 37.)
Type I corresponds to marked peripheral dilata-
ion, as after exercise, after meals, in shock, fevers, or in some nervous
individuals with vasomotor instability. This is the collapsing type of pulse,
rapid rise and rapid fall sometimes followed by a large dicrotic wave (see
page 45). The rise is, however, about two hundredths of a second slower
than normal, but this difference is not within the limits of perception. It
FIG. 36. — Diagram showing the time rela-
tions of ventricular volume and pressure curves
to pulse tracings from the aorta, carotid and
radial arteries. Time divisions in one-tenth sec-
onds. (Schematic.) Dotted lines represent curve*
taken with high peripheral resistance.
THE ARTERIAL PULSE.
45
feels more sudden because it is sharply followed by the sudden fall. The
fall in this type of pulse is almost complete before the end of systole, i.e.,
before the dicrotic notch which marks that point (Marey, Huerthle).
no
Fio. 37. — Three types of arterial pulse-curve corresponding to the same pulse-pressure and same pulse-
rate. (Johns Hopkins Hosp. Bull, xviii.) I, vasodilation; II, normal; III, vasoconstriction.
In T y p e II only about half the fall occurs during systole. This
corresponds to moderate degree of dilatation and is
the type present in normal individuals.
In Type III the wave soon rises to the summit and remains there,
forming a sustained plateau (outflow = inflow) until the end of systole, when
it gradually falls. This corresponds
to peripheral constriction,
preventing the outflow from the aorta
from exceeding the inflow into it,
as is the case where a normal degree
of dilatation is present. The normal
pulse in man may be converted into
this type by compression of both
femoral arteries (Marey) or of the ab-
dominal aorta (Stewart). The mere
increase of the blood-pressure is not
a cause, because after exercise the
blood-pressure is increased and yet
the pulse becomes more collapsing
than before.
FIG. 38. — Effect of inhalation of amyl nitrite
upon the pulse-form. (After v. Kries.) Curves
taken in succession. Vasodilation reaches its
maximum at c and diminishes at d and e. Well-
marked dicrotism at d. ft and a indicate second-
ary waves due to elasticity of the artery.
These general outlines of the pulse-
waves are further modified by smaller wave-
lets due to the elastic vibrations of the artery
wall, or to the rebound of the percussion
wave at the periphery (v. Kries). The most important of these is the dicrotic wave
following immediately upon the closure of the aortic valves and due either to
a centrifugal wave from the blood impinging against them, or to
a reflected centripetal w a ve from the periphery toward the
heart (v. Kries). Whichever theory may be correct, the essential fact remains that
the dicrotic wave is a secondary one and is dependent upon arterial elasticity. V. Kries
has shown that the dicrotic wave is most marked when the peripheral vessels are consider-
ably dilated, but not when they are dilated to their fullest extent (Fig. 38).
The other waves may occur upon either upstroke (anacrotic) or upon the downstroke
(katacrotic, Fig. 38, a /?) and are designated accordingly. Small secondary waves of this
46
DISEASES OF THE HEART AND AORTA.
type are most marked when the pressure is high and the heart action strong (e.g., pulsus
bisferiens), but their occurrence is often due to twitching of the tendons near the pelotte
of the sphygmograph, and too great weight must not be attached to them.
+ + + +
JJjH^
™|i||nflnn*™"n™'TO^
D+ Dt JH
yyTOryyymrK>ryVy>^^
Fio. 39. — Mercury manometer tracing from the carotid artery of a dog, showing rhythmic varia-
tions in blood-pressure and rhythmic increase in dicrotism. (Kindness of Prof. Abel and Dr. Rowntree.)
The dicrotic wave increases at the points (D + ) at which the blood -pressure is lowest ( — ) and the peripheral
arteries are dilated. Time in seconds.
Too much information should not be sought from the sphygmogram.
All that should be looked for is whether the upstroke is sudden (p. celer)
or gradual (p. tardus) ; whether the main fall in the wave begins early or
late in systole, or not until the beginning of diastole; also whether the
fall is quite or nearly complete before the end of systole. All possible
mental reservations should be made
for fling of the lever, incorrect appli-
cations of sphygmograph, etc., before
a judgment is made.
THE PULSE-RATE.
The normal pulse varies consid-
erably in different individuals, being
in general more rapid in those of
small stature and slower in persons
of larger stature, hence, more rapid
in women than in men. It also
varies considerably according to age,
being dependent upon the relative
tone of vagi and accelerators. The
pulse-rate is also more rapid (tachy-
cardia) in fevers, varying in general
according to the temperature — each
degree Fahrenheit increase corresponds
to an acceleration of about four to five
beats per minute. C. D. Snyder, as
the result of a long series of experi-
ments upon the heart-rate in different
vertebrates, finds that the rate is
influenced by temperature in the same degree as is the velocity of simple
chemical reactions and follows the logarithmic formula
Fio. 40. — Diagram showing various forms
of pulse-curve encountered clinically. Systolic
portions of the curve are underlined. HYPER-
DICROT, hyperdicrotic.
In typhoid fever there is often an exception, a temperature of 103° to 105° being
accompanied by a pulse-rate of about 90 per minute, owing to a toxic stimulation of the
THE ARTERIAL PULSE.
47
TYPES OF PULSE IN VARIOUS DISEASES.
The following types of pulse are associated with various pathological
conditions and corresponding states of the heart and vessels.
of pulse.1
Shown in Fig.
Characteristics.
Clinical condi-
tions in which it
is most fre-
quently observed.
Blood-pressure associated with it.
Vascular
condition.
Maximum.
Minimum.
Pulse-
pressure.
Normal....
40
Sudden rise, sharp
Normal individ-
Normal
Normal.
apex, slight pre-
uals
di erotic fall; then
slow fall, small
Some cases of aor-
High : Normal.. .
Increased .
Dilated.
dicrotic wave,
tic insufficiency
gradual fall in di-
astole
A few cases of
Normal or
Pulse -rate
Dilated.
fever
d i m in -
qui c k-
ished
ened
AnB-crotic .
40
Sudden rise or
Arteriosclerosis ;
High
High
Slightlyin-
Vaso con-
slightly rounded
chronic nephritis
creased
striction.
plateau top last-
or u n -
ing almost to di-
Some cases of aor-
changed
crotic notch
tic insufficiency
which is small;
gradual diastolic
Some normal indi-
Normal . . .
High
Slightly di-
Vasocon-
fall
viduals
minished
striction.
Bisferiens .
40
Resembling ana-
Arteriosclerosis;
High
High
Increased
Vasocon-
erotic except
chronic nephritis
rtriotion.
that the small
predi erotic fall is
Hypertrophied
followed by rise
heart acting
equal or above
strongly
that of the per-
cussion wave,
making the sum-
mit bifurcate
Tardus
40
Gradual slow rise,
Aortic stenosis . . .
Slightly or
Elevated..
Increased
Vasocon-
percussion wave
oblique, summit
greatly
elevated
or nor-
mal
striction.
round, gradual
fall
Collapsing.
40
Steep rise, apex
sharp, sudden
Aortic insufficien-
cy (water-ham-
L. o w or
normal
Increased
Vaso dila-
tion.
steep fall, di-
mer or Corrigan
crotic notch in
pulse)
lower half of
curve often level
Fevers
Normal or
Normal or
Nornuil or
Vasodila-
after the predi-
low
low
increased
tion.
crotic wave *
Normal individ-
Normal or
Normal or
Normal or
Vaso dila-
uals, neuras-
low
low
increased
tion.
thenics
Some cases of
Increased
Slightly in-
Increased .
Vaso dila-
Basedow's dis-
creased
tion.
ease
Dicrotic. . .
40
Collapsing in qual-
ity but dicrotic
Fevers, especially
typhoid
Normal or
subnor-
Normal or
s u b n o r-
Normal or
increased
Vaso dila-
tion.
wave very pro-
mal
mal
nounced and pal-
pable, as a small
Normal individ-
Increased
Normal or
Increased
Vaso dila-
wave regularly
uals during or
increased
tion.
following, soon
after exercise
after the percus-
sion wave
Neurasthenics,
Normal or
Normal. . .
Increased
Vasodila-
after amyl ni-
increased
tion.
trite or nitro-
glycerin
dicrotic
40
Dicrotic wave oc-
curs at the foot
Any of the condi-
tions in which
Normal or
increased
Normal . . .
Increased
Vasodila-
tion.
of the ascend-
di erotism may
ing instead of
occur, but with
descending limb
more rapid pulse-
rate.
'For forms of ii regular pulse see page 63.
48 DISEASES OF THE HEART AND AORTA.
vagus; while in meningitis the high intracranial pressure may bring the rate down to a
great deal lower (50 to 60) and may cause irregularity. In tuberculosis the pulse is rapid
even in the early stages. The pulse-rate is also accelerated in the anaemias, in neuras-
thenia, Graves's disease, hysteria, shock and collapse, abdominal distention, peritonitis
and other diseases of the abdominal viscera, and in numerous cardiac diseases. In fevers
and in many other conditions of acceleration the pulse becomes extremely small and
barely palpable on the one hand, and extremely rapid, barely countable on the other — a
small and "running" pulse. Pulse-rates of over 160 per minute are not uncommon in
fevers, while 200 or even 300 is reached in paroxysmal tachycardia. At these great rates
the duration of systole is markedly, shortened, as well as that of diastole (the period of
systolic output falling from 0.26 sec. to 0.2 or even less).
Slow pulse (bradycardia) (below 60 per minute) is observed especially in conditions
with intracranial tension, in meningitis, in digitalis poisoning, chronic nephritis, chronic
myocarditis, in convalescence from some fevers, especially diphtheria and influenza, and
in Adams-Stokes disease. In the latter condition the auricles and ventricles are beating
independently (see chapter on Adams-Stokes disease).
BIBLIOGRAPHY.
PULSE.
Harvey, W.: Exercitationes anatomicae de motu cordis et sanguinis circulatione, Rotero-
dami, 1671.
For historical resume cf. Morrow, W. S.: "The Pulse," Reference Hand-book of the
Medical Sciences, Phila., 1903, vi, 797.
Vierordt, K.: Die Lehre vom Arterienpuls, Braunschweig, 1855.
Marey, E. J. : Recherches sur 1'etat de la circulation d'apres les caracteres du pouls fournis
par un nouveau sphygmographe, Journal de la physiol. de rhomme, Par., 1860, iii,
241.
V. Jaquet, A.: Studien ueber graphische Zeitregistrirung, Ztschr. f. Biol., Muenchen u.
Leipz., 1891, xxviii, N. F. x., 1.
Roy, C. S., and Adami, J. G.: Heart-beat and Pulse-wave, Practitioner, Lond., 1890,
xliv, 81, 161, 241, 347, 412, xlv, 20.
Athanasiu, J.: Methode graphique, Trav. Assoc. de ITnstitut Marey, Paris, 1905, p. 29.
Hirschfelder, A. D.: Graphic Methods in the Study of Cardiac Diseases, Am. Jour. M.
Sci., Phila., 1906, cxxxii, 378.
Gerhardt, D.: Beitrage zur Lehre vom Blutdruck, Rindfleisch Festschrift, Leipz., 1907.
Stewart, H. A.: An Experimental and Clinical Study of the Blood-pressure and Pulse in
Aortic Insufficiency, Thesis, Edinb., 1907; also Arch. Int. Med., Chicago, 1908, i, 102.
Sahli, H.: Ueber das absolute Sphygmogram und seine klinische Bedeutung nebst kriti-
schen Bemerkungen ueber einige neuere sphygmographische Arbeiten, Deutsch.
Arch. f. klin. Med., Leipz., 1904, Ixxxi, 493.
Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Par., 1881.
Huerthle, K.: Beitrage zur Haemodynamik, Arch. f. d. ges. Physiol., Bonn, 1891, xlix, 29.
Hirschfelder, A. D.: Some Observations upon Blood-pressure and Pulse Form, Bull. Johns
Hopkins Hosp., Baltimore, 1907, xviii, 262.
V. Kries, J.: Studien zur Pulslehre, Freiburg, 1892.
Snyder, C. D.: The Influence of Temperature upon the Rate of the Heart-beat in the
Light of the Law for Chemical Reaction Velocity, Am. J. Physiol., Bost., 1906,
xvii, 350.
IV.
THE VENOUS PULSE AND ELECTROCARDIOGRAM
IN HEALTH AND DISEASE.
THE NORMAL VENOUS PULSE.
As has been seen, the study of the blood-pressure and of the arterial
pulse conveys information regarding the strength of the heart-beat, the
condition of the peripheral arteries, and the velocity which the heart is
imparting to the blood stream. But it reveals the action of the left ven-
tricle only, and what occurs in the other chambers of the heart must be
sought for elsewhere.
In studying the heart from the four stand-points of Engelmann,
rhythmicity, irritability, conductivity, and .contractility ,
it is necessary to obtain a knowledge of the origination of the impulses
in or above the right auricle (atrium), of whether impulses other than
those causing the normal rhythm are acting upon that chamber, of whether
the right auricle (atrium) is itself contracting, and of whether all the
impulses are being properly conducted to the ventricle. Our knowledge
upon these points has been derived almost entirely from the study of the
pulsation in the jugular vein.
Visible Pulsation in the Veins. — Pulsation over the veins is visible in
80 per cent, of healthy individuals (Hewlett) and is as pronounced as that
over the arteries, but it is different in character. The latter shows the force-
pump, the former the suction-pump action of the heart. The pulsation over
the arteries is quick, sharply localized, easily palpable, and the impulse is
more marked than the collapse; that over the veins is diffuse, wavy, rarely
palpable, and the collapse is more marked than the im-
pulse itself. Further, the pulsations over the vein under normal con-
ditions are exactly twice the number of those seen over the artery, and the
first of the collapses is synchronous with the impact in the artery. Such a
pulsation over the vein is known as the "physiological," "negative," or
"double " venous pulse, in contradistinction to the other types of venous
pulse to be described later.
The pulsation over the veins is not, like the arterial pulse, to be seen
in every vein in the body, though Morrow has shown that in dogs it
can be detected by means of delicate manometers. To the eye and to
the recording apparatus available upon man, it is appreciable only in the
veins near the heart, the external and internal jugular, the cephalic, and
the axillary. Occasionally it is also to be seen in the brachiocephalic and
other veins in the arm.1 The site where it is most easily and uniformly
seen is in the right supraclavicular fossa, either over or just to the right of
1 Friedreich thought that this pulsation was transmitted from the arteries through
the capillaries to the veins, but such transmission probably never takes place and other
explanations must be sought.
4 49
50 DISEASES OF THE HEART AND AORTA.
the origin of the sternocleidomastoid. Sometimes it is a little more marked
in the supraclavicular fossa at about the mammillary line where the exter-
nal jugular vein enters the subclavian. The normal venous pulsation is
rarely to be seen when the subject is standing or when propped up high
upon pillows, but is most distinct after he has been in reclining posture
for some minutes with a single pillow under his head and neck. In patients
with venous stasis, on the other hand, it may be necessary for the patient
to sit upright before any undulations appear.
It must be borne in mind that the pulsation seen and recorded over
the veins represents the alternate filling and collapse of the latter. The
collapse, that is the obliteration of the lumen of the vein by the atmospheric
pressure, is usually the most important factor. It is evident that a wave
will occur during those periods in which the pressure
within the vein is greater than the atmospheric, and a
collapse will occur whenever it is less. If it is permanently less
(negative) , the vein will remain collapsed ; if it is permanently a little greater,
the vein will remain distended. In neither case will a pulsation be seen.
The normal pulsation is best seen when the pressure in the jugular vein is alternating
between a positive and a negative pressure during the different phases of the cardiac
cycle. The elastic distention of the vein is not called into play. The elastic distention of
the vein at systole occurs only at a much higher venous pressure, as in tricuspid insuffi-
ciency. Occasionally, especially in chronic heart cases with phlebosclerosis, the veins stand
out like large knotty cords, but no pulsation is to be discerned in them at all. The knotty
appearance (Fig. 41) is due to the closure of the valves within the veins, the dilatations
appearing just above the valves. Perhaps the closure of the valves prevents or dampens the
pulsation, or perhaps the rigidity of the vessel wall prevents it from collapsing and filling.
Normally the valves in the jugular do not close, but this closure is brought about by chronic
venous stasis, just as it is in quadrupeds where back pressure results from the head being
dependent. In such cases it is impossible to obtain any idea of the undulations nearer the
heart.
GRAPHIC RECORDS OF VENOUS PULSATIONS.
A far more exact idea of the nature of the jugular pulsation can be
obtained by recording it graphically than by mere inspection. With proper
apparatus this is not accompanied by any difficulty, and a satisfactory
record of both venous and carotid pulsations can be obtained in about the
same time as a radial sphygmogram. For the interpretation of the venous
tracing it is necessary to compare it with the other events of the cardiac
cycle, which is accomplished by using the pulse-wave from some artery
to fix the standard of time.
In order to interpret the waves upon the venous- pulse, it is necessary
to record simultaneously the venous pulse and either the arterial pulse or
the cardiogram, and to see at which point in the cardiac cycle each event
will fall. Accordingly, all forms of apparatus (polygraph) for obtaining
such records are arranged for taking at least two records simultaneously.
In all of these the pulsation from over the vein is received in the same way,
and the only difference in the various forms of polygraph lies in the method
of obtaining the arterial tracing and in the form of kymograph used.
Application of the Receivers. — The pulsation in the jugular vein is recorded by
holding over the skin above it a small glass funnel on special receiver (Fig. 41, c), which is
connected with a Marey recording kymograph tambour. The movements of the skin are
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 51
transmitted at once to the kymograph tambour and recorded by the lever. As a rule, the
most favorable conditions are obtained when the patient is lying with head and neck
supported on a single pillow that extends down just to the shoulders, with his head turned
well to the right and the neck definitely flexed. In this way the right sternocleidomastoid
is relaxed and a tracing over the pulsation from base of the internal jugular vein is trans-
mitted to the skin. When this is not obtainable the junction of the external jugular vein
with the subclavian should be tried in the same way. The funnel should be pressed against
the skin just enough to make the contact air-
tight without affecting the pulsation, but this
is effected without any great dexterity, and
oscillations due to the holding of the re-
ceiver rarely appear upon the tracing. When
they do so it is in the form of fine oscillations
bearing no relation to the cardiac cycle and
having a rate of from four to eight per
second, in contrast to the much slower and
larger movements in the veins. Such
tracings should be discarded.
In many cases the simple glass funnel
is not as satisfactory as a receiving device
introduced by Mackenzie (Fig. 41, c), con-
sisting of a shallow metal pan 3 cm. in
diameter with a tube leading off from it in
the form shown in Fig. 41, one portion of
the circumference being flattened instead
of round in order to fit closely above the
clavicle. It is convenient to have a small
hole in the top of the pan so that it may
be adjusted to the skin without moving
the recording lever, and after adjustment
is complete the hole is closed by placing
JUGUU* VElh
RtUIVCR FOR » I IN
x~~x
^_^/
KCtlVlRfORMlTl
the finger over it.
The tracing from the carotid artery is
obtained in a similar way, using for a
receiver a small tambour surmounted by a
button to fit over the artery (Fig. 41, D).
A small hole in the top of this tambour
serves the same purpose as before and is
also stopped by covering with the finger,
inside the sternocleidomastoid when the
Fio. 41. — Sites for recording the jugular and
carotid pulsations. A, distribution of the veins
(shaded in black), showing the sites for applying the
jugular receiver (truncated) and the carotid receiver
(concentric circles); B, appearance of the valves
within the jugular vein when closed by back pres-
sure; C, receiver for jugular vein; D, spring tambour
for recording the pulsation over the carotid artery.
The carotid artery is next to the skin just
head is turned toward the corresponding
side, the pulsation being most marked when the receiver is pressed heavily upon it.
Comparison of Carotid and Jugular Pulsation. — Since the jugular vein
and the carotid artery are at about the same distance from the heart, the
tracings from the latter must always be compared
with the former in order to exclude waves which might have been
transmitted to it from the artery, and also to indicate the relations of the
venous waves to the cardiac cycle.1
This comparison may be made by taking the jugular and the carotid tracings simul-
taneously and comparing them with each other directly,2 or, for the sake of convenience,
1 Where great accuracy is necessary the onset of the c wave must be compared with
that of the apex beat.
2 It is not necessary that the levers be exactly superposed, but it is preferable to
measure off the distance of the given point horizontally from the arc described by the
lever at the beginning of the tracing (e.g., Fig. 44). This distance is then laid off upon the
other curve in the same manner. Wherever the curve may begin the paper traverses the
same distance upon both curves in the same time.
52
DISEASES OF THE HEART AND AORTA.
i\
FIG. 42. — Apparatus for recording the respiration.
RUB, rubber tube; GL, glass tube.
a carotid and a brachial or radial tracing may be made simultaneously, and the point at
which the carotid wave begins marked off upon the latter. Then a jugular and a brachial
tracing may be made, and the time that the carotid wave occurs before the brachial marked
off before each brachial wave in this tracing, and these points then measured off upon the
jugular tracing. This is often the simplest and quickest procedure.
Respiration Recorder.— It is often of importance to determine the
relation of an arrhythmia to the phases of respiration. The simplest device
for recording the latter consists of a piece of rubber tube (Fig. 42,
RUB) connected with the tube to
the recording tambours by a short
L-shaped piece of glass tubing
(GL). A piece of string or tape is
attached to the rubber tube,
another to the glass tube. The
apparatus is then put on so as
to encircle the level of the nip-
ples. The strings are tied tightly
enough to just stretch the rubber
tube during expiration. Inspira-
tion then causes a downstroke of
the levers, expiration an upstroke.
Forms of Polygraph. — Several forms of polygraph for clinical purposes have been
devised to record these curves. Their relative value depends largely upon the delicacy of
the tambours. The oldest form is the polygraph of Marey, consisting of an ordinary kymo-
graph drum arranged to rotate horizontally
with two Marey tambours to write upon it,
so as to record simultaneously the curve
from the jugular and carotid or jugular and
cardiogram. This is fairly satisfactory, but
in mechanical perfection some others are
superior. Mackenzie has devised two forms
of polygraph. The first, a simple Jaquet
sphygmograph upon which a Marey tambour
is mounted in addition so as to record the
radial pulse and jugular or carotid, etc.,
simultaneously, the time being marked off
in i seconds by a small clock-work as well.
In the improved form of Mackenzie poly-
graph, the levers bear ink pens and write
upon an endless roll of white paper, so that a
very long series can be obtained. V. Jaquet's
cardiosphygmograph differs from the simple
sphygmograph only in bearing in addition
two Marey tambours whose double-jointed levers write just above the lever attached to
the radial pelotte. Both Mackenzie's and Jaquet's methods suffer from the inconvenience
of adjusting the sphygmograph to the radial artery and keeping it adjusted during the
entire observation, a factor which is very disconcerting to both patient and physician and
which prevents many important observations from being taken on restless patients.
This difficulty is obviated in the writer's modificaton of the Er-
langer blood-pressure apparatus (Fig. 22, page 21), in which two small
Marey tambours and a time-marker are arranged to write above the lever of the blood-
pressure apparatus. When the bag is inflated upon the arm, the brachial pulse is recorded
by the lever of the blood-pressure apparatus and used as the standard instead of the radial
pulse. Thjs entails no trouble and no expenditure of time, thereby saving much of the
trouble given by the other methods, and permits a set of records to be obtained very
FIG. 43. — V. Jaquet's cardiosphygmograph.
(Kindness of A. H. Thomas Co.) a, time marker
(& sec.); 6, c, levers of tambours for recording
venous tracing, carotid pulse, or cardiogram; d,
lever recording radial pulse-wave.
THE VENOUS PULSE AND ELECTROCARDIOGRAM.
53
quickly. It is also possible for the operator to work with one hand free and thus save the
necessity of an assistant. The curve thus obtained from the jugular vein is shown in
Fig. 44 and its relation to the other events in the cardiac cycle shown in Fig. 45.
SLOW
FAST
CAROTID
JUGULAR
FIG. 44. — Normal venous tracings, a, wave due to auricular contraction; c, wave at onset of
ventricular contraction (the vertical line c representing the beginning of the carotid pulse-wave); x, the
bottom of the mesosystolic collapse; d time of dicrotic notch in the carotid; v, wave at end of systole;
y, hollow at the end of the postsystolic collapse; t, d (Bard), telesystolic and protodiastolic waves
described by Bard. (The x and y depressions are not lettered on all tracings.)
Recently, Uskoff has constructed
a very compact form of this appara-
tus, bearing an Erlanger blood-
pressure apparatus, a tambour for
recording the height of the blood-
pressure objectively, a tambour for
apex or venous or carotid tracings,
and an excellent time-marker. This
seems to be a very good instrument of
wide applicability, suitable to all the
needs of the practitioner.
The choice of apparatus
depends chiefly upon the deli-
cacy of the tambours and upon
the portableness of the appara-
tus. In the latter regard the
Jaquet cardiosphygmograph is
particularly desirable, but in
the former it is excelled by
many. The possession of
extremely delicate tambours
enables the observer to proceed
rapidly and to obtain beautiful
and accurate records which
would be impossible with ordi-
nary apparatus. The horizon-
tally writing tambours of
French manufacture are partic-
ularly delicate.
AORTIC &PULMONIC
FIG. 45. — Diagram representing the various events in
a cardiac cycle. Letters as in previous figures. Time in
T\J seconds (vertical lines). Dotted lines represent curves
obtained when the peripheral resistance is high. The
pulse becomes anacrotic and the intraventricular increases
toward the end of systole.
INTERPRETATION OF WAVES UPON THE VENOUS TRACING.
The curve of venous pressure obtained clinically and in animals (Fred-
ericq, Morrow, Hering, Theopold) corresponds exactly to those obtained
within the auricles (Chauveau and Marey, Fredericq, Porter). The first
54
DISEASES OF THE HEART AND AORTA.
JUG
CAR
wave (a)1 in the venous pulse is due to the contraction of the right
auricle, and disappears when the auricle is paralyzed. It occurs about
one-fifth second before the contraction of the ventricle. The onset of the
ventricular contraction is marked on the venous tracing by a
small wave (c), caused in part by the pushing up of the tricuspid valve
when the intraventricular pressure rises
(Hirschfelder, 1. c., Bard, 1. c., Morrow,
Cushny and Grosh), and in part by the
flow of blood from the coronary veins,
which, as Porter has shown, are forcibly
emptied into the auricle at this instant
(Sewall and Hirschfelder). Mackenzie
thinks that it is due only to the carotid
pulsation transmitted to the vein, but
Morrow has obtained it after ligature of
the carotid in animals. Besides the wave
appears about -gV second before the ca-
rotid wave in many cases (Hirschfelder,
Bard). When the tracings are taken from the left jugular and right
carotid, the c wave in the vein may be later than that in the artery, owing to
longer time of transmission. The c wave is almost always present; but, as
Bard has shown, it may be very small or entirely absent in hearts whose ven-
tricles are failing (Fig. 46). The rise of the c wave is followed by a large
fall (z), which may be the largest fall of pressure in the whole cardiac
cycle. The exact mechanism by which this fall of pressure in the veins
(and also in the auricles) is produced, and especially why it should sometimes
represent the largest fall of pressure, is not clear. It is evident at this period
of the cycle that several events are taking place: (1) relaxation of the
auricle ; (2) a certain amount of downward pull which the papillary muscles
FIG. 46. — Venous tracing showing ab-
sence of the c wave in a case of heart fail-
ure. The tracing is otherwise normal.
JUG., right jugular vein; CAR., left ca-
rotid artery. Time in J seconds.
FIG. 47. — A. Venous tracing showing auricular paralysis (absence of a waye) with large (x) depression
during ventricular systole between c and v. B. Same tracing, faster speedl
exert upon the tricuspid and mitral valves; (3) at each systole, as can be
seen when the heart is exposed, the movements of the latter within the chest
are exerting a pull upon the venae cavse, thus pumping their contents into
the auricles; (4) the outflow of blood and the decrease in size of the heart
during systofe cause a slight increase in the negative pressure within the
1 Since Mackenzie's first nomenclature and lettering of the waves was introduced, a
great variety of lettering and of designation by numerals has been used by different authors;
but these serve to complicate rather than to simplify the question. The letters or numbers
are merely symbols, and a single uniform system would be better than a Babel of terms.
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 55
thorax which may be transmitted to the thin-walled veins. It is probable
that neither of these factors alone is responsible for the fall (x depression) ,
but that each is active. Certain it is that auricular relaxation is not the
sole cause, for as shown in Fig. 47 it may still be the largest depression in
cases in which the auricle is paralyzed.
Dr. Peabody has called the writer's attention to a small wave which is frequently
seen during midsystole, especially in tracings from vigorous hearts, occurring just at the
base of the x depression, and which in many cases cannot be due to fling of the lever. The
origin and significance of this wave are extremely uncertain. It may be really transmitted
from the artery; or, as Dr. Peabody suggests, may be due to slight insufficiency of the
papillary muscles studied by Sewall.
The fall which leads to the x depression usually lasts until about the
end of ventricular systole, d (instant of the dicrotic notch), after which it
is followed by a large rise (diastolic wave of Porter; v or ventricular wave
of Mackenzie; vs, ventricular stagnation (Ventrikelstauungswelle) , Hering;
telesystolic wave, t, Bard). This wave is very constant in its occurrence
and is usually supposed to represent stagnation within the ventricle lasting
from the end of systole until the tricuspid valve opens; the fall v-y indi-
cates the opening of the tricuspid valve.
As Bard has shown, two undulations are occasionally found (t, d; t, telesystolic,
occurring at the end of systole; and d, protodiastolic, occurring at the very beginning of
diastole). Bard states that the wave t is coincident with the first secondary (predicrotic)
wave of the arterial pulse, the second with the vibration of the ventricles due to the clos-
ure of the aortic valves, but this is not very satisfactory.
Sewall believes that the stagnation at the end of systole (when the upstroke of the
v or t wave occurs before the end of systole) is due to a fatiguing or stretching of the papil-
lary muscles, causing a slight tricuspid regurgitation at that instant; but in cases with no
murmur in the tricuspid region this explanation needs confirmation.
The rise upon the v wave outlasts the end of systole by about yV sec.,
which probably represents the time required to transmit this change of
pressure to the veins.
Most writers follow Mackenzie in believing that the upstroke of the v wave repre-
sents stasis within the ventricle lasting until the tricuspid valve opens, but cardiometer
tracings show that filling of the ventricles, or at least dilatation, begins at the instant
systole ends. Chauveau's tracings of the movements of the heart valves also show that
the triscupid valve opens before the time at which the crest of the v wave appears, so that
it is probable that this wave does not represent the very instant at which the tricuspid
valve opens, but that when the period x-v exceeds the transmission time the interval
represents a period during which the venous pressure remains greater than atmospheric
pressure. Or it may last until a sufficient amount of blood has entered the ventricle to
have relieved the venous engorgement which followed the cessation of the factors which
had produced the x depression.
The descending limb of the v wave continues as long as blood is rushing
in to fill the ventricle (Henderson's period of diastolic filling), after which
there is a gradual filling of the vein and a rise until the next auricular systole.
In slow hearts Hirschfelder and A. G. Gibson have shown that the inflow
into the auricles and the filling of the veins is no longer uniform but is inter-
rupted by a well-defined wavelet (h, Hirschfelder; b, Gibson) which follows
the v wave by a definite interval (Fig. 48, h). Both these writers indepen-
56 DISEASES OF THE HEART AND AORTA.
dently ascribed this wave to the snapping together of the auric-
uloventricular cusps at the end of ventricular fill-
in g in middiastole, and the former called attention to its correspondence
••••••^^••••••••••M
FIG. 48.— Venous tracing from a very slow heart, with loud third heart sound, showing the presence
of the h wave. Max, maximal blood-pressure; Min, minimal blood-pressure.
with the onset of Henderson's period of diastasis. This fact is further borne
out by the presence of a corresponding wave upon the tracing from the
oesophagus (Fig. 54, h). This wave
disappears when the pulse-rate be-
comes more rapid (Fig. 49).
G. A. Gibson, Eyster, and the writer
have occasionally seen a wave w in late diastole
of slow pulse preceding the wave of auricular
contraction (a wave) by a rather definite
FIG. 49.— Tracing from the same person interval (Fig. 50). The distance from the h
one hour later, after giving atropine and quick- wave varies. This wave is assumed by the
ening the pulse. The h wave is absent. former writer to represent a contraction origi-
nating in the sinus region of the heart. Since
the remnant of the embryonic sinus is actually incorporated within the body of the auricle
(atrium), this view is questionable and requires experimental confirmation.
FIG. 50. — Showing a wave w occurring shortly before the a wave. (From a tracing made in collaboration
with Prof. L. F. Barker.)
VISUAL EXAMINATION OF THE VENOUS PULSE.
Some of these events in the cardiac cycle may be 'clearly distinguished
with the naked eye. Upon looking carefully at the jugular pulsation in a
normal individual and placing the finger upon the carotid artery the vein will
be seen to fill twice (a wave and v wave) and to collapse twice (x depression
and y depression) for each beat felt in the carotid artery (" presystolic-dias-
tolic," "physiological," "negative," "double" venous pulse (Hirschfelder)).
These waves may be timed less accurately with the eye, but, although, as
Mackenzie states, visual examination may save the examiner many unnec-
essary tracings, it should not be relied upon in doubtful cases. For example,
a simple mesosystolic collapse (like that shown in Fig. 44) with absolute
paralysis of the auricles may simulate a normal venous pulso..
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 57
ABNORMAL TYPES OF VENOUS PULSE.
Auricular Paralysis. — Besides this normal (negative or double venous)
pulse several other types of venous pulse are seen. In venous stasis and
cardiac failure the auricles may soon become weakened and the a wave, due
to their contraction, may disappear entirely (Figs. 47 and 51). This phe-
J VJD
pv
pv
JUG
BRACK
FIG. 51. — Positive or ventricular type of venous pulse in tricuspid insufficiency, showing absence of the
a wave. VJD, right jugular vein; ACS, left carotid artery.
nomenon is readily demonstrable in animals (v. Frey and Krehl) and need
not be accompanied by any change in heart-rate, though arrhythmia is fre-
quently present in man. In animals auricular paralysis or marked weaken-
ing of the auricular contraction may also occur as the result of vagus stimu-
lation, so that the presence of
this phenomenon alone is not
always a bad omen, though
usually such is the case.
Positive Venous Pulse. —
When the auricle is paralyzed
or there is a leak at the tricuspid
valve, the entire form of the
pulse-wave usually changes.
The collapse during ventricular
systole disappears and is replaced
by a systolic plateau, or more
usually an M-shaped wave with
an early systolic wave c or p, a
midsystolic depression, and a
telesystolic wave v (Hewlett).
Mackenzie believes that the
first crest of the M represents a
contraction of the auricle simultaneous with that of the ventricle, and
that the depression in the middle corresponds to diastole of the auricle;
but this form of curve has been obtained by Knoll and Theopold in
animals when the auricles were stopped by vagus inhibition. This form
is known as the "positive," "ventricular," or, from the fact that it
appears to the eye as a single wave, the "single" type of venous pulse
(see chapter on Tricuspid Insufficiency). Though the ventricular type of
venous pulse occurs in tricuspid insufficiency, it is not pathognomonic of
the latter and may indicate merely paralysis of the auricle.
FIG. 52. — Positive or ventricular type of venous pulse
in tricuspid insufficiency, showing absence of the a wave.
JUG, right jugular vein; BRACH, right brachial artery.
58
DISEASES OF THE HEART AND AORTA.
Information furnished by the Venous Pulse.— It is apparent from the
above description that the following facts are to be learned from the normal
venous pulse-curve: (1) whether the auricle (atrium) is contracting, and
whether each auricular (atrial) contraction is followed by a ventricular con-
traction; (2) the time required for the conduction of the impulse from
auricle (atrium) to ventricle (the interval a-c on the tracing, about i second
in normal individuals — conduction time) ; (3) whether or not the tricuspid
valve is closing perfectly (shown by the fall of pressure during systole
and the subsequent v wave).1 In irregular pulses many more important
facts are to be learned from the venous pulses, which will be discussed in
connection with this disturbance of function.
(ESOPHAGEAL TRACINGS.
The venous pulse tracing reveals the conditions prevailing in the right auricle (atrium)
and the state of the tricuspid valve. A corresponding investigation of the state of the
left auricle (atrium) and of the mitral valve
was made possible by a method used by
Fredericq in animals and introduced into
clinical medicine by Minkowski. Minkowski
calls attention to the fact that at the level of
the seventh to the ninth thoracic vertebrae
(about 35 to 37 cm. from the teeth) the left
auricle is in contact with the oesophagus, and
when one introduces a stomach-tube to this
level it receives impulses from the left auricle
alone. Accordingly, an ordinary stomach-tube
is capped with a thin rubber finger cot, and
the latter secured by winding a silk ligature
several times around it. The stomach-tube is
then swallowed by the patient until it extends
down 35 to 37 cm. from the teeth. It is then
connected with a Marey tambour whose oscil-
lations record the contraction of the auricle
and ventricle (Figs. 53 and 54). The fall in
the wave occurs when the auricle moves away
from the oesophagus, the rise when it is
pressed against the latter by filling with blood. Under ordinary circumstances ven-
tricular as well as auricular systole draws the auricle away from the oesophagus so
that the falls and rises correspond to auricular and ventricular systole respectively.
(Esophageal Tracing in Mitral
Insufficiency.— When the mitral valve
does not close (mitral insufficiency),
blood is forced back into the auricle
during ventricular systole, and, instead
of a fall, there is a rise during systole.
Minkowski's method furnishes the
means for obtaining the missing link
in our knowledge of the cardiac impulse FIG. 54. — (Esophageal and carotid tracings from a
and the meaning of functional murmurs, normal man.
but unfortunately the swallowing of the
stomach-tube is so disagreeable to the ordinary patient and so dangerous in all very
severe cases as to preclude its adoption into general use. Patients can, however, often
be trained to swallow the stomach-tube without difficulty, or a rubb'er tube of small bore
may be substituted, and then very satisfactory results may be obtained.
1 This, as has been shown by Mackenzie and by Rihl, is not absolute.
FIG. 53. — Method of taking tracing from
the oesophagus to show the contractions of
the left auricle. The arrow points to the thin
rubber bulb at the end of the oesophageal tube.
ST., stomach.
CAROT.
CESOPH.
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 59
GAIWWOMLTLR
TAMBOUR
SHA-DOW
T!MC MARKER
FIG. 55. — Simplest form of apparatus for recording the electrocardiogram and cardiogram simultaneously.
LEFT RIGHT, jars filled with salt solution to receive the left and right hands respectively.
FIG. 56. — Patient with both hands placed in
jars of salt solution, ready for taking electrocardio-
gram. (After Einthoven.)
Fio. 57. — Course of the electrical variations due
to the heart-beat in man. (After Waller.) c-c,course
of the negative wave from auricles to ventricles; 6, b,
zones about the auricle becoming negative during
the auricular systole; a, a, zones about the ventricles
becoming negative during ventricular systole.
!if:t::;
Fio. 58. — Normal electrocardiogram showing
the time relations to the venous and carotid pulse-
waves. (After Einthoven.)
FIG. 59. — Normal electrocardiogram tracing
taken by the writer in collaboration with Prof.
L. F. Barker and Dr. G. S. Bond.
60 DISEASES OF THE HEART AND AORTA.
INTRANASAL TRACINGS.
Mosso and also the writer have obtained very satisfactory cardiographic curves from
the changes of air pressure within the thorax. These may be obtained by placing in one
nostril a cork perforated by a glass tube which is connected with the recording lever. The
lips are closed and the other nostril is closed by pressure. Or, the tube may be placed
in the mouth and both nostrils closed by pressure. The glottis must be open and the
breath held. Curves thus obtained closely resemble the oesophageal tracings in normal
individuals, though the waves are smaller.
THE ELECTROCARDIOGRAM.
Another very promising method of examination which, has not yet
become general is the use of the electrical variations due to the heart con-
traction (electrocardiagram of Einthoven).
Einthoven places the patient in a chair with both hands or one hand and one foot
immersed in a jar of 0.9 per cent, sodium chloride solution. Each jar is connected in the
circuit with a very delicate Einthoven (or Edelmann) thread galvanometer (Fig. 55).
The movements of the galvanometer are recorded photographically. At each heart con-
traction a series of electrical changes appear (Figs. 58 and 59), in which the first wave
P corresponds to the auricular (atrial), the second QR and third ST to the ventricular
systole. This method, at first sight the most difficult, is, when the appliances are once set
up, one of the simplest of all the graphic methods. Einthoven has connected the Leyden
physiological laboratory with the hospital by means of telephone wires specially laid, and
is able to make his diagnoses at a distance of a mile without ever seeing the patient.
In hypertrophy of the right ventricle the wave QR is much larger than usual and is
en the same side of the base-line as the auricular 'wave P. In cases of hypertrophy of
the left ventricle the QR wave is inverted and its altitude is also greater than normal.
Einthoven and Kraus and Nikolai have shown that extrasystoles and other irregular-
ities may be deciphered by this method better than by means of the venous pulse; and it
is probable that it will to a great measure supplant the latter as a means of diagnosis.
BIBLIOGRAPHY.
VENOUS PULSE.
Engelmann, Th. W.: Ueber den Ursprung der Herzbewegungen, Arch. f. d. ges. Physiol.,
Bonn, 1897, Ixv, 109.
Morrow, W. S.: Ueber die Fortpflanzungsgeschwindigket des Venenpuls, Arch. f. d. ges.
Physiol., Bonn, 1900, Ixxix, 442. The Rate of Propagation of the Venous Pulse,
Canad. Rec. Sc., 1900, viii, 205.
Friedreich, N.: Ueber den Venenpuls, Deutsch. Arch. f. klin. Med., Leipz., 1865, i, 241.
Marey, E. J.: La circulation du sang a Te"tat physiologique et dans les maladies, Paris, 1881.
Mackenzie, J.: The Venous and Liver Pulses, and the Arrhythmic Contraction of the
Cardiac Cavities, Jour. Path, and Bacteriol., Edinb. and Lond., 1893-94, .ii, pp. 84
and 273. The Study of the Pulse and Movements of the Heart, London, 1903.
Hirschfelder, A. D.: Graphic Methods in the Study of Cardiac Diseases, Am. Jour. M.
Sc., Phila., 1906, cxxxii, 378.
Bachman, G.: The Interpretation of the Venous Pulse, ibid., 1908, cxxxvi, 674.
Hay, J.: Graphic Methods in the Study of Heart Disease, Oxford and Lond., 1909.
V. Jaquet: Cardiosphygmograph, Ztschr. f. Biol., Muenchen, 1901.
Mackenzie, J.: Diseases of the Heart, Oxford and Lond., 1908.
Jskoff, L.: Der Sphygmotonograph, Ztschr. f. klin. Med., Berl., 1908, Ixvi, 90.
Fredericq, L.: La seconde ondulation positive (premiere ondulation systolique) du pouls
veineux physiologique chez le chien, Arch, intern, de Physiol., 1907. Historisch-
kritische Bemerkungen ueber die von klinischer Seite neuerdings anerkannte Identi-
tat der Venen- und (Esophaguspulsbilder mit den Vprkammerdruckkurven, Zentralbl.
f. Physiol., I^ipz. u. Wien, 1908, xxii, 297.
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 61
Morrow, W. S.: Various Forms of the Negative or Physiological Venous Pulse, Brit. M.
Jour., Lond., 1906, ii, 1807. The Venous Pulse, ibid., 1907, i, 777.
Knoll, P.: Beitrage zur Lehre von der Blutbewegung in den Venen, Arch. f. d. ges. Physiol.,
Bonn, 1898, Ixxii, 317, 621.
Theopold, P.: Ein Beitrag zur Lehre von der Arhythmia perpetua, Deutsch. Arch. f.
klin. Med., Leipz., 1905, Ixxxii, 495.
Marey, E. J.: La physiologic du sang a l'£tat physiologique et dans les maladies, Paris, 1881.
Fredericq, L., 1. c.
Porter, W. T.: Researches on the Filling of the Heart, Jour. Physiol., Cam., 1892, xiii, 513.
Bard, L.: Des divers details du pouls veineux les jugulaires chez Thomme, J. de Physiol.
et de Path, gen., Par., 1906, viii, 454.
Hirschfelder, A. D.: Some Variations in the Form of the Venous Pulse, Bull. Johns Hop-
kins Hosp., Bait., 1907) xviii, 265.
Cushny, A. R., and Grosh, L. C.: The Venous Pulse, Jour. Am. M. Ass., Chicago, 1907,
xlix, 1254.
Mackenzie, J.: The Venous Pulse, Brit. M. J., Lond., 1907, i, 112.
Sewall, H., and Hirschfelder, A. D.: Unpublished investigations.
Peabody, F. W.: Personal communication.
Sewall, H.: Safeguards of the Heart-beat, Am. J. M. Sci., Phila. and N. York, 1908,
cxxxvi, 32.
Hering, H. E.: Die Verzeichnung des Venepulses am isolierten Kiinatlich durchstromten
Saugetierherzin, Arch. f. d. ges. Physiol., Bonn, 1904, cvi, 1.
Chauveau and Marey: Quoted from Marey, La Circulation du Sang, etc.
Gibson, A. G.: On a Hitherto Undescribed Wave in the Venous Pulse, Lancet, Lond., 1907,
ii, 1380.
Mackenzie, J.: The Interpretation of the Pulsations in the Jugular Veins, Am. Jour. M.
Sc., Phila. and N. York, 1907, n. s. cxxxiv, 12.
Rihl, J.: Ueber den Venenpuls nach experimenteller Lasion der Trikuspidalklappe, Ver-
handl. d. Kong. f. innere Med., Wiesbaden, 1907, xxiv, 453.
Gibson, G. A.: Certain Clinical Features of Cardiac Disease, Johns Hopkins Hosp. Bull.,
Bait., 1908, xix^361.
Eyster, J. A. E.: Unpublished observations.
Hirschfelder, A. D.: Inspection of the Jugular Vein; Its Value and Its Limitations in
Functional Diagnosis, J. Am. M. Assoc., Chicago, 1907, xlviii, 1105.
V. Frey, M., and Krehl, L.: Untersuchungen ueber den Puls, Arch. f. Physiol., Leipz.,
1890, 31.
Hewlett, A. W.: On the Interpretation of the Positive Venous Pulse, Jour. Med. Re-
search, Bost., 1907, xvii, 19.
Minkowski, O.: Die Registrierung der Herzbewegungen am linken Vorhof, Deutsch. med.
Wochnschr., 1906, xxxii, 1248. Zur Deutung von Herzarrhythmien mittelst des
oesophagealen Kardiograms, Ztschr. f. klin. Med., Berl., 1907, Ixii, 371.
Rautenberg, E.: Neue Methode der Registrierung der Vorhofspulsation vom Oesophagus
aus, Deutsche med. Wchnschr., Leipz. and Berl., 1907, xxxiii, 364.
Young, C. L, and Hewlett, A. W.: The Normal Pulsations within the (Esophagus, J. M.
Research., Bost., 1907, xvi, 427.
Hirschfelder, A. D.: Observations on a Case of Palpitation of the Heart, Johns Hopkins
Hosp. Bull., Baltimore, 1906, xvii, 299.
Einthoven, W.: Le te"16cardiogramme, Arch, internal, de Physiol., Liege, 1906, iv, 132.
Weiteres ueber das Elektrokardiogramm, Arch. f. d. ges. Physiol., Bonn, 1908, cxxii,
517. (See also chapter on Alterations of Rhythm.)
ANALYSIS OF ALTERATIONS IN CARDIAC RHYTHM.
The irregularities ' in rhythm of the heart may be divided first into
three classes: (1) arrhythmias, in which there is no discernible order
in the occurrence of beats ; (2) allorrhythmias (altered rhythms) , in
which, though the rhythm is not regular, yet the irregular beats occur
according to a certain regular system, so that the arrangement of these
62 DISEASES OF THE HEART AND AORTA.
beats in one section of the tracing can be prophesied from a knowledge of
another ; and (3) pararrhythmias ( Wenckebach) , in which two separate
rhythms are going on in either the same chamber or in different chambers
at the same time.
ALLORRHYTHMIAS.
A. Of extracardiac origin.
I. Neurogenic, due to more or less rhythmic reflex stimuli pass-
ing through the vagi and accelerators (toxic, reflex from various
organs, respiratory reflexes from lungs).
a. Associated with the phases of respiration.
b. Not associated with respiration — Mackenzie's youthful type.
II. Due to disturbances in the filling and emptying
of the heart from traction upon the heart and
great vessel s — dropping of beats without heart-block, pul-
sus paradoxus and Riegel's pulse.
B. Of intracardiac origin.
I. Due to disturbance in the conduction of normal
impulse s — dropping of beats.
1. Auriculo- (atrio-) ventricular block.
2. Sino-auricular block.
3. Interventricular (?) block (hemi systole).
II. Disturbance of contractility — pulsus alternans, and
failure to open the aortic valves.
III. Occurrence of beats in response to abnormal
stimuli or increased irritability.
1. Extrasystoles. in which irregular beat is brought on by a single abnormal
stimulus.
a. Ventricular.
b. Auricular.
c. Auriculo- (atrio-) ventricular.
2. Permanently irregular heart.
3. Paroxysmal tachycardia (auricular fibrillation).
I. NEUROGENIC ALLORRHYTHMIAS.
Alteration in cardiac rhythm resulting from intermittent stimuli
passing down the cardiac nerves constitutes one of the most common forms
of cardiac allorrhythmias. As has been seen (Chapter III.), altera-
tions of the pulse-rate may result from any stimu-
lation of any afferent nerve, from skin, muscles, mucous
membrane, and viscera, or from stimuli arising in the vagal or accelerator
centres in the medulla.
As Reid Hunt and Hooker have shown, the reflex stimulation may cause a slowing
of the pulse-rate through stimulation of the vagus centre, or, under other circumstance-
and especially when of a different intensity, it may cause an acceleration of the pulses
Hunt has shown that this acceleration is due chiefly to momentary cessation. of the
tonic stimuli in the vagus; but Hooker proves that there is also a stimulation of the
accelerators. Such afferent or sensory stimuli may arise in the skin and muscles but
especially m die viscera and the serous and mucous membranes.
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 63
RESPIRATORY
ALLORRHYTHMIA
AURICULO-
VENTRICULAR
HEART-BLOCK
ALTERNATING
PULSE
AURICULAR
KXTR ASYSTOLE
VENTRICULAR
EXTRA8Y8TOLE
AURICULO-
VENTRICULAR
EXTRAS Y8TOLE
PERPETUAL
ARRHYTHMIA
PAROXYSMAL
TACHYCARDIA
FIG. 60. — Diagram representing various types of irregular pulse. The heavy white arrows indi-
cate the site of origin of the disturbance of rhythm. The heavy white lines indicate the course of the
abnormal cardiac impulses. RESP, respiration; AUR, auricle; A-V or AVB auriculoventricular bun-
dle; VENT, ventricle; CAR, carotid pulse; VEN, venous pulse; SIN, sinus region of the heart; SVC,
JVC, superior and inferior vense cavse, respectively.
Reflex Allorrhythmias. — Franc,ois-Franck and Koblanck and Roeder
have been able to produce such an arrhythmia by stimulating the mucous
membrane of the nasal septum at a point just opposite the middle turbinate
bone, and Stadler and Hirsch have done so by stimulating the walls of
the stomach and intestines. There is normally a reflex slowing of the heart
64 DISEASES OF THE HEART AND AORTA.
during swallowing, and similar periodic slowing of the rate from stimulations
of the vagus may account for many of the disturbances of rhythm in air-
swallowers. Moreover, Einthoven has shown, by recording the electrical
variations in the peripheral stump of the divided vagus, that, with each
inspiration, afferent stimuli are passing up the vagus, and these may evoke
reflex responses when the entire nervous system is abnormally sensitive.
Occurrence. — Neurogenic arrhythmias are particularly common in
children and in young persons, and hence are designated by Mackenzie
as the "youthful type/' but this is only because the cardiac, vaso-
motor, and respiratory centres are in more labile equilibrium in them than
in normal adults. However, whenever the nervous system becomes more
irritable, — from the occurrence of visceral reflexes, emotions, or toxic
influences (bacterial toxins, alcohol, tobacco, coffee, etc.), — stimuli (like
those passing up the vagus) which are normally subminimal become
effective. Hence allorrhythmias of this type arise in nervous individuals
and in the so-called functional cardiac diseases or cardiac neuroses (Part IV,
Chapter III). Since the afferent stimuli in the vagus are continually act-
ing, it is quite natural that they should add themselves to any other afferent
RESPIRATION
RADIAL
FIG. 61. — Respiratory arrhythmia. (After Hewlett.)
stimuli which may also be acting, and that the alterations of rhythm will
then be associated with respiration; and, since the nature of reflex
responses varies with slight variations in the intensity of the stimulus,
it is not surprising that there is in some cases a series of slow beats
associated with inspiration and a series of rapid beats in expiration (Fig.
54), while in others the slowing occurs during expiration and the rapid
beats are during inspiration. This latter type is often spoken of as normal,
but in perfectly normal individuals the rate may be absolutely regular.
Reissner has shown that the irregularity is sometimes of psychic
origin; or, in other words, that the stimulus exciting the cardiac nerves
may descend from the cerebral cortex instead of ascending by the usual
paths of afferent stimuli. This psychogenic arrhythmia is not extremely
uncommon. Indeed, the writer, whose pulse has been regular at all other
times, experienced such an irregularity upon one occasion of intense anxiety
lasting for several minutes. The pulse became regular as soon as the
anxiety passed off; and has remained so for five years, in spite of a severe
tonsillitis and tonsillectomy.
As Reyfisch has shown, similar neurogenic allorrhythmias occur in
meningitis and in conditions with increased intracranial ten-
sion and, as Eyster has shown, in association with Cheyne-Stokes breath-
ing. Mackenzie has also shown that there are many other cases in which
neurogenic irregularity is not associated with the phases of respiration. In
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 65
these it may be either periodic or entirely intermittent. It is most important
that the exact mode of origin of such stimuli and its characteristics should
be carefully studied, since this arrhythmia must be differenti-
ated from those of myocardial origin. In these cases, though
the relation of the allorrhythmia to respiration may be timed by palpation
and inspection, a careful venous tracing should be made lest an extra-
systolic irregularity be diagnosed when it does not actually exist.
Characteristics of Reflex Allorrhythmias. — The striking feature of
these neurogenic disturbances of rhythm is that they are often charac-
terized by instability of rhythm, by the occurrence of rhythmic
changes in rate rather than by the interpolation of beats which differ from
the others in character. The beats usually occur in short groups, the first
beat of the slower group being the longest, the rate of the more rapid series
showing a progressive increase. The last beat of the rapid series, with
the vagal pause following it, may be mistaken for an extrasystole; but, on
examining the few beats preceding, it will be seen that this beat was not
premature and not due to an abnormal stimulus. Moreover, the beats
are usually of full and almost equal strength, thereby differing from
the feeble beats of extrasystoles; and they do not occur, as do the latter,
abnormally early in the cardiac cycle. It is an irregularity in rhythm rather
than an irregularity in force, though a certain degree of the latter may be
present through the action of the vagus on the heart.
The rhythm usually becomes regular within half an hour after the
hypodermic administration of atropine, .0005 to .001 Gm. (T^ to ^ gr.).
This rule is not invariable.
When long pauses alternate with short series of rapid beats, the force
of the first large beat may be slightly below that of the smaller beats, as
shown by tracings with the Erlanger apparatus at or near the maximal
pressure. With extrasystoles the systolic pressure of the smaller beats is
usually less than that of the regular (large) beat. In both cases, however,
this depends upon too many factors (time at which the extrasystole occurs,
amount of systolic output, amount of peripheral resistance, factors causing
the extrasystole, etc.) to be regarded as absolute criterion for diagnosis.
II. Respiratory (Pulsus paradoxus and Riegel's Pulse). — As will be
seen in the chapters on adherent pericardium (page 506) and enterop-
tosis, traction upon the aorta during respiration may prevent the heart
from emptying itself and thus cause the dropping of a beat in the arteries.
Or, on the other hand, traction upon the great veins may produce the same
effect by preventing the heart from filling. When there are adhesions in
the posterior mediastinum or when the diaphragm is low, this dropping
occurs during inspiration (pulsus paradoxus, Kussmaul), whereas when
there are adhesions between the heart and the anterior chest wall it may
occur in expiration (Riegel).
ALLORRHYTHMIAS HAVING THEIR ORIGIN' WITHIN THE HEART.
III. Allorrhythmias due to Failure to Conduct Impulses generated
Normally — Heart-block.1 — Of this there are several types. (1) Auriculo-
1 A full disetission may be found in Part III, Chapter XI.
66
DISEASES OF. THE HEART AND AORTA.
ventricular Heart-block. — The more usual, or at least better known,
type of blocking the impulses is at the auriculo ventricular junction. In
this type no change occurs in the origination of the cardiac impulse or in
the contraction of the auricles (atria), but the conductivity of the impulse
to the ventricle by the bundle of His is impaired. Such impairment may be
(a) functional, from overstimulation of the vagus, of which frequent
A SEC.
JUG.
APEX
BRACK.
FIG. 62. — Venous tracings in heart-block. Partial heart-block (3 : 1 rhythm) during pressure on the
vagus, in a case of Adams-Stokes disease.
examples are seen in every laboratory experiment. Clinically this may be
seen also in the cases of digitalis poisoning and postfebrile bradycardia,
especially after pneumonia and influenza, occasionally also in cases in which
there is a tumor pressing upon the vagus. (6) Organic, from interrup-
tion of the bundle of His. In this case the block may be increased by giving
atropine or anything else that quickens the heart, or it may not be affected.
FIG. 63. — Venous tracings in heart-block. Complete heart-block in a case of Adams-Stokes disease.
(c) There may be a combination of the two effects (v. Tabora,
Gibson, Thayer) , the conductivity of the injured Purkinje fibres of the bundle
being still further diminished by the action of the vagus upon them, and
this effect outweighing the favorable action in slowing the auricular rhythm.
The block may be partial or complete, depending upon whether
the ventricles still follow the lead of the auricles or initiate their own rhythm.
Thus, in the partial block the ventricles may respond to only every second,
third, or fourth, or even only every sixteenth contraction, or may sometimes
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 67
respond to every second, sometimes to every fourth beat, etc. On the other
hand, they may fail to contract at all over a considerable period (stoppage)
during which syncope (Adams-Stokes syndrome), epileptiform seizures,
or death may set in (Erlanger), or, after a stoppage of greater or less dura-
tion, they may begin to beat at a rhythm of their own, bearing no relation
at all to the rhythm of the auricles (complete block). This constitutes the
permanent bradycardia of Adams-Stokes disease.
(2) Sino-auricular Block. — Sino-auricular block may also occur, the
cardiac impulse being generated as usual at the mouths of the great veins
and coronary sinus in the region homologous with the sinus vcnosus of the
frog, but may fail to be communicated to the auricles.
Keith and Schonberg have shown that this could scarcely be the result of a localized
lesion, and would therefore depend upon the difference in the properties and irritability
of auricular and venous musculature rather than organic block. The presence of such
blocks is assumed by August Hoffmann in paroxysmal tachycardia, in which there is
a sudden doubling or even quadrupling of the pulse-rate during the attacks, and by
Hewlett in digitalis poisoning. Experimentally they have been produced by Erlanger
and Blackman on the excised mammalian heart, but both Hirschfelder and Eyster and
the former observers failed to do so in the heart in situ. Gibson assumes the existence of
a similar block in a case of Adams-Stokes disease, which he cites, along with the block
at the auriculoventricular junction.
APEX
FIG. 64. — Occasional absence of apex impulse during inspiration simulating interventricular heart-block.
(3) Interventricular Block (Hemisystole). — v. Leyden in 1868 reported
a case of bigeminal pulse in which he assumed that one ventricle was con-
tracting without the other.
This case and other cases reported by the older writers, and which were undoubtedly
due to extrasystoles, are really not conclusive; but recently cases have been reported by
Kraus and Nikolai, and by Hewlett and Schmoll, in which the electrocardiogram and
venous tracings have furnished some evidence that the right ventricle and the left ven-
tricle may have been contracting alternately and not synchronously. For the present,
one is justified in an attitude of moderate scepticism upon this point until absolute proof
has been brought. Professor Barker, Dr. Bond, and the writer have repeatedly cut through
the left branch of the His bundle without injuring the right branch. No asynchronism
of the ventricles occurred. Extrasystoles produced in either ventricle were conducted
to the other without delay. It does not, therefore, seem probable that a patch of endo-
carditis or myocarditis, such as Aschoff and Tawara occasionally found invading a single
branch of the His bundle, would be able to block the impulse to one ventricle and thereby
prevent its contraction. Moreover, it is possible that, like v. Leyden's, Hewlett's tracings
may permit of a different and more conventional explanation.
IV. Diminution in Contractile Power— Pulsus alternans.— When the
contractile power of the heart diminishes, or, more frequently, when the
rate is increased to the point that the heart has some difficulty in carry-
ing out effectual contractions, it is found that the alternate contractions
68 DISEASES OF THE HEART AND AORTA.
are of different size, some larger, some smaller, giving rise to the condition
known as pulsus alternans or alternating pulse. This is especially common
in the tachycardias associated with some weakness of the heart muscle,
FIG. 65. — Alternating pulse in a case of paroxysmal tachycardia.
and especially with paroxysmal tachycardia; but wherever it occurs it is an
expression of disproportion between the rate and contractility of the heart
(or, in Engelmann's terminology, between the chrono tropic and ino-
tropic influences).
Experimentally this can be readily shown by throwing induction shocks into the
heart at a rate which it can barely follow. A pulsus alternans invariably results (Hirsch-
f elder, Hering). After a few seconds or minutes the heart has gained its full contractility
and the alternating character disappears, only to reappear when it begins to weaken.
The same phenomenon is also seen in attacks of paroxysmal tachycardia (Fig. 65). Pul-
sus alternans is also present in some cases of angina pectoris (Mackenzie). It then indi-
cates that the heart is in a weakened condition.
V. Dropping of Beat owing to too low Contractility. — If the auricle be stimulated
directly at a rate still more rapid, it can no longer follow every single stimulus, but occa-
sionally one beat is dropped out, just as is the case in a partial heart-block, although the
stimulus is being applied directly to the auricle,
which intermits a little more rapidly, and it fol-
lows only alternate stimuli. If the irritability of
the auricle be now suddenly increased, as by
pouring warm salt solution over it, it will sud-
denly respond with a contraction to each instead
of to alternate stimuli, or it may respond occa-
sionally to all and occasionally to only alternate
stimuli, giving an allorrhythmia 1:1 + 2:1.
Thus we may have allorrhythmias simulating
partial heart-blocks on the one hand, and extra-
systoles on the other, due merely to general
decrease in the irritability of the entire mus-
culature without any special disturbance in
conductivity; and just such inotrophic and
bathmotrophic variations may be responsible
for many of the so-called veno-auricular heart-
blocks, such as have been described by Hewlett
and Wenckebach.
EXTR ASYSTOLES.
Irregularities may be due to the
FIG. 66.-ResPonse of frog's ventricle to origination of abnormal cardiac im-
abnormal stimuli. (After Marey.) Electric pulses Or to abnormal response to
shock thrown into it at the instant marked by ,• r / j. i \ rrit, • i
the nick in the base line and by the dotted line. Stimuli (extrasystoles) . I he Simplest
form of this is seen in the occurrence
of single abnormal beats. Experimentally it has been shown (Marey)
that when a single electrical or mechanical stimulus is applied to the
heart at any time except the refractory period, the latter responds
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 69
almost immediately with a contraction (extrasystole, Engelmann;
premature systole, Mackenzie, Cushny, and Matthews).
Ventricular Extrasystoles. — If the extra stimulus be applied to the
ventricle, the latter responds with a premature contraction, then usually
but not always misses the next impulse from the auricle and pauses for a
C .. Q,C .. QiC
FIG. 67. — Tracing from the jugular vein (V. J. D.) and brachial art«ry (A. B. R.) in man, showing
ventricular extrasystoles. Time markings in J seconds. E, extrasystoles arising in the ventricle (not pre-
ceded by an a wave). Time of the bigeminus (regular systole 4- extrasystole + pause) 3-°"*"5-4 = 2X4.2
5 5
while, until the second impulse from the auricle reaches it. We have, there-
fore, a normal contraction, a premature contraction, and the subsequent
pause (which together may be termed a bigeminus), lasting as long as
two regular contractions. The bigeminus may be spoken of as a "full
bigeminus" when it lasts through two full cardiac
cycles, and a "shortened bigeminus" when the duration
of regular s ystole + ex trasy stole + subsequent pause
is less than two cardiac cycles.
Auricular Extrasystoles. — When, however, the extra stimulus is applied
to the great veins or the auricle, the bigeminus lasts less than two cardiac
cycles if the stimulus follows closely upon the regular contraction, and
exactly equal to two cycles if it is applied late (Hirschfelder and Eyster).
If the stimulus is applied early, the auriculoventricular (atrioventricular)
conduction time (a-c) interval is slowed. Later in the cycle it is unchanged.
JUG.
BRACK.
FIG. 68. — Tracings from the jugular vein and brachial artery of a patient with trigeminal pulse due
to the regular occurrence of two auricular extrasystoles (E, E) after each regular systole. The a wave
and general form of the venous pulse are the same for the regular and the auricular extrasystoles.
The two forms of extrasystoles occur clinically and may be differ-
entiated by the analysis' of the venous pulse; the extrasystoles of auricular
(atrial) origin often give rise to shortened bigemini, while ven-
tricular extrasystoles always cause full bigemini. In the
tracings of auricular extrasystoles one can see the auricular wave before
the ventricular even in the extrasystole; the ventricular showing a single
large wave due to ventricular systole, sometimes with the notch due to
the contraction of the auricle from reversed conduction of the impulse.
70
DISEASES OF THE HEART AND AORTA.
i n -
Occasionally ventricular extrasystoles can be dist
guished on inspection by the large flapping "single"
pulsation in the jugular vein which accompanies them, in
contrast to the double venous pulse of the
normal beats and the auricular extra-
systoles (Hirschf elder) .
RIGHT
LEFT
A further advance in the clinical study of
extrasystoles is due to the clinical use of the elec-
trocardiogram by Einthoven and his pupils, and more
recently by Kraus and Nikolai, Hering, and Lewis.
Einthoven called attention to the presence of
certain very peculiarly formed electrocardiograms
obtained from irregularly acting hearts. Kraus and
Nikolai were able to reproduce these abnormal waves
by producing extrasystoles in dogs; and found that
extrasystoles arising in the right and left ventri-
cles respectively produced curves which were the inverse of one another (Fig. 69):
Kahn in Bering's laboratory has been able to confirm these findings in great part.
However, he calls attention to the fact that they do not hold absolutely, and shows that
stimuli applied to neighboring points in right and left ventricles, near the apex, may elicit
electrocardiograms which differ only slightly from one another.
FIG. 69. — Diagrammatic reproduction
of the electrocardiogram obtained in the
dog as the result of extrasystoles arising
in the right and left ventricles. (After
Kraus and Nikolai.)
FIG. 70. — Electrocardiogram of a patient with mitral stenosis, showing extrasystoles, which
arise in the right side of the heart. Taken by the writer in collaboration with Prof. L. F. Barker and
Dr. G. S. Bond. Current led off from the right hand and left foot. Lettering of curves as in Fig. £9.
P R T represent normal waves; EXTRASYS, extrasystoles.
Stimuli which Cause Extrasystoles. — The question as to the nature of
the stimulus which gives rise to extrasystoles in man is of the greatest
practical importance, for many writers (especially Fr. Muller) are of the
belief that they never occur unless the heart muscle is diseased. On the
other hand, Mackenzie, whose observations have been extended over a
period of fifteen years, regards them as of no special significance either in
prognosis or in influencing the patient's manner of life. He mentions hav-
ing advised one of his patients to continue playing football in spite of his
extrasystoles, and adds that the extrasystoles disappeared!
Experimentally it has been shown by Knoll, Marey, Hering, and others that ventric-
ular extrasystoles may be produced whenever either the left ventricle or the right is pre-
vented from emptying itself (i.e., by clamping the aorta or the pulmonary artery). In
man they are also most common in conditions in which there is a high blood-pressure and
the heart is just beginning to fail (chronic nephritis, myocarditis, aortic insufficiency),
and probably fails to discharge a sufficient amount of its contents. This probably acts as
a stimulus for a second extrasystole, as is frequently seen (pulsus trigeminus). Ventricular
extrasystoles are most common in hearts whose rate is slow and hence which discharge
a large amount of blood. They are particularly common at the end of the first third of
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 71
diastole when the filling of the ventricle is nearing completion. The ventricular fibres are
stretched more or less by the influx, and in conditions of increased irritability the stretch-
ing of the fibres may act as a stimulus and give rise to the extrasystoles.
Similar conditions are observed with reference to the auricle. Dr. Cameron, in the
writer's laboratory, observed an instance of permanent bigeminal pulse in a dog due to
the presence of a bubble of air in the right auricle. The air had entered
VOLUME OF
VENTRICLES
BLOOD- PRESSURE
SECONDS
FIG. 71. — Volume curve of the ventricles, showing the dilatation which followed the entrance
of an air-bubble into the right auricle. (Kindness of Dr. Cameron.) The extrasystoles drive very little
blood into the aorta. DIL, dilatation.
from a hypodermic syringe during an intravenous injection. When the bubble was mas-
saged out of the auricle the bigeminal pulse disappeared. It seems not improbable that
mural thrombi may play a similar role, though it is certain that this is not always the case.
Auricular extrasystoles may also be produced experimentally by causing a steno-
sis at the auriculoventricular orifices (Hirschfelder). Clinically they occur quite com-
monly in mitral disease and most frequently begin at the time of the v wave, the very
instant in the cycle at which the auricle is most distended (Fig. 68). Nevertheless, it must
be confessed that much remains to be learned regarding the nature of the stimulus or
stimuli, and the actual functional significance of extrasystoles.
Palpitation with Extrasystoles. — Extrasystoles are very frequently
associated clinically with cardiac hypersesthesia in the form of palpitation,
so that many clinicians erroneously regard all irregularities with palpita-
tion as extrasystolic. However, it is possible that this hypersensibility
about the heart may have some causal relation, since Hornung has shown
that extrasystoles in the dog are most readily produced by stimulating in
the vicinity of the cardiac nerves — auriculo(atrio)ventricular and inter-
ventricular grooves — and that they cannot be produced after cocainizing
the epicardium. True extrasystoles cannot be produced experimentally by
stimulation of nerves (Hoffmann, Hering), and though it is occasionally
claimed that they occur in gastro-intestinal diseases the exact relation is
not clear. It is certain that they are often brought on by constipation
and flatulence in certain persons, but whether there is a myocardial lesion
already present in these cases is a still open question.
Diagnosis of Extrasystoles. — In some cases it is very difficult to dis-
tinguish between the neurogenic irregularities and the auricular extra-
systoles. Dehio has called attention to the fact that the former disappear
under the administration of atropine, while the latter remain unaltered.
Nevertheless one cannot always be certain that the dose of atropine, even
if it has given rise to symptoms, has been large enough to produce the effect.
72 DISEASES OF THE HEART AND AORTA.
An example of this type was present in a patient seen by the writer several years
ago, in whom palpitation and arrhythmia had been present for several years, the patient
being conscious not only of the occcurrene but also of the size of every beat, and noticing
especially a group of one large beat with two small ones followed by a pause (pulsus trigem-
inus). The tracing made while the patient was in the hospital showed that these were
due to a single beat followed by two smaller and earlier ones and then by a pause, all the
beats being preceded by an auricular contraction (a wave). This irregularity was much
more marked whenever the patient was constipated, but it also persisted after 0.5 mg.
(T^ gr ) atropine, which gave the patient marked symptoms but caused no change
inVate. In such a case it is very difficult to state whether we have to deal with auricular
extrasystoles or with a very rapid pulse interrupted by variations in diastole (youthful
type). The ineffectiveness of atropine and the extreme irregularity are against the latter
view. However, the diagnosis of extrasystoles can usually be made by means of the
electrocardiogram .
In the routine physical examination extrasystoles may often be diag-
nosed on auscultation by the abrupt change from a rhythm 1-2 — 1-2
- 1 - 2, etc., to 1-2-3-4- -1-2, etc. Accompanying this there may
be seen an early wave in the jugular pulse. In the case of auricular extra-
systoles the pulsation does not differ from the double pulse of the regular
beat, but with ventricular extrasystoles there is a single wave, large,
conspicuous, and flapping.
Ineffectual Contractions. — When the extrasystole occurs early in dia-
stole, the heart may not have recovered from the effect of the last systole
sufficiently to generate a forcible contraction. The aortic valves are not
opened. The aortic second of the extrasystole disappears and the sounds
change from 1-2-3-4- -1-2, etc., to 1 - 2 - 3 - - 1 - 2 , etc.
By beating time to the regular beats it is sometimes possible to note that
the total rhythm is unchanged by occasional ventricular extrasystoles.
Such extrasystoles correspond to impulses on the apex and jugular tracings
but not on the carotid.
The variations in the force of the extrasystoles or in the beats of the
absolutely irregular pulse are great. Occasionally, especially when the
extrasystoles occur early in the cardiac cycle and there is a high peripheral
resistance, the intracardiac pressure may not reach the aortic pressure and
the aortic valves are not opened. The systole has been ineffectual (Frus-
trane contractionen, Hochaus and Quincke). The compensatory pause
after these may be so long and the circulation may be so poor that actual
syncope simulating the Adams-Stokes syndrome (W. B. James) may take
place in the interval between the regular beats. On the other hand, a
great deal of cardiac energy has been expended without opening the cardiac
valves and without propelling any blood. This increases the cardiac fatigue.
Bigeminal and Trigeminal Pulses due to Extrasystoles. — Very common
forms of extrasystolic irregularity are those in which the extrasystoles
recur after each regular beat; thus we may find every beat followed by a
single extrasystole and compensatory pause, so that the pulse beats occur
in pairs separated by pauses (pulsus bigeminus), or there may be two
extrasystoles following regularly after each regular systole (pulsus trigem-
inus), as in Fig. 68. These may be of either the auricular or the ventricular
type, dependent upon the site of the origin of the irregularity or of the
so-called auriculo(atrio) ventricular type referred to below. As stated
above, it is sometimes difficult to differentiate the auricular extrasystolic
THE VENOUS PULSE AND ELECTROCARDIOGRAM.
73
groups from the youthful type of arrhythmia, but this may usually be
accomplished by the use of a sufficiently large dose of atropine.
As Hering has shown, ventricular extrasystoles frequently disappear
under atropine or any other influence by which the pulse-rate is accelerated,
E E E
FIG. 72. — Extrasystoles with shortened conduction time, supposed to arise in the auriculoventricu-
lar bundle.
so that the normal stimuli fall in at about the periods at which the abnormal
stimuli would have fallen. The form of the venous pulse in ventricular
extrasystoles is, however, characteristic.
VJO * c
FIG. 73. — Variations in conduction time (a-c) in a case of mitral stenosis.
Auriculo(Atrio) ventricular Extrasystoles. — It is also claimed by Her-
ing and Rihl, Mackenzie and Wenckebach, Lohmann, Schmoll, Mackenzie
and Morrow, and others that extrasystoles may arise in the Purkinje cells
of the conduction system, and that such extrasystoles are
characterized by a shortening in the conduction time
(a-c interval on the venous pulse). Extrasystoles with shortened conduc-
tion time are not extremely rare, and it is possible that this explanation
may be correct, but it is not founded upon any direct experimental proof.
Hering, who originated the doctrine, observed such extrasystoles occurring spon-
taneously in apes, but did not clear it up by any experiments. Gaskell has shown in frogs
that if the tissue at the auriculoventricular junction was touched with a probe a series of
extrasystoles set in in both auricles and ventricle. Lohmann also observed them per-
sisting after the tissue in the vicinity of the His bundle had been stimulated. In a later
investigation upon the excised heart Lohmann poisoned the region of the vena? cava; by
means of cotton soaked in formalin. He then sometimes saw extrasystoles set in spon-
taneously. The auricles and ventricles sometimes contracted simultaneously, some-
times there were ventricular extrasystoles.
Hirschfelder has repeatedly produced extrasystoles with shortened conduction time
by faradic stimulation of the auricular appendix. The appearance of such extrasystoles
after faradization, in excitable hearts, in the intervals between paroxysms of tachycardia
in man, etc., seems to correspond with a state of greatly heightened excitability. Whether
the actual stimuli arise in the cells of the sinus region or in those of the conduction system
is still uncertain. It is not improbable that there may be an increased irritability of all
the primitive cardiac tissue (sinus and conduction system), and that in the sinus this mani-
fests itself by the generation of abnormal stimuli, while in the conduction system it is
shown by increased speed of conduction.
Upon the clinical side there is little positive evidence. Peculiar extra-
systoles often occur between attacks of paroxysmal tachycardia, but occa-
sionally also in cases with simple valvular lesions. Keith has found patches
74
DISEASES OF THE HEART AND AORTA.
of fibrous myocarditis in the vicinity of the His bundle in cases which had
shown these extrasystoles, and thinks that they irritated the cells in the
vicinity, but such scars are very common, and elsewhere in the heart are
not known to act as irritative lesions. Moreover, the writer has never been
A SEC.
JUG.
APEX
BRACK.
FIG. 74.— Tracing showing absolute irregular with weak ineffectual systoles (7, 7, 7) which do not
open the aortic valves. S, onset of ventricular systole. Numerals refer to duration of cardiac cycle in
tenths of a second. The venous pulse is of the ventricular type.
able to produce them by pressure upon the bundle with an Erlanger clamp,
injection of mercury into the left branch of the bundle, etc. So that in
spite of the interest in the subject it must be admitted that the occur-
rence of extrasystoles with shortened conduction time cannot be as yet
regarded as absolute proof of a lesion near the His bundle.
CAR.
VES.
AES.
A-VES.
jv* v<*lc v
A-V BLOCK
SINO- AURICULAR BLOCK
VAGAL SLOWING
FIG. 75— Diagram showing the alterations of rhythm which may cause a pulsus bigeminus. The arrows
indicate the incidence of stimuli ori.
Various Types of Allorrhythmia which may Result in a Bigeminal Pulse.
—It must be borne in mind that the bigeminal pulse is not pathognomonic
f any single disturbance of function, but may occur in any of the following
conditions (Fig. 75): (1) recurring ventricular extrasystoles; (2) recurring
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 75
auricular extrasystoles; (3) recurring auriculoventricular extrasystoles; (4)
recurring slight auriculoventricular heart-block, the ventricle failing to follow
every third beat; (5) recurring sino-auricular block (?), the auricles failing to
respond to every third impulse; (6) recurring vagal prolongation of every
alternate diastole. Similar conditions hold for the trigeminal pulse except
that two extrasystoles or regular beats are interpolated before the pause.
It is evident that these conditions must be carefully differentiated
from one another by means of the venous tracing or electrocardiogram and
atropine tests before attempts to remedy them should be begun.
PARARRHYTHMIAS.
In some of the allorrhythmias separate rhythms may be noticed in the
different chambers, either conducted to one another and interfering peri-
odically, or not conducted (heart-block). Wenckebach, who first called
attention to this, has proposed the name pararrhythmia for these
forms. The simplest example of this would be the bigemini. Another
example would be seen if, without loss of conductivity, spontaneous con-
tractions would occur in the ventricles as the usual slow rate, and these
go on simultaneously with the regular beats following the auricles, though
with occasional pauses due to interference. Cushny has shown this to
occur in digitalis poisoning, and it is not improbable that it may explain
many otherwise undecipherable arrhythmias, though little work has been
done along these lines up to the present.
ABSOLUTE ARRHYTHMIA.
Next to the neurogenic allorrhythmias the most common form of irreg-
ular heart action is the permanent irregularity (disorderly rhythm, Macken-
zie; pulsus irregularis perpetuus, Hering; arrhythmia perpetua, Gerhardt).
CAR.
JUG.
Fio. 76. — Absolute permanent irregularity with a wave preserved in a case of mitral stenosis.
This represents, as Mackenzie has shown, the common type of chronic
arrhythmia seen in old cases of myocarditis and of valvular lesions. As the
result of chronic stasis there is a permanently high venous pressure which
brings about dilatation -and paralysis of the auricles. The a wave is absent
from the venous tracing (Mackenzie) (Fig. 76), from the oesophageal tracing
(Hewlett), and the corresponding wave has disappeared from the electro-
cardiogram (Hering) . There is probably a perpetual.or a transitory paralysis
of the auricles (atria). As Bering's electrocardiograms show, the arrhyth-
The term perpetual irregularity is inaccurate, since it is sometimes transitory.
76 DISEASES OF THE HEART AND AORTA.
mia is due partly to extrasystoles, which are shown by their characteristic
curves, and partly to periodic (respiratory) alterations in the regular beats.
The site at which the cardiac impulse originates in this irregularity
is a matter of some dispute. Mackenzie believes, without further proof,
that the site of automaticity is shifted from the sinus region of the auricle
(atrium) to the cells of the His bundle ("nodal rhythm"), but it has not
been shown that, just because the auricular contraction and the corre-
sponding negative wave are absent, the cardiac impulse is not arising in
the region of the sinus. According to Mackenzie, the auricle and ventricle
are beating simultaneously in such cases. Cushny (Heart, vol. i) has
shown that such simultaneous contractions actually occur in experimental
aconite poisoning. On the other hand, v. Frey has shown that ^the
auricles become paralyzed at about 20 mm. Hg pressure, and observations
by Dr. Hooker, as well as by Mr. C. C. Cody, indicate that in cases with
permanent arrhythmia the venous pressure often approaches this level.
FIG. 77. — Perpetually irregular pulse with absence of a wave.
Radasewsky, under Dehio's direction, was the first to call attention
to the occurrence of fibrous changes in the auricles under these conditions,
but the exact relations were shown by Schonberg, who studied careful
serial sections of the entire veno-auricular region in five cases that had
been studied clinically by Gerhardt during life. Schonberg confirms Rada-
sewsky and finds definite patches of infiltration about the veno-auricular
border. On the other hand, G. Miiller has reported a case in which the
entire musculature of the auricles had disappeared and the rhythm had
remained regular.
Clinically, one sometimes sees an acute onset of absolute arrhythmia
with paralysis of the auricles, especially in the acute heart failure of mitral
stenosis. This state may last only for a day or so and disappear under
treatment; on the other hand, it may last for weeks, perhaps for months,
and then disappear. The longer it persists the greater is the probability
of serious changes and the less that of recovery. On the other hand, the
presence of an absolute and apparently permanent arrhythmia with auricu-
lar paralysis is perfectly compatible with a fair degree of vigor.
This is shown by a medical student now under the writer's care, who has had an irreg-
ular pulse of this type for two years, during which only occasional auricular waves have
been obtainable upon his venous pulse, and these during his periods of greatest vigor. He
has had slight shortness of breath on exertion, but no enlargement of the heart, murmurs, or
other signs of organic heart disease. His arrhythmia did not disappear under .00075 Gm.
(sy gr-) atropine subcutaneously. The electrocardiogram does not reve'al any extrasystoles.
His trouble does not date from any acute infectious disease nor from any overstrain other
than the long hours of work in a hospital. The nature of the lesion and its significance
in cases like this are still mysterious, but it is possible that in such cases there may be a
patch of myocarditis in the sinus region of the auricle like those shown by Schonberg.
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 77
Permanent arrhythmia with persistence of the auricular contraction
(a wave upon the venous pulse) is met with occasionally in mitral disease,
especially in mitral stenosis; and represents one form of the so-called
.1 SEC.
JUGULAR
ELECTRO-
CARDIO-
GRAM
FIG. 78. — Electrocardiogram from a case of perpetual absolute arrhythmia, showing extrasystole.
(After Hering, Deutsch. Arch. f. klin. Med., xciv.) E, extrasystole; R, T, electrical waves. The P
(auricular) wave is absent.
" mitralized pulse." In such cases it may at first seem absolutely impos-
sible to analyze the arryhthmia, but from time to time definite groups
of systoles may be discerned. Sometimes these groups are produced by
the occurrence of varying numbers of auricular extrasystoles, sometimes
by the occurrence of a few beats in which there is doubling of the pulse-rate
and shortening of the conduction time, just as is seen in paroxysmal
tachycardia. Since Hering has demonstrated the extrasystolic origin
of the absolute arrhythmia with auricular paralysis (Mackenzie's "nodal
rhythm"); and since Hirschf elder has produced the latter in experimental
mitral stenosis by bringing about extreme stasis in the left auricle, it
seems not impossible that the question of auricular paralysis may be one
of the degree rather than of the character of the disturbance.
The prognostic importance of a permanent arrhythmia with auricular
paralysis depends, like all other cardiac conditions, chiefly upon its effect
upon cardiac function.
MECHANICAL EFFECT OF ARRHYTHMIA IX THE CIRCULATION.
The mechanical effect of any arrhythmia is to s 1 o w the circu-
lation, as may be easily seen from the volume curve of the heart during
a period of irregularity.
This slowing in itself tends
to bring on cyanosis, in-
crease the CO2 in the blood,
and, as Cameron has shown,
to diminish the tone of the
heart muscle in this way.
On the other hand, the long
pauses cause an increase of
pressure in the veins, and
the influx of venous blood under a relatively increased pressure acting
upon cardiac muscle, whose tone is diminished, tends to overdistend the
heart (as seen in Fig. 79). The overdistention, by increasing the diameter
VOLUME
CAROTID
PRESSURE
i SECONDS
FIG. 79. — Effect of arrhythmia on the circulation, blood-
pressure, and volume of the ventricles. Tracing from a dog's
heart stimulated irregularly with induction shocks. /, /, /,
ineffectual systoles; DIL, dilatation. Upstrokes on volume
curve represent outflow from the ventricles.
78 DISEASES OF THE HEART AND AORTA.
of the ventricular chamber, increases the hydrostatic pressure upon its
walls and causes it to work at a disadvantage. Thus is established the
vicious circle of the irregular heart:
Overfilling of heart
t 1
Slowing of circulation <- Irregularity
The effect is most marked in the auricles, where tone changes show themselves in more
marked degree than in the ventricles, and the diminution in their tonicity hastens their
paralysis. When the auricles are paralyzed, the genesis of efficient stimuli becomes more
difficult, it is harder to accelerate the pulse during excerise, etc., and consequently it
becomes easier for CO2 to accumulate in the blood in the irregular than in the regular heart,
and the heart in this condition is per se permanently weakened.
Effect of Digitalis in Absolute Arrhythmia. — The good effect of digi-
talis in this condition lies not in affecting the rhythmicity but particularly
in restoring tone and force of the heart-beat, thus re-
versing the vicious circle. The pulse becomes more regular, sometimes
entirely regular. When the rhythmicity is destroyed by permanent paraly-
sis of the auricles it never returns, but the general cardiac condition may
be benefited by increase in tone and strength. On the other hand, when
the muscle-fibres are in too bad condition, they are oversensitive to digitalis
and a small dose causes them to pass not into the first but into the second
or third stage of digitalis poisoning.
PAROXYSMAL TACHYCARDIA.
Another group of allorrhythmias which may be classed with the extra-
systoles is that in which there is more or less paroxysmal increase in pulse-
rate, frequently amounting to exact doubling of the rate,
suddenly taking place and suddenly subsiding.
This condition is seen in paroxysmal tachycardia (Hoffmann) and in paroxysmal
irregularity (Cushny and Edmunds), and in the latter condition has been shown to be
associated with fibrillation of the auricles. Experimentally it can be brought on by stimu-
lating the auricles with a strong faradic current, the auricles then going into very rapid
more or less fibrillary contractions, the ventricles following at a fairly regular
rate which is almost exactly double the previous rate, this rhythm persisting for several
minutes after the faradization has been stopped and then suddenly halving. During its
continuance it may or may not be stopped by maximal stimulation of the vagus, just as
is the case clinically in paroxysmal tachycardia, but seems to yield at once to strophan-
thus intravenously. The nature of this sudden doubling is peculiar. It also occurs in
the ventricle upon faradizing the ventricular muscle directly, and similar exact doubling
and exact halving of rate have been observed in the frog by Engelmann and in the
mammal by Trendelenberg. (See Part IV, Chapter I.)
BIBLIOGRAPHY.
For general discussions of alterations of cardiac rhythm the reader may consult:
Wenckebach, K. F.: Die Arhythmie als Ausdruck bestimmter Functionsstorungen des
Herzens, Leipz., 1903. Les irre'gularite's du cceur, Arch, des malad. du cosur., Par.,
1908, i, 65.
Mackenzie, J.: The Study of the Pulse and Movements of the Heart, Lond., 1903. New
Methods of Studying Affections of the Heart, Brit. M. J., Lond., 1905, i, 519, 587,
702, 759, 812. Diseases of the Heart, Lond., 1908.
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 79
Hirschfelder, A. D.: Graphic Methods in the Study of Cardiac Diseases, Am. Jour. M.
Sc., Phila., 1906, cxxxii, 378. Recent Studies upon the Circulation and their Im-
portance to the Practice of Medicine, Jour. Am. M. Assoc., Chicago, 1908, li, 473.
Hewlett, A. W.: Some Common Cardiac Arrhythmias, Internal. Clin., Phi.a., 1907, 17th
ser., iv, 47.
Gerhardt, D.: Die Unregelmassigkeiten des Herzschlages, Ergebn d. innere Med., Berl.,
1908, ii, 418.
Dock, Geo.: Recent Advances in the Study of Heart Disease, Wisconsin M. J., Aug., 1907.
Bard, L.: Des divers types d'arhythmie cardiaque observes en clinique, Sem. m6d., Par.,
1909.
Hoffmann, A.: Ueber die klinische Bedeutung der Herzarhythmie, Deutsch. med. Wchn-
schr., Leipz., 1906, xxxii, 1682. Neuere Fortschritte in der Diagnostik der Herz-
krankheiten, Deutsch. med. Wchnschr., Leipz., 1908, xxxiv, 13.
Hunt, R.: Direct and Reflex Acceleration of the Mammalian Heart, Am. J. Physiol.,
Bost., 1899, ii, 395.
Hooker, D. R.: May Reflex Cardiac Acceleration Occur Independently of the Cardio-
inhibitory Centre ? ibid., 1907, xix, 417.
Mackenzie, J.: The Study of the Pulse and Movements of the Heart, Lond., 1903.
Fran£ois-Franck, Ch. A.: Contribution a l'4tude experimentale des n6vroses reflexes
d'origine nasale, Arch, de physiol. de 1'homme, Par., 1889, 5 ser., i, 538. Contri-
bution a l'e"tude de 1'innervation vasodilatatrice de la muqueuse, ibid., 1889, i.
Koblanck and Roeder, H.: Experimentelle Untersuchungen zur reflektorischen Herz-
arhythmie, Arch. f. d. ges. Physiol., Bonn, 1908, cxxv, 377.
Stadler, E., and Hirsch, C.: Meteorismus und Kreislauf, Mitth. a. d. Grenzgeb. d. Med.
u. Chir., Jena, 1906, xv, 449.
Reyfisch: Klinische und experimentelle Erfahrungen ueber Reizungen des Herz vagus,
Berl. klin. Wchnschr., 1905, 1468.
Reissner, O.: Ueber unregelmassige Herztatigkeit auf psychischer Grundlage, Ztschr. f.
klin. Med., Berl., 1904, liii, 234.
Einthoven, W., Flohil, A., and Battaerd, P. J. T. A.: On Vagus Currents Examined with
the String Galvanometer, Quart. Jour. Exper. Physiol., Lond., 1908, i, 243.
Eyster, J. A. E.: Clinical and Experimental Observations upon Cheyne-Stokes Respira-
tion, Jour. Exper. M., New York and Lancaster, 1906, viii, 565.
Kussmaul, A.: Ueber schwielige Mediastino-pericarditis und paradoxen Puls, Berl. klin.
Wchnschr., 1873, x, 433, 445, 461.
Riegel, F.: Ueber extrapericardiale Verwachsungen, ibid., 1877, xiv, 657.
Keith, A., and Flack, and Schonberg: See Chapter I.
Hewlett, A. W.: Digitalis Heart-block, J. Am. M. Assoc., Chicago, 1907, xlviii, 47.
Erlanger, J., and Blackman, J. R.: A Study of the Relative Rhythmicity and Conduc-
tivity in Various Regions of the Auricles of the Mammalian Heart, Am. J. Physiol.,
Bost., 1907, xix, 125.
Hoffmann, Aug.: See chapter on Paroxysmal Tachycardia.
Hirschfelder, A. D., and Eyster, J. A. E.: Extrasystoles in the Mammalian Heart, Am. J.
Physiol., Bost., 1907, xviii, 222.
Kraus, Fr., and Nikolai: Ueber das Elektrokardiogramm unter normalen und patho-
logischen Verhaltnissen, Berl. klin. Wochnschr., 1907, 765, 811.
Kahn, R. H.: Ueber das Elektrokardiogramm kiinstlich ausgeloster Herzschlage Zentralbl.
f. Physiol., Leipz. and Vienna, 1909, xxiii, 444.
Hewlett, A. W.: Heart-block in the Ventricular Walls, Arch. Int. Med., Chicago, 1908,
ii, 139.
Barker, L. F., Hirschfelder, A. D., and Bond, G. M.: Effects of Cutting the Branch of the
Left His Bundle going to the Left Ventricle, Trans. Assoc. Am. Phys., Phila., 1909. Also
Barker, L. F., and Hirschfelder, A. D.: Arch. Int. Med., Chicago, 1909, iv, 193.
Aschoff, L., and Tawara, S.: See chapter on Acute Myocarditis.
Hirschfelder, A. D.: Observations upon Paroxysmal Tachycardia, Johns Hopkins Hosp.
Bull., Bait., 1906, xvii, 337.
Hering, H. E.: Ueber Herzalternans, Muenchen. med. Wochnschr., 1908, Iv, 1417.
Mackenzie, J.: See chapter on Angina Pectoris.
Wenckebach, K. F.: Beitrage zur Kenntniss der menschlichen Herztatigkeit, Arch. f.
Physiol., 1906; 1907, i.
80 DISEASES OF THE HEART AND AORTA.
Engelmann: Ueber die Leitung der Bewegungsreize im Herzen, Arch. f. d. ges. Physiol.,
Bonn, 1894, Ivi, 149. Ueber die Ursprung der Herzbewegungen, ibid., Ixv.
Cushny, A. R., and Matthews, S. A.: On the Effects of Electrical Stimulation of the Mam-
malian Heart, Jour. Physiol., Camb., 1897, xxi, 214.
Hirschf elder, A. D.: Inspection of the Jugular Vein; its Value and its Limitations in
Functional Diagnosis, Jour. Am. M. Assoc., Chicago, 1907, xlviii, 1105.
Lewis, T.: Single and Successive Extrasystoles, Lancet, Lond., 1909, i.
Muller, Fr.: Nervous Affections of the Heart, Arch. Int. Med., Chicago, 1908, i, 1.
Mackenzie, J.: Diseases of the Heart, Lond., 1908.
Knoll, Ph.: Ueber die Veraenderungen des Herzschlages bei reflectorischer Erregung des
vasomotorischen Nervensystems, sowie bei Steigerung des intracardialen Drucks
iiberhaupt, Sitzungsber. d. k. Akad. d. Wissensch., Wien, Abth. Ill, 1872, Ixv-lxvi, 195.
Marey: La circulation du sang a 1'etat physiologique et dans les maladies, Par., 1881.
Hering, H. E.: Zur experimentellen Analyse des unregelmassigen Herzschlages, Arch. f.
d. ges. Physio]., Bonn, 1900, Ixxxii. Ueber continuierliche Herzbigeminie, Deutsch.
Arch. f. klin. Med., Leipz., 1904, Ixxix, 175. Ergebnisse experimenteller und klin-
ischer Untersuchungen ueber den Vorhofvenenpuls bei Extrasystolen, Ztschr. f.
exper. Path. u. Therap., Berl., 1905, i, 26; also his pupils.
Rihl, J.: Experimentelle Analyse des Venenpulses bei den durch Extrasystolen verur-
sachten Unregelmassigkeiten des Saugethier herzens, ibid., 1905, i, 43.
Pan, O.: Ueber das Verhalten des Venenpulses bei den durch Extrasystolen verursachten
Unregelmassigkeiten des menschlichen Herzens, ibid., 1905, i, 56.
Hirschfelder, A. D.: The Volume Curve of the Ventricles in Experimental Mitral Stenosis
and its Relation to Physical Signs, Johns Hopkins Hosp. Bull., Bait., 1908, xix, 319.
Mackenzie, J.: The Extrasystole, Quart. J. M., Oxford, 1908, i, 481.
Gerhardt, D.: Beitrag zur Lehre von den Extrasystolen, Deutsch. Arch. f. klin. Med.,
Leipz., 1905, Ixxxii, 509.
Hoffmann, Aug.: Arhythmie des Herzens, Deutsch. med. Wchnschr., Leipz., 1906, xxxii,
1682. Ueber die Entsthung der Extrasystolen irregularitat, Muenchen. med.
Wchnschr., 1907, liii, 1987.
Dehio, K.: Einfluss des Atropins auf arhythmische Herztatigkeit, Deutsch. Arch. f. klin.
Med., Leipz., 1894, lii, 97.
Hering, H. E.: Experimentelle Untersuchungen ueber Herzunregelmassigkeiten an Affen,
Ztschr. f. exper. Path. u. Therap., Berl., 1906, ii, 525.
Hering, H. E., and Rihl, J.: Ueber atrioventrikulare Extrasystolen, ibid., 1906, ii, 510.
Gaskell, W. H.: The Properties of Cardiac Muscle, Schafer's Text-book of Physiology,
Lond., 1900, ii.
Lohmann, A.: Zur Automatic der Bruckenfasern des Herzens, Arch. f. Physiol., Leipz.,
1904, 431; and Supplbd., 265. Ueber der Funktion der Bruckenfasern an Stelle
der grossen Venen die Fuhrung der Herztatigkeit beim Saugetiere zu iibernehmen,
Arch. f. d. ges. Physiol., Bonn, 1908, cxxiii, 628.
Mackenzie, J.: Inception of the Rhythm of the Heart by the Ventricles, Brit. M. J., Lond.,
1904, i, 529. Abnormal Inception of the Cardiac Rhythm, Quart. J. M., Oxford,
1907, i, 39.
Mackenzie, J., and Wenckebach, K. F.: Ueber an der Atrioventrikulargrenze ausgeloste
Systolen beim Menschen, Arch. f. Physiol., Leipz., 1905.
Schmoll, E.: Paroxysmal Tachycardia, Am. J. M. Sc., Phila. and N. York, 1907, cxxxiv,
662.
Mackenzie, R., and Morrow, W. S.: Cardiac Arrhythmia due to Extrasystoles Originating
in the Bundle of His, Am. J. M. Sc., Phila. and N. York, 1908, cxxxv, 534.
Cushny, A. R.: See chapter on the Action of Drugs.
Hering, II . E.: Ueber die haufige Kombination von Kammervenenpuls mit Pulsus irreg-
ularis perpetuus, Deutsch. med. Wchnschr., Leipz., 1906, 213.
Gerhardt, D.: Arhythmis perpetua des Puls, Deutsch. med. Wchnschr., Leipz., 1907,
xxxiii, 448.
Hewlett, A. W.: On the Interpretation of the Positive Venous Pulse, J. M. Research,
1907-8, xvii, 119. Clinical Observations on Absolutely Irregular Hearts, J. Am. M.
Ass., Chicago, 1908, Ii, 655.
Theopold, J.: Ein Beitrag zur Lehre von der Arhythmia perpetua, Deutsch. Arch. f. klin.
Med., Leipz., 1907, xc, 77.
THE VENOUS PULSE AND ELECTROCARDIOGRAM. 81
Hering, H. E.: Das Elektrocardiogramm des Pulsus irregularis perpetuus, ibid., 1908,
xciv, 205.
Radasewsky: See chapter on Chronic Myocarditis. Ueber die Muskelkrankungen der
Vorhofe des Herzens, Ztschr. f. klin. Med., Berl., xxvii.
Schonberg, S.: Ueber Veraenderungen im Sinusgebiete des Herzens bei chronischer Ar-
rhythmic, Frankf. Ztschr. f. Path., 1908, ii, 153.
Miiller, G.: Ungewohnliche Dilatation des Herzens und Ausfall der Vorhofsfunktion,
Ztschr. f. klin. Med. Berl., Ivi, 520.
Quincke, and Hochhaus, J.: Ueber frustrane Herzcontractionen, Deutsch. Arch. f. klin.
Med., Leipz., 1894, liii, 414.
James, W.: Clinical Study of Some Arrhythmias of the Heart, «Am. Jour. M. Sc., Phila.
and N. York, 1908, cxxxvi, 469.
Hirschfelder, A. D.: Contributions to the Study of Auricular Fibrillation, Paroxysmal
Tachycardia, and the so-called Auriculo(Atrio)ventricular Extrasystoles, Johns
Hopkins Hosp. Bull., Bait., 1908, xix, 322.
Hoffmann, A.: Neue Beobachtungen ueber Herzjagen, Deutsch. Arch. f. klin. Med., 1903,
Ixxviii, 39.
Cushny, A. R., and Edmunds, C. W.: Paroxysmal Irregularity of the Heart and Auricular
Fibrillation, Am. Jour. M. Sc., Phila., 1907, cxxxiii, 66; and Studies in Pathology,
Quatercentenary Public., Aberdeen Univ.
Engelmann, 1. c.
Trendelenberg, W.: Untersuchungen ueber das Verhalten des Herzmuskels bei rhythm-
ischer elektrischer Reizung, Arch. f. Physiol., Leipz., 1903, 271.
V.
X-RAY EXAMINATION.
The discovery of the X-rays by Rontgen in 1895 introduced a new
era in cardiac diagnosis. By this means we can now actually see the heart,
observe its outlines with accuracy, and note the changes of position and
of contour with different phases of respiration, and even to a certain extent
the changes from systole to diastole. All these data, when obtained with
proper precautions, are absolutely accurate, and have greatly supplemented
the observations made by percussion.1
METHODS OF EXAMINATION.
Most of the facts desired in the study of the circulatory system with
the X-ray may be gained by means of inspection with the fluoroscope,
a screen of barium platinocyanide or calcium tungstate which is rendered
luminous wherever the X-rays strike it.
A tube of low vacuum ("soft tube") should be used, one
whic.h shows the bones of the hand black without re-
vealing their internal structure, and the tissues of the hand a
fairly dark gray. The patient's chest wall should be at least 50 cm. from
the screen. Recently the usual distance has been increased to 2 M. (6|
ft.), at which the rays are almost parallel.
It is sometimes best to interpose a lead screen, with adjustable opening, between the
patient and the tube in order to cut off all the rays except those emanating from a small
part of the anticathode, thereby securing the greatest possible definition of focus. Indeed,
Immelmann found greatest definition when the opening in the lead screen was only 1 cm.
Often a lead cylinder (Albers-Schoenberg) is very satisfactory. It is also important that
no large objects be placed near the cathode, as rays striking these may also generate
secondary rays which affect the fluoroscope or photographic plate and thus blur the outline
of the original image (Walter). For securing sharp images it is preferable to keep a
number of tubes with vacua of different degrees which may be interchanged, rather than
change the vacuum in each tube. Changing the latter shortens the life of the tube by
heating the platinum target and causing the latter ultimately to become bent, so that the
rays are not reflected uniformly from its surface.
The X-ray image is a true shadow formed by the cutting off of rays
and not by their refraction, and the shadow is magnified in proportion as
the object is nearer to the tube or farther from the fluoroscopic screen.
1 Examinations with the X-ray require a very special technic, for which the student
is advised to consult the special text-books upon the subject, especially:
Albers-Schoenberg: Die Rontgentechnik, Hamburg, 1906.
Gocht, H.: Handbuch der Rontgenlehre zum Gebrauche fur Mediziner, 2te Aufl.,
Stuttgart, 1903.
Williams, F. H.: The Rontgen Rays in Medicine and Surgery, New York, 1903.
Beck, C.: Rontgen-ray Diagnosis and Therapy.
Kassabian: Rontgen Rays and Electro-Therapeutics, Phila., 1909.
82
X-RAY EXAMINATION. 83
In fluoroscopic examination it is most important for the observer to accustom his
eyes to the darkness before turning on the current. It is a well-proved physiological fact
that the longer the sojourn in darkness the greater the delicacy of vision. Hence the exami-
ner's vision is improved by closing or blindfolding his eyes or by going into a dark room
some ten or fifteen minutes before the patient; and the examining room should be lighted
only enough to permit the patient to undress and assume the proper position. The exami-
ner may also keep his head under a dark hood or wear heavily smoked glasses during this
time so as to accustom his eyes to the darkness.
In looking over the areas of light and shadows each region should be
studied carefully and in detail,- the size and shape of the shadow, the clear-
ness of the outline, and the distribution of areas of half shadows as well as
of full shadows. Not of least importance are the so-called pulmonary
figures, the half-tone shadows of pulmonary vessels, of bronchial glands,
and of strands of adhesions.1 Not only the full shadows but especially
these half shadows should be examined with care, for an interpretation
not apparent at first may become clear after a few minutes' observation.
Radiographers are, moreover, in the habit of looking at the fluoroscope through half-
closed eyes in order to intensify the contrast. This may be further intensified by the use
of dark glasses. The writer has also found it very useful to look at the shadow or skiagraph
through a biconcave lens which at once sharpens the contours and intensifies the contrasts.
Often an area may be indefinite during quiet breath-
ing or expiration and become quite definite on forced
deep inspiration, or it may become so by simply turning
the patient so that the rays p.ass through his body in
a different direction. These and similar precautions, like a care-
ful physical examination, reveal the
unsuspected, and distinguish the
skilled examiner from the unskilled.
The Cardiac Shadow.— The heart
shadow thrown upon a screen at the
front of the chest is shown in Fig. 81.
It will be noted that the outline of
the shadow closely resembles the
area of relative dulness on percus-
sion, except that the former extends
upward over the manubrium sterni,
where it is due to the presence of
the latter and Of the great Vessels FIG. 80. — Radiograph of normal chest. (After
, . , , , f ,, v. Ziemmsen and Rieder.) Tube behind the chest
and not of the heart. In the second piate in front.
left interspace the shadow
of the pulmonary artery is seen, and in the second right
that of the aorta. Occasionally a small prominence is seen to the left
of the sternum arising at the arch of the aorta. This is sometimes mistaken
for an aneurism, but if the patient be turned a little it will be seen to be
due to the curving of the aorta (Holzknecht).
Oblique Illuminations. — Much can be learned by turning the patient
about and examining him in several planes, as was first performed
by v. Criegern and Holzknecht (1. c.), arid later by Rieder, who suggested the
1 See chapter on Adherent Pericardium.
84
DISEASES OF THE HEART AND AORTA.
following cardinal directions (Fig. 81): (1) dorso ventral ; (2) ventrodorsal ;
(3) sagittal from right; (4) sagittal from left; (5) from right posterior to
left anterior; (6) from left posterior to right anterior; (7) from left anterior
to right posterior; (8) from right anterior to left posterior.
FIG. 81. — X-ray shadows in different axes of the body. (Modified from Holzkrecht.) The
arrows show the direction of illumination and position of the tube corresponding to the shadow.
AO, aorta; PA, pulmonary artery; LA, left auricle; RA, right auricle; LV, left ventricle; RV, right
ventricle. In 3 there is a metal sound in the resophagus.
By the examination in these planes every part of .the heart can be
brought into view, even the left auricle, which escapes observation in almost
all other methods of examination but appears quite clearly when the tube
is placed at the back or behind the right scapula. The oblique and trans-
verse examinations should never be omitted.
X-RAY EXAMINATION.
85
THE ORTHODIAGRAPH.
The shadow of the heart and vessels upon the screen or plate is
always larger than the objects themselves. In order to obviate this
when measuring out the heart F.
Moritz devised an instrument known
as the orthodiagraph (Fig. 82).
FIG. 82. — A simple form of orthodiagraph.
(After Gillet.)
FIG. 83. — Diagram showing the use of the ortho-
diagraph. 1, first position; 2, second position; P,
pencil; FLUOR, fluorescent screen.
In the orthodiagraph the fluorescent screen and X-ray tube are fixed upon each arm
of a large [/-shaped frame in such a way that the patient may stand or lie between the
two arms of the U and the rays thus
pass through his body to the screen.
At the point upon the screen which is
exactly opposite to the centre of the
anticathode or target of the tube, a
small hole is pierced, and a skin pencil
is fixed in place here so that the site of
this spot can be marked upon the body
of the patient. The whole [/-shaped
frame bearing the tube and fluoroscope
is movable in two directions by any
one of a variety of mechanisms, so that
the perpendicular ray can be brought
opposite any desired point. A series of
points corresponding to the exact con-
tour can thus be marked off, and when
these are joined with lines the exact
O U 1 1 i n e Of the heart U repre- FlQ 84._Or(hodiaKraPhiC outline of normal heart,
8 e n t e d . As shown by Fig. 83, this showing Morit7.'s conjugates. MR, midline to right
border (greatest distance); ML, midline to left border;
/., oblique longitudinal; Q, transverse; numerals indi-
cate centimetres.
furnishes a means of determining the
size of the heart or any organ with
absolute accuracy.
The outlines and mobility of the heart thus obtained are discussed
on page 97.
It is also possible with the fluoroscope to watch the individual con-
tractions of the heart and to note the changes in size due to systole and
86 DISEASES OF THE HEART AND AORTA.
diastole, but this is very difficult and can rarely be done with satisfactory
accuracy. On the other hand, the contractions of the auricles can be seen
with considerable definiteness, and dissociation of rhythm, heart-
block, can often be diagnosed in this way by sim-
ple inspection (Kraus, Gibson).
PERMANENT RADIOGRAPHS.
For obtaining permanent photographs a " medium soft " tube (Moritz
scale W 6 B W 5) is used in connection with a Wehnelt electrolytic inter-
rupter and an induction coil with proper self-induction yielding a 40 to 60
cm. spark. The patient is laid upon a table with the tube above or below
him, as is most suitable to the purpose of the examination. In order to
absolutely immobilize him it is well to support the shoulders upon sand
bags. He may also be examined standing by immobilizing the shoulders
to prevent blurring of the picture. Magnification of the shadow may be
obviated by placing the tube at a distance of 2 M. Skiagraphs of the chest
made with very short exposures have proved particularly valuable, since
they give greater definition (Rieder).
BIBLIOGRAPHY.
Rontgen, W. K.: A New Form of Radiation, Science, N. York and Lancaster, 1896, N. S.
iii, 726 and 729.
Barker, Geo. F.: The Rontgen Rays. Memoirs by Rontgen, Stokes, and Thompson, N. Y.
and Lond., 1899.
Michelson, A. A.: Theory of the X-rays, Am. Jour. Sc., 1896, 4th ser., i, 312.
Rowland, H.: Notes of Observations on the Rontgen Rays, ibid., 1896, 4th ser., i, 247.
For details regarding the secondary rays see:
Walter, B.: Physikalisch technische Mitteilungen, Fortschr. a. d. Geb. d. Rontgenstrah-
len, Hamb., 1900, i, 82.
Faulhaber : Ueber eine durch Sekundarstrahlung bedingte Erscheinung auf Rontgen-
platten, ibid., 1903, vi, 93.
Holzknecht, G.: Die rontgologische Diagnostik der Erkrankungen der Brusteingeweide,
Hamb., 1901. Das radiologische Verhalten der normalen Brustaorta, Wien. klin.
Wchnschr., 1900.
Cotton, W.: Some Principles and Fallacies of X-ray Interpretation, Practitioner, Lond.,
1906, Extra No. on X-rays, 100.
v. Criegern: Ergebnisse der Untersuchung des menschlichen Herzens mittelst fluorescir-
enden Schirmes, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1899, xvi, 302.
Rieder, H.: Die Untersuchung der Brustorgane in verschiedenen Durchleuchtungsricr-
tungen, Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamb., 1902-03, vi, 115.
Moritz, F.: Ueber die Bestimmung der wahren Grosse von Gegenstanden mittels des
Rontgenverfahrens, Miinchen. med. Wchnschr., 1900, xlvii, 509, 902. Ueber ortho-
diagraphische Untersuchungen am Herzens, ibid., 1902, xlix, 1. Ueber Tiefenbest-
immungen mittels des Orthodiagraphen und deren Verkiirzungen bei der Orthodia-
graphie des Herzens zu ermitteln, Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamb.,
1904, vii, 169.
Levy-Dorn: Schutzmaassregeln gegen Rontgenstrahlen und ihre Dosirung, Deutsche
med. Wchnschr., Berl. und Leipz., 1903, xxix, 921.
For numerous forms of orthodiagraphs of Moritz and Albers-Schoenberg (1. c.), but what
seems to the writer to be the most convenient and simple form is the apparatus
described by:
Gillet: Ein Orthorontgenograph einfacher Konstruction, Fortschr. a. d. Geb. d. Rontgen-
strahlen, Hamb., 1906, x, 114.
X-RAY EXAMINATION. 87
For the examination of the heart cf. also
Moritz, F.: Einige Bemcrkungen zur Frage der perkutorischen Darstellung der gesam ni-
ton Vorderflache des Herzens, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxvii,
276.
Dietlen, H.: Ueber Grosse und Lage des normalen Herzens und ihre Abhangigkeit von
physiologischen Bedingungen, ibid., 1906, Ixxxviii, 55.
Levy, M.: Ueber Abkiirzung der Expositionszeit bei Aufnahmen mit Rontgenstrahlen,
Fortschr. a. d. Geb. d. Rontgenstrahlen, Hamb., 1897, i, 75.
Rieder, H., and Rosenthal, J.: Ueber Moment-Rontgenaufnahmen, Fortschr. a. d. Geb.
d. Rontgenstrahlen, Hamb., 1900, iii, 100.
Rieder, H.: Neue Ausblicke auf die weitere Entwicklung der Rontgendiagnostik, Mun-
chen. med. Wchnschr., 1908, Iv, 381.
VI.
PHYSICAL EXAMINATION.
While it is impossible to enter into a treatise upon physical exami-
nation, a few points which are of special importance in cardiac cases may
be discussed.
General Appearance. — The general appearance of the patient, expres-
sion and color, are of great importance. The position which he naturally
assumes in bed, the presence or absence of dyspnoea and orthopnoea, the
general degree of nervousness or dulness are all to be noted.
The typical appearance of the cardiac patient (cardiac facies) is
characterized by an anxious expression, bright eyes with moist, glistening
conjunctiva?, cheeks full rather than sunken as in the abdominal facies,
and as a rule a tinge of cyanosis about the lips.
There are two main types: (1) the mitral (or mitrotricuspid) facies, with
rosy, flushed cheeks, dilated capillaries, and cyanosis (most commonly seen in mitral
stenosis); and (2) the aortic facies, with pale, often sallow, rather sunken cheeks,
bright eyes, moist conjunctivas, and slight cyanosis of lips and fingers. To these might be
added (3) the subicteric facies of broken compensation, with pallor, subicteric conjunctive,
and cyanosis of the lips.
Nasopharynx. — The tonsils and posterior nasopharynx should always be carefully
examined. The former are the chief portals of entry for the germs of rheumatism, while
adenoids and affections of the nasal septum may of themselves induce
cardiac arrhythmia, and may also be an important contributing factor in the attacks of
asthma in organic heart disease.
Ophthalmoscopic Examination. — The eye-grounds should always be examined when
arteriosclerosis (page 260) or congenital heart disease (page 438) is suspected.
Neck. — In the neck especial attention should be directed to the visible
throbbing of the carotids, the fulness of the neck, and the size and consist-
ency of the thyroid gland (page 585), the presence of thrills and murmurs
over vessels or thyroid, or a tracheal tug (page 533). The jugular pulsation
is discussed in full in Part I, Chapter IV, page 49.
Chest. — The form of the chest is of considerable importance, not only
as regards kyphosis, but particularly as to its f u 1 n e s s or f 1 a t n e s s (see
Part III, Chapter III). In recording this, the width of the costal angle
should be noted, but the general obliquity of the ribs in quiet
expiration should be designated by noting the vertebral spines
which are on the same level with the s t e r n o xi p h oi d
articulation (normally at the level of the eighth thoracic spine)
(page 598). It should be noted whether the chest in quiet breathing ap-
proaches more nearly to the position of expiration, flat chest, or to that
of inspiration. Pulsations, bulgings, heaving, or retractions of the ribs or
interspaces, as well as the presence of abnormal shocks. and thrills, should
of course be noted.
Abdomen. — In the abdomen the important features to be noted are
presence or absence of ascites, enlargement of liver (systemic
88
PHYSICAL EXAMINATION. 89
stasis), pulsation of the liver, systolic impulse (tricuspid insuffi-
ciency), systolic retraction (dilated or hypertrophied right ventricle), the
nature and the time of epigastric pulsation (systolic elevation being trans-
mitted from the abdominal aorta, systolic retraction indicating dilated
hypertrophied right ventricle) . A palpable spleen of cardiac origin
points to infarction, septic or thrombotic. When aneurism or arterio-
sclerosis is suspected the course of the abdominal aorta should
be mapped out by deep palpation with both hands, one above each side of
the aorta and that vessel between them (page 550) .
The genitalia should of course always be examined for signs of gonor-
rhoea and lues, — urethral smears for the former and a Wassermann
reaction for the latter being made whenever possible.
Extremities. — Upon the extremities the presence of oedema and
arthritis, acrocyanosis or pallor, and the size, consistency, and
uniformity of the brachial, radial, femoral, popliteal, and dorsalis pedis
arteries are the chief points of importance.
THE CARDIAC IMPULSE.
Mechanics of the Cardiac Impulse. — The apex itself, as shown by
Ludwig and Dogiel, does not move appreciably up or down during systole;
and, as Hesse has demonstrated, the transverse diameter of the heart
shortens more than the longitudinal.
The chief movements which lead to the production of the apex
impulse are due more to the systolic erection of the heart upon the great
vessels than to its diminution in size.
If one watches the exposed heart of a dog,
cat, or rabbit, it is seen to execute two move-
ments in systole: (1) the general contraction
affecting chiefly the transverse diameter of the
heart, and (2) a twisting about of the
apex from left to right and forwards.
This torsion of the apex is the resultant of the
several lines of traction exerted by the muscu-
lature of the right and left ventricles upon the
base of the aorta and pulmonary artery, and
modified by the pivoting of the heart against Fjo M;iMovement8 of the heart leading
the vertebral column and by the shifting of its to the protrusions and retraction during sys-
centre of gravity owing to variation in its tole. Forces shown by the arrows,
liquid content. The tendency of this move-
ment is to push the apex of the left ventricle against the chest wall, while the left
wall of the left ventricle and the right (anterior) wall of the
right ventricle move inwards toward the septum. Wherever in
man these walls are in contact with the chest wall these inwa'rd movements give rise to
retraction of the interspaces above them. The surface of the thin- walled right ventricle
moreover is actually pulled inwards during systole, so that there may actually be an
indentation of its surface which still further contributes to the systolic retraction.
Protrusions and Retractions. — A variety of protrusions and retractions
of the interspaces may be seen to occur with each cardiac contraction.
Graphic records of the impulse have been taken by means of the polygraphs
described above, the receiving funnel being placed over the area of pulsation exactly
as for a jugular or carotid tracing. Tracings can be made either with a rubber-
90
DISEASES OF THE HEART AND AORTA.
covered spring tambour like that used for the carotid, or with an open funnel ;
the former exerting pressure upon the apex, the latter merely recording the com-
pression or rarefaction of the air in the funnel due to the impulse.
The writer also finds that a funnel, made from a soft rubber stethoscope tip stoppered
tightly with a perforated rubber stopper penetrated by
a glass tube and bearing a rubber tip, is very satis-
factory (Fig. 86).
The movements seen may be divided as :
(1) Lifting of the entire precordium,
which results, especially in flat-chested individ-
uals or in those with very large hearts, from
the systolic erection of the heart as a whole as
it pivots against the vertebral column behind
and pushes against the chest wall in front.
This is usually seen in hearts which from any cause whatever are
beating heavily, though it is most marked over large hearts.
(2) The normal type of apex beat consists of a large protrusion
synchronous with and lasting throughout the duration of ventricular systole
(Fig. 88, I, s-d), usually preceded by a small presystolic wavelet (a-s), due
FIG. 86. — Rubber funnel for car-
diographic tracings.
JUGULAR
.°- 87* A, tracing from the apex impulse and carotid artery: c, time of carotid wave; d. time
of dicrotic notch. Upper line gives the time in £ sec. B. cardiogram obtained over a normal apex.
C and D, cardiogram over the fourth left interspace 5 cm. from costal margin (systolic retraction), from
the same individual as B.
to systole of the auricles. The large ventricular wave is followed by a fall
in early diastole, coincident with the fall in intra ventricular pressure.
After this fall there is sometimes a small upstroke of the lever (passive
protrusion of the apex by the inrushing blood) which may terminate in a
small protodiastolic wavelet (p). This protodiastolic wavelet corresponds
PHYSICAL EXAMINATION.
91
to the shoulder upon the cardiac plethysmogram at the end of ventricular
filling (page 9), and is particularly marked in cases in which a third heart
sound can be heard (Thayer).
• In cases with hypertrophy of the left ventricle the protrusion is
usually very forcible and heaving throughout systole — dome-like protru-
sion, choc en dome (Bard).
Occasionally, however, especially when there is some hypertrophy
of the right ventricle, the systolic protrusion may not last throughout
ventricular systole, but may be represented by only a momentary protru-
sion, followed by a retraction during midsystole (Fig. 88, III). Such a
beat, which really represents the algebraic sum of the systolic protrusion
over the left ventricle and the systolic retraction over the right, may be
in.
IV.
v.
FIG. 88. — Various forms of apex tracings. I. Normal, showing presystolic (auricular) wave a.
systolic plateau s-d, and the curve of ventricular filling d-p, ending in the protodiastolic wavelet p. II,
Normal apex beat showing only systolic elevation. III. "Mixed " type of impulse showing an elevation
followed by a retraction during the period of systole. IV. Systolic retraction. Apex formed by the
right ventricle. V. "Mixed" type of apex beat showing protrusion during auricular systole and
retraction during systole of the ventricle.
termed a "mixed" type of apex boat. In other mixed types
there may be protrusion during auricular systole (presystolic protrusion)
followed by retraction during systole of the ventricle (systolic retrac-
tion) . The right ventricle plays the leading rdle in the production of
such an impulse.
(3) Systolic retractions over the entire right ven-
tricle (third, fourth, fifth left interspaces between the parasttrnal
line and sternal margin) when this chamber is h y p e r t r o p h i e d or
contracting strongly, sometimes also in second left interspace
(Mackenzie). Occasionally, especially in cases of mitral stenosis, the
presence of a systolic retraction of the interspaces over the right ventricle
and a systolic protrusion over the apex gives the cardiac impulse the
wavy appearance of a peristalsis. In reality, however, the two move-
ments are synchronous. It is not a peristalsis but a see-saw movement.
92
DISEASES OF THE HEART AND AORTA.
(4) Systolic impulse in the second right interspace in aortic
insufficiency .
(5) Systolic impulse in the second left interspace (pulmonic area) in
pulmonary insufficiency or vigorous contraction of the right ventricle.
(6) Systolic retraction at the apex in adherent peri-
cardium or when the apex is
formed by an hypertrophied
right ventricle.
(7) Systolic retrac-
tions in the interspaces
beyond the apex (left axilla) due
to negative pressure over those
areas of lung produced by con-
traction of a very large heart or
to pleuropericardial adhesions.
(8) Retraction of the
xiphoid process or ribs
from traction of costopericardial
adhesions during systole
(Broadbent's sign).
(9) Systolic impulses
in various abnormal sites
due to aneurisms, tumors, or
tortuous sclerotic arteries.
FIG. 89. — Areas of pulsation and retraction. t ,
protrusion; ^ , retraction. CAR, carotid artery; JUG,
jugular vein; CEPH, cephalic vein; AO, aorta; PA, pul-
monary artery; R V, right ventricle; APHD, apex with
high diaphragm; AP, apex; LIV.TR.INS, liver-pulsa-
tion in tricuspid insufficiency; LIV. HYP. RV, liver-
retraction with hypertrophy of right ventricle.
FIG. 90. — Eddies producing thrills as
illustrated by a stream of water. Arrows
show lines of force. The large arrow indi-
cates the pressure at the point of palpation.
PALPATION.
Palpation of the precordium and thorax is undertaken with a view
to determine, (1) the force of the apex impulse; (2) the presence and force
of any diffuse heave; (3) the intensity of the shock accompanying the
heart sounds; (4) the presence and distri-
bution of "thrills"; (5) the presence, dis-
tribution, and character of other pulsations.
Thrills.— Corrigan (1837) and, later, Marey
showed that thrills may be imitated by producing a
constriction in a rubber tube attached to a water
faucet. It will be seen that this causes the stream to
assume a corkscrew form, giving rise to eddies, twists,
and nodes below the constriction. These tend to produce zones of constriction and dilatation
in the tube itself and thus set it into vibrations which are palpable as thrills and audible as
murmurs. Above the constriction there are no eddies, hence neither thrills nor murmurs.
The thrill is best transmitted in the direction of the stream producing
it. It disappears when the constriction becomes too great or the pressure
falls too low, and increases with the force of the stream (blood-pressure).
PERCUSSION.
It is of the greatest importance to determine the exact outline of the
heart. As has been seen, this is done most accurately by means of the
orthodiagraph (page 85), but under ordinary clinical conditions this is
not available and the cardiac area is outlined by percussion.
PHYSICAL EXAMINATION. 93
In determining the area of cardiac dulness it is important to map out,
(1) the area of cardiac dulness, or, more accurately, the relative cardiac
dulness; (2) the area of absolute dulness or cardiac flatness.
RELATIVE CARDIAC DULNESS.
In mapping out the area of relative cardiac dulness it is important
to begin percussion as far away from the heart as possible, and then to
approach the heart, marking the points at which the very first change of
note can be recognized as the heart is approached. In this way one obtains
an absolutely resonant note as long as the plessimeter finger is over lung
tissue, and a sharp contrast to this as soon as one percusses over the borders
of the heart; whereas, if one were to begin percussion over the heart and
percuss outward there would be a gradual change of note,
becoming more and more resonant, until it finally faded
into the perfect resonance over the lung.
Choice of Methods. — In outlining the cardiac area one has the
choice of several methods:
(1) Direct or immediate percussion by tapping the chest wall
directly with the finger-tips of one hand.
(2) Heavy indirect or mediate percussion.
(3) M e d i u m - 1 i g h t percussion.
(4) Lightest audible percussion (threshold percussion of
Ewald, Goldscheider, Curschmann and Schlayer).
(5) Palpatory percussion (Ebstein) by note too low to be FIG. 91. — Gold-
heard at all. scheider's ortho-
(6) 0 r t h o p e r c u s s i o n (Goldscheider) (Fig. 91), distal Percussion-
phalanx of the plessimeter finger held perpendicular to the chest wall.
(7) Instrumental percussion with a mechanical plessimeter, the blow being
struck by either the finger or a hammer.
In selecting the method of percussion it should be borne in mind that,
though bodies near the chest wall on either side of the line of percussion
stroke may tend to damp the vibration of the lung and impair the reso-
nance of the note, this tendency is greater for heavy percussion and loud
resonance than with light strokes which set only small areas of lung in
vibration. Moreover, it is a well-known law of sense-perception that the
softer the initial sound the easier it is to detect variations in it. Indeed,
de la Camp goes so far as to recommend light direct percussion through a
single layer of blanket laid upon the chest as the most accurate method
of outlining the cardiac dulness.
Moritz, Dietlen, de la Camp, Goldscheider, Curschmann and Schlayer,
and a number of other writers have compared outlines made by the various
methods of percussion in hundreds of cases with those obtained by the
orthodiagraph, while Simon has marked out his outlines by percussion
upon the intact cadaver with pins and then tested his accuracy upon
opening up the thorax. All these observers are unanimous in
advocating very light percussion for outlining the left border
of the heart, but Moritz prefers a rather heavy palpatory percussion
for the right border.
Moreover, the sensations which percussion imparts to the finger are
more delicately graded for a light stroke than for a heavy one, since the
94
DISEASES OF THE HEART AND AORTA.
pressure of a heavy blow somewhat dulls the sensibility of the finger-tips,
and in this way also a light stroke is more satisfactory. The oft-made
claim that a light stroke does not penetrate deep enough for mapping out
the right border of the heart, though seeming plausible, is not warranted by
experience. On the contrary, the writer has observed that those clinicians
who rarely make out at all the area of cardiac dulness which lies to the
right of the midline were usually those who used heavy percussion.
Avoidable Errors in Percussion. — The exact method used is a matter of individual
preference and practice. The essentials for all forms are: (1) a loose wrist, loosely held
finger-joints, and a short sharp blow with immediate elastic recoil;1 (2) firm pressure of
the plessimeter finger against the chest wall, especially in the interspaces. In the writer's
experience the important point is not the method used but the care in discriminating the
first slight differences in note and sensation. The errors of percussion so frequent among
students and even experienced physicians are far more frequently due to in-
ability to detect differences in note than to inability to elicit
them. This inability to detect slight differences was due in most cases to a precon-
ceived notion as to the intensity of change
obtainable. The observer usually expected a
greater change and permitted his ear to neglect
the lesser, although once his attention was
called he was perfectly able to detect it.
Special Methods of Percussion. — The
method of choice varies somewhat with the
purpose. For ordinary purposes very light
direct percussion is quite satisfactory, or ordi-
nary threshhold percussion with barely audi-
ble note. Where accuracy is important,
as in determining the mobility of the heart
or of the lung borders, Goldscheider's or-
thopercussion or J. O. Hirschfelder's
orthoplessimeter is preferable.
Goldscheider believed that orthopercus-
sion was so delicate that dulness was given
only by bodies directly in the axis of the
plessimeter phalanx and that in this way the
plane of an oblique surface could be detected; but experience shows that this is rarely
possible. It succeeds much more frequently when the orthoplessimeter (Fig. 92) is
used; so that a resonant note may be obtained when the shaft is pointed parallel to the
heart surface, a dull note when it is pointed toward the heart.
Unavoidable Errors in Percussion Outlines. — In outlining the heart
by percussion the right and left borders present different problems. The
right border is situated deeply and recedes at once from the chest wall, so
that it represents the first point at which dulness could be obtained. The
left border is superficial and convex and the convexity sometimes follows
the curve of the ribs in the left axilla. Accordingly it may happen that in
round narrow chests or in persons with large hearts the left ventricle may
almost fill the left half of the thorax. The curve of the ribs follows the wall
FIG. 92. — Percussion with the orthoplessi-
meter. A. J. O. Hirschfelder's orthoplessimeter
and its mode of application. B. Supposed line of
transmission of the percussion impulse from the
orthoplessimeter. RES, resonant percussion note.
1 Some persons are possessed of a loose wrist at once, others acquire it only after
long practice. For the latter the writer recommends the following exercise practised two
to five minutes daily: Hold the wrist as loosely as possible, then vibrate the forearm very
rapidly to and fro from the elbow until the hand shakes about like a Hail upon the loose
wrist too fast for the eye to follow its movements. The improvement in percussion fol-
lowing this exercise is very gratifying.
PHYSICAL EXAMINATION.
95
of the left ventricle and the latter may remain near the chest wall through-
out the axilla. The outer border of dulness may thus be obtained not over
the apex but over the posterior wall of the left ventricle. In persons
with narrow chests or much
enlarged hearts the area of
dulness (Fig. 93, P- -P) ex-
tends around the heart and
not merely across the trans-
verse diameter (O- -O). The
transverse diameter ( O - - O ) corre-
sponds accurately to the point mapped
out with the orthodiagraph. Accord-
ingly there may be a discrepancy of
several centimetres between the percus-
sion and orthodiagraph estimations of
the distance from the midline to the
left border. In'broad flat chests where,
beyond the apex, the left ventricle recedes
from the chest wall, this discrepancy does not occur; and the findings by
percussion and by X-ray coincide closely. In a very large series of
cases Moritz found his percussion (light percussion for the right border,
threshold percussion for the left) to be correct for the right border in
86 per cent., for the left in 70 per cent.
FIG. 93. — Diagram to show the cause of
unavoidable error in percussion of the cardiac
outlines. P — P, outline on percussion;
O — O orthodiagraph outline.
DIAMETER OF THE CARDIAC AREA.
In mapping out the area of cardiac dulness the position of the apex is
given, designating the level of rib or interspace during quiet respiration, and
the number of centimetres to
the left of the midline (Figs. 84
and 94) (ML). The level of
upper border at the left sternal
margin is given and also the
distance to the right of the
midline (MR) in the fourth
right interspace. The acuteness
or obtuseness of the angle
formed between the hepatic and
the cardiac dulness (cardio-
hepatic angle, angle of Ebstein)
is also noted. In addition to
this Moritz and Dietlen call
attention to the importance of
recording the two diagonal di-
ameters of the heart (longitu-
dinal, L, from apex to the
aortic angle of the dulness, and transverse, Q, from the cardiohepatic
angle to the upper left border, as shown in Fig. 84). Normal figures for
these conjugates according to Dietlen arc:
FIG. 94. — Areas of cardiac dulness and flatness in a
normal man. The outer fine line represent* cardiac <lul-
nc»; the inner heavy line represents cardiac flatm--.
96
DISEASES OF THE HEART AND AORTA.
Height of individual.
Men.
Women.
Cm.
Feet and In.
MR.
Cm.
ML.
Cm.
L.
Cm.
Cm.
Cardiac
area.
Qcm.
MR.
Cm.
ML.
Cm.
L.
Cm.
Cm.
Cardiac
area.
Qcm.
145-154
4.7—5.
3.5
7.9
12.5
9.7
95
3.5
8.1
12.7
9.4
93
155-164
5.1—5.5
4.1
8.7
13.8
9.9
109
3.5
8.4
13.2
9.7
101
165-174
5.5—5.9
4.2
8.8
14.1
10.3
116
3.8
8.5
13.4
9.9
105
175-187
5.9—6.2
4.4
9.1
14.8
10.7
127
Dulness in Children. — In children the heart is proportionately larger and lies more
transversely than in adults. The apex is usually in the fourth interspace lateral from the
nipple. Veith has shown that the cardiac shadow in children extends exactly twice as
far to the left as to the right of the midline (ML : MR 2:1).
Changes in the Relative Dulness. — The relative proportions of the
various conjugates undergo quite typical changes in various forms of heart
disease. In weakening of the right
heart, in tricuspid insufficiency, and
tricuspid stenosis the conjugate MR is
increased (dulness increased to the
right) ; in hypertrophy of the left ven-
tricle and in mitral insufficiency, dulness
increases to the left (MR increased),
while in the latter condition as well as
in mitral stenosis the oblique transverse
diameter (Q) is increased. In aortic
disease there is lengthening of the
long axis (L).
CARDIAC FLATNESS.
FIG. 95. — Cardiac outlines in
nine years.
The area of absolute dulness or
cardiac flatness represents the portion
of the heart which is not covered by
lung (Figs. 93 and 94). It forms a
triangle extending from the fourth rib above to within 2-3 cm. of the
apex, or even just to the latter in the fifth left interspace.
It is best mapped out by very light percussion, beginning over in the
fifth left interspace at the left sternal margin, percussing lateralward
and upward, passing from the absolute flatness to the area of impaired
resonance instead of in the opposite direction).
Variations in the Area of Flatness. — In the primitive mammals (dog,
cat, rabbit) the heart does not lie in close apposition to the chest wall, but
is slung rather loosely between the folds of the mediastinum and com-
pletely covered by lung. There is no area of flatness. This same condition
is met with in many otherwise normal persons, especially in the long flat-
chested, and in those who have extremely movable hearts or general mo-
bility of all the viscera (visceroptosis, enteroptosis, page 598).
Entire absence of cardiac flatness is also found in the exact
opposite type of chest, in the barrel-chest patients with emphysema, in
PHYSICAL EXAMINATION.
97
whom the exaggerated efforts at inspiration have caused the lungs to be
sucked in gradually between the heart and the chest wall.
On the other hand, the area of cardiac flatness is often
enlarged in persons with flat, rhachitic, or tuberculous chests. In
hypertrophy of the right
ventricle the area of flatness
is enlarged and the right border
becomes oblique , extending
downward to the right margin
of the sternum, often interrupted
by step-like protrusions (Kroe-
nig). In pericardial effusion it
extends well into the fifth right
interspace.
Changes in Size of the
Heart. — As seen in the investi-
gations upon cardiac volume,
the size of the heart, and hence
the area of cardiac dulness, is
subject to a physiological in-
crease when the heart is slow
and decrease in size when it is
rapid (Henderson, see page 9).
This decrease in size is especially
noticeable in certain cases with
rapid hearts, like paroxysmal
tachycardia when there is no
heart failure nor vasodilation
(Hoffmann, Dietlen). An in-
crease in size may be associated
with a slow pulse (see page 9
and Fig. 12), hypertrophy of
the heart, or with a pathological
dilatation. The physiological
condition should first be con-
sidered before assuming the
pathological.
Changes in Position of the
Heart. — (1) Upon changes in
posture. Normally changes
in posture are accompanied by
considerable changes in the
position of the heart. The apex may move 3-5 cm. when the patient
turns from one side to 'the other, always moving towards the side which
is lower. On standing a similar but less marked change occurs. Moritz,
and, later, Dietlen have shown that the area of the cardiac shadow is from
ten to thirty per cent, smaller on standing than on lying down. The latter
observer confirms Erlanger and Hooker in stating that the pulse-pressure,
and hence the systolic output of the ventricles, diminishes correspondingly.
7
Fro. 96. — Diagrams illustrating the movements of
the normal heart on change of posture from side to side
(A), and in the various phases of respiration (B). Solid
black line, normal cardiac outline in quiet breathing;
dotted line (R), cardiac outline with patient lying on
right side; broken line (L), cardiac outline with patient
lying on left side; EXP (horizontal shading), outline in
expiration; IS SI' (vertical shading), cardiac outline in
inspiration. The movements shown in these figures
represent the upper limits of normal mobility.
98 DISEASES OF THE HEART AND AORTA.
The diminished filling of the heart is due also to the fact that the pressure
under which the blood enters it in diastole (venous pressure) is lower upon
standing than upon lying down.
In some people extreme mobility (6-8 cm.) of the apex is found (wan-
dering heart) — a condition often associated with cardiac neurasthenia
and palpitation, and even paroxysmal tachycardia. Changes in position
of the diaphragm, upon expiration, inspiration, or intestinal flatulence, also
affect the position of the heart, especially upon standing; so that in
expiration or flatulence the apex is pushed up and the heart
lies more transversely, while in inspiration the apex falls and
the heart lies more nearly in the long axis of the body (Fig. 96). As can
be readily shown with Henderson's cardiometer, the former position inter-
feres with the cardiac filling and hinders the circulation, while the latter
position facilitates both. The amount of change of position of the apex
is normally about 1-2 cm.
AUSCULTATION.
CHARACTER AND TIME OF THE HEART SOUNDS.
The beat of the heart is accompanied by two definite sounds ordinarily
likened to the syllables "hib-dub" or "ta ta." the first sound accompany-
12 12
ing systole, the second occurring just at the beginning of diastole.
Graphic Records. — The exact period of the cardiac cycle to which they correspond
was first investigated by Bonders (1856), who marked the onset of the sounds by tapping
upon a receiving tambour the instant he heard sound and recording this signal upon a drum
while simultaneously recording the cardiogram. This method was subsequently developed by
Martius and has furnished some interesting information, but even in regular pulses the results
are very fallible and the method cannot be used at all when the pulse-rate is irregular.
CAROTID
PHONOGRAM
FIG. 97. — Graphic records of the heart sounds. (Kindness of Prof. Einthoven.) Each vertical division
represents .02 sec.
During the past fifteen years several methods of recording the heart sounds graphi-
cally have been devised (Einthoven and Geluk, Huerthle, Holowinski). Einthoven,
Flohil, and Battaerd place a microphone over the heart, connect the microphone with the
thread galvanometer, and photograph the movements of the latter.
O. Frank attaches the tube of a stethoscope to a tambour over which there is
stretched a delicate condom membrane bearing a small mirror. A beam of light is thrown
upon this mirror, and its movements, coincident with the sound waves in the stethoscope,
are recorded photographically.
A still more delicate method is that of Weiss and Joachim. Instead of
the condom membrane used by Frank, these investigators register the, vibrations of a soap
bubble film blown over their receiving tambour. To prevent bursting this is kept in a
moist chamber of glass. The vibrations are magnified by means of a small L of glass cap-
illary which rests upon the film. The movements of the shadow cast by the end of the L
are recorded photographically. Weiss and Joachim's results are at least as good as those
PHYSICAL EXAMINATION. 99
of Einthoven. Their records are similar and quite as delicate, and add much to our knowl-
edge of heart sounds. Moreover, they are able actually to synthetize and reproduce these
sounds by transferring their curves to zinc strips which are rotated upon a drum and set
a stile in motion. The vibration gives rise to sounds which they state have been identified
by other clinicians with those of the cases recorded.
Several methods of recording the heart sounds by vibrations of a gas flame
(Marbe, Roos) have been only moderately successful, and though simple are not as
satisfactory as the photographic methods.
Clinical Diagram for Heart Sounds. — In many text-books the heart
sounds are represented graphically in various ways, but it seems to the
writer that the best is to indicate the occurrence of the sounds directly
upon a simple diagram which indicates the relation to the auricular and
ventricular contractions, as shown in Fig. 98. l
CARDIAC CYCLE
HEART SOUNDS
FIG. 98. — Diagram for representing the heart sounds in clinical notes. Upper curve represents
the events of the cardiac cycle, the small auricular contraction followed by the larger ventricular con-
traction. Lower line represents the heart sounds. True heart sounds are represented by solidly shaded
blocks, whose height indicates their intensity and whose breadth indicates their duration.
CAUSES OF THE HEART SOUNDS.
First Sound. — Harvey states that "when there is the delivery of a
quantity of blood from the veins to the arteries, a pulse takes place which
can be heard within the chest." Laennec (1819) was the first to describe
the character of the sounds. He regarded the first sound as due to ventric-
ular systole, though he thought the second to be due to the contraction
of the auricle. In 1836, C. J. B. Williams and a committee of the British
Medical Association investigated the heart sounds experimentally. He
believed that the first sound was largely of muscular ori-
gin, like the contraction sound of skeletal muscles, because it could be
heard upon the excised heart even when the auriculoventricular valves
were held open with the fingers, but the second sound could not be heard
unless the aortic or pulmonic valves closed. This view was substantiated
by Ludwig and Dogiel; but Sibson and Broadbent found that in the exposed
heart of the ass the first sound begins with a sort of rumble, which disap-
pears when the blood flow is shut off by tying the venae cavae. This
rumble they ascribe to the movement of the auriculo-
ventricular valves.
Graphic records of the heart sounds by Einthoven, Flohil, and Battaerd
have shown that the first sound in man begins at the beginning of ven-
tricular systole and lasts .07 to .10 sec. It is loudest at its very
beginning, is deerescendo in character, and is almost
completed before the aortic valves open, — i.e., before the
heart has begun to pump blood into the aorta. The first sound is followed
1 Thus in cases of mitral stenosis (see page 348) the first sound may be short aud
tapping in character, though tracings show the systole to be of duration no less than that
met with in the absence of tapping character ( Hi rschf elder).
100 DISEASES OF THE HEART AND AORTA.
by the short pause, which usually lasts .15 to .25 sec., and which is then
followed by the second sound. Einthoven's results have been confirmed
in man by the records of Weiss and Joachim, Hess and Frank, as well as
by Prof. Barker, Dr. Bond, and the writer. In the dog, R. H. Kahn has
shown that the duration of the first sound is exactly coincident with the
period during which the intraventricular pressure is rising, while the dura-
tion of the short pause is exactly coincident with the systolic plateau.
Sahli and other clinical observers believe that the first sound at the
aortic area begins later than that at the apex and is due to the rush of
blood from the ventricle into the aorta, but graphic records seem to indicate
that the sounds in the two areas are synchronous, and begin before the
aortic valves open.
However, the first sound heard on listening in the suprasternal notch
is often split; and it is possible that the latter portion of this sound is due
to just such a forcible distention of the aorta.
The valvular element of the sound is probably brought about when
the valves are thrown into tension by the ventricular systole. The normal
valves give no sound at all when they open spontaneously.1 There is no
evidence to indicate that the normal sound is brought about to any extent
by eddy currents as are thrills or murmurs, nor does systole of the auricles
produce any portion of the normal first sound (Einthoven) .
Hess and Frank believe that the movement of the heart within the
chest and perhaps against the chest wall (systolic erection) may be an
important factor in the production of the first sound. This might explain
why the heart sounds are occasionally inaudible in emphysematous per-
sons in whom the organ is separated from the chest wall by a layer of lung.
On the other hand, this factor is shown to play only a minor role by the
fact that the first sound may be heard in its normal intensity in the exposed
and even the suspended dog's heart.
Second Sound. — The second sound has been shown by C. J. B. Williams
and the British Commission to accompany the closure of the aortic and
pulmonary valves, to be modified when these valves are injured, and to dis-
appear when they are held against the vessel wall. It lasts about .05 second.
It is loudest when the blood-pressure is high, when the valves are thicker
and more rigid than normally, or when the vessel walls are more elastic
than usual, the intensity varying at different times of life and under patho-
logical conditions.
METHODS OF AUSCULTATION.
Monaural Stethoscope. — The monaural stethoscope, introduced by
Laennec, is a simple wooden tube surmounted by a flat disk acting as an
ear-piece and resonator. The tube is pressed against the chest and the ear
laid upon the disk, so that the observer receives at once the sound and the
thrill in the wood transmitted directly. Obviously this method accentuates
the notes of low pitch which are nearest to the essential tone of the
instrument (and constitute most of the normal sounds), as well as those
1 Both the valves and the cardiac walls are at that time extremely lax and the val-
vular opening is almost equal to the diameter of the ventricular chamber.
BAD GOOD
•sKSlRp ; ffeSffg? JsS^Sf?--
PHYSICAL EXAMINATION. 101
of relative loudness, which cause it to vibrate mechanically. Hence it
is particularly adapted to the detection of presystolic and other rum-
bling murmurs, and is the method used almost exclusively outside of the
United States.
Binaural Stethoscope. — In the United States the binaural stethoscope
is in more general use. This consists essentially of a small receiving bell
which is placed upon the chest wall, and from which two tubes lead off to
small rubber ear-pieces which fit tightly into the external auditory meatus.
The most important essentials in these three forms are, (1) a bell composed
of various materials — ivory, wood, celluloid, or hard rubber — provided with
a sufficiently large air space at the tip (Emerson) : (2) ear-pieces perfectly
fitting the ear of the individual. It is safe to say that more errors of auscul-
tation result from poorly fitting ear-pieces than from real inefficiency on
the part of the listener. (3) In stetho-
scopes in which the ear-pieces are held | GQOD
in the ears by a spring this should not
exert excessive pressure lest it produce
sounds within the ear from the pressure
on the drum.
There are three main forms of binau-
ral stethoscope: (1) those with rigid FIG. 99.— Choice of stethoscope bells,
tubes (Gannett Js), (2) those with soft
rubber tubes, (3) those with soft rubber tubes, flat bells, and a small elastic
disk of metal or celluloid to act as a resonator (Bowles). Of these three
forms it may be said that the rigid tubes certainly convey the sounds some-
what better, but this is often more than compensated for by the better
fitting of the ear-pieces in stethoscopes with soft rubber tubes. In steth-
oscopes with disks certain sound waves, and particularly those of high pitch
(soft blowing murmurs), are accentuated, while other sounds may be rela-
tively suppressed. Moreover, any movement of skin or hair over the disk
may give rise to a sound simulating a friction, and this source of error
must be carefully excluded. Hair should be moistened, and a small bell
should be used with perfect approximation to the skin throughout its
circumference.
Alteration of Sounds by Pressure. — Emerson has shown that many
murmurs, especially presystolic and snapping sounds, are diminished or
obliterated by pressure with the stethoscope, while certain others are inten-
sified by pressure, and that this is dependent upon the pitch of the sound
and not upon the site of its production. It is therefore important for the
observer to listen carefully, first with the lightest possible pressure upon
the stethoscope and then with gradually increasing pressure. He should
do this consciously and as a matter of routine, rather than allow such
sounds to escape him or stumble upon them by accident.
Moreover, since the monaural and binaural stethoscopes each intensify
different sounds, both should be used in any important or dubious case
before the examination is concluded.
Graphic Methods. — As stated above, the most accurate and reliable
information which has thus far been obtained is that obtained by means
of the recording microphone. Unfortunately, however, all the methods
102 DISEASES OF THE HEART AND AORTA.
thus far devised have been too cumbersome for the bedside or even for
routine hospital use. They are of value only in exceptional cases for re-
search, but there is no doubt that the future of scientific auscultation lies
in this field.
"VALVULAR AREAS" IN AUSCULTATION.
The various cardiac sounds are best heard over certain definite locations
corresponding more or less to the structures in which they arise, but par-
ticularly to the course of the blood current and to their mode of origin
(Fig. 100) . Thus the sounds produced in the left ventricle are best heard
at the apex; those produced at the aortic orifice, though produced behind
the sternum, are heard just to the right of it in the second interspace; the
pulmonary sounds are carried to the second left interspace at the sternal mar-
gin; while the sounds from the right ventricle are heard over the entire body
of the .sternum, over the greater part of the area of absolute dulness, and over
the base of the ensiform cartilage. Abnormal sounds, murmurs, etc., have,
however, a different distribution
which will be discussed later.
Normally the first sound at
the apex and everywhere else
below the third rib is louder
than the second sound. It is
also of longer duration than the
latter (.08 second as compared
to .05). Over the aortic and
pulmonic areas it becomes some-
what fainter, begins a trifle later,
and is of longer duration than
over the apex. The second sound
is then louder than the first.
FIG. lOO.-The "valvular areas." The S6COnd SOUnd at the
second left interspace (pulmonic
second) is usually louder than that over the second right (aortic second) up
to the age of 25 to 30, when the latter becomes the louder (Cabot).1 This
varies greatly in different individuals. Mere changes in blood-pressure are
not sufficient to account for all these conditions, since the pressure in the pul-
monary artery is never more than half that in the aorta, but proximity to
the sternum, greater elasticity of the walls, etc., combine to bring about
the relative loudness of the second pulmonic sound, . and therefore any
further increase in pressure in either artery alters the relation of the two
sounds to each other, increased pulmonary pressure increasing the pul-
monic second, increased general blood-pressure increasing the second
aortic, etc. The progressive thickening of the aortic semilunar valves
after the age of 30 also contributes to the intensity of the sound.
Other Sites for Auscultation. — Boy-Teissier has also recommended auscultation in the
suprasternal notch, pressing the bell of the stethoscope as far down behind the
manubrium as possible. In this way he states that he can hear aortic diastolic murmurs
1 Directly over the exposed aorta the sound is louder than over the exposed pulmo-
nary artery. (Thayer.)
PHYSICAL EXAMINATION.
103
Fia. 101. — The propagation of the heart sounds from valves to chest wall. A. Course of the sound
waves within the heart. B. Propagation of the heart sounds at the level of the second interspaces.
C. Propagation of the sounds at the level of the fourth and fifth interspaces.
104 DISEASES OF THE HEART AND AORTA.
not otherwise audible. He thinks that he is also better able to distinguish the character of
aortic systolic murmurs. The method has never gained general usage, and the writer is
unable to find in it any of the advantages claimed by Boy-Teissier. The chief value of
suprasternal auscultation is found in persons whose heart sounds are feeble or inaudible
over the precordium. It must be borne in mind, however, that the mitral murmurs are not
well transmitted to this region, and that the first sound heard there is frequently redupli-
cated or split.
Another form of auscultation not in general use is the auscultation
through the stomach-tube, introduced as for a tracing from the left auricle.
This method, first used by A. Hoffmann in 1892, has been revived by Gerhartz, but, though
it might throw some light upon the nature of an occasional mitral murmur, it is in general
difficult and very inconvenient to carry out; and in many cases at least the murmurs are
no better heard than over the chest wall. Nevertheless where it is important to know
whether a murmur is conducted back into the left auricle, a positive finding by this would
be conclusive.
EMBRYOCARDIA.
Ordinarily the diastolic pause between sounds is longer than the sys-
tolic period, and the interval between the second sound of 'one cycle and
the first sound of the next is longer than the interval between the first
and second sounds of the same cycle. However, when the heart-rate is
very rapid, the diastolic pause may become shortened to about the same
interval as that between the first and second sounds (long p a u s e =
short pause), so^that the sounds succeed one another at uniform inter-
2 12 i
FIG. 102.— Graphic records of the fetal heart sounds. (After Weiss and Joachim.)
vals like the ticking of a clock. This rhythm is heard normally over the
fetal heart and hence has been termed embryocardia or fetal rhythm. It
also occurs in adults when the rate is very rapid (120 and over), and hence
under conditions in which the heart is under an abnormal strain (see page
227), as in fevers with high temperature, acute heart failure, and acute
overwork of a chronically diseased heart, also in cases of paroxysmal tachy-
cardia and allied conditions. Its absolute significance is simply that of the
rapid heart-rate to which it corresponds.
ACCESSORY HEART SOUNDS.
REDUPLICATED SOUNDS AND GALLOP RHYTHMS.
Reduplicated Sounds.— Occasionally one or the other of the two normal
heart sounds is replaced by two clear sounds, or, in other words, there is a
reduplication. This reduplication may occupy the place of either the first
or the second sound, and, as already noted by Skoda, it may seem to be
PHYSICAL EXAMINATION.
105
due to, (1) splitting of the normal sounds into two distinct portions, or
(2) pressure of an accessory sound besides the normal^ sound, being in the
latter case presystolic (before the first sound) , protodiastolic
(shortly after the second sound), or mesodiastolic (in mid-diastole).
The relation of groups 1 and 2 to one another and to the cardiac cycle is
shown in Fig. 103.
INTRAVENTRJCULAR PRESSURE
VOLUME OF VENTRICLES
PRESYSTOLIC GALLOP
SPLIT FIRST SOUND
SPLIT SECOND SOUND
PROTODIASTOLIC GALLOP
LUB DDB — DA
Fio. 103. — Diagram illustrating the split sounds and gallop rhythms and their phonetic equivalents.
As to the causation of these abnormal sounds, little definite is known. A great deal
of the indefiniteness which permeates the enormous literature upon the subject is due to
the failure of the writers to distinguish clearly between the different forms with which
they are dealing. The presystolic and protodiastolic forms are grouped under one head
regardless of their relations to mechanism or etiology; it is mainly due to the writers of the
French school under the leadership of Potain that the differentiation has reached even its
present stage of development. L. Bard, of Geneva, has recently given an excellent analysis
of the subject from this stand-point.
According to Bard, the two main groups of accessory sounds are:
(1) The presystolic gallop reduplication (ta-ta-tat) or ta ta tat, to which the term
1 *
gallop rhythm should be limited, most commonly met in nephritics with cardiac hyper-
trophy and in other heavily beating hearts.
(2) The protodiastolic sound ta ta ta (lub-dub-da), called by Bouillaud bruit de
1 3
rappel, — "sound of recall" or "diastolic echo," — frequently heard at the apex in mitral
stenosis. Bard thinks that the above-mentioned accessory sounds are to be regarded as
merely the exaggeration of vibrations normally present but normally inaudible.
Split Sounds. — The sounds (tlat-tat; tat-tatl) are characterized by the
1212
absolute similarity and short interval between the two portions, and may
be due either to slight asynchronism of the two ventricles (C. J. B. Williams,
1836, Skoda, Gibson, 1874) or slight separation of two parts of the ven-
tricular sound, which are of different origin but ordinarily fused.
As has been seen, the ventricular sound contains both a valvular (auriculoventric-
ular) and a muscular element, and perhaps also an element due to the stretching of the
walls of the aorta. Bard thinks that variation in either the muscular or the valvular
element might give rise to their separation into two sounds. The question of asynchronism
of the two ventricles which arises in this connection is one which was long without an
experimental basis, but the recent observations of Stassen, Kraus and Nikolai, and Hew-
lett indicate the possibility that it may occur clinically. Stassen, in Fredericq's labora-
tory, has recorded asynchronous contractions of the two ventricles when the latter were
recovering from vagus inhibition, and also with ventricular extrasystoles produced during
periods of vagus inhibition. The writer has on one occasion heard a split first sound in an
animal in which the contractions of both ventricles were being recorded with myocardio-
106 DISEASES OF THE HEART AND AORTA.
graphs. The ventricular contractions were slightly asynchronous. In a number of other
instances in which no split first sound could be heard the contractions were absolutely
synchronous. However, no conclusions are justified from an isolated observation.
The splitting of the first sound is best heard over the base and body
of the heart, in contrast to the accessory sounds which are best heard at
the apex (see below). As to the splitting of the second sound, this likewise
may be due to slight asynchronism of the two ventricles, or to the fact that
even without this the semilunar valves may not close at exactly the same
instant. It is often possible, by passing the stethoscope along the second
right and left interspaces, to determine which second sound lags behind.
It must be added, however, that, as Bard himself states, no accurate
knowledge of either the split sounds or the accessory sounds can be gained
until they are registered graphically by cardiophonographic methods along
with simultaneous venous, arterial, or cardiographic tracings, so that their
APEX
PHONOGRAM
Ti5 SECONDS
PRE. 1 SYST. A 2 B
FIG. 104. — Graphic record of a split pulmonic second sound. (After Weiss and Joachim.) PRE.,
presystolic rumble; SYST., systolic murmur; 1, first heart sound; 2 A, B, two parts of split second sound
(.04 sec. apart).
exact relation to the cardiac cycle may be determined. So rapid is the
sequence of the sounds that in an individual case the differentiation between
split and accessory sounds is often difficult.
Reduplication of the First Sound from Pericardial Adhesions. — Reduplication of the
first sound is also heard in a number of cases in which old pericardial and pleura! adhesions
are found at autopsy (Sewall), which may be easily understood to give an abnormal sound
in systole. Just how commonly this group occurs has not been determined statistically,
but under these conditions it need not signify any disturbance of function.
Presystolic Gallop Rhythm. — As regards the accessory sounds, the
great majority of writers take the view suggested by Exchaquet in 1875
and Johnson in 1876 that the first sound of gallop rhythm (presystolic
sound) is due to the vigorous systole of the auricle, a view which is further
supported by the studies of Kriege and Schmall (1891), Friedrich Muller
(1906), G. C. Robinson (1908), and others. According to Muller, Marey
believed that the extra sound was produced by the auricle sending blood into
a defectively emptied ventricle, a view which has been revived by Sewall.
Moreover, the writer has been able to show on the excised heart that when
the ventricles are distended under a slight positive pressure the auriculo-
ventricular valves may open along only a small extent of their line of clos-
ure. This gives rise to a slight functional stenosis at the point where they
actually open, a fact which may account for the audible auricular con-
traction. Muller considers that the extra tone may be dependent upon a
PHYSICAL EXAMINATION.
107
delay in the time between the auricular and ventricular contraction, pos-
sibly due to lowered conductivity in the atrioventricular bundle of His,
and when the two contractions are abnormally separated two sounds
instead of one are produced. Tracings, however, do not usually show
delayed conduction.
All these writers base their views upon the fact that the sound appears to be pre-
systolic in time and that in many cases a well-marked auricular wave may be seen upon
the cardiogram at a corresponding point of the cycle. It must be added that this is also
seen in many cases in which there is no gallop rhythm, and that it seems to be dependent
more upon the prominence of the apex impulse in the interspace facilitating the record
than it does upon the existence of the sound. However, this wave is often quite as prom-
inent in the curves (protodiastolic sound) in which no presystolic sound was heard as in
those used to illustrate the gallop rhythm itself. The proof is therefore insufficient, but
that does not mean that the theory is necessarily wrong. It is not at all improbable that
the forcible contraction of an overloading auricle may give an audible sound just as it
does when forcing blood through a narrowed orifice (presystolic rumble), but this has not
yet been proved and will require careful investigation with the cardiophonograph. The
possibility of functional mitral stenosis like those mentioned on page 371 must also be borne
in mind.
Another explanation for the phenomenon is that the sound occurs during the ven-
tricular systole, as suggested by H. Chauveau, who thought it due to the tension of the
auriculoventricular valves. His apex tracings, however, are not carefully timed and might
quite as well be interpreted as evidence of the auricular sound.
The numerous reviews of the literature, such as those of Obrastow, Pawinski, Robin-
son, shed no further light upon the subject.
Clinically, the presystolic gallop rhythm is usually met with in cases
with rapid hypertrophied hearts which are under a slight overstrain, as in
the classical group of chronic nephritis, chronic cardiac disease, aneurism,
cases with arteriosclerosis, exophthalmic goitre, mitral stenosis, and acute
fevers. Occasionally it is heard in normal individuals (Krehl). It seems
in most cases to accompany slight
overwork of the heart, but its me-
chanical and physiological significance
is still not clear.
Protodiastolic Gallop Rhythm.
Third Heart Sound.— The role of the
protodiastolic sound (bruit de rappel,
diastolic echo) seems to be more
definitely established. Though
already heard by Bouillaud in 1835,
in mitral stenosis, its occurrence was emphasized by Duroziez (1874) and by
Sansom (1881), who term it the "opening snap" of the mitral valve, indi-
cating that it was brought about by the opening of the stiffened valve.
Barie (1893) and Thayer (1906) called attention to its occurrence in normal
individuals. In 1907 the writer observed this sound in a normal individual
with a slow and vigorous heart, whose venous pulse showed a peculiar extra
wave (Fig. 106, h) which follows the inflow of blood into the ventricle
(as indicated by the normal v wave, Fig. 106, page 108).
The writer also called attention to the fact that this wave bore a close relation to the
end of the rapid filling of the heart (or diastole proper) upon the volume curve of the ven-
tricles, and that Henderson had claimed that at this time the mitral valves and triscupid
were closed by the elastic recoil of the heart walls. That this actually takes place and is
FIG. 105. — Graphic record of the third heart
sound. (Kindness of Prof. Einthoven.)
108
DISEASES OF THE HEART AND AORTA.
dependent upon a high venous pressure can be shown on the dead heart by pouring water
into the ventricles from a beaker after the auricles have been cut off in the manner devised
FIG. 106. — Jugular and carotid tracings from a normal individual with a well-marked third heart
sound, showing a large h and a smaller preauricular wave (w). ? indicates a small wave in middiastole
following the h wave, occasionally found though perhaps an artefact.
by Baumgarten (1843). If the water is poured from just above the valves they merely
float out a little toward the middle of the orifice; if from the height of about 10 cm. they
float into apposition; if from 50 cm. above they are left tightly closed when the flow ceases.
These observations have been confirmed recently by C. Lian in Fran9ois-Franck's labora-
tory. Hirschfelder also suggested that this clos-
ure of the valves may be sudden and vigorous
enough to cause a sound.1 The relation of this
sound to this portion of diastole seemed quite
definite by comparison with a graphic record of
this sound made at about the same date by
Einthoven (Fig. 105), which shows it to occur
0.18 second after the second sound. This ex-
planation has also been supported by A. G.
Gibson and Professor Thayer. The tracings of
Robinson, who was investigating the subject
from a different stand-point, have also shown
the constant presence of the h wave upon the
venous tracings accompanying this sound. Rob-
inson and Thayer have also shown that it accom-
panies a wavelet p upon the cardiogram in early
diastole (Fig. 88, I, page 91), probably due to
the filling of the ventricles. They find this wave
upon the cardiogram in almost all cases of pro-
todiastolic gallop rhythm, and regard it as char-
acteristic of the latter. Thayer has demonstrated
that it cannot be an artefact, since it is often
both visible and palpable, and hence
can often be found by the ordinary simple
methods of physical examination. Some venous
tracings made from animals by Eyster, along
with the volume curves of the heart, show that
the rise at the foot of the h wave occurs at the
end of the rapid diastolic filling (Thayer). According to these explanations the sequence of
events would be as follows : The end of diastole is marked by the second heart sound and by
the fall in the cardiogram. The tricuspid and mitral valves open almost instantaneously, but
a period of about TV second is required before the fall of pressure is transmitted to the jugu-
lar vein and the pressure begins to fall (v—y collapse) . The inrush of blood into the ventricles
VOL
FIG. 107. — Forces supposed to be at work
in the production of the third heart sound.
Diastolic closure of the auriculoventricular
valves. Dotted lines indicate the direction
of inflow. Black arrows indicate the recoil
waves tending to push the cusps together.
1 The assumption of such a slapping together of the auriculoventricular valves at the
end of ventricular filling is not at all incompatible with the fact that a small separation (1-3
mm.) may reappear between them in the latter part of diastole, when the accumulation of
blood in the auricles has become sufficient to just force the cusps apart (page 371).
PHYSICAL EXAMINATION. 109
rapidly distends the latter until they reach their full diatention, at which the inflow ceases and
the cusps of both mitral and tricuspid valves slap together (closing slap in diastole).
The end of this inflow may be accompanied by a slight recoil or similar movement of the
ventricle, giving rise to the small wave and shock noted at this moment. The intensity
of this recoil is probably dependent to a great extent upon the elasticity (elastic tissue)
of the ventricular walls; hence its absence in old persons. Whether the feeble
third heart sound is due to the slapping together of the valves
or is due to some other cause cannot be stated with certainty. After the period of
diastasis (slower inflow) has set in, the blood begins to accumulate in the veins, which
are distended at first rapidly and later in diastole more gradually.1 The angle made by
these two portions of the venous curve forms the h wave. The foot of the p wave com-
mences at the end of the period of rapid ventricular filling and corresponds to the crest
of the protodiastolic wave upon the cardiogram.
A priori, according to this explanation a protodiastolic sound should
be heard in slow hearts because in them the ventricular walls are distended
to their full extent early in diastole ; in cases of aortic insufficiency because
of the high intraventricular pressure which tends to slap the cusps of the
valves together early in diastole; in mitral stenosis owing to the peculiar
events in the filling of the ventricle (vide page 9), and perhaps in cases
in which there is a large amount of residual blood in the ventricle (dilata-
tion) which tends to diminish and shorten the period of inflow. These
represent the chief conditions in which it is actually heard. Thayer
states that it can be heard at the apex in about 30 per
cent, of normal individuals lying upon the left side.
By decades its frequency was as follows; First decade heard in 58.9
per cent.; second decade 84.4 per cent.; third decade 50.9 per cent.; fourth
decade 42.3 per cent.; fifth decade 14 per cent.; sixth decade and after 0.
It seems to occur in practically every condition, especially in cases with
slow hearts, and seems to bear no definite relation to cardiac weakness.
MURMURS.
MECHANICAL FACTORS IN THE PRODUCTION OF MURMURS.
As has been seen above (page 92), when a narrowing occurs in the
lumen of an elastic-walled tube through which liquid is flowing, eddies are
formed which set the walls of the tube into vibration and give rise to a pal-
pable thrill. Accompanying the thrill a blowing sound known as a " mur-
mur" may be heard over the tube; which, like the thrill, is heard much
better below the obstruction than above it, and is transmitted in the direc-
tion of the flow. The character of a murmur depends upon the width of
the orifice at which it is produced, upon the nature of the walls of the
orifice, upon the velocity and tension under which the fluid passes through
it, and upon the direction in which the flow occurs.
In this way a valvular orifice may be compared to the larynx
with its vocal cords. When the cords are lax and wide apart, the air moving over them in
even forced respiration gives no sound; when the cords are approximated a little but still
held loosely, it gives a whispered "ch" sound, and when they are held very tense true
vocal sound is heard. Similarly, no sound can be heard over the excised heart when the
fluid regurgitates through an absolutely patent mitral orifice (Fig. 108) ; if one of the chord®
tendineaj be stretched and the regurgitation takes place through a small slit whose walls
1 It is not improbable that, though the cusps are in apposition along the greater part
of their line of closure, they are separated at a few points during diastasis.
110
DISEASES OF THE HEART AND AORTA.
are flabby (relative insufficiency, Fig. 108), a soft low blowing murmur will be heard (the
smaller this orifice the higher pitched and more distinct the murmur); while if some more
or less hard irregular body, like calcified vegetation, is situated at the orifice, this acts more
or less as a resonator, increases the sound, and may even give it a roaring or a squeaking
(musical) character.1
FIG. 108. — Similarity between production of voice sounds and the production of murmurs. (Kindness
of the J. Am. M. Asso.) A, B, C, vocal cords; D, E, F, auriculoventricular valves; G, H, I, aortic and pul-
monic valves. A (high note), D, G, small leaks producing high-pitched murmurs; B (low note), E, H,
larger leaks producing low-pitcned murmurs ; C, F, I, very large leaks, producing no murmurs.
Occasionally murmurs become so loud as to be heard several feet away
from the chest or even across the room. Such murmurs are usually systolic
in time and are often due to calcified vegetations, arterial plaques, or aortic
or mitral stenosis. As in the larynx, the character of the sound produced
at a valvular orifice is due not only to the size and shape of the orifice, but
also to the tenseness of the walls and velocity of blood flow through it, and
hence is largely dependent upon the height of the blood-pressure. All
these factors, both the widening of the leak and the decreased force of the
beat, explain the fact that as the heart weakens under the influence of the
lesion the murmur may acutally disappear.
CHARACTER OF MURMURS.
Murmurs may be roughly divided into the following classes: (1) Direct mur-
murs best transmitted in the direction of the blood flow, as from stenoses or calcified
plaques; (2) Regurgitant murmurs due to a flow in the direction opposite to the
1 Musical or squeaking murmurs are sometimes due to the presence of tense mod-
erator bands stretching across the ventricular cavity and resounding like banjo strings,
although usually these bands do not cause murmurs at all.
Very frequently they arise in dilated right ventricles in association with functional
tricuspid and perhaps functional pulmonary insufficiencies. They are usually systolic,
but sometimes diastolic in time. They are often cardiopulmonary.
PHYSICAL EXAMINATION. Ill
usual blood flow (as in mitral and aortic insufficiencies); (3) To-and-fro " machinery "
murmurs which occur in both systole and diastole in congenital heart lesions; (4) Rum-
bling murmurs.
Of these 1, 2, and 3 are more or less blowing or roaring in character;
while the rumbling murmurs are devoid of this character, and are rumbling
or echoing, more like a series of heart sounds which vary in intensity (mitral
stenosis, Flint murmur) than like murmurs due to the passing of a stream
through an orifice.
Brockbank claims that these may be produced upon a model by means of a stream
flowing through a conical valve from apex to the base of the cone. The mechanism of the
production of such murmurs is still very obscure, and further researches are necessary
before satisfactory elucidation can be given.
"ACCIDENTAL," "H.EMIC, " AND " CARDIOPULMONARY " MURMURS.
Murmurs over the heart without the presence of valvular lesions are
so common that autopsy evidence led Laennec to the erroneous belief that
murmurs (bruits de soufflet) were of no diagnostic importance whatever.
Such murmurs are designated by various terms : "Haemic,"on
the assumption that they are always due to anaemia, hydraemia, or other
changes in the quality of the blood; "Functional" or "inorganic,"
because they are not associated with organic lesion; "Cardio pulmo-
nary" or "cardiorespiratory," on the assumption that they arise in the
lung above the heart and not in the heart itself; and "Accidental," since
they are not associated with any discernible alteration in form or function.
These terms are not mutually exclusive; but, since the term "functional"
has been used to designate conditions in which there is actual leakage
owing to muscular weakness, and since " inorganic" should include both
"functional" and "accidental," the term "accidental" appears to be
the one most generally useful. Thus, one murmur may be said to be an
accidental murmur of haemic origin, while in another case the accidental
murmur may be of cardiopulmonary origin.
Occurrence of Accidental Murmurs. — Potain, who has made the most extensive inves-
tigations upon the subject, found such murmurs in one-eighth of all the patients seen in his
hospital service. It was present in almost all his cases of Basedow's disease (exophthalmic
goitre). In chlorosis the frequency was 50 per cent.; in rheumatism, measles, and scarlet
fever, 20-25 per cont.; in typhoid, 16 per cent.; in pulmonary affections, 5-10 per cent.
These murmurs were common in subjects in the first three decades of life, reaching maxi-
mum frequency at the ages from 20 to 30, and gradually decreased in frequency after the
age of 3,0. For description of the murmurs Potain divided the precordium into the fol-
lowing regions: 1. About the apex (apical zone); 2. Above the apex (supra-apical); 3.
Lateral from the apex (para-apical); 4. In front of the infundibulum and conus arteriosus
of the pulmonary artery (pre-infundibular); 5. A zone between the pre-infundibular
region and the apex (left preventricular) ; 6. An area behind the sternum (sternal region);
7. A region behind the xiphoid (xiphoid region). The murmurs are most common in the
region lying between the pulmonary area and the apex (Potain's left ventricular region),
— that is, in the region above the right ventricle and the interventricular septum.
Character of Accidental Murmurs. — T hese murmurs usually
are soft and blowing, and often seem rather super-
ficial. They vary greatly when the patient changes
his position. Sometimes they are best heard when the patient is
112 DISEASES OF THE HEART AND AORTA.
lying down and diminish or disappear entirely when he stands or sits
up; sometimes they appear only when the patient's position is vertical
and disappear on his lying down. They also vary with the phases of
respiration.
Time of Accidental Murmurs. — As regards their occurrence in the
cardiac cycle, accidental murmurs are most commonly systolic in time,
though occasionally diastolic. Potain calls attention to the fact that mur-
murs may occupy either the whole of systole (holosystolic) or only
a portion of it. The latter may occur only at the very beginning of systole
(protosystolic), so that they accompany or replace the first heart
sound. Or, they may be heard in midsystole (mesosystolic), in
which case they follow the first sound but are separated from the second
sound by the short pause, which is then somewhat shorter than usual.
Or, they may occur at the very end of systole (tele systolic) and
end, without interruption, in the second sound. According to Potain,
the murmurs of mitral and tricuspid insufficiency
are heard throughout the entire duration of systole,
a view which is confirmed by the graphic records of Einthoven and Weiss
and Joachim. The accidental murmurs, however, are con-
fined to only a portion of systole. Potain believes
that, as a rule, they are entirely mesosystolic; while
Weiss and Joachim, from both auscultatory and graphic evidence (Fig.
110), believe that they also accompany and modify the first sound though
they do not replace it; in other words, that they occupy both the proto-
systolic and the mesosystolic portions of the systole.
Sahli states that accidental murmurs never occupy the very end of
systole (telesystolic, Potain; prediastolic) , but Potain has shown that
though such murmurs are rare they occur occasionally.
Accidental diastolic murmurs are also rather common, and may occur
either in the aortic region, behind the sternum, or along the upper left
border of cardiac dulness. Occasionally they are heard at the apex. They
are usually short superficial puffs following a well-marked second sound
and lasting during only a short portion of early diastole.
Differential Diagnosis of Accidental Murmurs. — Potain gives the following points in
which other murmurs differ from the cardiopulmonary.
1. Pulmonary Stenosis: loud, rough holosystolic murmur, maximum in
second left interspace, transmitted toward left clavicle; always accompanied by a thrill.
The accidental murmur is soft, often mesosystolic, devoid of thrill.
2. Pulmonary Insufficiency: diastolic murmur, maximum in second left
interspace; pulmonic second sound absent or diminished. The accidental diastolic murmurs
very rarely have their maximum in the second left interspace.
3. Aortic Stenosis: rough holosystolic murmur, maximum in second right
interspace, propagated toward right clavicle; accompanied by thrill. The heart is hyper-
trophied. The accidental or cardiopulmonary murmur in this region is more superficial,
soft, and changes on change of position.
4. Anaemia: murmur very similar to that of aortic stenosis, but the thrill is less
marked and the heart is small or dilated rather than hypertrophied.
5. Aortic Insufficiency: murmur commences exactly at the beginning of
the second sound and almost entirely fills diastole; whereas the cardiopulmonary diastolic
murmur follows the second sound, often after a short intervening pause (i.e., the murmur is
mesodiastolic). Both aortic and accidental murmurs are of wide distribution, embracing
the entire precordium, and varying greatly with change of position.
PHYSICAL EXAMINATION 113
6. Patent Septum of the Ventricles: holosystolic murmur loudest at
the third left interspace; rough, always accompanied by a thrill; whereas the accidental
and cardiopulmonary murmurs are not.
7. Mitral Insufficiency: murmur holosystolic, usually rather rough, maxi-
mum at the apex. The cardiopulmonary murmur may have its maximum two or three
centimetres lateral wards from the apex; and this is usually associated with a systolic retrac-
tion at the apex.
8. Tricuspid Insufficiency: murmur maximum over sternum and xiphoid
process. There is an increased area of flatness (hypertrophy of ventricles). This murmur
is also increased by leaning forwards so as to throw the heart against the chest wall.
Nature and Causation of Accidental Murmurs. — The facts mentioned
above apply to a large number of cases in which murmurs have been heard
during life, but in which no leaks and no lesions of the heart were demon-
strable at autopsy.
A large variety of factors have been mentioned to explain these accidental murmurs:
H.-umic Murmurs. — Bouillaud was the first to call attention to the fact that mur-
murs were more readily produced in the less viscous blood of
anaemia than under normal conditions; a fact which was subsequently
verified by Cohnheim; but Bouillaud himself realized that, though anaemia might give rise to
some of the accidental murmurs, there were many cases in which it could not be a factor.
The blood counts made in later decades have entirely substantiated Bouillaud's conserva-
tism. However, numerous observers from Bouillaud's time to the present have adhered
to the "hsemic" origin of the accidental murmurs. Sahli goes so far as to state that
they may in reality be only venous hums transmitted to the
ventricles, though he does not explain why they should be systolic in time. Even
though this explanation is inadequate, it is certain that in cases of grave anaemia such trans-
mitted murmurs do arise. They are heard very loudly over the aorta and second right
interspace, but are loud, rough, and superficial, quite different from the gentle blow of the
usual accidental murmurs.
Functional Insufficiency of the Auriculoventricular Valves, especially of the mitral,
was supposed by Naunyn to be the chief cause of the accidental murmur in the pulmonary
area. Naunyn believed that this murmur was transmitted from the left auricle directly to
the pulmonary artery and thence to the chest wall in the pulmonary area. However, in
these cases the murmur may not be heard at all in those areas in which the definite mitral
and tricuspid murmurs are best heard. Functional insufficiency of the tricuspid valve
has also been assumed, but this is rendered improbable by the fact that these murmurs have
a very different distribution from those of the tricuspid and are rarely heard over the
xiphoid process. In dogs the writer has found accidental murmurs very common; but,
in contrast to the murmurs in tricuspid or mitral insufficiency, these accidental
murmurs cannot be heard over the right or left auricle. In man
also they are not heard over the region of the right auricle, even when the patient is made
to lean forward and the walls of that chamber are thus pressed against the chest wall.
Functional Stenosis of the Pulmonary Artery and Infundibulum has been assumed by
Luethje in order to explain the production of systolic murmurs in the pulmonary area.
It is true that the pulmonary artery makes a sharp bend just behind the second left inter-
space; and also, as Romberg and others have shown, that often the accidental murmur is
increased by pressure with the stethoscope. Against this view are the softness of the
murmur, the absence of a thrill, and the fact that it is not transmitted toward the left
shoulder, but is well heard over the right ventricle. Moreover, in dogs the accidental mur-
mur may persist in practically every position in which the heart may be held.
Eddy Currents within the Ventricles.— Hilton Fagge has called attention to the fact
that eddy currents may arise within the ventricles, as the blood passes between the papillary
muscles and the trabeculse carneae: that these may strike against the bases of the papillary
muscles and the chorda? tendineae, set them into vibration while they are tense during
systole, and thus give rise to a systolic murmur. Although Fagge himself believed that
this would apply only to a dilated heart, it seems also applicable to a small heart, since
during systole the apertures between the walls and the papillary muscles are smaller and
more slit like. However, the explanation lacks confirmation.
8
114
DISEASES OF THE HEART AND AORTA.
Similar to this view is the old-time assumption that accidental blowing as well as
musical murmurs indicated the presence of a moderator band across the chamber of the
right ventricle, but this is not borne out by autopsy experience.
Cardiopulmonary Factors.— Laennec in 1826 wrote: "In certain persons the pleurae
and the anterior borders of the lungs extend in front of the heart and cover it almost entirely.
If one examines such a person when his heart is beating more forci-
bly than usual, the diastole of the heart, compressing these
portions of the lungs and forcing the air out of them, alters the
breath sounds in such a way that it imitates a blowing murmur or the sound of wood file.
But with a little skill it becomes easy to distinguish this sound from a cardiac murmur.
It is more superficial; one hears the normal heart sounds be-
low it; and it disappears almost entirely when the patient is
made to hold his breath for a few moments."1
Physiological experiments have borne out Laennec 's claim that the lung moves to and
fro with each cardiac cycle (Buisson, Voit, van der Heul, Landois, Meltzer). but have demon-
strated that the most sudden movement of the air accompanies the rarefaction of the air
within the lung during systole, rather
than its extrusion during diastole.
The cardiopulmonary murmurs
formed the subject of an exhaustive
study from 1865 to 1894 by Potain,
many of whose data have been given
above. Potain controlled the findings
by auscultation with carefully made
cardiograms and experimental studies
and found that:
1 . The cardiopulmonary murmurs
are loudest and most frequent in
those regions (infundibulum and vicin-
ity of the pulmonary artery) where
the movement of the heart is greatest.
2. They occur in regions
and in phases of the car-
diac cycle at which the car-
diogram shows retractions
of the interspace (areas of
negative pressure with sudden expan-
sion of the lung).
Hence, the systolic murmur is most common over the infundibulum and right ven-
tricle, over which there is usually a systolic retraction (see page 91 and Fig. 89).
If the retraction (fall in the cardiogram) occurs in the middle of systole, the murmur
is found to be mesosystolic; if at the end of systole, the murmur is telesystolic ; if the fall is
in diastole, the murmur is diastolic. Indeed Potain encountered several cases in which
the form of the cardiogram changed upon alteration of the position of the patient; and
corresponding to the period of greatest retraction the murmur over the area changed from
mesosystolic to diastolic.
This is a surprising confirmation of the theory of cardiopujmonary murmurs. There
can indeed be no doubt that cardiopulmonary murmurs are frequent, and that they form
a very considerable proportion of "accidental" murmurs. Besides the blowing murmurs
referred to above, it is probable that many of the so-called "musical" or "squeak-
ing" murmurs are of cardiopulmonary origin, and are really piping rales produced by the
1 "Chez quelques sujets, les plevres et les bords ante"rieurs des poumons se prolongent
au-devant du coeur et le recouvrent presque entierement. Si Ton explore un pareil sujet
au moment oil il eprouve des battements du co3ur un peu energiques, la diastole du cceur
comprimant ces portions du poumon et en exprimant Pair, altere le bruit de la respiration
de maniere a ce qu'il imite plus ou moins bien celui d'un soufflet donne par le coeur lui-
meme: il est plus superficiel; on entend au dessous le bruit naturel du coeur; et en recom-
mandant au malade de retenir pendant quelques instants sa respiration, il diminue beau-
coup ou cesse presque entierement."
FIG. 109. — Distribution of the accidental murmur.
PHYSICAL EXAMINATION. 115
toand-fro movement in the lung during either phase of the cardiac cycle. Other rales of
cardiopulmonary origin more closely resembling the sonorous and crepitant rales
of respiration are also very common along the margin of the left lung. Moreover, the breath
sounds themselves are frequently modified by the cardiac movements, giving rise to the so-
called cog-wheel type of breathing; in which inspiration is interrupted by a series
of small clicks and pauses coincident with and due to the effects of cardiac contractions
upon the air in the lungs. The cog-wheel type of breathing is often associated with slight
changes in the overlying lung and is thus often a premonitory sign of pulmonary tuberculosis.
Differentiation between Cardiopulmonary and other Accidental Mur-
murs.— However, in spite of the frequency of cardiopulmonary murmurs,
it is probable that Potain erred in ascribing all accidental or non-valvular
murmurs to this origin. In the first place, many such murmurs are audible
over the area of cardiac flatness several centimetres from the lung borders,
when breath sounds which are of equal loudness over the lung cannot be
CAROTID
PHONOGRAM
Fio. 110. — Graphic record of an accidental murmur. (After Weiss and Joachim.)
heard at all at these sites. Secondly, the murmurs can be well heard directly
over the exposed dogs' hearts when the lung has been entirely retracted,
and when valvular insufficiencies and stenoses can be absolutely excluded.
For the present, therefore, it must be admitted that there are still
many uncertainties in the differentiation between cardiopulmonary and
other accidental murmurs. The diagnosis of the former must
be confined to murmurs of distinctly superficial
quality which are heard loudest over thelung bor-
ders and are absent or much diminished over the area
of cardiac flatness, and which vary with change of position.
The diagnosis may be considered as rendered probable if the area over
which the murmur is heard moves toward the sternum in inspiration and
away from it in expiration, corresponding to the movement of the marginal
strip of lung. If the reverse is the case and the area of intensity extends
lateralward in expiration and recedes toward the sternum in inspiration,
the murmur is more likely to arise within the heart.
Imitations of the Heart Sounds. — A remarkably accurate method for imitating the
heart sounds, reduplications, and rough or blowing murmurs has been used for the past
three years by the writer's colleague, Dr. Charles W. Larned. This is carried out by placing
the palm of the observer's hand tightly over his ear, and then tapping upon the elbow
with the finger tips of the other hand. The blow must be struck with loose finger-joints.
Its force can be varied to suit variations in the loudness of the sound. Dull :m<l
distant sounds may be imitated by light blows of the finger or by raising the palm of the
hand from the ear, snapping sounds by pressing the hand tightly upon the ear and
executing a sharp stroke. Blowing murmurs are reproduced by a gentle stroking of the
116
DISEASES OF THE HEART AND AORTA.
elbow. Dr. Henry Lee Smith has modified this procedure by striking the blows directly
upon the back of. the hand, instead of the elbow, a method by which sharper and more
snapping sounds can be produced. He is able to give a very accurate reproduction of the
presystolic rumble and snapping first sound of mitral stenosis by bringing all the four fingers
down upon the knuckles or metacarpals in as rapid succession as possible, a manoeuvre
which is best executed by a quick pronation from the elbow. The blow struck with the
index finger (snapping first sound) should be somewhat louder than the rest.
While these methods are excellent for demonstrating to one student at a time, they,
cannot be used for demonstrating to a whole group simultaneously. For this purpose the
writer has resorted to the somewhat cruder method of executing the same taps and strokes
upon the top of a derby or even a soft felt hat. This imitation is not quite so accurate,
and the snapping and rumbling quality are not reproduced, but nevertheless it enables
the instructor to point out the salient features to all and to illustrate their main variations
and relations to the events of the cardiac cycle.
INTRAVENTRICULAR
PRESSURE
VOLUME OF
VENTRICLES
MITRAL 5Y5TOLIC
AORTIC 5Y5TOLIC
AORTIC DIASTOLIC
PRESYSTOLIC
FIG. 111. — Diagram showing the relation of the more common simple murmurs to events of the
cardiac cycle. Solid black bars indicate the heart sounds. Vertical parallel lines reaching to the base
indicate blowing or rough murmur. Wavy vertical lines not reaching to the base indicate a rumble.
The exact method for the reproduction of each sound or murmur can thus be indi-
cated schematically by designating the finger to be used (I = index, M = middle, R = ring
finger, L = little finger) and the accent of the sound'. Time intervals may be shown by
dashes, and rapid succession of the split sounds by bracketing the corresponding letters.
Murmurs are indicated by stroke.
Thus: V — I = Normal first sound at the apex; I — I' = Normal first sound at aorta;
stroke I' = Mitral murmur; I — (I'M) = Split second sound; (IM — I)=Split first sound;
(I-M' — I) = Presystolic gallop; I — P-M = Protodiastolic gallop; I stroke I = Mesosystolic
murmur; LRMP — I = Presystolic murmur; I — stroke = Diastolic blowing murmur replac-
ing second sound; I — I stroke = Diastolic murmur following the second sound; LRMP
stroke I = Presystolic systolic murmur of mitral stenosis; Gentle to-and-fro rubbing of
skin = Pericardial friction.
Relations of the Simple Murmurs to Events of the Cardiac Cycle. — The relations of
the simple cardiac murmurs to the contractions of the cardiac chambers, as well as to the
filling and emptying of the ventricles, is shown in Fig. 111. The mechanism of their
production will be discussed in detail in connection with the valvular lesions to which
they correspond. It will be seen, however, that the mitral systolic murmur begins
coincidently with the first heart sound before the blood flows into the aorta, and that
it continues throughout systole; that the aortic systolic murmur follows the first sound
and is loudest in midsystole; that the aortic diastolic murmur is loudest in early diastole,
when the filling of the heart and the regurgitation are most rapid; and that the presys-
tolic rumble is produced by the inrush of blood into the ventricles during auricular systole.
PHYSICAL EXAMINATION.
SINGLE MURMURS.
117
Time.
Character.
Phonetic l
equivalents.
Distribution.
Clinical condition.
it is
Presystolic
Rumbling, occasion-
ftat-ta; trat-at; tr-
Apex only, lower
Mitral stenosis ; t ri-
ally blowing
r-rub-dub
precordium be-
cuspid .stenosis.
1 * 2
tween parasteroal
line and sternum
i 2
Systolic
Blowing or roaring.
shush-dub; jjje-dub;
Over body of heart,
M 1 1 nil insufficiency "
Enters into or re-
places as well as
ssh-dub; faf-tam
at apex and to ax-
illa, often at back.
tri cuspid insuffi-
ciency.
follows first, sound.
Over lower ster-
Uniform or decres-
num and neighbor-
cendo
ing precordium
1 212
Blowing or roaring;
luzsch-dub; taf-dub
Loudest over 2d
Sclerosis of aorta;
follows first sound;
right interspace;
aortic stenosis- con-
has a crescendo
thrill also in ves-
genital heart lesion.
character in mid-
sels of neck. Not
systole and decres-
so loud at apex
cendo in late sys-
tole
1 212
Similar in character
lujsch-dub; taf-dub;
2d left interspace
Pulmonary stenosis.
to aortic systolic
1 2
and to left of ster-
congenital heart le-
murmur
taf-tam
num (thrill). Else-
sion, aneurism.
where over chest
(thrill)
12 12
Mesosystolic or tel-
esystolic (predi-
Soft blowing, uni-
form or decres-
lupff-dub; taf-tat;
1 2
Over en tire precord-
ium, esp. 2d and
Functional, accident-
al, or anaemic mur-
astolic)
cendo
luff -dub
3d left interspace.
mur. Anaemic fever;
Varying with
neurasthenia etc. -
change of position.
sometimes organ-
Not transmitted
ic (?).
beyond apex
1 2
Diastolic
Blowing
lupd-shsh; tam-taf;
At 2d rib near ster-
Aortic insufficiency.
lup-dush; lup->!i-li
nal margin; loud-
est over sternum
at level of 2d left
interspace and in
the latter near the
sternal margin
At 2d left inter-
Pulmonary insuffici-
space and r i g h t
ency.
sternal margin ;
also to right of
sternum
At 2d left interspace
and sternal margin
With no other marked
signs of valvular in-
sufficiency. Abnor-
mal murmur (Potain,
Graham, Steele).
1 2
Mid-diastolic
Rumble
lub-dub-tra
At apex only
Mitral stenosis; some
cases with pericard-
ial adhesions, etc.
'These phonetic equivalents most closely imitate the cardiac sounds when the consonants are
prolonged as much as possible.
COMBINED MURMURS.
Time.
Character.
Phonetic
equivalents.
Distribution.
Clinical condition.
Presystolic (Flint
murmur), systol-
ic, and diastolic
Presystolic rumble;
systolic blow; di-
astolic blow
I 2 1
ftaftash; tr-r-rub-
2
dush
Blow loudest at 2d
right and 2<1 left in-
terspaces; at apex
and out in axilla.
Rumble over apex
only
Vegetation at aortic
valve, aortic insuf-
ficiency. Sometimes,
but not necessarily,
mitral insufficiency,
occasionally also
mitral stenosis.
118
DISEASES OF THE HEART AND AORTA.
COMBINED MURMURS (Continued).
Time.
Character.
1
Phonetic
equivalents.
Distribution.
Clinical condition.
Systolic and di- Systolic and dias-i taf-tash; lush-dush; 2d right and left in- j Aortic
astolic
Same . .
tolic blow
Same.
Irregularlyinboth: Soft, superficial,
systole and di- scratchy
astole
shush-shush
Same. . .
slush -dush; slush-
2
dush-da
Accompanies both ! Pleuropericardial .
heart sounds and !
both breath'
sounds
Crepitant; small ex-
plosive rales
terspace, sternum,
left sternal mar-;
gin, transmitted to
arteries
insufficiency
with aortitis; aortic
stenosis.
Loudest at left ster- Pulmonary stenosis
nal margin; thrill and insufficiency;
maximum to first open ductus arterio-
and second left, sus; other congeni-
interspace tal heart lesions.
Over the entire pre-i Fibrinous pericarditis,
cordium. especial-
ly over the area of
absolute dulness;
increased by pres- '
sure with stetho-
scope
Over relative cardi- Pleuropericarditis.
ac dulness only;|
scratch simultane-!
ous with respira-
tion as well as
cardiac cycle. In-
creased by pres-
sure with stetho-
scope
Over relative cardi-
ac dulness only
Emphysema. Inter-
stitial emphysema.
VASCULAR SOUNDS AND MURMURS.
Arterial. — Besides the murmurs transmitted from the heart, murmurs
also occasionally arise in the arteries themselves/ A systolic murmur and
an audible first sound (pistol-shot tone) may be produced by pressure with
the stethoscope over the arteries, but without exerting a definite pressure
it may often be found accompanying the dilatation of markedly pulsating
arteries, as in aortic insufficiency and with dicrotic pulses, etc. The eddies
arising in an aneurism usually give rise to a rough or blowing systolic
murmur which may be transmitted for a considerable distance along the
arteries. In aortic insufficiency a double murmur (sytolic and diastolic)
may be heard over the arteries (Duroziez).
Venous. — A sound is heard over the jugular vein, especially over the
jugular bulb just above the clavicle, in cases of marked anemia, chlorosis,
etc. (Camac). The murmur is humming or roaring in character and
occurs during both systole and diastole (humming-top murmur, "bruit
du diable," etc.). Weiss and Joachim have registered the sound and have
shown that it never ceases. As shown by Cohnheim the anemic blood
flows more rapidly than does normal blood, probably owing to its lower
viscosity; and both these factors facilitate the production of a murmur.
However, it has not yet been shown that the murmur is loudest at
those periods of the cardiac cycle during which the flow in the veins is
most rapid.
PHYSICAL EXAMINATION. 119
MURMURS AS AN AID TO DIAGNOSIS.
It is evident from what has gone before, as well as from the consensus
of medical practice, that auscultation furnishes a most important means
of diagnosis of cardiac lesions. It is equally evident that each abnormal
sound may be associated with any one of several clinical conditions, which
must be still further differentiated from one another, not only by the mur-
mur but by its distribution, transmission, and variations, but particularly
by the other methods of physical examination, graphic methods, and
X-ray examination. The examiner should not content himself with a
simple designation of the lesion, but should become fully conversant
with the disturbance of function in all parts of the circulatory system,
and with its remote secondary effects.
BIBLIOGRAPHY.
PHYSICAL DIAGNOSIS.
Herz, M.: Herzmuskel insuffizienz durch relative Enge des Thorax oppressio cordis, Ver-
handl. d. Kong. f. inn. Med., Wiesbaden, 1908, xxv, 292.
Selling, T.: Untersuchungen des Perkussionschalles, Deutsch. Arch. f. klin. Med., Leipz.,
1907, xc, 163.
Muller, Fr. : Studies in Percussion, paper read before the Johns Hopkins Hospital Medical
Society, Mar. 21, 1907.
De la Camp, O. : Zur Methodik der Herzgrossenbestimmung, Verhandl. d. Kong, f . innere
Med., Wiesbaden, 1904, xxi, 208.
Curschmann, H., and Schlayer: Ueber Goldscheider's Methode der Herzperkussion,
Deutsch. med. Wchnschr., Leipz., 1905, xxxi, 1996.
Ebstein, W.: Zur Lehre von der Herzperkussion, Berl. klin. Wchnschr., 1876.
Moritz, F.: Einige Bemerkungen zur Frage der perkutorischer Darstellung des gesamten
Vorderflache des Herzens, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxvii, 276.
Dietlen, H.: Ueber die Grosse und Lage des normalen Herzens und ihre Abhangigkeit von
physiologischen Bedingungen, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxviii, 55.
Die Perkussion der wahren Herzgrenzen, ibid., 1906, Ixxxviii, 286.
Simon, A.: Die Schwellenperkussion des Herzens an der Leiche, ibid., 1906, Ixxxviii, 246.
Hoffmann, A.: Die paroxysmale Tachycardie.
Dietlen, H.: Orthodiagraphische Beobachtungen ueber Veraenderungen der Herzgrosse
bei Infektionskrankheiten, exsudative Perikarditis und paroxysmale Tachykardie,
Munchen. med. Wchnschr., 1908, Iv, 2077.
Williams, F. H.: Rontgen Rays in Medicine and Surgery.
Veith, A.: Ueber Orthodiagraphische Untersuchungen bei Kindern im schulpflichtigen
Alter, Jahrb. f. Kinderh., Berl., 1908, Ixviii, 205.
Donders: Quoted from L. Hill, Schafer's Text-book of Physiology, Edinb. and Lond.,
1900, ii.
Martius: Graphische Untersuchungen ueber die Herzbewegung, Ztschr. f. klin. Med.,
Berl., 1888, xiii, 327, 453, 558.
Einthoven. W., and Geluk, M. A. J.: Registrierung der Herztone, Arch. f. d. ges. Physiol.,
Bonn, 1894, Ivii, 617.
Huerthle, K.: Ueber die mechanische Registrirung der Herztdne, ibid., 1895, be, 263.
Holowinski, A.: Physikalische Untersuchung der Herztone, Ztschr. f. klin. Med., Berl.,
1901, xlii. 186.
Einthoven, W, Flohil, A., and Battaerd, P. J. T. A.: Registrirung der menschlichen
Herztone, Arch. f. d. ges. Physiol., Bonn, 1907, cxvii, 461.
Marbe, K.: Registrierung der Herztone mittelst russender Flammen, Arch. f. d. ges.
Physiol., Bonn, 1907, cxx, 205.
Roos, E.: Ueber die objective Aufzeichnung der Schallerscheinungen des Herzens, Ver-
handl. d. Kong. f. innere Med., Wiesbaden, 1908, xxv, 643.
120 DISEASES OF THE HEART AND AORTA.
Frank, O., and Hess, O.: Ueber das Cardiogramm und den ersten Herzton., Verhandl. d.
Kong. f. innere Med., Wiesbaden, 1908, xxv, 285.
Weiss, O.: Das Phonoskop, Mediz. naturw. Arch., Berl. and Vienna, 1908, i, 437.
Weiss, O., and Joachim, G.: Registrierung und Reproduktion der menschlichen Herztone
und Herzgerausche, Arch. f. d. ges. Physiol., Bonn, 1908, cxxiii, 341.
Hess: Entstehung der Herztone, Deutsche med. Wchnschr., Leipz., 1908, xxxiv, 1611.
Kahn, R. H.: Weitere Beitrage zur Kenntniss des Elektrocardiogrammes, Arch. f. d. ges.
Physiol., Bonn, 1909, cxxix, 291.
Sahli, H.: Lehrbuch der klinischen Untersuchungsmethoden.
Harvey, Wm.: De motu cordis.
Williams, C. J. B.: Rep. Brit. Assoc. Adv. Sc., Lond., 1836, p. 269.
Ludwig, C., and Dogiel, A. S.: Ber. d. k. sachs. Gesellsch. math. nat. Cl., Leipz., 1869,
xx, 89.
Sibson and Broadbent: In Sibson's Medical Anatomy, 1869, p. 89.
Emerson, C. P.: The Effect of Pressure of the Stethoscope on Intrathoracic Sounds, Bull.
Johns Hopkins Hosp., Baltimore, 1908, xix, 49.
Cabot, R. C.: Physical Diagnosis.
Boy-Teissier: L'auscultation retrosternale dans les maladies cardio-aortiques, Marseilles
meU, 1892, xxix, 303; Rev. de med., Par., 1892, xii, 169.
Hoffmann, A.: Ueber cesophageale Auskultation, Centralbl. f. klin. Med., Leipz., 1892,
xiii, 1017.
Gerhartz, H.: Zur Frage des Stethoskops, Deutsch. Arch. f. klin. Med., Leipz., 1907, xc, 501.
Bard, L.: Du bruit de galop de 1'hypertrophie du coeur gauche, Sem. me"d., Paris, 1906,
xxvi, 229. Also De la multiplicite anormale des bruits du coeur, ibid., 1908, xxviii, 3.
Kriege and Schmall: Ueber den Galopprhythmus des Herzens, Ztschr. f. klin. Med., Berlin,
1891, xviii.
Miiller, F. : Ueber Galopprhythmus des Herzens, Miinchen med. Wchnschr., 1906, liii, 785 .
Marey, E. J.: La Circulation du sang a P6tat physiologique et dans les maladies, Par., 1881.
Sewall, H.: On a Common Form of Reduplication of the First Sound of the Heart, Contrib.
Sci. Med. (Vaughan), Ann Arbor, 1903, 29; also, A Common Modification of the First
Sound of the Normal Heart Simulating that heard with Mitral Stenosis, Am. J. M.
Sc., 1909, cxxxviii.
Robinson, G. C.: Gallop Rhythm of the Heart, Am. J. M. Sci., Phila., 1908, cxxxv, 670.
Chauveau, H. : Etude cardiographique sur la mecanisme du bruit de galop, Thesis, Paris,
1902.
Pawinski, J.: Die Entstehung und klinische Bedeutung des Galopprhythmus des Herzens,
Ztschr. f. klin. Med., Berl., 1907, Ixiv, 70.
Duroziez and Sansom: Quoted from Bard.
Hirschfelder, A. D.: Some Variations in the Form of the Venous Pulse, Bull. Johns Hop-
kins Hosp., 1907, xviii, 265.
Einthoven, W.: Ein dritter Herzton, Arch. f. d. ges. Physiol., Bonn, 1907, cxx, 31.
Gibson, A. G.: Upon a Hitherto Undescribed Wave in the Venous Pulse, Lancet, Lond.,
1907, ii, 1380.
Thayer, W. S.: On the Early Diastolic Heart Sound (the So-called Third Heart Sound),
Bost. M. and S. J., 1908, clviii, 713; Further Observations on the Third Heart Sound,
Arch. Int. Med., Chicago, 1909, iv, 297.
Potain: La Clinique me'dicale de la Charite', Par., 1894.
Laennec, Bouillaud, Hilton Fagge: quoted from Potain.
Luethje: quoted from Brugsch and Schittenhelm, Lehrbuch Klinischer Untersuchungs-
methoden, Berl., 1908.
Buisson, Voit, van der Heul, quoted from Meltzer, S. J. : On the Nature of Cardio-pneu-
matic Movements, Am. J. Physiol., Bost., 1899, i, 117. Also, Sanders, G.: Cardiopul-
monary Murmurs, Edinb. M. J., 1897, N. S., i, 522.
Stengel, A.: The Significance of Systolic Murmurs over the Apex and Base of the Heart,
Cleveland J. M., 1898, iii, 191; and Foshay, P. M.: A Case of Cardiopulmonary Mur-
mur Illustrating the Importance of Differentiation, ibid., 1901, vi, 236.
Putnam, J. J.: The Clinical Associations and Significance of the Cardiopulmonary Murmur,
Tr. Ass. Am. Phys., Phila., 1903, xviii, 157.
PART II.
i.
PRIMARY CARDIAC OVERSTRAIN.
IT has long been known that heart failure may arise from simple over-
strain of the heart without the intervention of any actual cardiac symptoms.
This condition usually remains acute and ends in rapid recovery, but it
may also become chronic and reduce the patient to lasting invalidism. In
its worst form such a purely functional weakening of the heart may result
in death.
This conception was first introduced by Stokes in 1854, and was con-
firmed later by studies of Clifford Allbutt, A. R. B. Myers, and Peacock in
England, and da Costa in America. Their articles were collected, trans-
lated into German, and published, along with an excellent monograph
upon the subject, by Johannes Seitz, of Zurich, in 1875, bringing them to
the cognizance of the German writers. In 1886 v. Ley den added important
contributions. In 1898 the matter was subjected to clinical experiment
by Theodor Schott, whose conclusions have been disputed by a host of
later and more careful observers.
The most interesting, extensive, and complete of all these papers are
those of da Costa, based upon several hundred cases occurring among
Union soldiers of the Civil War. It is impossible to do justice to these
studies in a brief abstract. His presentation is so complete and so nearly
a model of clinical study for its time that the reader is urged to consult
the original publication.
CLINICAL CASES.
A very typical case of da Costa's series is illustrated by the following
history.
CASE I. — Irritable heart, chiefly from hard service; recovery.
— Wm. Henry H., private 68th Pennsylvania Vol., admitted into the Turner's Lane Hospital
in Philadelphia, November 2, 1863, having just returned from a furlough. He enlisted in
August, 1862, at the time in good health, though he had suffered occasionally from rheu-
matism. He did a great deal of hard duty with his regiment. Some time before the battle
of Fredericksburg, he had an attack of diarrhoea; after the battle, he was seized with
lancinating pains in the cardiac region, so intense that he waa
obliged to throw himself clown upon the ground, with palpitation.
These symptoms frequently returned while on the march, were attended with dimness of
vision and giddiness, and obliged him often to fall out from his company and ride in the
ambulance. Yet he remained wjth his regiment until J u 1 y 4, 1863, when he was wounded
at the battle of Gettysburg. The wound healed in about one month; but the cardiac
symptoms became worse, and violent palpitations ensued upon the slightest exertion,
sometimes also whilst in bed, obliging him to rise. There was soreness in the cardiac
121
122 DISEASES OF THE HEART AND AORTA.
region, and a constant dull pain. The impulse was extended, slightly jerky, 96, and of
irregular rhythm, some beats following one another in rapid succession; the first sound was
feeble, the second very distinct. The man did not look sick. Height 5 feet 7 inches;
measured 31 inches around the chest one inch below the nipple; he did not smoke; chewed
tobacco in moderation.
The patient did not improve under aconite; but under digitalis the impulse became
quiet and 78, and on March 23, having previously done duty as orderly, he was detailed
on police duty, and his treatment stopped^. The heart continuing to act regularly,
he returned to his regiment May 3, 1864.
Another case, quoted from v. Leyden, illustrates the various phases
of the malady very well.
CASE II. — Carl Timm, butcher, aged 30. Family history negative. Syphilis ten years
before, quiescent for several years. Otherwise always healthy. Performed military service
for 5 years without any trouble. In the fall of 1880 became a butcher in the Charite Hospital
where he had to lift and chop sides of beef weighing 200 Ibs. The
first symptoms appeared suddenly on the afternoon of December 30, 1880, during an
ordinary day's work, when he felt a severe pressure in the pit of the stomach,
preventing him from taking a deep breath and causing him to stop in his work. 'At this
time he noticed palpitation and irregularity of the heart. For several days
after this he did no heavy work and then felt well. When he tried to do heavy
lifting again the same pain and sensation of pressure returned, and
though he continued his work he was compelled to stop for breath from time to time. On
Feb. 17, 1881, the pain became very intense and he entered the hospital on Feb. 21.
Physical Examination. — Patient is a very well-built young man, well muscled, well
nourished but not fat. Complexion florid but healthy looking. No dyspnoea or
cyanosis. Moderate oedema of lower extremities. Patient complains only
of palpitation of the heart. The pulse is strikingly irregular so that it is im-
possible to count. The radial arteries are small, blood-pressure apparently low. The
cardiac impulse is intense, vibratory, and very irregular. Apex impulse is in
5th left interspace 2 cm. beyond mammillary 1 i n e , well marked, read-
ily palpable. Cardiac dulness begins above at 3d rib, extending below to 6th rib, and
reaching just to the right of the sternum. Heart sounds are feeble and unequal but
clear. Lungs clear. Liver and spleen are not enlarged. Urine 500 c.c., sp. gr. 1023. no
albumin.
Ordered rest in bed, ice-bag over heart, infusion of digitalis every
2 hours. Within a few days symptoms and oedema had subsided, but the
irregular heart action persisted. By March 20 he was well enough to be discharged, with
the following note: Apex beat 0.5 cm. to left of mammillary line; first sound at apex
loud and ringing, second sound distant but clear; pulse irregular; examination otherwise
negative.
This represents the first stage of his illness, in which the following
features are noteworthy: 1. A very strong and perfectly healthy young
man suffers from heart failure as the immediate result of overstrain. The
first attack came on suddenly while at work and passed off soon, but attacks
recurred whenever the patient did heavy work, and he was compelled to
enter the hospital. 2. Physical findings: heart dilated especially in the
longitudinal axis, weak apex beat (dilatation of left ventricle), great cardiac
irregularity. 3. Relatively rapid improvement after rest in bed and digi-
talis. 4. The heart then returned to almost normal size, but the irregu-
larity in rhythm persisted.
Second Stage. — Patient returned to his old work in spite of warning,
and within two months oedema of the legs had agjain set in and he was confined to
bed for eight weeks more. Returning to work again, he could perform only
very light labor, and very soon returned once more to the hospital for seven weeks,
with still mdre marked oedema. Once more these disturbances disappeared after rest and
PRIMARY CARDIAC OVERSTRAIN. 123
digitalis, but thereafter the slightest work caused palpitation and the feeling as though
there were a t i g h t c o rd about the chest. He also felt pain in the region of the
liver. At this point he re-entered the hospital. Pulse ISO, small, irregular. Face flushed,
no cyanosis. Expression depressed. Skin normal; oedema of feet and legs. Gangrene of
l>i.u; toe of right foot. Respiration a little rapid, dyspnoea only on exercise, but while walk-
ing he often stops to catch his breath. Occasionally he has attacks of dyspnoea lasting
about 10 minutes, beginning with a feelirg of pressure in the region of the heart. He
then feels as though hot liquid were pouring from the heart upwards to each side of
the neck.
Physical Signs. — A pex beat in 6th left interspace in anterior axillary
line, soft and easily compressed. Heart therefore much enlarged, sounds clear and fairly
loud, action markedly irregular. Liver enlarged and tender.
Ordered rest in bed, digitalis, morphine at night. Patient became much better
within twenty-four hours, pulse then 68 per minute. The attacks of dyspnoea almost
disappeared. Urine 1300, sp. gr. 1020. Within six days all cardiac symptoms had dis-
appeared. March 11: Pulse 52. Feels well, no pain. Apex beat in 5th left interspace
3 cm. beyond mammillary line, moderately forceful. Heart sounds clear but irregular.
He still occasionally has feeling of pressure in chest.
Features of second stage: 1. Dilatation of heart much
more marked than before. 2. Very rapid and very irregular
heart action. 3. Definite attacks of pain in heart and feeling of pressure
(anginoid in character), with radiating pains in slioulder and arm. 4. Swell-
ing of liver (failure of right heart). 5. Return to almost normal under
treatment, diminution in size of left ventricle. 6. Intercurrent affections:
small infarct of lung, pressure gangrene of great toe, recovered from,
Third Stage. — Returned to the hospital in July, 1885 (two years later). He has been
able to do very little since last admission. Now much emaciated, face thin, ap-
pears depressed. Cheeks and lips slightly cyanotic. Respiration dyspnoeic and
stertorous. No orthopnoea. Moderate oedema of shins.
Cardiac impulse seen in 5th to 7th left interspaces, apex beat felt in 7th in axillary
line, forcible. Heart rate about 132, irregular. Cardiac dulness 19 cm. from left sternal
margin. (Upper limit of cardiac dulness as before begins at 3d rib.) Liver readily pal-
pable. Sounds loud, more or less short but no murmur. Did not remain in hospital, but
on October 4, 1885, was brought in again in collapse. Marked cyanosis, extremities cold,
oedema of legs up to knees. Heart as before, sounds still clear. Pulse 150. Liver a hand's
breadth below costal margin. Ordered digitalis, also camphor subcutaneously, tea with
cognac. At midnight collapse more marked, very marked dyspnoea and cyanosis; threw
himself to and fro, groaned loudly. Pulse not palpable, not revived by camphor or ether
injection. At 2 A.M. became quiet; stertorous breathing set in at 3 A.M.; died quietly at
3.15A.M.
Autopsy. — Marked oedema of legs. Both lungs slightly retracted, slightly adherent
over apices. Pericardium distended, little fluid. Heart markedly enlarged (more
than twice the size of patient's fist), especially in the longitudinal axis. Left ventri-
cle more dilated than right. Distance from insertion of pulmonary artery
to apex 13 cm., to right border of heart 10 cm. Length of left ventricle 15 cm. Little
epicardial fat. Valves normal, aortic valves close perfectly. Papillary muscles well devel-
oped, some trabecula? flattened and undergoing fibrous changes. A fibrous patch is seen
on the interior surface of the left ventricle. Endocardium otherwise delicate, showing
some yellow areas of fatty, degeneration of the endocardium and papillary muscles. Cut
surface of heart muscle shows cloudy swelling. Left auricle markedly di-
lated. Right ventricle appears pale with spots of yellow. Lungs, oedema of bases.
Liver, markedly enlarged; definite nutmeg liver. Kidneys, large, dark red, harder
than normal.
Microscopic examination shows extensive fatty degeneration of muscle-fibres, but
only in the inner layers. No interstitial changes, no changes in blood-vessels
or nerves of the heart. Here and there the interstitial strands of connective tissue
appeared thicker than normal but without cellular infiltration.
124 DISEASES OF THE HEART AND AORTA.
ETIOLOGY.
In da Costa's 200 soldiers, well-marked fever preceded the overstrain
in 17 per cent.; diarrhoea (among which there may have been many mild
cases of typhoid fever) 30.5 per cent.; hard field service, particularly exces-
sive marching, 38.5 per cent.; wounds, injuries, rheumatism, scurvy, ordi-
nary duties of soldier life, and doubtful cases 18 per cent. Contrary to the
belief of many observers, tobacco did not seem to be an etiological factor
in his series.
Allbutt gives the following etiological factors of cardiac overstrain:
gymnastics, rowing, Alpine climbing, long-distance running, intense fits
of anger or emotion, sexual excesses. Overstrain is very frequent among
miners, metal workers, carriers of heavy burdens, blacksmiths, moulders.
Morton Prince calls attention to the development of cardiac dilatation
under severe mental strain, as in a civil service examination. Anaemia and
chlorosis (Henschen), apparently mild illnesses, intestinal disturbances,
acute alcoholism, and febrile diseases (Dietlen) are also frequent causes.
Sexual excess is an important factor, especially in men; but its effects
are usually more marked in hearts already weakened from other diseases
or from valvular lesions than in perfectly healthy hearts.
Myers, Allbutt, and Schott have shown that tight belts, uniforms,
and corsets displace the heart upward, embarrass its action, and predispose
to overstrain. Indeed Myers found that cavalry soldiers with tight belts
suffered more from long rides than infantry from marching the same dis-
tance.
SYMPTOMS, SIGNS, AND CLINICAL COURSE.
The chief symptoms are dulness, excitability, nervousness, loss of
sleep, loss of appetite, restlessness, buzzing in the ears, vertigo, musca3
volitantes, palpitation of the heart, usually very severe and often asso-
ciated with a feeling of pressure or constriction over the chest. This may
be very distressing, but does not, as a rule, cause the patient to remain
absolutely still nor give him the fear of sudden death, though da Costa
mentions cases in which the precordial distress was great enough to cause
soldiers to fall to the ground in the midst of battle.
Pain over the precordium and the left shoulder, occasionally down
the arm, increased on inspiration and on coughing.
Dull headache, dizziness, especially on bending over, sleep-
lessness, indigestion, tympanites, and diarrhoea are common.
The patient often wears an anxious expression and there are usually
pallor and more or less cyanosis. Pulse is usually small, feeble, rapid, and
often irregular. The cardiac impulse may be barely or not at all visible,
but on percussion the area of relative cardiac dulness is usually found to be
enlarged considerably to the left both downward and upward, and often also
to the right as well. This corresponds to the dilatation of the left ventricle
and of both auricles (i.e., diameters MR and ML, Fig. 84, are much increased).
On the other hand Katzenstein has shown that in just these cases the impulse
may be exceptionally strong and impart a heaving to the whole
chest, even though the heart be much dilated, failing, and devoid
of the slightest trace of hypertrophy. A systolic retraction is usually seen over the greater
PRIMARY CARDIAC OVERSTRAIN.
125
part of the precordium of these overworking hearts (Fig. 89), corresponding to the con-
traction of the right ventricle (page 91). Occasionally in rapid and irregular hearts this
appearance is somewhat puzzling and has led some clinicians to dictate notes of " delirium
cordis" where this condition was not present at all.1
The area of relative cardiac dulness is much enlarged (Fig.
112), especially to the left, both downwards, corresponding to the dilata-
tion of the ventricle, and upwards, corresponding to the auricle. In more
severe cases, especially with marked cyanosis, the dulness is enlarged
also to the right from dilatation of the right auricle. Occasionally this
dilatation may have passed off before the patient has been seen by the
physician and only the other
symptoms and signs persist, but
it is safe to assume that it has
been present at an earlier stage
of the disease.
The heart sounds may
be either very distant and feeble
or very short and sharp, corre-
sponding to the two types of
cardiac impulse. They are usu-
ally unaccompanied by mur-
murs, but in an irregular heart
may be of uneven intensity.
The second pulmonic is usually
the loudest sound heard. The
clearness of the first sound is
often altered by a reduplication,
especially in rapid hearts, or by
the presence of a soft blowing systolic murmur, which is usually loudest
over the pulmonic or tricuspid area, but occasionally also heard to the
anterior axilla. These sounds do not always but may sometimes corre-
spond to the presence of functional insufficiency of the mitral valve
(vide page 323), in other cases to anaemia. It is, however, extremely
difficult or sometimes impossible to decide absolutely whether such an
insufficiency is present.
The pulse is usually rapid, ranging from 80 to 160 per minute,
small, and weak, in many cases irregular in both force and rhythm. In
less severe cases there are only occasional extrasystoles (Schott); in the
more advanced there is an absolutely irregular rhythm which persists
even after the rate slows. There is often persistent tachycardia without
dyspnoea, lasting for even weeks or months.
Clinical Course. — In some cases, however, all the signs and symptoms
of overstrain may be present without any irregularity whatever, but often
associated with a rapid and regular pulse. Occasionally the pulse may be
regular only while it is rapid, but becomes irregular as the rate diminishes.
In many cases no murmurs or other signs of valvular insufficiency are
1 The term delirium cordis is used rather indefinitely to designate conditions
varying between extreme irregularity with tachycardia and true fibrillation of the heart.
The onset of the latter is, however, not consistent with the existence of life.
Fio. 112. — Cardiac dulness in v. Leyden's case upon hi*
three successive admissions (I, II, III).
126 DISEASES OF THE HE^RT AND AORTA.
encountered, while in still others a relative or functional insufficiency of
the mitral or tricuspid valve results from the cardiac dilatation, with some
embarrassment of the heart resulting therefrom in addition to the original
failure. Systolic (functional) murmurs are heard in these areas, and the
stasis is still further increased by the regurgitation of blood. The O3dema
becomes extreme, hydrothorax may set in, and death soon results. As in
the case of da Costa' s patient under discussion, the progress may be stayed
somewhat by occasional treatment and rest. If the latter is sufficient and
the disease not too far advanced, the patient's life may be saved.
The liver, as in Case II, enlarges when the condition becomes severe
and tricuspid insufficiency has set in. Its edge is then smooth and varies
in consistency from being rounded and so soft as to be palpable only
with the side of the index finger to almost board-like hardness. It is
always smooth. In severe cases jaundice may be present and the liver may
pulsate.
The abdomen is often distended with gas, a factor which contrib-
utes largely to the cardiac discomfort by pushing up the diaphragm. In
the later stages of heart failure ascites may be present.
The g e n i t a 1 i a show oedema only in the later stages of the disease.
The lower extremities are often oedematous, the swelling first mani-
festing itself about ankles and shins.
The urine during the period of heart failure is usually scant, — less
than 900 c.c. (30 ounces) for 24 hours, — owing to diminished rapidity of blood
flow. It is then of high specific gravity (1020 and over), and often contains
albumin and casts. In extreme stasis numerous epithelial, coarsely and
finely granular, and hyaline casts are seen in every field of the microscope.
Blood. The blood picture may vary from a moderate anaemia to
a real polycythaemia, dependent upon the condition of the patient before
the over-exertion.
The sputum may be scanty and mucous, or profuse, frothy, and
albuminous, dependent upon the relative strength of the right and left
ventricles. In rare cases haemoptysis results during the exertion from
engorgement of the pulmonary capillaries.
Transitory Cardiac Dilatation. — A particularly instructive series of
cases studied with modern methods are those reported by Harming (1908).
Among 1100 cases which he watched with the X-ray during the past seven
years he has met with a number who usually showed perfectly normal
hearts but were subject to acute dilatation after overstrain. This was
particularly frequent in persons who had used alcohol "to excess, in those
who had recently suffered from infectious diseases, and in anaemic indi-
viduals. The attacks of dilatation are brought on by fright,
high altitudes, excitement, over-exertion, etc. Sexual ex-
citement might -be added to this list. Hornung returns to the old view of
Seitz, Allbutt, and v. Leyden, that cardiac overstrain with acute
dilatation is much more common than might be supposed
from the work of Moritz and his pupils.
For a long period, however, he may be expected to be more subject
to other attacks than before, although by care he may remain free from
them. Just how long this susceptibility may last varies with each case,
PRIMARY CARDIAC OVERSTRAIN. 127
but da Costa has shown us that after carefully sparing the patient from all
severe effort for weeks or even months, he may again perform even such
severe efforts as are entailed on cavalry charges and forced marches without
injury and may lead a life of perfect health.
The other side of the picture is shown by v. Ley den's case. This man
returned to work in spite of the discomfort. The latter became worse, and
after bearing it for three months he entered the hospital with a heart already
dilated and permanently irregular, and with well-marked cedema of the
limbs. Definite heart failure had set in. From this he recovered under
rest and treatment with digitalis. His heart resumed almost normal size,
his oedema disappeared. The circulation once more returned to almost
normal, but one permanent injury had been done for which the treatment
was of no avail. The heart action had become irregular and remained so.
The commencement of permanent absolute irregularity in rate (pulsus
irregularis perpetuus) (see Part I, Chapter IV) at this stage is a very com-
mon occurrence in overstrained hearts, and seems to be one of the most
important factors in determining the subsequent course of the disease (see
page 123). When the irregularity persists it adds its own mechanical effects
on the circulation to those already present and increases the overstrain.
When a life of strenuous muscular work is continued by such a patient
the result is inevitable. Strain follows strain, and the condition brought
about by the first failure is exaggerated with each successive day's work.
The attacks of pain and pressure in the thorax (anginoid attacks) increase
in severity and frequency. The heart dilates more and becomes corre-
spondingly weaker. Blood stagnates in the veins, first in the more depend-
ent portions, causing cedema of the ankles, shins, thighs, genitalia, then
enlargement of the liver and ascites from -stasis in the portal system, finally
cedema of the face and arms. The heart dilates still more; the mitral and
tricuspid orifices no longer close. After each attack he is less vigorous
than before, and greater care must be taken to avoid exertion. For the
manual laborer such a life may be at once impossible and intolerable, but
the litterateur, the scholar, the scientist, and the man of affairs may be
saved for years to a life of quiet but none the less useful activity in spite of
a considerable degree of cardiac break-down.
DIAGNOSIS.
The diagnosis of primary overstrain of the heart is not always simple.
It is always a question not of whether the heart has been overstrained but
of whether this weakening is primary, and whether the heart was perfectly
healthy before the effort was made. If the heart, muscle, or valves were
in any way diseased before the effort, the overstrain may be considered as
secondary to that lesion. Accordingly the diagnosis rests upon the pre-
vious history, upon the nature, duration, and sequelae of previous infec-
tious diseases, upon the degree of arteriosclerosis, and upon the general
health of the patient before the onset of the trouble.
Latent myocarditis, fatty degeneration, and arteriosclerosis are par-
ticularly difficult to exclude. A mild grade of myocarditis may have given
no symptom whatever in daily life, but become apparent when exercise
is violent. A mild grade of arteriosclerosis is practically universal among
128 DISEASES OF THE HEART AND AORTA.
persons past middle age, but if considerable efforts had been made without
symptoms of cardiac insufficiency these may be disregarded. When symp-
toms of heart failure occur suddenly in a robust individual during or after
some intense muscular or nervous effort, acute cardiac dilatation and over-
strain may usually be diagnosed with certainty, but, like hysteria among
the nervous diseases, it should be arrived at only after a process of careful
exclusion.
BIBLIOGRAPHY.
Stokes, W. : Diseases of the Heart and Aorta, Dublin, 1854.
Allbutt, T. Clifford: The Effect of Overwork and Strain on the Heart and Great Blood-
vessels, St. George's Hosp. Rep. (Lond.), 1870, v, 23.
Da Costa, J. M.: On the Irritable Heart; a Clinical Study of a Form of Functional Cardiac
Disorder and its Consequences, Am. J. M. Sci., Phila., 1871, Ixi, 17. Medical Diagnosis,
Phila., 1864. Also, Observations upon Heart Diseases in Soldiers, etc., Mem. U. S.
Sanitary Commission, Washington, 1867, ch. x, p. 36.
Maclean, W. C.: On the Diseases of the Heart in the British Army and the Remedy, Brit.
M. J., Lond., 1867, i, 161.
Myers, A. R. B.: Etiology and Prevalence of Diseases of the Heart among Soldiers, London,
1870.
Peacock, T. B.: Lectures on Diseases of the Heart, Med. Times and Gaz., Lond., 1873,
ii, 1, 57, 113, 169, 221, 319, 349. On Some of the Causes and Effects of Valvular Dis-
eases of the Heart, Lond., 1865.
Seitz, Joh.: Die Ueberanstrengung des Herzens, Berl., 1875. (A monograph by the author
containing translations of the articles of Allbutt, da Costa, and Myers.)
V. Leyden, E.: Ueber die Herzkrankheiten in Folge von Ueberanstrengung, Ztschr. f.
klin. Med., Berl., 1886, xi, 105.
Schott, Th.: Zur acuten Ueberanstrengung des Herzens und deren Behandlung, Wies-
baden, 1898.
Hornung: Beitrage zur Frage der acuten Herzerweiterung, Berl. klin. Wchnschr., 1908,
xlv, 1769.
Henschen, S. E.: Ueber die Herzdilatation bei Chlorose und Ansemie, Mitth. a. d. med.
Klin, zu Upsala, 1898, p. 27.
Katzenstein, J.: Dilatation und Hypertrophie des Herzens, Miinchen, 1903.
II.
PATHOLOGICAL PHYSIOLOGY OF EXERCISE, CARDIAC OVER-
STRAIN, HEART FAILURE, AND COMPENSATION.
.PHYSIOLOGY OF EXERCISE.
It is evident from the foregoing examples that muscular efforts which
lead to cardiac overstrain are in themselves merely the exaggeration of
ordinary exercises. To understand these effects it is necessary first to
understand those of ordinary exercise.
McCurdy has classified exercises as—
1. Exercises of speed, like running, chest weight exercises, etc., in which
the individual movements require little effort, but the main effort lies in the rapidity with
which they are repeated.
2. Exercises of endurance, as in long-distance running, prolonged walk-
ing, forced marches, etc., in which the movements are neither difficult nor especially
rapid and the element of strain sets in only with the onset of fatigue.
3. Exercises of strain, as lifting heavy objects, wrestling, etc.
Exercises of Speed. — The cases of cardiac overstrain reported by All-
butt and da Costa represent overstrain from exercises of endurance; those
by v. Leyden and Miinzinger represent exercises of strain.
Masing, Erlanger and Hooker, Dawson and Eyster, and Gordon
have investigated the effect of exercises of speed such as rapid weight-
lifting, running, etc., upon man. The three last named have found that
in individuals in training, whose circulation is least affected, mild exercise
causes either no change or else a fall of blood-pressure. Tangl and
Zuntz also found this in horses and a similar period, though of short
duration, in dogs running on a tread-mill.
In all muscular work an increased amount of CO2 is given off from the
muscles and acts as a hormone l which sets into play the following physio-
logical mechanisms:
1. Vasodilation in the muscles, diverting four or five times as much blood through
this channel (Chauveau and Kaufmann).
2. Acceleration of the heart, at first through diminution in the vagus action, and in
the later stages of prolonged severe exercise chiefly through stimulation of the accelerators
(Hering, Bowen).
3. Vasoconstriction, especially in the splanchnic vessels, which tends to counteract
the effect of the vasodilatation in the muscles.
4. Stimulation of the aiigmentor fibres, and perhaps also of the heart muscle, directly,
causing an increased force of contraction (higher maximal pressure) and an increased
systolic output (higher pulse-pressure). Stimulation of the augmentor fibres also, as a
rule, causes increased cardiac tonicity.
1 Hormone, a substance generated in one part of the body which circulates in the
blood, reaches and sets into activity another organ, thus playing the r61e of a "chemical
messenger." (Cf. Starling, E. H.: On the Chemical Correlation of the Functions of the
Body, Lancet, Lond., 1905, ii, 391, 423, 501, 579.)
9 129
130 DISEASES OF THE HEART AND AORTA.
The heart of the trained athlete is habitually throwing out
an amount of blood suited, not to the needs of the moment, but to the
needs of the periods of exercise to which he has accustomed himself. The
systolic output is above normal when the exercise (and hence the increased
production of CO2) is slight. The heart is thus able to take care of the
excess CO2 production in exercise without increasing its output; and hence
the vasodilatation in the muscles is the only factor influencing the blood-
pressure. When the exercise becomes severe the other mechanisms begin to
play a role.
In normal but not trained young men Masing found
that upon lifting and lowering a weight with the feet the blood -pres-
sure (maximal) and pulse-rate rose at once to a con-
stant height, where they remained until the exercise
ce a&ed. They then fell almost immediately to the original level. The
EXERCISE EXERCISE
FIG. 113. — Alterations of blood-pressure due to rapid lifting of light weights with the feet. (After Masing,
Deutsches Arch. /. klin. Med., vol. Ixxiv.) A. Noimal young man. B. Man aged 68.
writer has found that the minimal pressure rises also, but less than the
maximal, the pulse-pressure being increased. In middle-aged persons
Masing found that the pressure rose higher, and on cessation of the exercise
required several minutes to reach the original level; while in very old persons
the rise was still greater and neither pressure nor rate returned to normal
for a considerable period. The response is proportional to the effort.
When exercise is continued in normal young persons and
the organism re^adapts itself to the effort (the "second wind" setting in),
blood-pressure and pulse-pressure again fall to a fairly constant level
(Dawson and Hatfield). This probably explains why the heart-rate of
well-trained Marathon racers is sometimes slow at the finish. In animal
experiments it finds its analogy in the improved cardiac action observed
as a result of clamping the thoracic aorta, and represents the response of
the heart to a strain which is not excessive.
The weaker the individual or the more severe the
exercise the more prominent become factors 2, 3, and
4, the greater the rise of bloo d-p ressure and the
greater the pulse-rate. The slowness at which conditions return
to normal is more or less proportional to the exertion and the fatigue.
It is also true that for a given amount of exercise performed in a given
time the amount of CO2 formed is least when it is done with least effort
by trained individuals and increases when the effort becomes marked.
PHYSIOLOGY OF EXERCISE.
131
Zuntz and Schumburg have shown upon German soldiers that a certain
short march used up only 554.8 calories of energy when the subjects were
fresh, but required 635.5 calories when they were fatigued. This is prob-
ably due to the fact that with the increase in effort accessory muscles are
called into play, many of which contract and give off CO2 without mate-
rially improving the execution of the exercise.
FIG. 114. — Effect of walking on a level on
patient with badly broken compensation. (After
Cabot and Bruce, Am. J. M. Sc., cxxxiv.)
FIG. 115. — Effect of prolonged exercise upon
the blood-pressure of men in various degrees of
muscular ftrength. The arrows indicate the point
at which symptoms of exhaustion set in. COM-
PENSATED, compensated heart lesions; FAIL-
ING, broken compensation with heart failure.
Exercises of Endurance. — The point at which an exercise of speed
becomes converted into an exercise of endurance is more or less relative
and depends chiefly upon the condition and the training of the individual.
The most typical exercises of endurance, the forced march, the long-dis-
tance runs (Marathon races), and long-distance bicycle races, have been
carefully studied by Zuntz and Schumburg, Blake and Larrabee, Dietlen
and Moritz, and R. T. Abercrombie. In these exercises the least changes
occur in the best-trained individuals in whom the amount of effort put
forth is least or least prolonged.
The pulse-rate of the men who finished in the Marathon races at Boston showed sur-
prisingly little increase, the greatest rise during the race of 1900 being from 76 before to
144 after; but the average rate after the race was 103 (Blake and Larrabee). There was
frequently a moderate grade of irregularity. Zuntz and Schumburg found similar effects.
The blood-pressure after the race was usually found to be a trifle lower than before the
start, though it varied greatly in different individuals. J. Barach has recently obtained
similar results with the Erlanger apparatus upon another set of trained Marathon racers.
The orthodiagraph showed dilatation of the heart in all his cases. Quite different are
the results in long-distance races run by amateurs. Dr. R. T. Abercrombie has recently
made a careful study of the condition of contestants in a twenty-mile road race before
and immediately after the race. Before the race the average blood-pressures with the
Erlanger apparatus were: maximal 120-130, minimal 75-80; pulse-rate 80. Immediately
after the race the pulse was in almost every instance too feeble to be counted, as were
also the heart sounds; and neither these nor the blood-pressure could be satisfactorily
estimated until one-half hour after the finish, when the pulse-rate was usually about 120
per minute, the maximal pressure about 75-100 mm. Hg. The heart sounds were still
132
DISEASES OF THE HEART AND AORTA.
rapid and feeble. Nevertheless all of these men felt quite well, and were able to enjoy a
cold plunge immediately after the examination. Within an hour after the finish they
were all feeling quite active. The blood-pressure was usually found to be lower than be-
fore the start, but this varied greatly in individual cases.
Not all the results of endurance tests are as mild as these. During the amateur
athletic contests in the United States the past five years there have been several cases of
permanent heart failure following directly upon overstrain in
long-distance runs. As in da Costa's series, the persons whose hearts were injured
were usually boys under twenty who were poorly trained and whose hearts were not fitted
for the strain put upon them.
As regards the metabolism during such exercise Zuntz and Schumburg, and also A.
Loewy and L. Zuntz, found that both the amount of CO2 given off per minute and the
respiratory quotient were markedly lessened (CO2 falling from 802.3 c.c. to 743.0 c.c. per
minute; respiratory quotient falling from 0.855 to 0.780) at the end of the exertion, though
the O2 used was unchanged. This is due to formation of intermediate oxidation prod-
ucts, sarcolactic acid, /3-oxybutyric acid, etc., the pressure of whose salts may add to
the fatigue. Moreover, the lessened output of CO2 indicates a lowCO2 content of the blood
(acapnia), and, as Henderson has shown, this in turn causes dilatation of the veins and
causes the blood to gradually leave the arteries, stagnate in the venous reservoir (see
page 31), and thus diminish the rapidity of the blood flow.
Corresponding to the variations in rapidity of blood flow, the urine
is increased in amount during mild exercise, decreased during severe exer-
cise. After boat races and after the Marathon races it often contains
albumin, casts, and even traces of
blood, probably as a result of stasis
or high pressure in the renal veins
and capillaries.
Exercise of Strain.— The effect of
exercises of strain, lifting, etc., is totally
different. McCurdy, Bruck, and others
have shown that these exercises cause
a far greater rise of blood-pressure than
do the exercises of speed; and, on the
other hand, the pulse-rate does not rise
rapidly but is at first either slowed or
unchanged. The rise in blood-pressure
is greater in arteriosclerotics, old per-
sons, and weak individuals for the
same amount of work than in well-
developed normal individuals. In per-
sons already suffering from broken
compensation, on the other hand, the
heart absolutely fails to respond with
increased effort, and may be so greatly
weakened by the strain that the blood-
pressure may fall.
All the factors which are called into play by the hormone action of CO2
in exercises of speed and of endurance are also acting in exercises of strain;
but, since the latter are usually intermittent or of short duration, their
effects are at first overshadowed by others which are more intense.
In carrying out any exercise involving muscular
strain the individual in vpl u-n t ar il y closes his glottis
FIG. 116. — Rise of blood-pressure during
Valsalva's experiment and during exercise.
Normal individual. (Schematic, after Bruck.)
ARTERIOSCLER, curve of blood-pressure in
man with arteriosclerosis performing the same
exercise.
PHYSIOLOGY OF EXERCISE. 133
and executes an attempt at forced expiration. The
result of this is a tremendous increase in intrathoracic pressure, which
hinders the outflow of bood from the right ventricle as well as the inflow
into the right auricle.
The result of these two factors is dilatation of the right ventricle and stasis in the
systemic veins, which is still further shown by the cyanosis of the face and distention of the
veins that accompany all such exercises even in trained athletes. The venous stasis is
further increased by the sudden squeezing out of blood from the large masses of skeletal
muscles, which are being forcibly contracted simultaneously, as well as from the vessels
of the splanchnic area.
The high pressure within the lungs stimulates the sensory endings of the vagus; which
in turn reflexly stimulate the motor nucleus of the vagus and the vasomotor centre in the
medulla and cause both slowing of the pulse and rise of blood-pressure. The general result
is the same, but less marked when the Valsalva experiment only (forced expiration with
glottis closed) is carried out, and depends very largely upon this factor.
SIZE OF HEART AFTER EXERCISE.
Diminution in Size in Healthy Hearts. — Examined with the X-ray
the auricles are seen to dilate greatly, but the ventricles do not, as a rule,
show any dilatation whatever. This again is a question of tonus, and here
also the latter factor seems to determine whether dilatation shall set in
or not. All exercises when sufficiently severe lead to dilatation of hearts
whose myocardium has suffered injury, especially during the course of
r ,
Fio. 117. — Semi-schematic drawing showing variations in size of the heart of a long-distance
bicycle rider, as the result of a very long race; reconstructed from the orthodiagraphic outline. A. Before
the race. B. Immediately after the race, showing the gieat diminution in size of the heart. C. Four
weeks later. (After Moritz and Dietlen, Miinchen med. Wchnschr., 1908, Iv.)
infectious diseases (da Costa, Zuntz and Schumburg, de la Camp, Moritz
and Dietlen) or during the first few weeks following them. On the other
hand, Schott has claimed to have seen cardiac dilatation in healthy wrestlers
and bicycle riders as a result of short wrestling bouts. This fact has been
disputed by 'a number of observers who have carefully controlled the more
or less subjective findings of percussion by outlining the heart with the
orthodiagraph.
The following exercises have been studied: bicycle riding, by Mendelsohn, Albu,
Beyer, Schieffer, Dietlen and Morita; marching, by Zuntz and Schumburg, Albu and
Caspari, Balders, Heichelheim and Metzger; football playing, by F. Pick and by Selig;
ski running, by Henschen; wrestling, by Levy-Dorn, Selig, Mendl and Selig; swimming.
by Kienbock, Selig and Beck.
The results of these observations quite uniformly confirm those of
de la Camp in showing that exercise, even to the point of exhaustion and
134 DISEASES OF THE HEART AND AORTA.
fainting, does not bring about cardiac dilatation in otherwise healthy men.
In most cases the X-ray and orthodiagraph show an actual diminution in
the volume of the heart * (see Fig. 117). De la Camp also found that healthy
dogs could run upon a tread-mill until they dropped from exhaustion with-
out causing dilatation of the heart; whereas the hearts of dogs which had
been poisoned with phosphorus and which were in a state of mild fatty
degeneration dilated greatly from the same exercise.
Dilatation and Myocardial Injury. — On the other hand, Hornung,
who has watched the course of 1100 cases of weak heart with the X-ray,
states that in such persons acute dilatations (demonstrable with the ortho-
diagraph) are very common as the result of slight overstrain. It may
require comparatively little strain to bring this about. For example, he
cites the case of a woman with a weak heart who acquired a dilatation by
taking a short cut instead of a gradual ascent while climbing a hill (Oertel's
Terrainkur). The dilatation lasted for several days and gradually passed
off. Persons whose hearts are in this labile equilibrium are liable to have
repeated attacks. But the cardiac condition rarely stands still. It grad-
ually becomes either better or worse, according to the treatment and the
mode of life of the patient.
Thoracic and Abdominal Constriction as a Factor in Cardiac Over=
strain. — A high diaphragm due to tight belts or corsets is one of the most
important factors which predispose to cardiac overstrain. This was already
shown by A. R. B. Myers in 1867. Myers observed that certain cavalry
regiments in the Indian Arniy were particularly subject to cardiac over-
strain and to chronic cardiac disease, even more so than the infantry regi-
ments which were doing more arduous work under the same conditions of
climate and diet. He noticed that the uniforms of this cavalry regiment
were very tightly belted and had tight cuirasses compressing the chest.
Upon experimentation he found that the men in this regiment, when not
wearing their uniforms, were quite as strong as those of other regiments
in the service. He also found that the same men were able to withstand
much greater exertion in the same uniforms if only the belts were worn
looser. This has been shown with somewhat greater exactness by Th.
Schott. Schott demonstrated with the orthodiagraph that wrestlers could
withstand much greater exertion before the onset of acute dilatation or of
cardiac symptoms if they wore no belts than if they were tightly belted.
This is, of course, not surprising, and is simply another way of demonstrat-
ing the every-day experience of most healthy women that they can do
more work without a corset or with a loose one than when wearing one
that is tightly laced.
The reason for this is twofold. The belt interferes with the respira-
tory movements of the abdomen and diaphragm, and hence diminishes the
rhythmic alternation of positive and negative pressures, of force-pump and
suction-pump action, in one of the largest of the vascular reservoirs, thus
1 The syncope (cerebral anaemia) under these conditions is probably due to the exactly
opposite condition, diminished cardiac filling and hence diminished
cardiac output; arterial anasmia due to rapid pulse-rate in a heart whose tonicity
is increased. (This condition is fully discussed in the chapters on Paroxysmal Tachycardia
and Miscellaneous Heart Diseases.)
PHYSIOLOGY OF EXERCISE.
135
diminishing the rapidity of blood-flow. Moreover the viscera are pushed
back and the diaphragm is pushed upward by the belt, and this causes the
heart to assume a more transverse position, in which kinking of the great
veins, the aorta, and the pulmonary artery sets in, and both the filling and
the emptying of the heart are impeded. This mechanism is readily demon-
strated upon the exposed heart of the living animal. A comparatively
slight upward or downward displacement of the heart from its natural posi-
tion may cause tremendous fall in blood-pressure and interference with
the work of the heart.
PHYSIOLOGICAL FACTORS BRINGING ABOUT DILATATION.
The diminution in the size of the heart which was found so uniformly
by the above-mentioned observers seems to be due, in part, to diminished
filling of the ventricles when the heart is rapid, but chiefly to the fact that
the cardiac tonicity was increased by the strain.1 This clinical observa-
tion has its analogue in experimentation on animals. O. Frank has shown
that, other things being equal, a moderate increase in intra ventricular
pressure acts as a stimulus and causes an increase in the force of the next
beat. If the pressure is raised further it reaches an optimum; but if it
VOL.
LATED
A i
I. A M E_
B. P.
FIG. 118. — Effect of strain upon the dog's heart whose tonicity is good. Volume curve (VOL.)
and blood-pressure curve (B.P.) of an animal whose heart is in good condition. Descending thoracic
aorta clamped at the moment indicated by the arrow. Momentary dilatation followed by a diminution
in size. The heart becomes smaller than before the clamping. Tonicity is increased (T +). Blood-
pressures maximal and minimal are also increased.
becomes too high the force of contraction becomes much weaker than if
there were no load at all. There is a similar effect upon cardiac tonicity.
Hirschfelder has shown that if the thoracic aorta of the dog is clamped the
ventricles at first dilate rapidly and the systolic output diminishes. If the
heart is in good condition the systoles soon begin to increase, the excess
of blood is pumped out of the ventricular cavities in systole, and on the
other hand, in spite of the high pressure in the veins, less blood enters the
ventricles than before.
1 It is possible that acapnia (page 31) may play a r61e under these conditions.
136 DISEASES OF THE HEART AND AORTA.
The amount of blood which enters the ventricles depends upon two
factors: 1. As Howell and Donaldson have shown for the excised heart,
and Roy and Adami for the dog's heart in situ, it is more or less propor-
tional to the venous or intra-auricular pressure. 2. Roy and Adami,
Hirschfelder, Cameron, and others have shown that it is also dependent
upon the cardiac tonicity, being greater when tonicity is low (dilatation)
and least when tonicity is high. It is therefore evident that a heart whose
tonicity is high will withstand a comparatively high venous pressure with-
out dilating, whereas when the tonicity is low it readily overfills.
Several factors contribute toward diminishing the strength of an over-
filled heart: 1. With the increase of the cubical contents and the internal
surface of the ventricles the mechanical work necessary to exert a normal
VOL.
B. P.
SEC.
FIG. 119. — Volume curve of a dog whose cardiac tonicity is low. Clamping the aorta is followed
by permanent dilatation and only a slight momentary increase in blood-pressure. The systolic output
is diminished, owing to inability of the heart to force the usual quota of blood against the increased
resistance.
pressure is increased (Roy and Adami). 2. In the dilated beart the blood
flow through the coronary arteries and hence the nutrition of the cardiac
walls is diminished (Hyde) . Moreover the dilatation of the ventricles may
or may not be permanent, dependent upon the tonus of the heart muscle
(Hirschfelder, Cameron). If the latter is low the dilatation remains and
increases, whereas if it is high the increased pressure acts as a stimulus.
It is usually a high venous pressure which keeps the heart dilated and a
low tonicity which permits it to remain so.
Since the venous pressure is certainly highest in the exercises of strain,
it is not surprising that permanent heart trouble arising in previously
healthy persons as a result of primary cardiac overstrain is particularly
common among persons (butchers, porters, stevedores, etc.) who lift the
heaviest weights.
EFFECT OF THE STRAIN UPON THE HEART.
The response of the heart to a muscular exertion which just fatigues
may be of three grades: 1. The heart becomes smaller or the cardiac
outlines are unchanged — tonicity high (normal hearts-). 2. There is a
transitory dilatation (after acute infections and in hearts with myocardial
or some other cardiac disturbance). 3. The overstrain leads to perma-
nent injury of the heart, often with permanent arrhythmia (chronic car-
PHYSIOLOGY OF EXERCISE.
137
diac overstrain, myocardial changes). These three conditions find their
analogues in the effects of clamping the thoracic aorta upon the volume
of the ventricles (Fig. 119).
As has been seen in the cases quoted above, the repetition of the strain
is quite as important a factor in heart failure as is the overstrain itself.
Even a heart with extremely low tonicity will, in most cases, recover and
gradually return to normal volume after the strain has been removed, but
during the period when it is still dilated it is much more susceptible to a
further overstrain. On the other hand, after a sufficient period of rest it
regains its former volume and still later its former tonicity, and once more
reaches its original strength. That this is probably the case in man also is
shown by the fact that Poynton did not regard an occasional overstrain
FIG. 120. — Effect upon the volume of the dog's heart produced by clamping the descending tho-
racic aorta. Ascent of curve = diminution in volume; descent = dilatation. 1, normal and vigorous heart;
2, slightly weakened heart with diminished tonicity; 3, very weak heart with much diminished tonicity.
as of any special significance in boys, provided it were followed by a period
of sufficient rest. Moreover, Meylan has found that the lives of oarsmen
upon the Harvard boat-crews were somewhat longer than the average for
normal individuals, in spite of the fact that albuminuria and other signs
of cardiac overstrain are quite common just after such races. Indeed
not a single case of cardiac disease developed among the 152 oarsmen
of his series, which comprised members of the intercollegiate crews from
1852 to 1892. There was only one case in which enlargement of the heart
was noted and one case of irregularity, but neither of these inconvenienced
the patient.
These individuals, in contrast to cases like that of v. Leyden, had rested
sufficiently between the periods of strain, and the second strains had not
been imposed upon their hearts until long after their strength and tonicity
hud returned to normal. In v. Leyden's case and other cases of permanent
138 DISEASES OF THE HEART AND AORTA.
heart failure, the heart was still dilated at the time of renewed strain. This
condition seems to determine the border-line between heart failure and
recovery.
The border-line conditions may therefore be summarized as follows:
Dilatation of the heart during or after exercise represents a pathological,
though not a very infrequent, condition in which the heart has overstepped
its limits. The condition usually recedes and leaves no traces unless the
heart is again overstrained while still in a dilated condition.
As regards the anatomical changes induced by the condition of over-
strain, Roy and Adami have shown that, when the dog's heart begins to
fail after clamping the aorta, stasis occurs in the coronary veins and the
heart muscle becomes oedematous. This oedema is especially marked in
the regions which are richest in connective tissue, the auricles and the
auriculoventricular valves. They believe that when the strain is con-
tinued the cedema is replaced by infiltration, the infiltration by connective
tissue, and that fibrous myocarditis results. Indeed, a fibrous myocarditis
(cardiosclerosis) is a common autopsy finding in cases of long-continued
cardiac overstrain in which there has been no severe infectious disease to
account for the lesion. On the other hand, Pearce and Fleisher and Loeb
have found exactly the stages mentioned by Roy and Adami in animals in
the various stages of adrenalin myocarditis (see page 226) .
BROKEN CARDIAC COMPENSATION.
As long as the heart is able to maintain a certain velocity of blood
flow throughout the circulation, the latter may be said to be compensated;
but when the blood stagnates to such a degree as to give rise to the signs
and symptoms of stasis, compensation may be said to be broken.
There are two forms of broken compensation. When the blood stag-
nates in the systemic veins from failure of the right side of the heart, the
condition may be termed broken systemic compensation;
when stasis occurs in the lungs because the left side of the heart is not
acting as strongly as the right, broken pulmonary compensation
results. Each of these two forms brings with it a characteristic group of
symptoms: The broken systemic circulation (usually designated simply as
" broken compensation ") manifests itself in the signs and symptoms which
are seen in tricuspid insufficiency — breathlessness, cyanosis, cedema, begin-
ning in the feet and legs, enlargement of the liver, and systolic pulsation
of the liver and veins, etc. Broken pulmonary compensation is accom-
panied by the signs and symptoms of an acute severe mitral insufficiency —
intense respiratory disturbance, dyspncea, cough, occasionally pulmonary
hemorrhage, and the sputum containing the characteristic cells of passive
congestion (Herzfehlerzellen).
Broken Systemic Compensation.— From the physiological stand-point,
the cardinal features of broken systemic compensation are dilatation and
weakening of the right ventricle, dilatation and paralysis of the right
auricle, increase :n CO2 and decrease in O2 in the venous blood, functional
insufficiency of the tricuspid valve, rise in venous pressure (often to as
high as 20 mm. Hg) (Fig. 121, III). The signs are cyanosis, engorgement
and systolic pulsation of the veins, enlargement of the liver, cedema of the
BROKEN CARDIAC COMPENSATION.
139
feet and legs, and sometimes venous stasis in the medulla, vasoconstriction,
high blood-pressure, and dyspnoea of medullary origin.
Broken Pulmonary Compensation. — The characteristics of broken pul-
monary compensation are dilatation and weakening of the left ventricle,
dilatation and usually paralysis of the left auricle, rise of pressure and
stasis in the pulmonary veins, engorgement of the pulmonary capillaries,
and "erection" of the lung tissue (v. Basch) (Fig. 121, IV). Welch has
shown that when the stasis is very intense, pulmonary redema sets in.
V. Basch and his pupils have applied this idea to the milder pulmon-
ary manifestations and have shown that a moderate erection of the lung
tissue brings on cardiac dyspnoea and leads to bronchitis and cough. His
pupil, Kauders, has shown that the position of the diaphragm is affected
reflexly by the amount of blood in the lungs, congestion causing the
•diaphragm to descend, depletion causing it to ascend. It is thus usually
lower than normal in mitral lesions, higher in pulmonary and tricuspid.
NORMAL
ii
BROKEN
PULMONARY
COMPENSATION
III
BROKEN
SYSTEMIC
COMPENSATION
• IV
FAILURE OF
BOTH
VENTRICLES
FIG. 121. — Diagram showing changes in the circulation. I, normal; II, broken pulmonary com-
pensation; III, broken systemic compensation; IV, both compensations fail; stases in lungs and veins.
AO, pressure in the aorta, PA.
V. Basch also believed that the congestion of the lungs causes the elastic-
ity of the lungs to diminish and to become so rigid as actually to diminish
the respiratory expansion, but the experiments of D. Gerhardt have thrown
doubt upon this phase of his conclusions. As regards the changes of pres-
sure and the distribution of the blood, however, v. Basch's conclusions
have been confirmed, not only by Gerhardt in Germany but by W. G.
MacCallum and McClure in America.
In badly weakened hearts both forms of broken compensation may
be present, sometimes features of one, sometimes of the other, predomi-
nating.
Functional Valvular Insufficiency in Broken Compensation.— Although
it has not been absolutely proved, it seems almost certain that the occur-
rence of broken compensation from acute dilatation is accompanied by a
functional insufficiency of the tricuspid or the mitral orifice which may
be of transitory duration. Indeed this functional insufficiency of the tri-
cuspid valve in heart failure is much more common than organic lesion of
140 DISEASES OF THE HEART AND AORTA.
the valve, and in long-standing cases is accompanied by actual stretch-
ing of the tricuspid orifice (T. W. King, G. A. Gibson, Mackenzie, Keith).
T. W. King, in 1837, demonstrated that such functional insufficiencies
occur at the triscupid valves, and even that they were dependent upon the
tonicity of the ventricular fibres; since the valves which had been in-
sufficient a few hours after death held water perfectly after rigor mortis
had set in (quoted in full on page 396). These observations have been
confirmed and extended by G. A. Gibson, Frangois-Franck, Mackenzie,
Friedreich, Marey, Hirschfelder, Keith. Hering demonstrated the same
phenomenon for the mitral valve in rabbits, but found that in dogs the
mitral valve did not leak even after clamping the aorta. Stewart and the
writer have been able to demonstrate the occurrence of such an insuffi-
ciency of the mitral valve when the aorta was clamped, in dogs whose
aortic valves had been rendered insufficient. In man Morton Prince and
Broadbent have noted the presence of transitory mitral systolic murmurs
(sometimes transmitted to the axilla) in men who were being subjected
to the strain of civil service examinations, and in cases with similar signs
Minkowski has obtained tracings from the oesophagus which have the form
characteristic of mitral insufficiency.
In the earlier stages of cardiac overstrain the dilatation of the auricles
is a more or less passive phenomenon which exerts little influence upon the
circulation, but in the more severe stages it may play a leading role.
Auricular Paralysis and Arrhythmia in Cardiac Overstrain. — Condi-
tions which affect tonicity and filling of the ventricles have a still greater
effect upon the tonicity and filling of the auricles. It was demonstrated
by Ludwig's pupils, Waller (1878) and v. Frey and Krehl (1890), that
when the ventricles began to fail, the auricles soon became overloaded
with blood and ceased to contract entirely when the pressure reached
15-20 mm. Hg. As a rule this does not affect the cardiac rhythm, but
Hirschfelder has shown in dogs that when this is brought about by nar-
rowing the mitral orifice; an absolute irregularity (disorderly rhythm)
may set in without any apparent contractions carried out by the auricles.
It seems probable that, under these circumstances, the contraction stimuli originate
in the auricle and are transmitted but are not carried out by these chambers; just as
Biedermann has shown that muscle in water rigor can originate and transmit a stimulus
without itself contracting. Mackenzie and others believe that under these circumstances
the stimulus no longer originates in the sinus portion of the auricle but in the Purkinje
cells of the His bundle (at Tawara's nodal point, Knotenpunkt) , and hence designates,
this absolute irregularity as nodal rhythm. They believe that the auricle and ventricle
are 'contracting simultaneously under these circumstances. Since Retzer has traced the
bundle directly into the sinus region and believes that there is no nodal point, this view
seems open to question.
Arrhythmia. — Whatever may be the origin of the arrhythmia it is very common in
severe overstrains. This not infrequently arises in the course of valvular lesions as well, as
Mackenzie has proved. The case cited on page 350 gives an example of such an irregularity
arising during such an attack and subsiding a few days later after rest and digitalis. Five
days later the rhythm became regular and the auricles were contracting once more. When
the overstrain is more protracted the auricular contraction may remain absent for weeks
and even months, and most frequently, if it has persisted for a considerable length of time,
permanent changes set in in the musculature of the sinus region (Keith, Schonberg), and
regularity is never regained. The pulse has become permanently irregular (pulsus irregu-
laris perpetuus, arrhythmia perpetua). As has been seen on page 77, the arrhythmia
BROKEN CARDIAC COMPENSATION. 141
itself slows the blood stream and the diseased condition of the sinus prevents the heart
from compensating for this by a greater number of contractions. The velocity of the
circulation is thus self-limited. Only a certain amount of CO2 per minute can be taken care
of and any excess brings on overstrain.
Changes in Venous Pressure. — Changes in pressure in the systemic
veins, which show how well the right ventricle is pumping, often afford
an excellent index of the break in systemic compensation, rising from
normal pressure of 5-10 cm. H2O to a height of 20 or 25 cm. It usually
rises when the patient's condition becomes worse and falls as improvement
sets in (Hooker and Eyster).
The arterial pressure, on the other hand, is affected by too many
factors to show characteristic changes. It may be kept up until shortly
before death, by asphyxia of the medullary centres and resultant vaso-
constrictor and augmentor stimulation; or, on the other hand, when this
mechanism is not brought into play, the arterial pressure may be low and
the pulse may be small and weak.
CARDIAC FAILURE WITH A SMALL HEART.
There is another form of failure of the circulation which sometimes
occurs as the result of exertion, even in trained athletes. This form is
accompanied by pallor, a small rapid pulse, and sometimes even by syncope.
However, as Dietlen and Moritz have shown, it is not accompanied by a
dilatation of the heart, but, on the contrary, the latter is smaller than
normally. It is a failure of the rest of the circulation rather than of the
heart.
It must be admitted that this condition has not attracted much attention, and but
little can be said of the mechanisms involved. The pallor, small pulse, and small heart,
however, are features which are also common to the condition of shock and the cardiac
neuroses. In these conditions, the important mechanical factors are the accumulation of
blood in the dilated abdominal veins, giving rise to a low venous pressure, the diminished
filling of the heart, and consequently the diminished output into the aorta. The symp-
toms are symptoms of "arterial anaemia."
The causal factor in bringing about this condition may be dilatation of the veins.
In the case of exercise this veno- and vasodilatation may result either reflexly from dis-
turbed digestion, or, perhaps, as Henderson suggests for somewhat similar conditions, it may
set in when the rapidity of breathing exceeds that necessary to aerate the blood, even to
meet the increased needs of the body. Under these conditions CO2 leaves the lungs, and
hence also the blood, a little too rapidly, acapnia results, and, as its first effect, allows the
veins to dilate (see page 31). The blood thus stagnates in the veins. As a matter of fact,
Kraus, Zuntz and Schumburg, and also A. Loewy have shown that at this stage of exercise
less CO2 is given off from the lungs than before, and the respiratory quotient CO2is lessened.
They believe that oxidation is less at this stage and hence less CO2 is present in the blood.
In other words, from a totally different stand-point, and years before Henderson's experi-
ment, it was rendered probable that a state of acapnia is present at the stage of fatigue
in exercises of endurance, and therefore that the mechanism which he observed to be active
in acapnia is largely responsible for this form of circulatory failure.
FUNCTIONAL TESTS OF CARDIAC EFFICIENCY.
It is evident from the facts discussed above that the most important
question in the functional study of heart failure is to determine accurately the
border-line between fatigue and overstrain, to distinguish between the nor-
mal and the pathological. Various tests have been devised for this purpose.
142 DISEASES OF THE HEART AND AORTA.
1. Postural Change in Pulse=rate. — The rise in the pulse-rate which oc-
curs when the patient stands after lying down is of some importance. Under
normal conditions the acceleration is not more than twenty beats per minute, the average
acceleration for normal individuals being seven. However, this depends upon many
factors, one of which is the length of time during which the patient has lain down, his state
of mental excitement or quiet, etc. The psychic element plays a particularly important
role in this test.
2. Contraction of Antagonistic Muscles. — Herz has introduced another procedure,
the self-checking or self-antagonizing test (Selbsthemmungsprobe) . He
counts the pulse over a period long enough to assure a reasonably constant rate per minute.
The patient is then made to sit down and very slowly flex and extend the right forearm,
putting, all the while, his full attention upon the movement, but contracting simultaneously
the flexor and extensor muscles of the arm, and attempting to antagonize his own move-
ment with as much force as possible. This converts the exercise into a mild exercise of
strain. Herz states that in normal individuals this causes no change in pulse- rate,
while in those with feeble hearts the pulse-rate is slowed 5-20 beats per minute. (Per-
haps this is due to the morq vigorous expiratory effort which accompanies this procedure
in persons with diseased hearts.) Cabot and Bruce have repeated Herz's observations,
and find that they are correct in at least a certain number of cases, but they are unwilling
to subscribe to his general rule. The writer also has found a number of perfectly strong
and healthy individuals who give Herz's pathological reaction.
3. Rise of Blood=pressure on Constricting the Femoral Arteries. — Marey (1881)
demonstrated that in normal individuals the blood-pressure rose when both
femoral and both brachial arteries were compressed. Katzenstein found that on com-
pressing both femoral arteries alone, in
Blood-pressure Pulse-rate
Normal individuals Rose 5-15 mm Fell.
Compensated cardiac lesions Rose 15-40 mm Unchanged or fell.
Slight cardiac insufficiency Unchanged Unchanged or rose.
Very weak hearts Fell Fell.
Hoke and Mende and others have repeated Katzenstein's observations, and find that,
though these results hold true in general, the method is unreliable as a test and in bad
cases is too dangerous for use.
4. Rise of Blood=pressure upon Exercise. — Another method, introduced by Graupner,
of Nauheim, depends upon the rise of blood-pressure which occurs dur-
ing exercise. Graupner found that, as Masing had shown, mild rapid exercise, such
as walking up and down stairs rapidly, etc., caused a rise of blood-pressure in normal indi-
viduals but a fall of pressure in those with failing hearts. His observations have been
repeated on a considerable series of patients by Baur (also of Nauheim). Baur used the
stationary bicycle as a test, regulating the effort by applying a loaded brake to the wheels.
He found that in normal individuals there was at first a rise of 5-10 mm. Hg and later a
fall of 5-10 mm., while in insufficient hearts there was a fall of 5-20 mm. Hg. The limit
of performance of the latter was 45-300 Hg of work, however, only a small fraction of that
which could be done by the normal individuals. Cabot and Bruce also have repeated and
confirmed Graupner's observation, and believe that it will prove of assistance as an aid in
functional diagnosis.
That a close relationship exists between the increase in blood-pressure
and the increase in tonicity (stimulation of augmentor fibres) , which results
from strain put upon the heart, may be seen from. the curves of Hirsch-
felder and Cameron in the dog's heart (quoted on page 135, and shown in
Figs. 118 and 119). It is probable that, in most cases, rise of pressure cor-
responds to increased systolic output and concomitant increase in tonicity.
It must be realized, however, that in some cases the rise may be second-
ary to stimulation of the vasoconstrictor centre from medullary stasis or
asphyxia, but may represent an unfavorable condition.
FUNCTIONAL TESTS OF CARDIAC EFFICIENCY. 143
Several objections may be made to the value of this test:
1. G. A. Gordon in G. A. Gibson's clinic and also Professor Dawson, in collaboration
with Professor Eyster and also with Mr. Hetfield, have shown that the blood-pressure
in trained athletes falls during mild exercise exactly as it does in broken
compensation ; also that it falls when the " second wind " is acquired and while the
person's functional power is increasing rather than decreasing.
2. As already shown by Masing, the greatest rises of blood-pressure
occur in old and feeble persons, whom the exercise brings near to the border-line of cardiac
overstrain.
3. In persons in whom the fall in blood-pressure occurs as a result of the test exercise,
the general symptoms, respiratory distress, cyanosis, etc., to say nothing of the diminished
decrease in the size of the pulse, tachycardia and arrhythmia resulting, are more than suf-
ficient evidence that the patient's strength has been overtaxed.
4. These simpler clinical manifestations are more delicate indices and are less ambig-
uous signs than are the changes in blood-pressure.
The recent studies of Schott, de la Camp, v. Criegern, Hornung, Moritz and his pupils,
taken in conjunction with the physiological experiments of
Frank, Hirschf elder , and Cameron, indicate that the only true
numerical criterion of cardiac efficiency is whether a given
strain causes it to diminish in size ( inc rease in t on i ci ty= stimu-
lation) or to dilate (decrease in tonicity — overs train).
Functional studies upon the border-land between functional suffici-
ency and cardiac failure are of the most fundamental importance, and all
the facts added to our knowledge of the subject are of the greatest value
in adding to our understanding of the subject.
Observation versus Estimation. — However, it must be admitted that,
in order to be decisive, all these tests usually have to be pushed to a point
at which the appearance, sensations, and signs of the patient are in them-
selves perfectly characteristic of cardiac insufficiency, and at which, for
diagnostic purposes, a little common-sense observation is at least as unam-
biguous as observation with elaborate apparatus. This does not mean
that exercise tests are unimportant. On the contrary, they are of the
greatest value; and no change in the patient's mode of living during con-
valescence or during after life should be undertaken without them. But their
importance depends more upon the care with which the physician watches
the general appearance and condition of the patient, the rapidity with which
he recovers from the exercise, his general condition, and whether nervous-
ness, irritability, cough, or insomnia have set in during the twenty-four
hours following it, than in the numerical changes which occur at the moment
of exercise. The symptoms to be looked for as evidence of overwork are
discussed in more detail in the instructions for giving Schott exercises (page
195). These are subtler manifestations resulting from smaller changes
than may be detected by even the most refined observations by mechan-
ical methods, and which are less easily masked by ambiguities. Moreover,
it must be realized that any one form of exercise furnishes data which
may depend as much upon the condition of the skeletal muscles as upon
the heart. The blacksmith with a diseased heart may be able to do more
work than the book-keeper with neurasthenia, and yet under the conditions
in which he lives, even if not under the strength test arranged for the average
man, the blacksmith's heart may be failing.
Relation of Functional Test to Mode of Life. — In diagnosis, prognosis,
and therapy, the testing of functional insufficiency is a matter of sociology
144 DISEASES OF THE HEART AND AORTA.
as well as physiology. The important question is not what the
patient can do in a gymnasium, but what he can do and
what he can not do in every-day life. Each man must be fit
for his own mode of life or must be made to change it. His cardiac power
must be studied with reference to that mode of life rather than with ref-
erence to a rigid scheme.
Probably the most thorough system of routine functional testing ever
instituted was that resorted to by J. M. da Costa during the Civil War before
he permitted his convalescents from cardiac overstrain to return to active
duty with their regiments. He subjected them first to light camp duties,
then to guard duty, then to provost duty, and later made them run frequent
races comparable to charges upon a battlefield — each test commensurate
with the mode of life which the patient was about to live. Step by step
he ascertained the endurance of his patients without overstraining them,
and thus obtained a series of permanent cures which stands as a worthy
monument to one of the most careful and brilliant of American clinicians.
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Zur Pathologie und Therapie des Lungenoedems, Arch. f. exper. Path. u. Pharmakol.,
Leipz., 1885, xix, 433.
Klinisch-experimentelle Untersuchungen aus dem Laboratorium von S. v. Basch, Berl.,
1891, vol. i; 1892, vol. ii; 1896, vol. iii. Vol. i. Grossmann, M.: Das Muscarin-
10
146 DISEASES OF THE HEART AND AORTA.
Lungenoedem, p. 7 (also Ztschr. f. klin. Med., Leipz., 1887, xii, 550). V. Basch, S.:
Ueber eine Function des Capillardrucks in den Lungenalveolen, p. 49; Pathologie
der cardialen Dyspnoe, p. 53. Grossmann, M.: Experimented Untersuchungen zur
Lehre vom acuten allgemeinen Lungenoedem, p. 80 (also Ztschr. f. klin. Med.,
xvi). Bettelheim, K., and Kauders, F.: Experimented Untersuchungen ueber die
kiinstlich erzeugte Mitralinsufficienz und ihren Einfluss auf Kreislauf und Lunge,
p. 144. V. Basch, S.: Ueber Lungenschwellimg und Lungenstarrheit, p. 171; Zur
Lehre von der cardialen Dyspnoe, p. 183; Ueber Lungenschwellung bei der cardialen
Dyspnoe des Menschen, p. 198. Kauders, F.: Ueber einige Experimente zur Lehre
von der Cardialen Dyspnoe, p. 211. Vol. ii. Zerner, Th. J.: Ueber den Einfluss der
Digitalis auf die Respiration, p. 19. Grossmann, M.: Ueber Stauungshypersemie in
den Lungen, p. 30. Kornfeld, S.: Experimenteller Beitrag zur Lehre vom Venen-
druck bei Fehlern des linken Herzens, p. 126. Vol. iii. Hegglin, C.: Experimented
Untersuchungen ueber die Wirkung der Douche, p. 1. Zerner, Th. J.: Klinisch-
experimentelle Untersuchungen ueber die cardiale Dyspnoe, p. 77. Buday, K.:
Ueber die Herzfiillung wahrend des Lebens und nach dem Tode, p. 106. Winkler, F.:
Experimentelle Studien ueber die Funktionelle Mitralinsufficienz, Ztschr. f. klin. Med.,
Berl., 1899, xxxvii, 456.
Gerhardt, D.: Ueber die Compensation von Mitralfehlern, Arch. f. exper. Path. u. Phar-
makol., Leipz., 1901, xlv, 186.
MacCallum, W. G., and McClure, R. D.: On the Mechanical Effects of Mitral Stenosis and
Insufficiency, Trans. Ass. Am. Phys., Phila., 1906, xxi, 5; and Johns Hopkins Hosp.
Bull., 1906, xvii.
Hering, H. E. : Zur experimentelle Analyse des unregelmassigen Pulses, Arch. f. d. ges.
Physiol., Bonn, 1900, Ixxxii, 1.
Minkowski, O.: Zur Deutung der Herzarhythmien mittelst des oesophagealen Kardio-
gramme, Ztschr. f. klin. Med., Berl., 1906, Ixii.
Prince, M.: Physiological Dilatation and the Mitral Sphincter as Factors in Functional
and Organic Disturbances of the Heart, Am. J. M. Sc., Phila., 1901, cxxi, 188.
Broadbent. Quoted from Prince.
Waller: Die Spannung in den Vorhofen des Herzens wahrend der Reizung des Hals-
markes, Arch. f. Physiol., Leipz., 1878, 525.
V. Frey, M., and Krehl, L.: Untersuchungen ueber den Puls, ibid., 1890, p. 31.
Biedermann, W.: Electrophysiology, transl. by F. A. Welby, Lond., 1896.
Kraus, Fr.: Die Ermudung als Mass der Constitution, Bibliothec. Med. Cassel. Abth. D.,
1897, Heft 3.
Stephens: Blood-pressure and Pulse-rate as Influenced by Different Positions of the
Body, J. Am. M. Assoc., Chicago, 1904, xliii, 955.
Herz, M.: Eine Funktionspriifung des Kranken Herzens, Deutsch med. Wchnschr.,
Leipz., 1905, xxxi, 215.
Cabot, R. C., and Bruce, R. B.: The Estimation of the Functional Power of the Cardio-
vascular Apparatus, Am. J. M. Sc., Phila. and N. York, 1907, cxxxiv, 491.
Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1881.
Katzenstein: Ueber eine neue Functions prufung des Herzens, Deutsche med. Wchnschr.,
Leipz. and Berl., 1905, xxxi, 695.
Hoke, E., and Mende, J.: Ueber die Katzensteinsche Methode zur Prufung der Herz-
kraft, Berl. klin. Wchnschr., 1907, xliv, 304.
Levy: Ueber Kraftmessung des Herzens, Ztschr. f. klin. Med., Berl., 1906, Ix, 74.
Fellner, B., and Riidinger, C.: Beitrag zur Funktionspriifung des Herzens, Berl. klin.
Wchnschr., 1907, xliv, 417, 475.
Graupner: Die Messung der Herzkraft, Mimchen, 1905.
Baur, Fr.: Zur Bestimmung der Leistungsfahigkeit des gesunden und kranken Herzens
durch Muskelarbeit, Verhandl. d. Kong. f. inn. Med., Wiesb., 1904, xxi, 620.
III.
SYMPTOMS OF CARDIAC DISEASE.
The symptoms for which a patient suffering from cardiac disturbance
presents himself to the physician are variable, and frequently seem so far
removed from the site of disease as to mask their real origin and even to lead
to mistakes in diagnosis. Accordingly, it is important to consider the
symptoms early and the conditions giving rise to them, remembering that
in general they are due to (1) slowing of the circulation and local anaemia
or accumulation of C02; (2) overfilling of the veins with blood; (3) disturb-
ances in the nervous system, of circulatory origin.
The following are the main symptoms associated with cardiac diseases:
(1) shortness of breath; (2) cough; (3) swelling of the feet and legs;
(4) urinary disturbances; (5) palpitation of the heart, precordial pain,
pain down the arms; (6) digestive disturbances, indigestion, vomiting,
abdominal pain, jaundice; (7) general nervousness, occasionally transitory
delusions and hallucinations, sometimes fainting spells.
All these symptojns are liable to be increased after exercise,
excitement, or worry, on account of the increased heart-rate and
often increased blood-pressure that accompany them, and the conse-
quent increase in the work of the heart. They are also much increased
by damp and sultry weather when there is little air stirring. The patient's
color is then usually pale, showing a vasoconstriction to which some of the
embarrassment is probably ascribable. The symptoms usually improve
when the weather becomes clear.
RESPIRATORY DISTURBANCES.
DYSPNCEA.
Shortness of breath is usually the earliest and most common sign of
cardiac failure and especially of failure of the left ventricle (broken com-
pensation). The foundation for this doctrine was laid by the classical
experiments of Welch under Cohnheim's direction. Welch demonstrated
that in conditions in which the force of the left ventricle was impaired
without impairment of the right, oedema and congestion of the lungs set in.
V. Basch and his pupils, Grossman, Bettelheim, and Kauders, have
shown — in a very careful series of investigations upon animals — that
dyspnoea and the other respiratory disturbances of heart
failure are due chiefly to stasis in the pulmonary capil-
laries and veins, and are associated with rise of pressure in the left
auricle. Under these circumstances the elasticity of the lungs is probably
diminished and the volume of lung tissue increases. The respiratory
excursion decreases. These conditions disappear when the output of the
left ventricle (and hence the suction-pump action of that chamber) in-
147
148 DISEASES OF THE HEART AND AORTA.
creases sufficiently to pump out the excess of blood from the lungs and
remove the stasis. Accordingly, as is the common clinical experience,
severe dyspnoea is an early sign of mitral lesions, which readily comes
and goes with slight overstrains; while in aortic disease it is a sign of a
severe break in compensation, and often indeed of a secondary mitral
insufficiency.
This group of symptoms — cough, dyspnoea, cardiac
asthma, pulmonary oedema, pulmonary hemorrhage-
constitute a group of symptoms characteristic of stasis
in the pulmonary veins (broken pulmonary compensa-
tion), just as cyanosis, enlargement of the liver, and
ascending oedema are characteristic of failure of the
right heart. In Wilkinson King's "safety-valve action of the right
ventricle " failure of the latter substitutes a state of broken systemic com-
pensation for one of broken pulmonary compensation.
Rubow has shown by spirometric investigations that in cardiac dys-
pnoea there is a tendency for the lungs to assume the greatest possible vol-
ume (diaphragm descends lower and lower) just as is the case in emphysema.
According to Kraus the amount of O2 taken up by the blood and of CO2 given off per
minute is practically unchanged in cardiac failure. The conditions are therefore practically
analogous to Zuntz and Schumburg's experiment, in which increasing the CO2 in the inspired
air caused polypnoea and caused the total amount of air taken into the lungs per minute
to rise tremendously without altering the amount of oxygen taken up by the blood. It
is probable that stasis in the pulmonary capillaries stimulates the vagus endings in the
same way as does CO2.
Orthopnoea. — One of the most striking features of cardiac dyspnoea is
the fact that it is increased in the reclining posture and relieved by sitting
up (o r t h o p n o e a) , although this position favors the accumulation of
oedema in the legs, and, as Erlanger and Hooker have shown, impedes the
total velocity of the circulation. For this fact there may be several expla-
nations, or, more accurately, there may be several factors involved:
1. As Rubow has shown, when the patient is propped up, his liver and diaphragm
descend, and there is thus more air space available in the thoracic cavity.
2. Since the head up and feet down position tends to impede the return of venous
blood from the lower extremities, trunk, and abdomen, it thus tends to equalize the activi-
ties of the right and left ventricles. By slowing the inflow of blood into the lungs it enables
the weakened left ventricle to deplete the pulmonary capillaries more effectually than
would occur if more blood were thrown into them by the relatively stronger right ventricle.
3. In the head up position the veins of the -medulla drain more readily, thus diminish-
ing venous stasis in the medulla and consequently also diminishing the effect of direct CO2
stimulation of the vagus and respiratory centres. This effect of the erect position in dimin-
ishing the volume of (i.e. the blood in) the brain is well known to brain surgeons, who some-
times make use of it for penetrating to otherwise inaccessible places.
Cardiac dyspnoea is particularly marked during sleep, partly because
the diminished sensitiveness of the respiratory centres allows CO2 to accu-
mulate (if only momentarily) with greater ease than during periods of wake-
fulness, and partly because the muscles of the larynx relax, the laryngeal
slit is narrowed, and air enters the lungs with more difficulty, thus allow-
ing a slight asphyxia to set in.
Cardiac Asthma. — Occasionally the respiratory distress takes the form
of a definite paroxysmal dyspnoea or cardiac asthma. These paroxysms
SYMPTOMS OF CARDIAC DISEASE. 149
are particularly common in aortic insufficiency or coronary sclerosis. They
frequently occur at the moment of awakening; or, more accurately, the
patient is awakened by the need of air, CO2 having accumulated during
sleep, owing partly to the slower respiration, partly to the above-men-
tioned relaxation of the laryngeal muscles. This factor may also give rise
to an acute failure of the left ventricle from impaired cardiac tonus which
arises during the mild asphyxia that has preceded. Perhaps the dyspncea
is due partly to heart failure and partly to respiratory failure.
While the patient is awake, such attacks are sometimes brought on
by the act of defecation. This is not surprising, since defecation presents
a typical Valsalva's experiment, in which, as previously shown, a great
strain is thrown upon the left ventricle, sometimes severe enough to pro-
duce a functional mitral insufficiency.
Morphine and Strychnine in Cardiac Dyspnoea. — Such attacks of car-
diac asthma may be relieved by morphine, but the continued use of
morphine for this purpose often has a bad effect. Though it momenta-
rily relieves the distress, it also diminishes the irritability of the respira-
tory centre and thus allows still more CO2 to collect in the blood. The
patient then requires still more morphine to quiet him, and a vicious
circle is introduced:
Accumulation of CO 2
in the lungs Paroxysm of dyspnoea
t I
Diminished irritability _ MQ
of respiratory centre
On the other hand, the patient so quickly acquires the morphine
habit that frequently he brings on a paroxysm of dyspncea voluntarily in
order to get the drug, and does himself considerable harm by this effort.
Under these conditions strychnine is the drug indicated by its pharma-
cological action in stimulating the respiratory centre (as Eyster has shown).
Where strychnine (.002 to .005 Gm. =gr. -fa to gr. Ty or with atrcpine
(.0005 Gm. to .001 Gm. = gr. T|^ to gr. -fa) does not suffice, morphine may
have to be given, but it is best to give some strychnine along with it. After
the first dose it is frequently possible to obtain the quieting psychic effect
by injections of distilled water or of strychnine alone without giving rise
to the morphine habit.
Cardiac Asthma from Nasal Disease. — Another form of asthma with cardiac symptoms
has its origin not within the heart but in the nose. Frangois-Franck in 1889 was able to
demonstrate that cough, laryngeal spasm (false croup), asthma, and a reflex bronchitis
arise reflexly from stimulation of the nasal mucosa. He was able to reproduce these phe-
nomena in animals by stimulating the mucosa of the septum. They were accompanied
by acceleration of the heart and vasoconstriction. They did not appear when the latter
had been cocainized; or if they had once set in, they disappeared on cocainization. He
found that these effects were much more pronounced in animals with experimental aortic
insufficiency than in normal animals, and he believes that such exaggerated responses to
nasal reflexes are responsible for many of the paroxysmal respiratory disturbances in car-
diac patients suffering from cardiac disease, and especially from aortic insufficiency. It
is possible that they may give rise to some of the vasomotor crises.
It is important to differentiate cardiac asthma from the bronchial form.
Both may be accompanied by bronchitis and by the presence of rales.
In the cardiac form there is no impediment to either expiration or inspira-
150 DISEASES OF THE HEART AND AORTA.
tion, and hence only a simple polypncea is observed, while in bronchial
asthma there is stenosis of the smaller bronchi with hinderance to both
expiration and inspiration, and hence a peculiar labored and wheezing
breathing with prolongation of expiration which is quite characteristic.
C. M. Cooper (The Respiratory Ratio: A Preliminary Note, J. Am. M. Asso., Chicago,
1909, lii, 1182), suggests that the differential diagnosis in doubtful cases may sometimes
be made by noting the ratio between the periods during which the breath can be held in
full inspiration and those in which it may be held in full expiration. In normal individ-
uals the breath may be held in inspiration from 40 to 70 seconds; in expiration from 20 to
(40—70 \
i.e., ratio - — ). In patients with cardiac insufficiency this ratio is pre-
20-oo / /25 \
served, though the periods are shortened ( TF )• In bronchial asthma, on the other
hand, the breath can be held longer in expiration than in inspiration and the ratio
A
is reversed
It seems probable that this ratio will prove of great value in differentiating be-
tween asthmatic attacks due to acute failure of the left ventricle and those which arise
in cases of cardiac diseases, from reflexes of nasal or visceral origin.
PULMONARY (EDEMA.
Occasionally the attack of cardiac failure is very severe and is accom-
panied by oedema of the lungs. The above-mentioned experiments of
Welch and Cohnheim, and later of v. Basch and his pupils, have shown
that this is due to pulmonary stasis from acute failure of the left ventricle.
It is most frequent in cases of mitral stenosis in which pulmonary stasis
readily sets in, and is the complication particularly to be feared during
pregnancy and labor.
Experimentally, pulmonary oedema is readily produced by overstraining the left
ventricle through an overdose of adrenalin (L. Loeb1)- Besides conditions of cardiac
disease it is occasionally encountered after operations in which adrenalin has been used,
especially when in large amounts or upon surf aces, from which it is readjly absorbed. Oc-
casionally, as in a case recently known to the writer, sudden death results from this cause
from an operation otherwise trivial.
J. J. Miller and S. A. Matthews have recently investigated the action of numerous
poisons in producing pulmonary cedema, and have found that mechanical factors in the
circulation (failure of the left ventricle) are the immediate cause of the pulmonary cedema
after adrenalin, iodides, and iodine, but that acetic ether, nitric oxide, and ammonia cause
it to appear without any evidence of disproportion between the action of the two ven-
tricles, 'these substances apparently act entirely by injuring the walls of the pulmonary
vessels and by increasing the secretion of the alveolar walls, cells, and pulmonary lymph.
Signs of Pulmonary (Edema. — The onset of pulmonary cedema is
marked by pallor, cyanosis, cough, coarse moist rales throughout the chest,
and often by a frothy serous expectoration which may be very profuse.
Friedrich Miiller has shown2 that this expectoration contains considerable
1 Haven Emerson has shown that this occurs only when the chest is closed, not when
the chest is opened and artificial respiration substituted, and that it can often be cured
by artificial respiration with bellows inflation. Barringer reports good results from artificial
respiration in one patient.
2 To demonstrate the presence of albumen add dilute acetic acid to the sputum to
precipitate all the mucin, filter, and then precipitate the albumen from the filtrate by the
addition of potassium ferrocyanide.
SYMPTOMS OF CARDIAC DISEASE. 151
albumen, a fact of great diagnostic importance in doubtful cases. These
symptoms constitute a signal for immediate action.
Treatment. — The strain upon the left ventricle may be relieved by
inhalations of amyl nitrite, and its strength may be increased within a few
minutes by intravenous injection of strophanthus. The most certain pro-
cedure, however, is venesection, since it diminishes the work of the
right heart at once and thus enables the left ventricle to equalize conditions.
Accordingly pulmonary ce'dema is the signal for venesection in any except
the most anemic persons.
For the oedema itself atropine (0.5-1.0 mg., ^ to ^V gr. hypodermati-
cally) should be given, inasmuch as it diminishes the bronchial secretions
and thus does away with the cedema. In desperate cases larger doses
should be used.
HEMORRHAGE FROM THE LUNGS.
As a result of engorgement of the pulmonary capillaries or of per-
manent injury to their walls, hemorrhages from the lungs may occur in
any acute cardiac overstrain, but they are most frequently seen in cases
of mitral disease. In itself such a pulmonary hemorrhage is of no impor-
tance, although by relieving the congestion it may bring a great deal of
subjective relief to the patient. On the other hand, the conditions which
bring them on acutely are frequently those of severe overstrain. They
are particularly common in mitral disease, in pulmonary insufficiency
and sclerosis, and congenital heart diseases.
It is always of the greatest importance to differentiate between such an haemoptysis
and that of an early pulmonary tuberculosis, and only the most careful repeated examina-
tions, coupled with the presence of the cardiac lesion and the absence of signs of pulmonary
disease, give sufficient grounds to exclude the latter. It is particularly important to exam-
ine for tubercle bacilli in the blood spit up, since after a hemorrhage they may not be pres-
ent again in the sputum for several months.
Rest and the general measures which diminish pulmonary engorgement
constitute the treatment.
PULMONARY EMBOLISM AND HEMORRHAGES.
Pulmonary embolism with infarction is a not uncommon complica-
tion when a clot forming in the right auricle or ventricle is loosened into
the circulation and lodges in some branch of the pulmonary artery. These
infarcts may be large or small, dependent upon the artery occluded, and
upon their size depends the severity of the symptoms and the onset of
dyspnoea.
In all these cases there is an area of dulness, tubular breathing,
and increased vocal fremitus over some parts of the lung, and the expectoration of a slimy,
bloody or prune-juice sputum, which differs from that occurring in brown
induration in being much richer, deeper in color, and in containing a great deal of more or
less changed blood intimately mixed with the mucus instead of somewhat separate from it.
Pulmonary embolism is sometimes fatal when a large vessel is occluded, but usually not
so in the first instance. Exactly when a single embolus will be followed by a shower of
emboli and a fatal result cannot be foretold, and the patient lives continually under a
sword of Damocles, although in some cases he may live for several years without further
disturbance.
152 DISEASES OF THE HEART AND AORTA.
CHEYNE-STOKES BREATHING.
Cheyne, of Dublin, described a peculiar form of respiration in which
there are occasional pauses of variable duration, from several seconds to
half a minute, followed by inspirations at first slow, then more rapid, then
again lapsing into a pause. It was again described by Stokes in 1846 and
is very common in bad cases. This phenomenon is particularly frequent
in heart cases, especially in aortic disease, and is usually seen when the
patient is asleep. It is also common in cases of brain tumor, apoplexy, or
any condition where there is an increased intracranial tension. Not infre-
quently, in cardiac disease, the patient is in a state of coma or semicoma
during the periods of apncea but fully conscious during the periods of
dyspnoea. During the former the pupils are contracted and do not react;
during the latter they widen and react once more.
FIG. 122. — The two types of Cheyne-Stokes respiration in their relations to the blood-pressure
curves. (After Eyster.) A. Intracranial pressure type — apncea accompanies slowing of the pulse and
fall of blood-pressure. B. The cardiac type — apnoea associated with rise of blood-pressure and quick-
ening of the pulse-rate.
Eyster has found that the occurrence of Cheyne-Stokes respiration is always asso-
ciated with the slow periodic changes of blood-pressure known as Traube-Hering waves.
He distinguishes two types: In the first, which is always associated with increased intra-
cranial tension, as in brain tumor, meningitis, uraemia, the period of respir-
atory activity is associated with a rise of blood-pressure and quickening
of the pulse, the period of apnoea with a fall of blood-pressure and s 1 o w-
ing of the pulse (Fig. 122, A).
In the second type, the common form in cardiac and arterial disease, the respir-
atory activity is associated with a fall in blood-pressure and slowing of
the pulse, and the apnoea is associated with rise in blood-pressure and quick-
ening of pulse-rate (Fig. 122, B). Eyster was able to reproduce the first group in animals
by raising the intracranial tension, and found that whenever the intracranial pressure
was above the mean blood-pressure apncea occurred. Then the blood-pressure rose through
asphyxial stimulation of the vasomotor centre, and when it overtopped the intracranial
pressure, respirations again set in. The converse was not true of the second group of
cases, and neither he nor any other observer has been able to reproduce this more com-
mon type or analyze its causal factors.
Biot has described another type of respiration, in which a series of inspirations equal
in rate and in size are punctuated by long apnoeic pauses. This is only a small variety of
the cases showing the Cheyne-Stokes type, and its occurrence and causal factors seem
to be about the same as the latter.
Mosso has also depicted another group of periodic respirations occurring at high
altitudes, apparently from low CO2 content of the blood reaching the vasomotor centre
(acapnia), in which there is with each respiratory group rise of blood-
pressure and slowing of the pulse. This does not seem to occur in cardiac or intra-
cranial cases.
SYMPTOMS OF CARDIAC DISEASE. 153
Eyster concludes that in the intracranial pressure type the Cheyne-Stokes respiration
is due to the fact that the respiratory centre is more sensitive to anaemia than is the vaso-
motor centre, and rapidly loses its irritability, regaining it when circulation is reestablished.
Therapeutically Eyster has attempted to remedy the condition by
increasing the irritability of the respiratory centre, (1) by injections of
strychnine (1.5 mg., tV gr-)> and (2) by inhalations of CO2. Both of these
measures seem fairly successful, but more observations are necessary be-
fore conclusions can be reached. Pembrey was able to cause the periodic
breathing to return to normal by causing the patient to breathe either
pure 02 or O2 containing an excess of CO2 , demonstrating that in this
case the action of the respiratory centre could be restored by either im-
proving its condition and increasing its irritability through increased
aeration, or by increasing the strength of the respiratory stimulus by in-
creasing the concentration of CO2 in the lung alveoli.
The occurrence of Cheyne-Stokes respiration is a very grave symptom.
It is often a harbinger of death, as claimed by some authors, but the writer
has seen many patients recover from it and even live for several years. It
should therefore be classed with several other symptoms as indicating a
grave weakening of the circulation but not necessarily an incurable one.
COUGH.
Patients with chronic cardiac trouble are very apt to suffer from a
mild cough, even during their periods of remission, and especially every
winter. Sometimes this may even be mistaken for a primary bronchitis.
Primarily the condition is due to engorgement of the pulmonary vascular
system, with increased secretion of the bronchial mucous glands as a result.
It represents a state of mild loss of pulmonary compensation.
In somewhat worse form, and particularly in bad cases of chronic mitral disease,
the alveolar capillary walls become so much injured that there is diapedesis of red blood-
cells into the alveoli. These die and are taken up by phagocytes which find their way into
the sputum in the form of " Herzfehlerzellen " — large endothelial cells containing vacuoles
and numerous brown granules of hsemosiderin. The expectoration of "Herzfehlerzellen"
is usually associated with a condition of brown induration of the lungs, a chronic interstitial
pneumonia with dilatation of the pulmonary capillaries, tortuous condition of the vessels,
and deposition of haemosiderin in the tissues.
ACCUMULATIONS OF FLUID IN CARDIAC DISEASE.
(Edema.— When a case of heart disease reaches the stage of broken
(systemic) compensation and the right heart fails to perform its function
properly, oedema of the feet and legs sets in. This occurs at some stage
of almost every case of heart disease, but not always at stages of equal
severity, sometimes setting in quite early, sometimes only as a terminal
event. Consequently, although a grave symptom, the presence of oedema
need not indicate a desperate condition.
The distribution of oedema of cardiac origin differs characteristically
from the nephritic type. This is readily comprehensible when it is recalled
that, as Cohnheim has shown, oedema occurs only when there has been some
injury to the walls of the vessels and capillaries. In nephritis Heinecke
and Meyerstein have proved the existence of a substance in the blood which
154
DISEASES OF THE HEART AND AORTA.
injures the capillaries, and Kast has demonstrated that the blood of nephrit-
ics contains a substance with lymphagogue action. As might be expected
from a poison circulating in the blood, the injury occurs simultaneously
throughout the body. Hence in nephritis the cedema begins quite irre-
spectively of the action of gravity and is especially marked in the face and
eyelids. In cardiac cedema there is no such lymphagogue poison at work,
and the injury to the capillary walls is the result of local stasis, lack of
oxygen in the cells of the capillary walls under the influence of the slowed
circulation. Accordingly it begins where circulation is slowest, i.e., in the
dependent portions, — the feet and legs, — and either remains localized there,
or, if the condition becomes worse, progresses upward to the genitalia, to
the abdominal cavity (portal stasis),
giving rise to intense ascites, to the
subcutaneous tissue of the body wall,
and finally to the production of fluid
in the chest (hydrothorax).
Occasionally when the oedema has been
long continued the limbs reach tremendous
proportions. Some four years ago the writer
had under his care at the Johns Hopkins
Hospital a patient who reached the ward in
a condition of very marked dyspnoea, with
legs swollen to a diameter of 1(H inches and
absolutely elephantoid in appearance (Fig.
1 23) . The skin over the entire legs was covered
with papillomatous outgrowths so suspicious
that the diagnosis of elephantiasis vera was
seriously entertained by some members of the
hospital staff. The patient had been suffering
•from a severe aortic insufficiency for about
a year, and for six months had been so ortho-
pnceic that he had not been able to go to bed,
but had rested sitting bolt upright in a chair
and usually with feet down. There were
tremendous crypt-like ulcers about 10 cm. (4
inches) in diameter in both legs, each covered
with a deep layer of necrotic tissue. The patient was placed in bed with feet raised to the
horizontal, and the wound dressed with a 1-10000 potassium permanganate solution and
tr. digitalis m. xv administered every four hours. He was purged freely with Epsom salts.
He improved so rapidly that within twelve hours the circumference of the legs had appre-
ciably diminished and within a few weeks they were almost normal. The patient has
remained quite well ever since and is at present managing a farm in western Maryland.
Unfortunately, cedema does not always disappear so satisfactorily.
It has been shown that the cedema fluid is richer in salts than is the blood,
and that resorption of the cedema is somewhat favored by a practically
salt-free diet, such as one consisting of milk, sugar, eggs, meats, bread,
sweet butter, and cereals prepared without the addition of salt. The diu-
retics, especially those of the caffein group, also favor resorption;1 free
1 Fleisher, Hoyt, and Loeb have shown that the presence of calcium salts in infusion
fluid diminishes the formation of cedema, but this observation had not yef received an
application in therapeutics, and these observers have found that this does not apply to
cardiac oedema.
FIG. 123. — Legs of a patient with extreme
oedema (simulating elephantiasis) and tremen-
dous ulcers. Diameter of the left leg 10^ inches
(25.5 cm.). (Drawn from photographs lent by
Dr. W. Preston Miller, of Hagerstown, Md.)
SYMPTOMS OF CARDIAC DISEASE.
155
purgation aids in removing fluid from the body, sometimes as much as 3000
c.c. per day, and digitalis does the same by increasing heart action. Besides
this, the oedema can be combated by raising the legs to the horizontal or if
possible a little above it, thereby increasing the drainage from them.
Drainage of Legs. — Sometimes also a light spiral elastic bandage of rubber dam
may be applied to the legs, beginning at the feet and ascending to the groin, thereby
assisting the drainage and replacing the lost elasticity of the skin. When these means are
insufficient, several incisions may be made aseptically in the skin of the legs and drainage
aided by applying Bier's suction cups, or a large trocar with sides perforated (Curschmann's
modification of Southey's tubes) may be inserted to bring about free mechanical drainage.
The best results are obtained by the following method, described by Romberg :
Boil a long rubber tube fitted with a pinch-cock in physiological salt solution. After
removing the point from the trocar, attach the rubber tube to the metal tube of the latter
and place the lower end of the rubber tube in a basin
of boiled water upon the floor next to the bed. In
this way a siphon is established, helping the drainage
of the fluid. The tube of the trocar should be kept
in place in the leg by tying with a silk ligature, the
ends of which are then inserted in a strip of adhe-
sive placed loosely about the leg above the trocar.
Romberg states that from 2 to 15 litres of fluid may
be removed in 24 hours !
The oedema often involves the scrotum
and penis until they are enlarged to two or
three times the ordinary size, and phimosis
or paraphimosis may cause considerable
difficulty in micturition.
Ascites. — Ascites is common and may
cause distress by pushing up the diaphragm
as well as by impeding the abdominal circu-
lation. It is often advisable to remove it
mechanically by introducing a trocar in the
midline midway between the umbilicus and
the symphysis, under aseptic precautions (after first emptying the patient's
bladder), and allowing the fluid to drain out. In so doing care must be
taken to keep a many-tailed (Scultetus) bandage tight across the abdomen,
readjusting it several times during the tapping for fear too much blood
may enter the relaxed 'abdominal vessels when the pressure about them is
diminished and shock result therefrom (see page 31).
Hydrotherax. — In cases with severely impaired compensation hydro-
thorax (usually right sided) is common. Starling and Leathes, Stengel, and
Dutton Steele have demonstrated that its frequency upon the right side is
due to the position of the great azygos vein, which drains the intercostal
spaces and the pleurae. One of the factors producing stasis in this vein is
the fact that the latter enters obliquely into the superior vena cava (Fig. 5)
and thus its mouth is readily closed off. Another is probably the fact,
which the writer has noted, that the mouth of the vein is not as distensi-
ble as the walls of the vein above it, and hence imposes some obstruction
to the blood flow. In all cases of heart failure in animals the azygos vein
may be seen to be dilated above its entrance into the vena cava. The
heart in hydrothorax is usually displaced to the left. The respiration shows
FIG. 124. — Curschmann's modifica-
tion of the Southey tubes for draining
oedema of the legs. (After Romberg.)
156 DISEASES OF THE HEART AND AORTA.
much embarrassment: (1) from removal of a considerable part of the
right lung, (2) from compression of the left lung by the displacement of the
heart, (3) from embarrassment of the heart itself from the displacement,
(4) from compression of the venae cavsa especially during defecation and
exertion. This may prevent inflow into the heart and cause sudden
death. (Calvert.)
The fluid should always be removed promptly by paracentesis thoracis.
This process is unfortunately not without danger, sudden death occasionally
resulting in spite of the greatest care.
The writer has seen two deaths of this kind, and they occur with about the same
frequency in the experience of most clinicians. A very valuable contribution to this field
has been made by the studies of Capps and Lewis, showing that the visceral layer of the
inflamed pleura is especially sensitive, and upon handling or touching it two reflex
phenomena result, a vagal inhibition, sometimes so intense as to s t o p the
heart, and a paralysis of the vasomotor centre which gives rise to a marked fall of blood-
pressure. According to these observations it is therefore advisable to diminish vagal tone
with a preliminary hypodermic injection of 0.5 to 1 mg. atropine (gr. Tso to sV) about
15 minutes before beginning the tapping, and to have at hand a hypodermic syringe loaded
with 1-10000 adrenalin chloride solution to restore promptly the vasomotor tone in case
of collapse.
RENAL COMPLICATIONS OF CARDIAC DISEASES.
RENAL CHANGES.
Albuminuria and diminished secretion of urine are invariable results
of broken compensation. They may also occur after severe exertion,
probably as the result of excessive pressure in the veins. The stasis in the
vena cava and renal vein has been shown to give rise to albuminuria, and
the slowing of the circulation through the kidney is sufficient to account
for the diminution of the urine secreted. Such urine, though diminished
in amount, is highly colored, normal or increased in specific gravity (1016
to 1026), and contains a normal concentration of NaCl and urea. The total
excretion of the latter in 24 hours is, of course, decreased. As in the experi-
mental stasis numerous finely granular and hyaline casts may be excreted.
The kidneys of such cases (Osier's arteriosclerotic kidneys) are usually of the large
red or "beefy" type, with both cortex and medulla increased in size, the capsule adherent,
and diffuse interstitial changes as well as some parenchymatous degeneration. The red
color is probably due to the venous congestion. >
It is of great importance to differentiate between a primary cardiac
disease. with secondary renal involvement and primary chronic nephritis
with secondary arteriosclerosis, cardiac hypertrophy, and cardiac insuffi-
ciency. At an early stage of the disease a careful study of the chloride
metabolism and its relation to urine concentration may be of great help.
In cardiac cases the power of excreting NaCl is, as a rule, not
as much impaired as in renal cases. If 5 Gm. NaCl be added to the diet on
one occasion there should be an abrupt rise in the NaCl content of the urine. If the kidney
cells are damaged it will be gradually excreted during 2-4 days. However, it must be
remembered that in many cases of primarily cardiac origin the kidney cells may be im-
paired. The urinary findings, as sh ow n in the cases cited on page
240 and page 335, may be practically identical; and hence all the fea-
tures in etiology, history, and metabolism must be thoroughly considered before a decision
is reached.
SYMPTOMS OF CARDIAC DISEASE.
157
SENSORY SYMPTOMS ABOUT THE HEART.
Palpitation. — Under normal conditions one is not conscious of sensory
impressions from the region of the heart. Einthoven, Flohil, and Bat-
taerd have shown, however, that an afferent impulse is transmitted up the
vagi by each heart-beat, and there are probably similar impulses transmit-
ted through the intercostal nerves from the parietal pleura, mediastinum,
and chest wall, against which the heart is beating. Under normal condi-
tions these sensations do not reach consciounsess, but they occasionally
do so when the general nervous sensibility is increased, as by coffee, tobacco,
or hyperthyroidism, in neurasthenic and hysterical states, or when the
beat of the heart is more forcible than usual, The distinct sensation caused
by each beat of the heart is known as palpitation. It is frequently associated
with cardiac weakness and irregularities, and has been thought by some
writers to be clearly associated with B
extrasystoles. But while it is true that
VAG.
RKSR
CAROT.
Fro. 125. — Electrical record of afferent impulses travelling up the vagi. (After Einthoven, Flohil,
and Battaerd.) VAG., record of centripetal electrical wave in the vagus ; RESP., respiration ; CAROT.,
carotid tracing. A. In quiet breathing. B. In apncea. The large electrical waves are due to respiration ;
the small ones to the cardiac contraction.
extrasystoles frequently give rise to palpitation and also that the patient
can often distinguish between strong beats and weak beats, nevertheless
there are many cases of extrasystoles without palpitation and of pal-
pitation without extrasystoles. Hirschfelder has shown that palpitation
may occur without any motor disturbance in the heart's action and with-
out any change in the reflex response of the heart to various stimuli.
Hewlett has found the c wave unusually large and sudden in a case of
palpitation, and believes that the "earlier movements of the ventricle
were exerted with unusual speed." However, this finding is not uniform
in cases of palpitation, and, moreover, would not explain the occurrence of
palpitation from wreak extrasystoles in which these movements are executed
slowly. Such changes in the venous pulse are often found in vigorously
beating hearts without any palpitation whatever. Palpitation is therefore to
be regarded as a purely sensory phenomenon, which, though it is frequently
associated with cardiac disturbances, may occur quite independently.
The category of sensations in which palpitation should be placed and the path which
the sensation traverses are not perfectly clear. It is evidently a pressure or touch sensation,
perfectly distinct and limited to the period of systole. It is always sharply localized,
usually referred to either the apex or the bifurcation of the trachea — the two sites at which
158 DISEASES OF THE HEART AND AORTA.
the heart exerts direct pressure or traction upon the surrounding structures. In this dis-
tinctness it differs entirely from other visceral sensations, which are less definite in time
and in site, and also, as a rule, more nearly allied to pain sensation. It thus differs greatly
from the pain sensations arising in and about the heart, and hence suggests that it should
be placed in a different category. Whether the path of the sensation is up the vagi or
through the thoracic nerves cannot at present be stated.1
Another point in favor of the view that palpitation is an extracardiac sensation is the
fact that quite similar sensations may be felt in the abdominal aorta and radial arteries
when there is visible pulsation (to-and-fro motion) of the latter with pressure and traction
upon the skin and surrounding structures.
The continuance of the sensation is very wearing upon the patient,
especially when the heart is irregular. Often he is able to distinguish be-
tween large and small beats, and is constantly reminded of the pathological
condition and usually much worried about it. The sensation is not entirely
dependent upon psychic phenomena; for in one case under the writer's obser-
vation (I.e.) it disappeared for five minutes, while the blood-pressure and pulse-
rate rose after exercise when the patient was under examination, although
he had his mind fixed upon the disturbance throughout the entire procedure.
Palpitation is frequently the result of tea or coffee drinking, smoking,
digestive disturbances; it often occurs with various forms of cardiac diseases,
but seems to have no relation to the latter. Relief is very difficult to obtain.
Except for removing the causal factor, application of an ice-bag or a cold-
water coil over the heart is about the best remedy. The bromides of potas-
sium, ammonium, and strontium are of some value, as are also vibratory
massage and the application of sinusoidal currents.
Precordial Pain. — Precordial {)ain is a less definite sensation than
palpitation. It is continuous throughout the cardiac cycle, is less definitely
localized, and more commonly associated with referred sensory disturb-
ances resembling other types of visceral sensation. It seems to bear a
somewhat closer relation to dilatation of the heart, and, as a rule, accom-
panies more severe organic diseases, being especially common in aortic and
mitral lesions. There is sometimes, but not always, precordial tenderness.
The most severe form of precordial pain, angina pectoris (see page
285), in which there is, besides intense pain, a feeling as though the heart
were held in a vise, seems to be associated with sclerosis of the coronary
arteries, but a definite relation between this and other forms of precordial
pain has not yet been established.
Frequently in heart diseases, and especially in cases of aneurism and angina, there is
marked pain radiating down either or both arms. In fact these may be the
first symptoms given by an aneurism. It is easily seen from the distribution of the cardiac
nerves (page 14, Fig. 16) that a lesion in the vicinity of the sympathetic fibres might give
sensations which, reaching one of the cervical spinal ganglia, would be referred to its
peripheral distribution in the cutaneous region innervated by that segment, usually down
the arm. Hence the frequency of these pains. Not only cardiac condition, but high blood-
pressure in the aorta may cause this distress. It is difficult to relieve this symptom. If
lowering of the blood-pressure with nitroglycerin fails to bring it about, codeine, 15 to
20 mg. (£ to % gr.) should be tried, and, if that does not suffice, morphine may have to be
resorted to, but should always be avoided as long as possible.
1 In this connection it would be interesting to note whether palpitation occurs in cases
of transverse lesion of the cord in the lower cervical or upper thoracic region, or whether
it can be brought on in such persons by large doses of coffee.
SYMPTOMS OF CARDIAC DISEASE. 159
DIGESTIVE DISTURBANCES.
One of the first effects of weakening of the heart is engorgement of
the veins of the portal system, and this in turn brings about a catarrhal
condition in the mucosa, and especially the gastric mucosa, with consequent
symptoms of indigestion. Fermentation frequently takes place, and the
inflation of the stomach with gas, displacing the diaphragm upwards and
shifting the heart more towards the horizontal, tends to increase its embar-
rassment. Overloading the stomach, the transdiaphragmatic neighbor
of the heart, should therefore always be avoided; and the patient will be
saved much suffering if he is kept on a light, easily digestible diet, consist-
ing largely of eggs, milk, and carbohydrates, just enough in quantity to
keep him from losing weight. Friedrich Miiller has shown a diminished
power of absorption of fats in heart disease. Perhaps this may be due to
the fact that the high venous pressure prevents the thoracic duct from
emptying itself properly, or perhaps because, as H. M. Evans has shown,
a high portal pressure causes the lymphatics of the intestines to collapse.
On the other hand, meats and other foods containing purin bodies in
large quantities (sweetbreads, lungs, liver, etc., also coffee and tea, and
alcohol in all forms) do distinct harm by raising the blood-pressure and by
increasing the viscosity of the blood (page 39).
The engorgement of the gastric and oesophageal veins sometimes leads
to exudation of blood into the stomach and to vomiting of blood.
Abdominal Pain from Distended Liver. — One of the commonest symp-
toms of failing compensation is very intense abdominal pain felt over the
region of the liver. This organ may become much distended, and, as shown
by Salaman, may be expanded until its blood content is several degrees
above the normal. Under this expansion there is marked tension upon
the capsule of the liver (Glisson's capsule) which, in turn, gives rise to
pain. This symptom is really so clearly bound up with the failure of com-
pensation itself that it subsides with resumption of the latter, or after some
time the capsule of the liver will have become sufficiently stretched and it
will then cease to be painful.
Abdominal pain also results from arteriosclerosis of the gastric and
mesenteric arteries, from vascular crises as well as from abnormally great
pulsation of the abdominal aorta.
Catarrhal Jaundice. — Like the gastric mucosa, the bile passages undergo
catarrhal inflammation from the venous engorgement, and a definite
catarrhal jaundice may accompany the failure of compensation. Usually,
the jaundice is mild and barely perceptible, the color being sallow and icte-
roid rather than icteric. The presence of this slight icteric hue in a patient
with heart disease should always lead to the suspicion of broken compen-
sation or tricuspid insufficiency, and is always a sign of danger.
PSYCHIC DISTURBANCES.
An anxious expression is so commonly manifested by patients suffer-
ing from heart disease that a certain type is spoken of as "the cardiac
fades." This facies is difficult to describe, but may be said to be character-
160 DISEASES OF THE HEART AND AORTA.
ized by bright watery, somewhat staring eyes, wide palpebral slits (without
definite exophthalmus or other signs of Basedow's disease), rather tensely
held mouth, and the rest of the face a little sunken, though not to the degree
present in the "abdominal facies." Many cardiac cases, perhaps from the
difficulty which they are constantly experiencing in getting their breath, feel
irritable and peevish to a considerable degree, and not infrequently the onset
or increase of peevishness is an early sign that the cardiac condition has
become worse.
DELUSIONS.
Occasionally, especially in patients with irregular heart action, definite
psychoses set in. These are especially common during the night and early
morning, disappearing again during the waking hours.
The patient usually awakens from his sleep unable to recognize the place where he is,
which he usually locates somewhere else, and then regards the doctors, nurses, and attend-
ants as inhabitants of the more familiar scenes, often mistakenly recognizing them as
people of his acquaintance in those places. He usually regards his confinement in bed as
a sign of some attempt upon his life, and the administration of medicine as a certain at-
tempt to poison him. Of this fact he is always certain, although he may admit that there
is some doubt in his own mind as to the correctness of some of his other ideas. For
example, one delirious patient under the writer's care as house physician mistook him for
an old friend from home and said, " He liked , and had great confidence in him, but
he could not see why — — did want. to poison him." But he would recognize no other
possible motive.
Occasionally when daylight comes or some one familiar object appears, the patient
suddenly recognizes his surroundings, wakes up as from a dream, and may even explain
exactly the nature of and reasons for his delusions. Under the influences of these
delusions, patients are often very hard to manage, but their attitude is more commonly a
defensive than an offensive one, resisting confinement and treatment, and attempting to
leave the ward or room peaceably, rather than showing maniacal pugnaciousness primarily.
They can usually be persuaded by gentle means to remain where they are for a time,
especially as their minds are almost always confused ; they realize that they are not
perfectly well, and the nurse or physician can lead the argument along its logical
conclusions to a reason why they should return to bed and to rest for the time being.
After some minutes' argument of this kind the patient can usually be given a hypo-
dermic of morphine and gotten back to bed with much less injury to himself than if
forcible means were attempted. He can then usually be kept in bed by an attendant
constantly present.
The reason for these delusions is not very certain, but in some cases
they may be regarded as "waking dreams" not very different from those
of somnambulists, and perhaps like the night terrors of children with ade-
noids. They may be asphyxial in origin, associated more or less with
cerebral arteriosclerosis and cerebral ansemia, of which perhaps the frequent
high blood-pressure may be another expression. This delusional insanity is a
bad omen, and its onset often precedes the fatal outcome by only a few days
or weeks. Duroziez and H. O. Hall have called attention
to the fact that in some cases these delusions may be
due solely to the digitalis and may disappear entirely when the
drug is discontinued.
HALLUCINATIONS.
Definite hallucinations of sight and hearing are also not uncommon.
Henry Head has observed that these are especially common in aortic disease about
the time of twilight, and are usually quite simple in character, the auditory hallucinations
SYMPTOMS OF CARDIAC DISEASE. 161
consisting in simple rhythmic sounds (associated with the heart-beats?), such as of knock-
ing or of bells tolling, the visual hallucinations usually taking the form of the face
of a man or woman seen stationary at the foot of the bed or slowly stalking across
the room. The face is ashy white, the eyes black and staring, and the contour invariably
indefinite and surrounded by a mass of wavy black hair. If the body is seen at all, it is
poorly outlined as though draped in a black gown. Head found this hallucination quite
constant and seen by many patients, though they, as a rule, recognized the hallucinatory
character and spoke of it only after the physician had gained their confidence. The writer
has also elicited the same answers from a number of patients, after prefacing the question
by a statement that visual hallucinations were not uncommon in their disease and were
to be regarded merely as troublesome but not significant features of the disease itself.
All who gave positive answers accurately described the hallucinatory vision as above.
Head states that highly colored and rapidly moving visions do not
occur frequently in heart cases, but the writer has seen one very marked
exception to this rule.
This was in the case quoted on page 508 — a young railroad engineer, 23 years old,
of temperate habits and excellent family history, who had a very adherent pericardium.
For several years, especially when his cardiac condition became worse, he suffered from
seeing a few feet before him swarms of large animals, lions, tigers, etc., all highly colored,
leaping rapidly about. He recognized these as hallucinations at the time, but stated that
the sight irritated him so that he lost his self-control, and he begged to be placed in soli-
tary confinement for a few days until the hallucinations passed off. He was then once
more a perfectly rational being.
Like the delusions, these cardiac hallucinations are probably due
either to anaemia or venous stasis in brain, but especially in the special
centres, or in the retina, middle ear, visual or auditory centres, giving rise
to rudimentary sensations which the mind translates or distorts into the
above-mentioned pictures.
Syncopal attacks also occur in some forms of heart disease as a result
of cerebral anaemia and will be discussed in detail in Part III, Chapter XI,
under the head of Adams-Stokes disease. The feeling of faintness and
weariness unaccompanied by syncope will be discussed under "cardiac
neuroses," etc. (Part IV, Chapter III).
BIBLIOGRAPHY.
SYMPTOMS OF CARDIAC DISEASE.
Grossmann, Bettelheim, and Kauders. Quoted on page 146.
Eyster, J. A. E.: Clinical and Experimental Observations upon Cheyne-Stokes Respira-
tion, J. Exper. Med., N. York and Lancaster, 1906, viii, 265.
Welch, 1. c., page 145.
Emerson, H.: Artificial Respiration in the Treatment of (Edema of the Lungs. A Sug-
gestion based on Animal Experimentation, Arch. Inter. Med., Chicago, 1909, iii, 368.
Barringer, T. B.: Pulmonary (Edema Treated by Artificial Respiration, Report of a Case;
ibid., 1909, iii, 372.
Miller, J. L.: Trans. Assoc. Am. Phys., Phila., 1909. Also, Miller, J. L., and Matthews,
S. A.: A Study of the Mechanical Factors in Experimental Acute Pulmonary (Edema,
Arch. Int. Med., Chicago, 1909, iv, 356.
Muller, Fr.: Die Erkrankungen der Bronchien, Die deutsche Klinik., Berl. and Vienna,
iv, 279; quoted from Romberg.
Mosso, A.: Fisiologia dell roma sulla Alpi, Arch. Ital. de Biol., 1905, xliii; and other
articles quoted on page 35.
Pembrey, M. S., Beddard, A. P., and French, H.: Observations on Two Cases of Cheyne-
Stokes Respiration, Proc. Physiol. Soc., Lond., 1906, p. vi.
11
162 DISEASES OF THE HEART AND AORTA.
Kast, A. : Ueber lymphagoge Stoffe im Blutserum Nierenkranken, Deutsch. Arch, f . klin.
Med., Leipz., 1902, Ixxiii, 562.
Heineke and Myerstein: Experimentelle Untersuchungen ueber den Hydrops bei Nieren-
krankheiten, Deutsch. Arch. f. klin. Med., Leipz., 1908, xcii, 101.
Frangois-Franck, Ch. A.: Contribution a 1'etude experimentale des nevroses reflexes
d'origine nasale, Arch, de physiol. des hommes et des anim, Par., 1889, 5e se>., i, 538.
Starling, E. H.: Physiologic Factors Involved in the Causation of Dropsy, Lancet, Lond.,
1896, cl, 1407.
Meltzer, S. J.: (Edema, Am. Med., Phila., 1904, iii, 19, 59, 151, 161.
Pearce, R. M.: The Production of (Edema, Arch. Int. Med., Chicago, 1909, iii, 423.
Pearce, R. M.: An Experimental Study of the Influence of Kidney Extracts and of the
Serum of Animals with Renal Lesions upon Blood-pressure, J. Exper. M., 1909, xi, 430.
Fleisher, M. S., Hoyt, D. M., and Loeb, L.: Studies in (Edema. I. Comparative Investi-
gation into the Action of Calcium Chloride and Sodium Chloride on the Production
of Urine, Intestinal Fluid, and Ascites, J. Exper. Med., N. York and Lancaster, 1909,
xi, 291.
Fleisher, M. S., and Loeb, L.: The Influence of Myocarditic Lesions on the Production of
Ascites, Intestinal Fluid, and Urine in Animals infused with Solutions of Sodium
Chloride and of Sodium Chloride and Calcium Chloride, J. Exper. Med., N. York and
Lancaster, 1909, xi, 480.
Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart,
1906.
Capps, J. A.: Some Observations on the Effect on the Blood-pressure of Withdrawal of
Fluid from the Thorax and Abdomen, J. Am. M. Assoc., Chicago, 1907, xlviii, 22.
Starling, E. H., and Leathes, J. B.: The Arris and Gale Lectures on Some Points in the
Pathology of Heart Disease, Lancet, Lond., 1897, i, 569.
Stengel, A.: Right-sided Cardiac Hydrothorax, Univ. Penn. M. Bull., Phila., 1901, xiv,
103.
Steele, J. D.: Pleural Effusion in Heart Disease, J. Am. M. Assoc., Chicago, 1904, xliii,
927.
Calvert, W. J.: Sudden Death in Pleurisy with Effusion due to Change of Position, Johns
Hopkins Hosp. Bull., Bait., 1908, xix, 44.
Capps, J. A., and Lewis, D. D.: Observations upon Certain Blood-pressure-lowering Re-
flexes that Arise from Irritation of the Inflamed Pleura, Am. J. M. Sc., Phila. and
N. Y., 1907, cxxxiv, 868.
Einthoven, W., Flohil, A., and Battaerd, P. J. T. A.: On Vagus Currents Examined with
the String Galvanometer, Quart. J. Exper. Physiol., Lond., 1908, i, 243. Ueber Vagus-
strome, Arch. f. d. ges. Physiol., Bonn, 1909, cxxiv, 246.
Hirschf elder, A. D. : Observations on a Case of Palpitation of the Heart, Johns Hopkins
Hosp. Bull., Bait., 1906, xvii, 299.
Hewlett, A. W.: The Venous Pulse, Science, Lancaster, 1909, xxix, 515.
Miiller, F. Quoted from Romberg.
Evans, H. M.: Personal communication.
Salaman, R. N.: The Pathology of the Liver in Cardiac Disease, Lancet, Lond., 1907, i, 4.
Duroziez, P.: Du delire et du coma digitaliques, Gaz. hebdom., Par., 1874, xi, 780.
Hall, H. O.: The Hallucinations of Digitalis: Does Digitalis Cause Hallucinations, Delir-
ium, or Insanity under Certain Conditions? Am. Med., Phila., 1901, i, 598. The
Delirium and Hallucinations of Digitalis, ibid., 1905, ix, 489.
Head, H.: Certain Mental Changes that Accompany Visceral Disease; Brain, Lond., 1901,
xxiv, 345.
IV.
GENERAL PRINCIPLES OF TREATMENT OF FAILURE
OF THE HEART.
The best index of the treatment of the patient is his own condition,
sensations, and general appearance. Physical examinations, determina-
tion of blood-pressure and pulse-rate, as well as of increase in the product
of pulse-pressure by pulse-rate (velocity coefficient), venous tracings, and
gas analysis aid in the interpretations of the condition, and particularly
in discovering where the fault in the mechanism of the circulation lies;
but the changes of conditions themselves are often very subtle and mani-
fest themselves in the general condition of the patient before they can be
detected on examination.
QUIET.
The most important element in the treatment of cardiac failure is
rest as complete as possible. In all cases of heart failure or disease in the
heart the patient should be confined to bed, if necessary propped up with
pillows, and should be kept there until the acute symptoms have subsided
and have remained quiescent for several days.
As Morton Prince has shown, mental excitement and worry are impor-
tant factors in bringing about acute dilatation of the heart; but they are usually
contributing factors rather than sole causes.
The effect of mental activity upon the circulation is to bring about vasoconstriction,
of both extremities and viscera, a slight rise of blood-pressure, and increase in the pulse-
rate; all of which taken together considerably increase the total work of the heart (i.e.,
roughly speaking, the product of maximal pressure by pulse-rate).
A good night's sleep is often the best remedy for the patient with a
weak heart, and almost any method by which it may be procured may prove
a. good therapeutic procedure. Small doses of bromides, if necessary aided
by a little trional, veronal, or other hypnotic, often suffice for this purpose
and allow the heart a few hours respite in which the other therapeutic
measures may have opportunity to act.
However, it must be borne in mind that in persons who are much
worried, mental rest and absence of distractions or occu-
pation are not necessarily synonymous. Indeed, the removal
of other subjects for thought may serve only to centre the patient's mind
upon himself and his ailments and may increase rather than diminish the
nervous strain. This should be carefully guarded against. The daily routine
should therefore be accommodated to both the general condition and the
temperament of the patient. If possible absolute rest and isolation should
be secured for the worst cases of heart failure, but even for these patients
a few minutes' conversation with a cheerful friend, whose demeanor is quiet
and soothing, may be of actual benefit. Reading should not be allowed to
163
164 DISEASES OF THE HEART AND AORTA.
patients in the worst stages, but a little reading of the lightest and least
exciting sort may otherwise be allowed.
Rest, Distraction, and Spa Treatment. — As Mackenzie states, it is chiefly
due to the element of mental distraction combined with the judicious
supervision of a physician and the favorable climatic conditions, which
make the Spa treatments of cardiac disease so successful; although, as
he states, each Spa physician has evolved some method of treatment which
he regards as of special benefit, when the actual benefit has been due to the
air and restfulness itself. Nevertheless, it must be confessed that the treat-
ments at Nauheim by the late August Schott (page 194) have been of great
benefit, and being founded upon sound physiological doctrines have been
applicable elsewhere as well. The physician must always realize that,
however little there may be in the Spa treatments per se, the combination
of the mental rest and change of air with the baths and dietetic treatment
is one which the patient whose condition warrants a trip, should not forego.
Rest in Bed. — The bed should not be so high above the floor as to make
it hard to get in and out ; it should if possible have a metal frame and a good
rather firm mattress. It should be provided with a good back rest ready
for use in case the patient finds it more comfortable, and plenty of pillows
should be available.
In dealing with cases of mild cardiac failure it may be impossible in
private practice to compel the patients to remain in bed all the time, and
then it may suffice to insist upon their lying down for several hours a day
without absolutely remaining in bed. Under these circumstances the
physician must insist that the patient remain quiet all day upon a sofa
or in a wheel chair with legs raised. A short period of such absolute rest
is better than a much longer period of relative invalidism, for it enables,
the dilated heart to bail itself out, to regain its former dimensions and
tonicity, and permits the heart-rate to return to normal. It is important
that the patient should remain horizontal rather than in sitting or in stand-
ing posture, since the latter tends to slow the circulation (cf. Erlanger and
Hooker, quoted on page 26) . The rest should continue until all symptoms
have subsided, until cardiac distress, pain, and palpitation have disappeared,
and respiration has again returned to normal. If possible the subsidence
of tachycardia or irregularity of the pulse should be awaited; but these may
persist for some time even in spite of the improvement in the patient's
general condition, and may have to be disregarded. After the symptoms
have subsided (in severe cases after the symptoms have remained quies-
cent for a few days), the patient may be allowed to get out of bed and sit
up in an arm chair or wheel chair for a little while. At first this period
should be very short, to avoid exhaustion, but it may be gradually increased
and he may soon be allowed to walk. (For exercises to be taken by patient
with cardiac disease see page 199.)
COLD APPLICATIONS OVER THE HEART.
The application of cold to the precordium is of value both for the
cardiac symptoms (palpitation and pain) on the one hand, and for diminu-
tion of the heart-rate on the other. This may be carried out by the applica-
TREATMENT OF FAILURE OF THE HEART. 165
tion of a simple ice-bag (especially containing a mixture of ice and salt)
which may be kept in close application to the skin by tying it around the
chest and shoulders with a strong elastic four-tailed bandage. The ice-bag
should be changed every hour or two in order to keep up an intense cooling.1
In hospital use or in well-supplied houses the use of the cardiac tube is most satisfac-
tory. This consists of a coil of thin-walled rubber or aluminum tube applied over a wet
compress to the precordium. A stream of cold water from a cooler is kept flowing slowly
through the tube. The cooling of the skin thus obtained is excellent and without any
discomfort to the patient. Its effects have been tested both clinically and experimentally
by Winternitz and da Silva.
These observers found that the application of cold to the precordium brought about
in dogs a cooling of both the anterior and posterior surfaces of the pericardium, amount-
ing to l°-5°, and was accompanied by a slowing of the pulse and rise of blood-pressure
from 120 to 190 mm. Hg. In man the pulse-rate did not begin to fall for fifteen minutes
after the application, and reached its height within an hour, lasting in turn about an hour
after removal of the cold. In normal individuals they found the pulse-rate falling from
72 to 64, 68 to 52, 78 to 68; in other cases, chlorosis 84 to 72, pericarditis 84 to 78, mitral
stenosis 60 to 40. Simultaneously the blood-pressure rises and the pulse increases in vol-
ume. There is evidently both a reflex vasoconstriction from stimulation of the vasomotor
centre and a reflex stimulation of the vagus. Besides this, da Silva thinks that there is a
direct stimulation of the heart muscle. It will be noted that these effects are exactly those
brought about by digitalis, and hence enthusiastic hydrotherapists are in the habit of
speaking of the ice-bag as ''physiological digitalis."
Its use is attended with less danger, but in cases of extreme
fibrous or fatty degeneration of the heart, cyanosis
and collapse occasionally occur. Hence it should be ap-
plied very mildly in cases where these conditions are suspected.
There can be no doubt that the ice application is not as efficient as the use of digitalis
in slowing and strengthening the heart, but when the two are vigorously used at the same
time they may greatly reinforce one another, and the vigorous use of a good ice-bag may
enable satisfactory effects to be obtained with smaller doses of digitalis than would other-
wise suffice.
VENESECTION.
When the patient' is in very bad condition, deeply cyanotic, and rest-
less or nervous, and the area of cardiac dulness is increased to the right,
a free venesection will often bring the greatest relief.2
Technic of Venesection. — Venesection is best performed in the following manner:
The skin over the flexor surface of the elbow-joint is scrubbed with green soap and washed
with warm water, then with alcohol, and lastly with 1-2000 bichloride solution. An elastic
or gauze bandage is tied about the upper arm tightly enough to cause the veins to stand out
but not to obliterate the pulse at the wrist. The largest vein visible (usually the median
cephalic) is selected and a small slit in the skin just alongside of (not over) the vein is made
with a curved bistoury, which is then pushed in through the slit in the skin and under the
vein. It is then twisted so that the edge is turned upward towards the skin against the
vein and the vein cut through without again piercing the skin. A very free flow of blood
is obtained, especially by keeping the arm dependent and if the patient is made to clench
and open his hands rapidly. From 300 to 1200 c.c. (12 ounces to 2* pints) can thus be
removed in less than twenty minutes, usually with great relief to the patient. Breathing
1 When a mixture of ice and salt is used it is possible to actually freeze the skin, an
accident which must be carefully avoided.
2 The haemoglobin should always be tested before performing a venesection; and it
should not, as a rule, be performed if the haemoglobin is below 70 per cent.
166
DISEASES OF THE HEART AND AORTA.
becomes easier, the head clearer, and the general condition better, but the crucial point is
reached when the color changes and the cyanosis gives way to a healthy rosy color in the
lips and elsewhere. This indicates that the overstrained heart has been unburdened, and
the bleeding need not be pushed much further. Indeed it should not be, for to cause an
angemia is dangerous. All that is desired is to relieve the distention of the right heart.
FIG. 126. — Insertion of the knife in venesection. A. Lateral view. B. Cross section of arm.
Effect of Venesection on the Circulation. — The value of venesection can often be seen
in experiments upon animals. It is not at all uncommon to find a heart failing and an
auricle already paralyzed from overdistention, in which a free venesection gives immediate
relief, and the auricle as well as the ventricle resumes forcible contractions. The effect of
this procedure upon the blood-pressure is variable and depends to a certain extent upon
the phenomena present before the venesection.
Before Venesection.
Blood- pressure.
Condition.
After Venesection.
1. Normal or elevated
2. High.
3. Low or normal
Heart distended but circulation
still sufficient
Circulation slowed. Vasocon-
striction through stimulation
of medulla by excess of CO2
in the blood
Circulation slowed; heart fail-
ing. Unable to keep up cir-
culation through medulla in
spite of vasoconstriction
Fall of blood-pressure from emp-
tying of vascular system and
diminished viscosity of blood.1
Fall of blood-pressure; occasion-
ally compensated by increased
force of heart-beat and dimin-
ished viscosity of blood.
Blood-pressure .rises on account
of marked increase in force of
heart-beat in spite of empty-
ing of vascular system and of
relaxation of peripheral vessels.
Quite independently of these changes the right border of cardiac dul-
ness recedes one or more centimetres toward the sternum, the venous pressure
should fall, and the general condition should improve (cf. Fig. 127 and case on page 239).
Contraindications to Venesection. — However, it must be borne in mind
that venesection can do harm as well as good. Gushing has shown that in
conditions with increased intracranial tension, among them apoplexy, the
1 Heubner has shown that two-thirds of the viscosity of the blood is due to the cor-
puscles, hence venesection cannot fail to reduce the viscosity.
TREATMENT OF FAILURE OF THE HEART.
167
high blood-pressure is a phenomenon of physiological compensation, which
is necessary in order to maintain the circulation through the medulla. In
conditions with long-continued high blood-pressure, especially chronic
nephritis, this may also be the case. In these conditions venesection with
a view to lowering the arterial
pressure is contraindicated ; but
in these, as in other conditions,
it is still the procedure of choice
to relieve pulmonary oedema or
acute dilatation of the right heart.
The venesection should be carried
only to the point of relieving the
venous stasis, not to that of low-
ering the arterial pressure.
DIET.
FIG. 127. — Effect of venesection on the cardiac out-
line, showing diminution in size of right heart. (Case
of G. G.) Solid line indicates cardiac outline before
venesection, broken line after venesection. «
BEFORE VENESECTION AFTER VENESECTION
Rest for the gastro-intestinal
tract is quite as important for
the heart as is rest for the mus-
cles. Erlanger and Hooker have
shown that " an increase in pulse-
pressure becomes manifest within
a few minutes after the beginning of the meal, reaches its maximum within
one or two hours, and, as a rule, declines somewhat more slowly. It seems
to pass off within one or two hours after the maximum has been reached.
The pulse-rate is always distinctly increased with the ingestion of meals.
.... The product P. P. X
P. R., representing the velocity,
follows the curve of the pulse-
pressure/' hence the velocity
of flow and the work of the
heart are increased. Accord-
ingly, the diet should be light,
just enough to keep the patient
nourished without ever giving
him a sense of fulness or to
allow gas to form in the stom-
ach and intestines. Distention
of the stomach pushes up the
diaphragm and causes the
heart to lie more transversely
in the thorax, embarrassing
its action, causing a diminution in the systolic output and an increase
in the pulse-rate. Not infrequently this is also associated with onset
of precordial pain and constriction. Accordingly a very light diet
is necessary for the patient suffering from heart failure. The lac to-
cereal diet is the best, consisting mainly of milk, eggs, custards,
junket, toast, zweiback, crackers. The numerous prepared cereal foods,
FIG. 128. — Typical effect of venesection upon the circu
hit ic >n . Arrows indicate change in blood-pressure.
168 DISEASES OE THE HEART AND AORTA.
which consist of partially toasted flakes of wheat, corn, or rice, are
particularly good, since much nourishment may be given in small bulk
and in a form which does not tend to form thick, impenetrable, doughy
masses. Besides they contain the bran as well as the starch, and hence,
by leaving considerable fecal residue, tend to keep the bowels moving. Meat
should be given sparingly, partly because the purin bodies (xanthin, hypo-
xanthin) tend to raise the blood-pressure and increase the work of the heart,
and more particularly because the meat fibres are relatively slow in diges-
tion. For this reason it is better to take the proteid food in the forms men-
tioned above. Finely hashed Hamburg steak, lamb chops, or chicken are
the best forms of meat.
Liquid and Salt. — Liquids should be limited to 1500 c.c. (three
pints) a day in cases where oedema is present, since an excess of liquid
ingested causes further accumulation of oedema as well as bringing on a
slight overfilling of the blood-vessels, and thereby increasing the work of
the heart.
Salt should also be withheld from the food as far as possible, since
Widal and Javal, Strauss and Richter have shown that it is a contributing
factor in the production of oedema, and Barie reports good results from the
diminution of NaCl in the diet in diseases of the circulation.
Barie recommends the following articles as a basis for a diet low in
sodium chloride: Type I— Unsalted bread 500 Gm. (18 oz.), raw meat 400
Gm. (14 oz.), butter 80 Gm. (2i oz.), sugar 100 Gm. (3J oz.). Type II— Pota-
toes 1000 Gm. (32 oz.), raw meat 400 Gm. (14 oz.), butter 80 Gm. (24 oz.),
sugar 150 Gm. (5 oz.).
Sample Diet. — An excellent diet for severe heart cases, which may at
least serve as a basis for other variations, is the following, slightly modified
from that used for cardiac cases in the wards of the Johns Hopkins Hospital:
8 A.M. Cereal, soft egg, toast, coffee 200 Gm. (vi oz.).
10 A.M. Milk 200 c.c. (vi oz.), soft egg, crackers.
Dinner (noon). Soup, chicken, potatoes.
4 P.M. Milk 200 c.c. (vi oz.).
Supper, 6 P.M. Milk 200 c.c. (vi oz.), soft egg, crackers, prunes.1
9 P.M. Milk 200 c.c. (vi oz.), bread.
Limited Milk Diet. — In cases of broken compensation, with extreme
oedema great success has sometimes been attained by limiting the diet to
600 to 800 c.c. of milk in 24 hours (Carell, Hoffmann, Jacob and Hirsch-
feld), even in cases in which all other therapeutic measures have failed.
Professor Barker has occasionally obtained excellent results by increasing
the proteid intake upon this diet through the addition of nutrose to the
milk. However, striking results with this method are by no means the
rule, and it is to be used with caution.
Alcohol. — A very little alcohol, either as wine, or as brandy or whiskey,
may be allowed to persons accustomed to its use. Beer is less advisable,
1 It is important to avoid giving stewed fruits which contain much acid, such as peaches
and apricots, along with the milk, as the digestion of patients with broken compensation
is very easily disturbed, and an attack of vomiting places a considerable strain on the heart.
TREATMENT OF FAILURE OF THE HEART. 169
since it carries with it large quantities of liquid and often disturbs the
digestion as well, whereas, wine, whiskey, or brandy in small quantities
improves it. Against this is balanced the deleterious effect of alcohol upon
the heart muscle. Large quantities tend to produce fatty degeneration of
the latter. Whether small quantities have any such effect in the individual
case is uncertain, but it must be borne in mind that the injured organ is
much more susceptible to deleterious influences than is the healthy organ.
It is a safe rule that, in persons not already addicted to its use, brandy or
whiskey be given only in doses which serve as carminatives, and not in
doses intended for stimulation. Even the psychic effect may often be
secured as well by small doses as by large ones. One point in favor of alco-
hol in man as against animal experimentation lies in the fact that in such
persons it greatly increases the sense of well being and removes psychic
depression and worry. The latter may be especially straining upon the
heart, and hence every effort should be made use of to ward it off, especially
during certain crises; but it should be borne in mind that the patient may
easily become dependent upon the drink to arouse his spirits and in this
state more harm than good is done. The greatest judgment should be used
in the administration of alcohol even in small quantities, and it should even
then be reserved for crises when the stimulation of every fibre is all-impor-
tant. On the other hand, alcohol should never be withdrawn suddenly from
persons addicted to its use, since this procedure often precipitates an attack
of delirium tremens, but moderate doses (whiskey 15 c.c. or £ oz. every
four hours) should be given.
Tea and Coffee. — Whether tea and coffee should be given depends
largely upon the patient. In some persons these cause marked general
nervousness, sleeplessness, tremor, and even palpitation and irregularity;
others have established a tolerance such that no effect at all is produced.
The caffein itself is an excellent cardiac tonic of the digitalis order, and
where its effects on the nervous system are not manifest it may prove an
excellent adjuvant to the treatment. (A cup of coffee or of strong tea
contains about 0.1-0.2 Gm., 1£ to 3 gr.; the pharmacological dose of pure
caffein being 0.05 to 0.25 Gm.) As a rule it is safer to remove them from
diet, but in this as in all other rules individual exceptions can be made.
Tobacco should not be used under any circumstances. Besides the
nervous symptoms, it produces vasoconstriction, and often irregularities,
palpitation, and even precordial pain. Hence it is particularly
to be avoided in cases of cardiac disease.
PURGATION.
In patients with cardiac disease, and especially in those with broken
compensation, the question of purgation assumes unusual importance. In
these patients purgation seems to have a threefold beneficial action: first,
by eliminating the products of waste and putrefaction, to which they are
particularly sensitive; secondly, by relieving the distention of the bowels
from gas which tends to push up the diaphragm and to embarrass the heart
by placing it in a more transverse position ; and thirdly, by removing fluid
from the body through the bowels. This last effect is probably of con-
170 DISEASES OF THE HEART AND AORTA.
siderable importance, since Askanasy, Kast, and others have shown that
broken compensation is accompanied by hydrsemic plethora. Hydrsemic
plethora causes a rise in venous pressure and a dilatation of the heart (Roy
and Adami, Cameron), thus embarrassing the circulation. Moreover, in
broken systemic compensation the venous stasis also affects the kidneys
and diminishes the excretion of fluid, so that the bowel becomes an impor-
tant accessory channel of elimination. It is therefore the hydragogue
purgatives which are indicated in cardiac failure and not merely the pur-
gatives which increase peristalsis.
In most cases the best method of procedure is to start movement of the
bowels with calomel in either large single doses (0.3-0.6 Gm., grs. v-x) or in
small divided doses (.006 Gm., gr. TV half-hourly). The dose of calomel
should always be accompanied by a small dose of bicarbonate of soda
(0.3-0.6 Gm., gr. v-x) to avoid disturbing the digestion. Still more certain
purgation is obtained by giving a single dose of calomel and rhubarb in
equal quantities (0.3 Gm., gr. v), given at night. In all cases the calomel
should be followed by a saline purgative the next morning. Epsom salt
or some aperient water is preferable to Seidlitz powders or effervescent
citrate of magnesia, partly because of the action of the organic acids upon
the residium of calomel, but chiefly because the carbonic acid in the drug
distends the bowels and pushes up the diaphragm, thus embarrassing the
action of the heart. However, Epsom salts and aperient waters sometimes
cause nausea, and in such cases the advantages gained from the mildness of
the Seidlitz powder may outweigh its deleterious effects.
After constipation has been overcome purgation with salines should be
continued vigorously until the cedema has completely disappeared. Just
how vigorously this purgation should be maintained is a matter of some
dispute. Some clinicians, who regard presence of fluid as the most dele-
terious factor, believe that the best- results are obtained with ten to fifteen
fluid stools in twenty-four hours, with the elimination of two or three litres
by the bowel. Most observers, however, believe that the beneficial advan-
tages of such extreme purgation are more than counterbalanced by the
strain which they place upon the patient, not only by disturbing his rest,
but also by causing a considerable rise of both arterial and venous pressure
with each movement of the bowels. Indeed, each effort at stool constitutes
a typical Valsalva's experiment, which, as has been seen (Fig. 116, p. 132), is
accompanied by tremendous rises in blood-pressure and in weakened hearts
by acute dilatation.
Mr. W. E. Dandy has shown that the rise of arterial pressure during
the act of defecation is from 30 to 50 mm. Hg, and Mr. C. C. Cody has found
a corresponding rise in the venous pressure. These observations are sup-
ported by the fact that sudden death at stool is by no means uncommon in
cases of cardiac disease, especially in cases of aortic insufficiency, and
occurs even when the movements have been kept soft by daily purgation
with salts.
In this, as in most other therapeutic procedures, extreme measures
are to be avoided and treatment should be directed to secure a few easy
bowel movements without too much disturbance to the patient. In many
cases one or two compound cathartic pills (colocynth, jalap, gamboge, and
TREATMENT OF FAILURE OF THE HEART. 171
calomel) at night and a dose of Epsom salts or aperient water in the morn-
ing maintain just the correct number and quality of stools. Compound
jalap or compound licorice powders are also useful from time to time. In
stubborn cases elaterium or a drop of croton oil may be resorted to, but
should be used with extreme caution.
On the other hand, cascara, aloes, strychnine, belladonna, castor oil,
phenolphthalein, and the other purgatives which purge by increasing peris-
talsis, are of less value in the stage of broken compensation, since they do
not deplete the portal system nor relieve the hydraemia, though they are
satisfactory enough when compensation has been reestablished.
BIBLIOGRAPHY.
GENERAL PRINCIPLES IN THE TREATMENT OF CARDIAC DISEASES.
Erlanger and Hooker. Quoted on page 35.
Winternitz and da Silva. Quoted from Buxbaum, Lehrbuch der Hydrotherapie, Leipz., 1903.
Widal, F., and Javal, A.: La cure de dechloruration; son action sur l'oedeme,sur 1'hydra-
tation et sur 1'albuminurie a certaines pe>iodes de la nephrite epitheliale, Bull, et mem.
Soc. MeU d. hop. de Par., 1903, 3 s., xx, 733.
Widal, F., and Lemierre: Pathogenic de certaines cedemes brightiques; action du chlorure
de sodium ingeVe", ibid., 1903, 3 se>., xx, 678.
Widal, F.: Die Kochsalzentziehungskur in der Brightschen Krankheit, Verhand. d. Kong.
f. innere Med., Wiesbaden, 1909, xxvi, 43.
Strauss, H.: Zur Frage der Kochsalz und Fliissigkeitszufuhr bei Herz und Nierenkran-
ken., Therap. d. Gegenwart, Berl.-Wien, 1903, N. F. v, 433; Symposium on Thera-
peutics, Med. News, N. Y., 1903, Ixxxiii, 673; also, Die Chlorentziehung bei Nieren-
und Herzwassersucht, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1909, xxvi, 91.
Die Chlorentziehung bei Nieren- und Herzwassersucht, Verhandl. d. Kong. f. innere Med.,
Wiesbaden, 1909, xxvi, 91.
Richter, P. F.: Experimentelles ueber Nieren wassersucht, Berl. klin. Wchnschr., 1905,
xlii, 384.
Bane", E.: The Dechloridation Treatment in Diseases of the Heart, Internat. Clin., Phila.,
1906, 16th ser., i, 26'. Cf. also Symposium in Verhandl. d. Kong. f. innere Med.,
Wiesb., 1909, xxvi.
€arell, quoted from Romberg.
Hoffmann, F. A.: v. Leyden's Handbuch der Ernahrungs therapie, 1898, i, 579.
Jacoby, L.: Ueber die Bedeutung der Karellkur bei der Beseitigung schwerer Kreislauf-
storungen und der Behandlung der Fettsucht, Muenchen. med. Wchnschr., 1908,
Iv, 839.
Hirschfeld, F.: Die Karell'sche Milchkur und die Unterernahrung bei Kompensations-
storungen, ibid., 1908, Iv, 1587.
V.
THE EFFECTS OF DRUGS IN CARDIAC DISEASE.
It does not lie within the scope of this work to enter into a detailed
discussion of the pharmacology of the drugs used. The reader is referred
to the text-books upon this subject, especially —
Cushny, A. R.: A Text-book of Pharmacology and Therapeutics, Philadelphia and
New York.
Sollmann, Torald : Text-book of Pharmacology.
Hatcher, R. A., and Wilbert, M.: The Pharmacopoeia and the Physician, Chicago,
1907 (published by the American Medical Association).
Heinz, R.: Handbuch der experimentallen Pathologic und Pharmacologie, Jena, 1905.
However, since it is frequently inconvenient to refer to such books, a brief summary
of the action of each drug will be given with especial regard to its clinical application.
The drugs used in the treatment of cardiac disease may be of value
through their action on the following systems:
I. UPON THE HEART MUSCLE — digitalis, strophanthus, strychnine, squills, caffeine.
II. UPON THE PERIPHERAL VESSELS — constrictors: camphor, strychnine, adrenalin,
ergot, digitalis, nicotine (tobacco), caffeine; dilators: amyl nitrite, nitroglycerin, sodium
nitrite, erythrol tetranitrate.
1. ACTING UPON THE CARDIAC NERVES.
A. Slowing the heart through stimulation of the vagus: aconite, digitalis, strophanthus,
sometimes strychnine and caffeine, nicotine, veratrum viride, muscarin, very large doses of
potassium salts, bile salts, blood in jaundice.
B. Increasing the heart-rate through paralyzing the vagi: atropine, cocaine, amyl nitrite
and other nitrites.
C. Increasing rate through stimulation of accelerators: adrenalin, amyl nitrite, and
other nitrites.
D. Paralyzing accelerators: apocodein.
- , • 2. DIMINISHING VENOUS PRESSURE AND STASIS BY DEPLETING PORTAL SYSTEM:
purgative series, especially calomel, the saline and the vegetable purgatives.
3. DRUGS WHICH INCREASE THE TONICITY OF THE CARDIAC MUSCLE in pharmaco-
logical doses: digitalis, strophanthus, strychnine, amyl nitrite, nitroglycerin, calcium
chloride (transitory effect).
4. DRUGS WHICH DECREASE TONICITY: potassium salts, chloroform, formic acid, salt
infusion, ether, adrenalin.
Toriicity is practically unaffected by small doses of aconite, though slightly diminished
by larger on.es.
DIGITALIS.
Foremost among the drugs used in treatment of circulatory diseases
are the preparations of digitalis, introduced into medical practice by Wither-
ing in 1785. He says of it: "In the year 1775 my opinion was asked
concerning a family receipt for the cure of the dropsy. I was told that it
had long been kept a secret by an old woman in Shropshire, who had some-
times made cures where the more regular practitioners had failed. . . .
The medicine was composed of twenty or more different herbs, but it was
not very difficult for one conversant in these subjects to perceive that
172
THE EFFECTS OF DRUGS IX CARDIAC DISEASE. 173
the active herb could be no other than the foxglove. ... I soon found
the foxglove to be a very powerful diuretic. . . I use it in ascites,
anasarca, and hydrops pectoris." He then cites the results obtained in
the treatment of over 100 cases, many of which would be worthy of
modern therapeutics.
Drugs of Digitalis Series.1 — Digitalis, strophanthus, apocynum, convallaria majalis,
squill (scilla), erythrophlceine, helleborein, antiarin (antiaris toxicara).
DIGITALIS consists of the dried leaves of Digitalis purpurea collected from the flower
at the commencement of the second year's growth. It should not be kept more than one
year.2 Average dose pulv. digitalis = 0.05 Gm. (1 grain).
PREPARATIONS. DOSE.
Gram. English.
Fluid extractum digitalis 0 . 05 n\, 1
Extractum digitalis 0.01 gr. 1/5
Infusum digitalis
(1.5% digitalis + 10% alcohol + 15% cinnamon water) 8.00 5 ii
Tinctura digitalis 1 . 00 K\, xv
(10% of crude digitalis in dil. alcohol)
A very satisfactory form for administering digitalis and a purgative at once is
Addison's (or Niemayer's) pill, made up according to the following prescription:
Pulvis digitalis ) ..
Pulvis scilla,.. I"" °'6 *r'x
Hydrarg. chloridi mit 0.08 gr. 1 1/4
M. fiat in pil. x sen capsulas x.
Sig. One pill every three hours.
The calomel may be increased to gr. x, or may be replaced by blue-mass (massa
hydrarg.) or gray powder (hydrargyrum cum creta) in capsules.
The efficacy of Addison's pill depends upon the care taken to secure an active prepa-
ration of digitalis in making it. Moreover, its action may be uncertain, owing to the fact
that a certain amount of digitalis is eliminated with the stool without having been absorbed.
DERIVATIVES OF DIGITALIS. — Digitoxin — the most active substance derived from
digitalis, producing all the digitalis effects; soluble in alcohol; insoluble in water, except
in the presence of digitonin. Prepared in soluble form with digitonin under the trade name
"Digalen" (Cloetta). "Digalen," dose 1 c.c.
Digitalin (digitalinum verum Kiliani) — a white amorphous glucoside, less toxic than
digitoxin but otherwise resembling it in physical properties and pharmacological action.
Dose 2-6 mg. (gr. drfis)-m
Roughly, digitoxin is six times more potent than an equal weight of digitalinum
verum (Fraenkel).
Digitalin " German" — amorphous powder, soluble in water and alcohol; a mixture
of pure digitalin, digitalein, and digitonin. Dose 2-6 mg. (gr. ^V~iV)-
Digitalein and digitonin are other somewhat similar substances which have no phar-
macological action.
STROPHANTHUS — the ripe seeds of Strophanthus Kombe". Tinctura strophanthi, 10
per cent, of the drug in 65 per cent, alcohol. Dose 0.5 c.c. (n^viii).
1A very full discussion of these drugs is given in Cushny's article.
2 It is most difficult to obtain a preparation of digitalis leaves of which one can be
certain, and upon this alone the result 6f the whole treatment depends. Owing to the varia-
tions in leaves it is best to obtain preparations from manufacturing chemists who have
standardized them from physiological effects upon frogs or mammals. (The term "frog
unit," "Froscheinheit," refers to the amount of drug which will kill an average frog,
leaving the heart in systole; cf. also Sowton and especially Edmunds and Hale.)
Edmunds and Hale have shown that in frogs the drug acts chiefly on the heart, in mam-
mals largely on the nervous system.
174 DISEASES OF THE HEART AND AORTA.
Derivative and Active Principle. — Strophanthin — a white crystalline glucoside of con-
stant composition and action, soluble but undergoing decomposition in water. Hence
best prescribed in dilute alcohol:
Strophanthin 0.01 gr. 1/5
Alcohol dil 1.50 5 v
Sig. Teaspoonful p. c. in half glass of water.
R. A. Hatcher has shown recently that the absorption of strophanthus and strophan-
thin from the gastro-intestinal tract is very uncertain, and that it is liable to set in suddenly
after tremendous doses have been given without effect. Hence these drugs should be
administered intravenously or intramuscularly.
For intravenous or intramuscular injections Strophanthin (amorphous) is put up in
small sterile phials (Boehringer & Co.). It is very useful for the physician to carry a few of
these in his emergency case.
Strophanthin (Thorns) is said to be crystalline and is a more stable and more uni-
form preparation. It acts in doses of \ to \ mg. (gr. ^ to T^).
EFFECT OF DIGITALIS ON THE NORMAL HEART.
Fraenkel and Schwartz and also Cloetta have shown that in thera-
peutic doses digitalis has no effect upon the normal heart, either in affect-
ing the strength of the beat or in bringing about hypertrophy. Neither
has it any effect upon the perfectly compensated, undilated heart with a
valvular lesion. Its chief effects are seen in dilated hearts whose myo-
cardium still retains some reserve power. In the severest stages of cardio-
sclerosis and fatty degeneration it may stimulate the fibres to the limit of
their power, and thus do actual harm, and even hasten the end.
ACTION OF DIGITALIS.
Digitalis has the following actions: (1) it stimulates the vagus, both
centrally and peripherally, brings about slowing of the heart, and diminishes
conductivity; (2) it increases the irritability, force of contraction, and
tonicity of the cardiac muscle in both auricles and ventricles, slightly
diminishing conductivity by direct action upon the cardiac muscle even
in atropinized hearts; (3) it causes the peripheral blood-vessels to constrict,
thereby raising the blood-pressure; (4) a diuretic action, mainly through
increase in the rate of general blood flow; (5) it causes a constriction of the
coronary blood-vessels and diminished flow through the walls of the heart.
As shown by Cushny, the action of digitalis may be divided into three
stages, characterized by the following phenomena:
I. Therapeutic Stage. — Slowing of entire heart, increase of blood-pres-
sure, increase of systolic output and of cardiac tonicity, peripheral vaso-
constriction, dilatation of coronary arteries, slowing of conductivity.
II. Stage of Irregularity. — The heart-rate becomes somewhat accel-
erated and irregular. Cushny thinks that this irregularity is due to the
fact that, besides following impulses from the auricles, the ventricle begins
to beat with a rhythm of its own. A para'rrthymia thus sets in, and
the two independent rhythms occasionally produce interference and pro-
longed pauses. In this stage the blood flow becomes slowed, although
the output of individual systoles is much increased.
III. Stage of Incoordination. — Extreme irregularity of both auricles
and ventricles has now set in, both beating independently of one another
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 175
(absolute heart-block). The blood flow has now markedly slowed and beats
become irregular in force and rhythm. Death sets in.
Action of Digitalis on the Coronary Arteries. — Another effect of digitalis, namely,
marked constriction of and lessened blood flow through the coronary vessels, has been
demonstrated by Oswald Loeb upon the excised heart. This is due mainly to the digi-
toxin, and occurs even at a time when the size and force of the cardiac contractions are
definitely increased. Although Dr. G. S. Bond in the writer's laboratory has been unable
to obtain any such change in flow through the coronary arteries of the dog's heart in situ
after administration of digitalis and strophanthus, there is considerable clinical evidence
that digitalis sometimes does distinct harm in patients whose
myocardium has undergone extensive fatty degeneration, or
cardiosclerosis, or whose arteries are sclerotic. Strophanthin pro-
duces the same effects though in less marked degree.
ATVWVWWVWW
. A „
WWIM
A B C D E
FIG. 129. — Tracings sho.wing the action of digitalis upon the dog's blood-pressure. (After Cushny.)
A, normal; B, therapeutic stage, with increased blood-pressure and moderate slowing of the pulse, but
quickened blood-flow; C, excessive inhibition, causing low blood -pressure and slowed circulation; />, still
further slowing, with slight arrhythmia; E, third stage, irregularity with further rise of blood-pressure
from excessive vasoconstriction.
Effect on the Blood-pressure. — The rise of blood-pressure due
to digitalis is in part due to the increased force and out-
put of the heart, in part to the constriction of the periph-
eral and, especially, the abdominal blood-vessels. The
velocity of blood flow (as shown by product of pulse-pressure X pulse-
rate1) is usually increased when this effect is brought about (Fellner,
Fraenkel). Strophanthus causes less vasoconstriction than digitalis, and
hence usually affects the minimal pressure less than the maximal, but
increases the velocity of blood flow without causing so great a strain upon
the heart. Unfortunately, the preparations of strophanthus are less-
reliable for continuous action.
Occasionally it is found that both digitalis and strophanthus actually
lower the maximal blood-pressure. This occurs especially
in the cases where the circulation through the medullary centres ia
impaired by venous stasis or arteriosclerosis, or failure of the heart,
1 Janeway has reported cases in which digitalis produced great improvement without
increasing P. P. x P. R. Considering the error which may be involved in this calculation,
such exceptions are not surprising (see page 24).
176
DISEASES OF THE HEART AND AORTA.
and the high blood-pressure is merely the result of general reflex vaso-
constriction from the ischsemia of the centre (high-pressure stasis). When
the force of the heart is increased and the blood passing through the
centre is better aerated, the vasoconstrictor influence is no longer exerted
and the general blood-pressure then falls.
Effect of Digitalis on Tonicity. — C linically the most important
action of digitalis is its effect upon the tonus of the
cardiac muscle, in preventing and in
overcoming dilatation, and it is in dilated
hearts that the beneficial action of digitalis
is most pronounced. Frangois-Franck (1882)
demonstrated that the administration of
digitalis did away with the transitory func-
tional tricuspid insufficiency which resulted
from stimulation of the vagus. Cushny and
Cameron have shown marked increase in
tonicity, as shown by diminution in cardiac
volume. Moreover, Cloetta has demon-
strated that the prolonged administration
of digitalis prevents the heart from dilating
in experimental aortic insufficiency (posi-
tive intraventricular pressure during dias-
tole). The hearts of animals which have
been treated with digitalis are smaller and
stronger than those which have not been so
treated (see page 377). Colbeck, Gossage,
arid others have also emphasized the impor-
tance of this effect on cardiac tonus.
CHOICE OF DIGITALIS PREPARATIONS.
The first question arising is, What form of
digitalis to administer? Numerous attempts to iso-
late and administer the purified active principle of
digitalis have demonstrated that, though several such
substances (digitalin, digitoxin, digitalein, digitonin)
have been used, digitoxin comes closest to the crude
drug. Unfortunately, pure digitoxin is insoluble in
water and in the tissue juices, but becomes soluble
in the presence of digitonin. The mixture of the two
substances known as "digalen" (Cloetta) or "soluble
digitoxin" is on the market, and is widely used, especially for intravenous injection, when
rapid effects are desired. Digitalin, especially the so-called "German" digitalin, has
been much more widely used than digitoxin, but, as is also Kiliani's digitalinum verum,
is far less certain and less active.
However, the recent critical studies of Albert Fraenkel have demon-
strated that the crude digitalis is at least as satisfactory as any of its deriva-
tives, provided its toxicity (lethal dose for a frog) has been determined
and the therapeutic dose standardized accordingly. This is all important,
since digitalis leaves from different sources vary greatly in their content of
digitoxin, digitalin, etc., and a mere knowledge of the weight of powdered
leaves, which is all that is necessary for the pharmacopceial preparations,
FIG. 130. — Variations in blood-pres-
sure in a patient under the influence of
digitalis and nitroglycerin. MAX, max-
imal blood-pressure ; MIN, minimal
blood - pressure ; PP, pulse - pressure ;
P P X PR, pulse - pressure X pulse-
rate: DISC. DIGITALIS, discontinue
digitalis.
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 177
gives no idea of the actual potency of the drug. Fraenkel also found little
or no difference between digitoxin and crude digitalis as regards the time
at which their effects set in, both becoming manifest in twelve to twenty-
four hours after administration by mouth or intravenously. The absence
of immediate effects from digitalis preparations may be obviated by the
use of strophanthin intravenously. This drug acts with great certainty
and its action usually sets in within less than half an hour, so that it is
very useful in cases where immediate effects are desired. Fraenkel recom-
mends a single dose of strophanthin intravenously to be followed within
twenty-four hours by digitalis by mouth, so that the effect of the latter
may begin as that of the strophanthin wears off. Of course if the patient
has recently received digitalis, strophanthin should not be used for fear of
cumulative effect.
VASOCONSTHICTION
VOL. LEG I
SECONDS
FIG. 131. — Effect of digitalis on cardiac tonicity in the dog. (Experiment by Dr. Cameron.) Upper
curve, volume of the hind leg, taken with a plethysmograph, showing vasoconstriction; second curve,
volume of the ventricles; lower curve, blood-pressure taken with the Huerthle membrane manometer.
Time in seconds. A small dose of tincture of digitalis injected into the jugular vein at the arrow. The
effect upon tonicity, T + , outlasts both the rise in blood -pressure and the vasoconstriction.
An example of Fraenkel's remarkable therapeutic effects may be quoted here:
Patient, aged 57, male, admitted to Strassburg Hospital November 17, 1905. Had
rheumatic fever in 1869 and again in 1886. Palpitation when at work, and occasional
swelling of legs since 1900. Drinks considerably.
Present Condition. — Considerable redema of legs, thighs, and scrotum. Moderate
ascites. Dulness and diminished breath sounds over right base. X-ray shows heart
shadow enlarged to left and right: dynamic dilatation of aorta. Pulse irregular, 104 per
minute, maximum pressure 180. Pulv. folia digitalis 0.1 Gm. (U gr.) three times a day
brought pulse down to 86 in 4 days, to 76 in 6 days, increasing diuresis from 2000 to 4500
and 5800 respectively.
Another attack of pain in joints on December 1; left clinic "improved " on December
11. Returned January 25, 1906. (Edema as before; ascites marked — abdomen 108 cm.
in circumference. Liver palpable four fingers' breadth below costal margin. Spleen pal-
pable. Dulness and diminished fremitus over base of right lung. Heart dilated more than
before; impulse not palpable; first sound at apex reduplicated; second accentuated, espe-
cially over pulmonic area. Slight gallop rhythm. Heart action rapid and regular. Marked
orthopnoea and very distressing cough. Patient has had no sleep for several nights.
The following table shows the effects of the intravenous administration of strophan-
thin upon his blood-pressure, urine output, and symptoms. The product of pulse-pres-
sure and pulse-rate furnishes a very rough index of the velocity of blood-flow.
12
178
DISEASES OF THE HEART AND AORTA.
Time.
Blood-pressure.
Pulse.
Pulse-pressure
X Pulse- rate.
Urine in
24 hours.
Max.
Min.
Jan. 27, 10.30
10.40
10.45
268
286
206
206
92
84
1 mg. stro
Diuresis b
80
5640
7490
phanthin intn
egins
7904
1600
Dyspnoea increasing.
Pulse feels larger.
No feeling of constric-
tion. Sleeps well.
ivenously
6050
11.00
Jan. 28
260
156
Jan. 31
Feb. 1..
(Edema almost disappeared.
(Edema completely disappeared.
Patient makes uninterrupted recovery with no further medication.
PRECAUTIONS AND METHODS OF ADMINISTRATION.
Flavoring. — Gastric disturbances, such as nausea and vom-
iting, occasionally result from the administration of digitalis prepara-
tions or derivatives. This is in part due to the direct irritating action upon
the gastric mucous membrane and in part to the extremely unpleasant taste
and after taste of the drug. In order to obviate the former the drug should
always be given in a large quantity (at least half a tumbler) of water. The
intensely disagreeable taste of the digitalis and strophanthus preparations
may be disguised by the addition of bitter orange peel (tinctura aurantii
amari), compound tincture of either gentian or cardamom, or tincture of
quassia or calumba. It may also be given in albumin water flavored
:with lemon so that its taste is barely noticeable. The use of any of
these disguises greatly lessens the discomfort of the patient and frequently
minimizes the gastric disturbances resulting from the drug.
Rectal Administration. — When the gastric symptoms persist in spite
of. these precautions, the drug may be administered per rectum, being given
in 100 c.c. physiological salt solution with a little starch. This method is
very satisfactory (Janeway). Dr. Finley informs the writer that he has
seen the pulse-rate slowed and the patient's condition greatly improved
within two hours after the administration of digitalis per rectum,
whereas the effect rarely follows administration by mouth in less than
twenty-four hours.
Period of Administration. — In the administration of digitalis it is impor-
tant to obtain a definite effect and yet not to push the drug beyond the first
stage of its activity, — that of slowing and increase in size of the pulse, — and
to avoid the onset of the second stage, i.e., of irregularity. Since different
hearts vary in their susceptibility to digitalis, and since, on the other hand,
the drug begins to act only after twenty-four hours and may have a cumula-
tive effect, this task is by no means easy. To avoid the onset of toxic effects
various routine methods may be resorted to. Thus, Professor Osier and
other authorities recommend giving the drug in "courses" consisting of
eight doses of 15 minims of the tincture (0.1 Gm. or 1^ gr. digitalis) every
four hours. The course is to be repeated if necessary. It may be said that
this method often falls short of the effect or brings it about too slowly.
The writer has found it very satisfactory to order "0.3 c.c. (5 minims) of
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 179
the fluidextract three times a day until the pulse-rate reaches 80, when it
should be discontinued without the necessity of a special order." Albert
Fraenkel suggests giving several strong doses equivalent to 0.1 Gm. (2 gr.)
of powdered digitalis (about twice the usual dose, 2 c.c. or 30 minims of
the tinctura digitalis) to insure prompt effect (slowing of the pulse), and
thereafter dropping to steady dosage of .03 Gm. (£ gr., 0.5 c.c., or 7J
minims of the tincture) to prevent cumulative but retain the therapeutic
effect. This seems to be the most satisfactory method, since it insures
not only the immediate but a permament effect. Indeed in many chronic
cases " the strength of the heart begins to fail a short time after leaving off
the digitalis. Here the continuous use of digitalis (0.05 Gm. or 1 gr. digi-
talis), as recommended by Kussmaul, Naunyn, and Groedel, for months and
even years, has an admirable effect in keeping the cardiac activity at its
necessary height" (Romberg).
Digitalis and Nitrites. — In many cases digitalis and nitro-
glycerin, sodium nitrite, or erythrol tetranitrate may
be given together with great advantage (J. O. Hirschfelder). This com-
bination of drugs does more than merely annihilate the constrictor effect
of the digitalis, for the nitrites also increase cardiac tonicity and the two
drugs unite in bringing about this beneficial effect. Moreover, it is a well-
known principle in therapeutics that the combined effect of two equivalent
doses of drugs having a common action is often greater than would be pro-
duced by using double the dose of either one. As will be seen, this combined
action is particularly important in the treatment of aortic insufficiency.
ARRHYTHMIA AND HEART-BLOCK CAUSED BY DIGITALIS.
Mackenzie and later Hewlett have investigated the nature of arrhyth-
mias which have been produced clinically by slight cumulative action of
digitalis. They found two forms:
First, the ventricle occasionally fails to respond to contractions of the auricle (par-
tial heart-block). V. Tabora has found in animals that this block is brought about mainly
by stimulation of the vagi. If the vagi have been sectioned or paralyzed with atropine,
it appears only after a much greater dose has been administered. Hence this digitalis
block may be regarded as belonging to the first stage of digitalis effect. To obviate this,
Hewlett recommended giving atropine along with the digitalis, a combination suggested by
Cushny but discarded by him in favor of digitalis and spartein, a drug which paralyzes the
vagus without the unpleasant action of atropine (Cushny and Matthews). Neither of these
combinations has been used extensively, and, moreover, Cameron's experiments show that
atropine prevents digitalis from improving the cardiac tonicity, and hence robs it of its
most important effect. The second form of irregularity following digitalis is the occurrence
of ventricular extrasystoles, such as were observed in animals by Cushny. As stated by
this observer, this effect belongs to the second stage of digitalis action, and accordingly is
a more urgent sign for discontinuing the digitalis than is even the partial heart-block.
ADMINISTRATION OF DIGITALIS IN WEAKENED HEARTS.
The relation of digitalis to the arrhythmias has recently been investi-
gated by Dmitrenko, who claims that drugs of this series are always con-
traindicated in cases where the heart is irregular. This is certainly an
extreme view. Hering has shown that certain irregularities, due to extra-
systoles arising in the ventricle, disappear under the use of digitalis. Mac-
180 DISEASES OF THE HEART AND AORTA.
kenzie has shown that where the irregularity arises in the auricle digitalis
may sometimes do positive harm by diminishing conductivity; but this is
comparatively rare. On the other hand, da Costa, Leyden, and the later
writers have shown that in the permanent irregularities digitalis does not
cause the arrhythmia to disappear, but usually increases the force of the
individual contractions, causes them to become less unequal, and increases
the velocity of blood flow. The effect depends largely upon the condition
of the heart and its susceptibility to the drug. In general, the more diseased
the organ the more sensitive it is to the action of small quantities. A very
weak heart with intense myocardial change may therefore pass to the second
stage of digitalis action under smaller doses than would bring about a
physiological effect in one whose fibres were less intensely degenerated.
The effect ofvdigitalis upon the patient must always be carefully watched,
and if the rhythm becomes more irregular it must be discontinued. On
the other hand, where the myocardium is reduced to small amount in ex-
treme fatty or fibrous myocarditis, the increased strain (and perhaps also
the coronary vasoconstriction) caused by digitalis is often too great, and
the failure of the heart is increased and the drug does distinct harm. At
present no absolute rule can be laid down for the border-line cases in which
there is doubt, except that when an irregularity is present, especially one
which has its origin in the auricle or great veins, digitalis should be used
only to treat cardiac dilatation, and even then with great hesitancy and
extreme precaution. When any disturbance of conductivity occurs, digi-
talis is absolutely contraindkjated.
HALLUCINATIONS FROM DIGITALIS.
Another toxic effect of digitalis lies in the production of mental symp-
toms, delirium and delusions, through its action on the central nervous
system (Duroziez, Hall, see page 160). The onset of these symptoms
therefore constitutes a contraindication to continuing the drug.
CHOICE OF DRUGS.
As between digitalis and strophanthus, the choice lies with the former
except in the following conditions: (1) when rapid action is needed, in
which case strophanthin should be given intravenously; (2) in cases of
myocardial weakness or fatty degeneration, when it is important not to
increase peripheral resistance; (3) in cases of aortic insufficiency and of
mitral stenosis, where the same is true ; (4) in some cases with aneurism and
broken compensation.
Besides digitalis and strophanthus numerous other drugs and their
derivatives enumerated above have been introduced, but none seems to
have any decided advantages which warrant supplanting these two.
SUMMARY OF CLINICAL APPLICATION OF DIGITALIS.
Professor Osier's epigram, "Broken compensation is the signal for
digitalis/7 about summarizes the use of the drug. Its applicability in indi-
vidual diseases will be discussed under the separate chapters, but in general
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 181
it may be said to be useful in three classes of conditions : (1) in cases where
compensation is broken; (2) in cases where acute dilatation is present and
has persisted after rest and other modes of treatment; (3) in cases with
persistent or distressing tachycardia, which does not yield to other means.
It is in general absolutely contraindicated : (1) in cases with heart-block;
(2) where the amount of heart muscle has been diminished by fibrous or
fatty myocarditic changes, or in a case in which digitalis has been known
to fail already. It should be used with caution: (1) in arrhythmias due to
disturbances arising in the auricles or sinus region; strophanthus is equally
contraindicated; (2) in cases with coronary sclerosis, owing to the constrict-
ing action upon those vessels, strophanthin is here less undesirable.
STRYCHNINE.
PREPARATIONS.
Strychnine (strychnina) is an alkaloid obtained from nux vomica. Tinctura nucis
vomicae contains 2 per cent, extract of nux vomica and is assayed to contain 0.1 per cent,
strychnine. It is useful more as a stomachic bitters than as a cardiac stimulant. Dose,
1-2 c.c., 15 to 30 minims.
Strychninae sulphas contains 5 molecules of water of crystallization and 78 per cent,
of strychnine, soluble in 3 parts of water. Average dose, 0.0015 Gm. (?V gr.)-
Strychninae nitras is soluble in 42 parts of water and 120 parts alcohol. Dose, same
as sulphate.
PHARMACOLOGICAL ACTION OF STRYCHNINE.
There are many cases in which the circulation is beginning to show
some signs of slight weakening and yet where it does not seem necessary
to use digitalis. In these cases other drugs are resorted to, — in America
usually strychnine,1 in Germany usually camphor; both apparently yielding
good clinical results. It must be added, however, that according to most
pharmacologists strychnine has no effect whatever upon the heart and
produces the rise in blood-pressure only by the vasoconstrictor action.
Effect on Cardiac Tonicity. — Dr. P. D. Cameron has* recently investi-
gated the subject under the writer's direction, and has found in the dog
that strychnine in doses of .00003 Gm. per kg. or TsW gr- per lb., corre-
sponding to .002 Gm. (^V gr.) hypodermically for a man, always produces
an increase in tonicity of the heart muscle, though without affecting the
force of the beat or markedly changing maximal pressure. Mean and
minimal pressures are usually slightly increased (by 10-15 mm. Hg) and
pulse-rate a little slowed. Larger doses increase the systolic output, raise
the blood-pressure, slow the heart, and increase the tonicity.
Clinical Effects. — In view of the wide-spread and often indiscriminate
use of this drug, it is important to realize exactly its clinical use before
prescribing it. As has been stated, strychnine stimulates both vasocon-
strictor and vagus centres, hence raises the blood-pressure and slows the
pulse-rate. These effects, however, have been observed mainly in animals,
and few exact clinical studies have been made upon man in connection
1 In view of the wide use of strychnine in heart diseases in English-speaking countries,
it is quite striking that this drug is not mentioned in connection with therapy of the cir-
culatory system in such extensive German text-books as those of Romberg and Heinz.
182
DISEASES OF THE HEART AND AORTA.
with observations of the change of blood-pressure. Briggs and Cook, who
were most enthusiastic over the use of the drug, did not obtain rises of
blood-pressure exceeding 10 mm. Hg from doses of 1 to 6 mg. (^5- to TV gr.)
and in no case slowing of the pulse. Cabot and F. P. Drayer, on the other
hand, failed to note any changes whatever in many cases. The writer has
made a considerable number of observations, determining the blood-press-
ure with the Erlanger apparatus. He injected strychnine in doses which
BEFORE
AFTER
BEFORE
AFTER
SECONDS
II
FIG. 132. — Curve showing the effect of strychnine upon cardiac tonicity. (Experiment by Dr.
Cameron.) Lettering as in Fig. 131. Fig. I shows increase in systolic output and maximal blood-pressure.
Fig. II shows increase in tonicity, with a diminution in the systolic output and a fall in the minimal, but no
change in the maximal blood-pressure. The effect upon tonicity is the most constant effect of the drug.
rose to 15 mg. (i gr.) hypo, without obtaining any effect upon maximal
or minimal pressure, pulse-rate, or rate of respiration, and from single
doses scarcely any increase in reflexes. These tests were made upon hearts
which were not dilated, and hence no effects upon tonicity could be noted.
Since the rank and file of English and American physicians entertain
an almost superstitious belief in the efficacy of this drug, it is evident that
effect in each case should be controlled by blood-pressure determinations.
Cameron's experiments upon animals have shown that a distinctly bene-
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 183
ficial effect upon tonicity may be obtained with but little change (5-10 mm.)
in the maximal blood-pressure, but that often when these changes are
very slight the effect may be much more distinctly shown by a rise in
the mean or minimal pressure. Both should be carefully watched in cases
in which strychnine is given, and the dose should be sufficient to be effec-
tive. If no effect is obtained it should be discarded for some more potent
drug.
INDICATIONS FOR STRYCHNINE.
It is probable that strychnine is of particular value in the disturbances
of respiration following extreme heart failure, such as Cheyne-Stokes breath-
ing, cardiac asthma, etc., as claimed by Eyster; and in such cases it should
be given whether digitalis is being administered or not.
By virtue of its stimulating action upon the vasomotor centre, strych-
nine is particularly indicated in cases in which this centre is beginning to
fail. This is particularly the case in all infectious diseases, in many cases
of neurasthenia, in mild shock, in some cases of anaemia, asthenia, and in
many convalescents. Strychnine should be used not to replace digitalis,
but may be given as a prophylactic to prevent the heart muscle from wear-
ing itself out upon a relaxed vascular system. When the heart muscle
once shows signs of giving way, when marked cardiac dilatation, etc.,
have set in, its period of usefulness is over. Small doses of digitalis will
then do the same work better and will do more. It is also valuable when
given along with digitalis. The value of strychnine again becomes mani-
fest in the later stages of heart failure through its action as a stimulant
for the respiratory centre. Eyster believes that it is particularly useful in
warding off Cheyne-Stokes respiration and also in the treatment of the
latter. It is probably still more useful in cardiac asthma, more as a pro-
phylactic measure in maintaining the activity of the respiratory centre
than in stopping individual attacks; and it may also prove of value in
warding off the distressing dreams that result from mild asphyxia dur-
ing sleep, as well as the attacks of tachycardia and other unpleasant con-
ditions which may occur as the result of waking " with a start " (asphyxia
during sleep).
CAMPHOR.
Camphor is a white substance, soluble in alcohol, ether, and chloro-
form, whose structural formula is—
C(CH3)
CH3
Average dose 0.12 Gm. (2 gr.), best given as linimentum camphor® (camphorated
oil), which contains 20 per cent, of camphor dissolved in cotton-seed oil. Average dose
0.75 to 2.0 c.c. (20 to 45 minims), available for hypodermic use or by mouth.
Spiritus camphorse, a 10 per cent, solution of camphor in alcohol. Dose 1 c.c. (15
minims).
184 DISEASES OF THE HEART AND AORTA.
Camphor, like strychnine, is a stimulant to the vasomotor centrer
but, according to Cameron, does not seem to have so pronounced an effect on tonic-
i t y . Like strychnine it also varies in its effects on different individuals. Some persons
require doses twenty times as large as do others before an effect sets in, especially when
the drug is given by mouth. Camphor is most important for its use in shock. It is given
deeply into the muscles in order to avoid subsequent inflammations. It is not so valuable
for continuous use. As recently shown by Winterberg, Seligmann, and Gottlieb and
Magnus, camphor has also a very distinct action upon the heart muscle, causing the fibril-
lating excised heart to revive from fibrillary contractions. After camphor has been ad-
ministered to a dog the ventricle (in situ) can be thrown into fibrillary contractions by
weak faradic stimuli and yet recover. On the other hand, a direct therapeutic effect upon
the heart muscle in man has not yet been proved.
CALCIUM SALTS.
Calcium chloride and other salts of calcium have been recommended recently as
cardiac stimulants by Lauder Brunton and other English clinicians. Although the action
of calcium upon the excised heart is indisputable, its effect upon the heart in situ has been
supposed to be too transitory to be of practical value. The writer has been unable to find
any effect upon the maximal and minimal blood-pressures and pulse-rates of a number of
cases of typhoid fever who were receiving calcium lactate in sufficiently large doses to
hasten coagulation. Sladen also found in a large variety of cases that calcium lactate had
no effect upon pulse-rate or blood-pressure. On the other hand, in animals calcium chloride
has an effect, especially upon tonicity, which closely simulates that of strychnine. Injec-
tion of considerable quantities directly into the cavities of the heart revives that organ as
nothing else appears to do. The writer has found that in some cases dogs' hearts that had
actually stopped beating and even lost their mechanical irritability revived to such an
extent as to resume a regular rhythm with a moderately high blood-pressure. The matter
is, however, still in the experimental stage.
CAFFEINE.
From the results of experiments, upon animals, caffeine would take
rank next to digitalis in cardiac therapy. Like digitalis it acts upon the
cardiac muscle, increasing the size and force of the contraction; like digi-
talis it has a vasoconstrictor action, and raises the blood-pressure by bring-
ing about constriction of the peripheral blood-vessels. It is therefore par-
ticularly valuable in conditions of collapse and shock. In this regard it is
more reliable than camphor (Romberg) or strychnine.
On the other hand, caffeine does not exert a constricting action upon the coronary
arteries (O. Loeb), and hence is not contraindicated in cases of coronary sclerosis. Upon
the pulse-rate caffeine exerts a variable effect, in relatively small doses (0.1 Gm., 2 gr.)
slowing the pulse by stimulating the vagi, in larger doses accelerating. The acceleration
is apparently due to direct action upon the heart muscle, since it occurs also in the excised
heart when caffeine is added to the Locke's solution. However, as regards the effects of
a given dose, there is the greatest variation among different individuals, some persons
being extremely sensitive to small doses, others extremely resistant. Even in the same
individual tolerance varies. Thus a considerable degree of tolerance may be developed by
the constant use of coffee, so that* three or four cups (0.15 to 0.2 Gm., 3 to 5 gr. caffeine)
a day may be taken with no symptoms whatever. Thus, in a case under the writer's ob-
servation, after several months of absolute abstinence from coffee, marked palpitation,
tachycardia, and sleeplessness resulted from a single cup in twenty-four hours; a few weeks
later one cup and after a few months two cups could be taken without any apparent effect.
Unfortunately, the therapeutic use of caffeine is often accompanied by
palpitation, sleeplessness, and even nausea, vomiting, vertigo, and delirium,
which occur with particular ease in cases with cardiac disease. In using
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 185
caffeine one is therefore usually in a dilemma between a hypersensitiveness
and an habituation. Unfortunately, the palpitation and discomfort usually
set in at about the same point as the therapeutic effect, or even earlier;
but there are certainly many cases in which this is not the case, and in
which caffeine is a valuable therapeutic agent.
THEOBROMINE.
Theobromine has a much less effect upon the cerebral cortex and upon
the vasomotor centre than caffeine, but has a very strong diuretic action.
As shown by O. Loeb it possesses a much more powerful action in dilating
the coronary arteries of the excised heart. Upon the heart in situ its action
does not seem to be pronounced. Indeed, G. S. Bond, in the writer's
laboratory, has been unable to detect any effect upon the outflow from the
coronary veins as the result of intravenous injection of agurin (theobromine
sodium acetate). The stimulating action of theobromine upon the heart
muscle, though not as intense as that of caffeine, is still very marked. It
has therefore been recommended as a cardiac stimulant, particularly by
the French clinicians, who found it of considerable value in the weak
hearts of fatty individuals. Kaufmann and Pauli, Brewer and v. Leyden
recommended the use of theobromine in attacks of angina
pectoris (stenocardia). Pineles advises theophyllin. Pal has
found that theobromine is occasionally useful in the treatment of vaso-
motor crises, but that it often fails in cases where iodine and potassium
thiocyanate help.. Romberg is not able to detect any beneficial action of
theobromine apart from its diuretic action. In using theobromine it is
preferable to use those compounds which are free from salicylates, since
this radical has a certain depressant action upon the heart and an irritant
action on the kidneys. Acettheobromine sodium ("agurin") and
acettheocin sodium are therefore preferable to theobromine sodium sali-
cylate ("diuretin").
ACONITE.
PREPARATIONS.
A c o n i t u m , the dried tuberous root of aconitum napellus, collected in autumn,
and yielding not less than 0.5 per cent, aconitin. Dose 0.05 Gm. (1 gr.).
Tinctura aconiti, U.S. P., now represents 10 per cent, of the crude drug,
formerly stronger. It is the most certain and most stable of all the aconite preparations.
Dose 0.6 c.c. (10 minims).
Aconitina, the crystalline alkaloid. Dose 0.00015 Gm. (0.15 mg. or TJu gr).
It is so irritating that it is usually preferable to prescribe the simple tincture of aconite,
since this is assayed according to the last pharmacopeia.
Pharmacological Action. — Aconite has three pharmacological actions
upon the circulatory system: (1) it stimulates the vagus promptly and to
a high degree; (2) it diminishes the size and force of the cardiac contrac-
tion, and also accelerates the heart when this organ is liberated from the
action of the vagus centre ; (3) it slightly stimulates the vasomotor centre
in very small doses. However, it also diminishes the activity of the respira-
tory centre, and may thus bring on dyspnoea.
Therapeutic Uses. — When carefully given in therapeutic doses aconite
slows the heart by stimulation of the vagus, and has little action upon the
186 DISEASES OF THE HEART AND AORTA.
heart muscle. It is therefore of value in the acceleration of the pulse in
fevers, where the heart muscle itself needs no stimulation and the heart
needs slowing. Owing to the variability of the tincture under the old
pharmacopoeia, the use of aconite has fallen into disrepute, and enough
time has not elapsed since the adoption of the last pharmacopoeia (1900,
adopted in 1905) for its real utility in physiological therapeutics to have
been investigated. There is no doubt that it is of value in many cases of
tachycardia, especially those of nervous or postfebrile origin. Da Costa, in
1864, found it of some value for the tachycardia of acutely overstrained
hearts, but particularly useful when given with digitalis.
This combination contains two drugs; both stimulate the vagi, the one
tends to diminish, the other to increase the force of cardiac contraction. If
the latter effects balance each other it may be possible to obtain in this
way the purest and most intense action in slowing of the pulse.
It is certain that the simultaneous use of two drugs having certain actions in common
often brings about an effect not obtainable with either drug alone; but since the reaction
against the polypharmacy that reigned during the middle of the last century, the tend-
ency has been toward the use of single drugs. There is no doubt that much can be learned
in the treatment of cardiac diseases by judicious combinations along the lines mapped out
by pharmacological experiments, just as is now found with hypnotics, analgesics, and
purgatives. This is radically different from the ancient polypharmacy, in which hetero-
geneous drugs were mixed without regard to their action or antagonism.
ADRENALIN.
Adrenalin (suprarenin, epinephrin) , the active principle of the
suprarenal gland, is also used occasionally to raise blood-pressure by its
constricting action upon the peripheral blood-vessels and slight stimulating
action upon the heart, but its action lasts only from one to two minutes
and hence it is of little value, except to tide over a sudden failure until
some other drug can become active.
ERGOT.
Ergot has been recommended by some writers for its vasoconstrictor
action exerted through stimulation of the vasomotor centre. It also stimu-
lates the vagal centre. Cronyn and Henderson have found that these effects
are very uncertain when the drug is given by mouth, but occur quite uni-
formly when it is given intravenously. Since this is rarely necessary, the
use of ergot may be confined to patients with vasomotor failure, in which,
like adrenalin, it is used as a last resort.
NITRITES AND NITROGLYCERIN.
PREPARATIONS. (PHARMACOPCEIAL, U. S. P.)
Amyl nitrite (amylis nitris), a liquid containing about 80 per cent, of amyl nitrite.
Average dose 0.2 c.c., 3 minims (inhaled). Usually to. be had in pearls, each pearl contain-
ing one dose.
Nitroglycerin CH2ONO2
CHONO2
CH2ONO2
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 187
is sold in tablets of varying size, usually one tablet containing ^ gr. (0.6 mg.). How-
ever, in tablet form the nitroglycerin is liable to undergo more or less rapid deterioration,
and hence administration in this form is unreliable. It is best given as spiritus glycerylis
nitratis (spiritus glonoini), a 1 per cent, solution of nitroglycerin in alcohol, which should
be freshly prepared from a 10 per cent, stock solution. Initial dose 0.05 c.c. (1 minim),
increasing if necessary 1 minim at a time.
Sodii nitris (sodium nitrite), NaNO2, a white fused mass, very deliquescent and
slowly becoming oxidized to sodium nitrate on exposure to the air, thus becoming
useless. Dose 0.06-0.12 Gm. (gr. i-ii).
There are also several non-pharmacopceial nitrates which are very
satisfactory. Erythrol tetranitrate, CH2ONO2-CHONO2-CHONO2-
CH2ONO2, has about the same action as nitroglycerin, except that it acts
more slowly (action lasting three to four hours) . Sold as tablets, each con-
taining .03 Gm. (i gr.). Dose one or two tablets every four to six hours.
In the cases in which the writer has used it erythrol tetranitrate has been
very efficient and satisfactory.
ACTION OF THE NITRITES.
In practical therapy the nitrites are drugs of great importance. In
animals they are found to act upon the muscles and nerves of the blood-
vessels to bring about an intense vasodilatation, thereby diminishing the
resistance to blood flow and lessening the resistance to the action of the
heart. As far as can be judged from the studies of O. Loeb, they do not
influence the vasoconstrictors of the coronary arteries unless present in
concentration which is absolutely toxic
to heart muscle. G. S. Bond has found . - MIN. HOURS
that the outflow through the coronary
veins of normal dogs is decreased rather
than increased by nitroglycerin and
amyl nitrite. It is therefore question-
able whether these drugs ever bring
about dilatation of the coronary arte-
ries, as has been supposed from their no. 133.— Effect* of drugs of the nitrite
fiflRpQnv in ano-irm rkAr>tr»ri<a series upon the blood-pressure in man. (Schema
jmcacy in angina pe< representing the findings of Hewlett and Mat-
The relation of the various nitrites thews.) MIN, minutes,
to one another as regards rapidity
of action is shown in Fig. 133. The effect of amyl nitrite sets in within
a minute and passes off within five minutes; that of nitroglycerin lasts
from about the seventh to the twentieth minute after administration,
sodium nitrite from the fifteenth to the thirty-fifth, while erythrol tetrani-
trate begins to exert an effect only after about fifteen to thirty minutes,
but this continues for three to four hours.
Amyl Nitrite.— Hewlett has recently made a careful clinical study of the effects of
amyl nitrite inhalation, and found, (1) an immediate fall of maximal pres-
sure, average 13 mm. Hg, lasting less than forty seconds, and accompanied by a less
fall of minimal pressure and an increase of pulse-rate. This is followed by a second-
ary rise (about 28 mm.) of maximal pressure to considerably above the original height,
accompanied by a less marked rise of the minimal pressure and by a return of pulse-rate
to the normal. These changes in blood-pressure correspond to an increased sys-
tolic output and increased force of heart -beat (augmentor effect), and Hewlett was
able to see with the fluoroscope that, "as the action of the heart slowed down the excur-
188
DISEASES OF THE HEART AND AORTA.
sions of the left ventricle became wider by one-half centimetre, but they soon returned to-
normal." In other words, besides being a vasodilator amyl nitrite is a very
active cardiac stimulant, more rapid than any except adrenalin. These
findings accord well with the results of Cameron on dogs, that nitroglycerin both
increases cardiac output and cardiac tonicity to a marked degree.
Relaxation of the peripheral blood-vessels under the influence of the amyl nitrite, as shown
by the plethysmograph, was present throughout all Hewlett's experiments in spite of the
peculiar variations of blood-pressure. The vasodilatation reaches its maximum within
the first minute and very gradually subsides after the second, but a definite effect is still
noticeable ten or twelve minutes after. In older persons Hewlett found that the pulse-
rate often did not change, probably owing to the absence of the tonic activity of the vagus.
The following represent typical effects in normal men as obtained in
the very careful clinical investigations of Hewlett and Matthew.
Dose.
Time when
action begins.
Average
fall in B.P.
Maximal
fall
occurs in
Duration.
Amyl nitrite (Hewlett)
15 sec.
20
1 min.
10 min.
Nitroglycerin 05 — Ice (gr i~ij)
1 min
28
4A- min
i hr
Sodium or potassium nitrate .15 Gm. (gr. ij) . .
Erythrol tetranitrate .03-.06 Gm. (gr. $-i)
Manitol tetranitrate 06 Gm (gr. i) ....
5 min.
5^ min.
12
32
35
35
14 min.
22 min.
100 min
Nitroglycerin. — As to nitroglycerin, there is tremendous variation in its effects upon
different individuals, A. Loeb having reported a case of collapse after 0.6 mg. (Tfo gr.),
whereas J. Stewart has given 20 grains a day to a single patient.
In some cases it is impossible to obtain a fall of pressure with any ordinary doses.
The writer's experience agrees with that of Matthew, that the effects are often lacking in
cases of nephritis in which high blood-pressure has persisted for some time. To this might
also be added a certain group of arteriosclerotics in which the renal symptoms do not pre-
dominate, although it is possible that arteriosclerotic changes may be present in the kidney.
In Prof. J. O. Hirschfelder's wards it was customary to begin with a
dose of 1 gtt. (-^V c.c., J minim) every half hour, increasing 1 gtt. at every
third dose until palpitation, headache, or buzzing in the ears warned that
the physiological limit had been reached. The next dose was then omitted
and a permanent dosage of 1 gtt. less than the dose last given was then
kept up. In some cases as much as 1 c.c. (15 minims) of the 1 per cent,
solution was given every half hour with only the mildest subjective symp-
toms, the average permanent dose being 0.3 to 0.6 c.c. (5 to 10 minims).
The effect of these doses is very variable.
Effect on the Circulation. — A fall in minimal blood-pressure is the
most constant, usually accompanied by a rise in pulse-pressure, and the
maximal pressure sometimes rising, sometimes falling. Hewlett thinks that
there is combined dilatation of the blood-vessels and increased systolic out-
put of the heart. In a series of observations upon the fluctuations of blood-
pressure after the administration of these drugs, made with the Erlanger
apparatus independently of and some years before those of Hewlett, the
writer had noticed effects quite similar to those above mentioned. There
seems no doubt, therefore, that, as stated by Hewlett, the beneficial effects
of the nitrites in man are due to something more than a simple vasodilata-
tion, and indeed it is possible that the latter may play often even a minor
THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 189
role. Certain it is that in many cases they are ideal drugs to relieve the work
of the heart over short periods when the blood-pressure is not already too
low to admit of their use. However, it must be borne in mind that indi-
vidual susceptibilities vary, and the patient should be tested with amyl
nitrite, whose effects can be controlled, before any other nitrite should be
given. When used over long periods of time, moreover, the production
of methaemoglobin in the blood may be brought on (shown by the spectro-
scope, or by a chocolate tint in the blood), which is distinctly harmful and
a sign for immediately stopping the use of the drug.
POTASSIUM IODIDE.
Potassium iodide is the drug which is most widely used in the treat-
ment of all forms of arteriosclerosis, and the clinical results are
so definite as to render its usefulness certain. The manner in which it
exerts this beneficial action is, however, much less definitely known. It
was at first supposed by Potain and others to lower the blood-pressure by
some direct action upon the vasomotor or cardiac mechanisms, but this
action is slight if any, and the writer does not recall ever having seen high
blood-pressure depressed by potassium iodide without the intervention of
some other factor. It was then supposed to have some effect in diminish-
ing the viscosity of the blood, as was claimed by Otfried Miiller and Jnada
in Romberg's clinic. A careful persual of their statistics shows that the
results were absolutely negative in about half of their cases and within the
limits of observational error in the others. Determann, who repeated their
•experiments, found the effect upon viscosity entirely negative.
It was then claimed by Koranyi and others that potassium iodide pre-
vented the production of adrenalin arterionecrosis, but this claim also fell
to the ground when tested upon a very large series of animals by Leo Loeb
and Githens.
The pharmacological action of potassium iodide is therefore still to
be classed among those mysterious actions termed "alterative."
Some light is thrown upon the action of potassium iodide by the recent studies of
Collins and Sachs and Longcope upon the vascular changes due to syphilis. These ob-
servers obtained a positive Wassermann reaction in many cases of aortic insufficiency
in which there was no other sign of active luetic lesion. In these cases and also in simple
arteriosclerosis of luetic origin, the potassium iodide probably facilitates the removal of
the luetic exudations and thus diminishes the ill effects of the arterial lesion. This would
explain why no action can be detected upon the healthy vessel or upon the mechanical
factors in the circulation.
It must be admitted that the mode of action is entirely unknown; but, on
the other hand, administration of potassium iodide does lessen the symp-
toms of stenocardia and other painful and disagreeable sympto/ns in many
cases of arteriosclerosis, and may even cause them to disappear permanently.
It may therefore be administered with advantage in all cases in which the
above-mentioned symptoms arise or even where they are threatened.
Potassium iodide is best given after meals in large amounts (half
glassful or glassful) of water or milk. The unpleasant taste may be dis-
guised by a little sherry, elixir of calisaya, or gentian. Dose potass, iodi
0.3 to 2.0 Gm. (gr. v to xxx) (reached by increasing doses).
190 DISEASES OF THE HEART AND AORTA.
When not well borne by the stomach or when the heart is very weakr
sodium iodide, the iodized fatty acid "iodipin," or new iodized organic
acid "sajodin" may be substituted. Their action does not seem to differ
much from that of potassium iodide.
POTASSIUM THIOCYANATE.
Another drug which tends to lower the blood-pressure greatly is potassium thiocya-
nate (KCNS). The use of this drug as a sedative to the nervous system was first suggested
by W. Pauli (1903), who believed that he obtained some excellent results in eleven arterio-
sclerotics and in two cases of heart failure. It was used more carefully by J. Pal (1905),
who writes: "I have been able to obtain a good effect from thiocyanate preparations in
some cases in which even potassium iodide was without effect. This cyanate often grad-
ually reduces a high blood-pressure, but often brings on symptoms of intox-
ication in arteriosclerotics, especially in those with renal complications. These toxic
symptoms are erythemata and mental confusion, which disappear, as I
have found, when the thiocyanate is left off and opium given. . . . Diuretin and iodide or
thiocyanate are of value (in vasomotor crises) only when administered over long periods."
BIBLIOGRAPHY.
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Schmiedeberg, O.: Untersuchungen ueber die pharmakologisch wirksamen Bestandtheile
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THE EFFECTS OF DRUGS IN CARDIAC DISEASE. 191
DlGITOXIN.
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Ueber die Kumulativwirkung des Digitalis, ibid., 1906, liii, 2281.
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Fraenkel, Alb.: Abhandlungen zur Digitalistherapie. II. Zur Frage der Kumulation,
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DIGITALIN.
Kiliani: Archives de Pharmacie, 1892-1899.
Deucher: Ueber die Wirkung des Digitalinum verum bei Cirkulationsstorungen, Deutsch.
Arch. f. klin. Med., Leipz., 1896, Ivii, 1. Vid. also Fraenkel, cited above.
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Fraser: The Action and Use of Digitalis and its Substitutes, Brit. M. J., Lond., 1885, ii,
904. Note on Tincture of Strophanthus, ibid., 1887, i, 151.
Popper: Ueber die physiologische Wirkung des Strophanthins, Zeitschr. f. klin. Med.,
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Fraenkel, Alb., and Schwarz: Ueber intra venose Strophanthintherapie bei Herzkranken,
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Hering, H. E.: Ueber kontinuierliche Herzbigeminie, Deutsches Arch. f. klin. Med., Leipz.,
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Da Costa, v. Ley den, see page 128.
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Janeway, T. C.: The Use and Abuse of Digitalis, Am. J. M. Sc., Phila. and N. York, 1908,
cxxxv, 781.
STRYCHNINE.
Heinz, R.: Lehrbuch, quoted on page 172.
Cook, H. W., and Briggs, J. B.: Clinical Observations on Blood-pressure, Johns Hopkins
Hosp. Rep., Bait., 1903, xi, 451.
Cabot, R. C.: Measurements of Blood-pressure in Fevers before, during, and after the
Administration of Strychnine, Am. Med., Phila., 1904, viii, 31.
Drayer, F. P.: Personal communication.
Eyster, J. A. E.: Personal communication.
CAMPHOR.
Heubner: Ueber die Wirkung des Kampfers auf die Leistung des Froschherzens, Arch.
d. Heilk., Leipz., 1870, xi, 334.
Harnack and Witkowski: Pharmakologische Untersuchungen ueber das Physostigmin
und das Kalabarin, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1876, v, 401.
Maki : Ueber den Einfluss des Kampfers, Kaffeins, und Alkohols auf das Herz, In. Diss.,
Strass., 1884.
192 DISEASES OF THE HEART AND AORTA.
Passler, H. : Experimentelle Untersuchungen ueber die allgemeine Therapie der Kreislaufs
storungen bei acuten Infektionskrankheiten, Deutsch. Arch. f. klin. Med., Leipz., 1899,
Ixiv.
Winterberg, H.: Ueber die Wirkung des Kampfers, Arch. f. d. ges. Physiol., Bonn, 1903,
xciv, 455.
Seligmann: Zur Kreislaufwirkung des Kampfers, Arch. f. exper. Pathol. u. Pharmakol.,
Leipz., 1905, lii, 333.
Gottlieb, R., and Sahli, H.: Herzmittel und Vasomotorenmittel, Verh. d. XIX Kong. f.
innere Med., Wiesb., 1901.
ACONITE.
Matthews, S. A.: A Study of the Action of Aconitin on the Mammalian Heart and Cir-
culation, J. Exp. Med., Baltimore, 1897, ii, 593.
Da Costa, J. M.: On Irritable Heart, Am. J. M. Sci., Phila., Ixi, 17.
Hirschfelder, A. D.: Observations upon Paroxysmal Tachycardia, Bull. Johns Hopkins
Hosp., Bait., 1906, xvii, 337.
CAFFEINE.
Wagner: Experimentelle Untersuchungen ueber den Einfluss des Kaffeins auf Herz und
Gefassapparat, In. Diss., Berl., 1885.
Glupe: Ueber die Wirkung der Kaffeinsalze bei Herzkrankheiten, In. Diss., Berl., 1884.
Cushny and van Naten: On the Action of Caffein on the Mammalian Heart, Arch. int. de
Pharmacodyn., 1901, ix, 169.
Cushny, A. R.: A Contribution to the Pharmacology of the Mammalian Heart, Brit. M.
J., 1898, i, 1068.
Fraenkel: Klinische Untersuchungen ueber die Wirkung von Kaffein, Morphium, Secale
cornutum und Digitalis auf den arteriellen Blutdruck, Deutsch. Arch. f. klin. Med.,
Leipz., 1889-90, xlvi, 542.
Bock: Ueber die Wirkung des Kaffeins und Theobromins auf das Herz, Arch. f. exper.
Pathol. u. Pharmakol., Leipz., 1900, xliii, 367.
CALCIUM SALTS.
Brunton, T. Lauder: Use of Calcium Salts as Cardiac Tonics in Pneumonia and Heart
Disease, Brit. M. J., 1907, i, 616.
Stark, J.: Calcium Salts as Cardiac Tonics, Lancet, Lond., 1907, i, 1701.
Barr, J.: On the Use of Calcium Salts as Cardiac Tonics in Pneumonia and Heart Disease,
Brit. M. J., Lond., 1907, i, 717.
Sladen: Personal communication.
Boggs, T. R.: Variations in the Calcium Content of the Blood following Therapeutic
Measures, Johns Hopkins Hosp. Bull., Baltimore, 1908, xix, 201.
NITRITES.
Brunton, T. L. Quoted on page 184.
Hewlett, A. W.: The Effect of Amyl Nitrite Inhalations upon the Blood-pressure in Man,
J. Med. Research, Bost., 1906, xv, 383.
Cameron. Quoted on page 145.
Matthew: Vasodilators in High Blood-pressure. Quart. J. M., Oxford, 1909, ii.
Loeb, A.: Klinische Untersuchungen ueber den Einfluss von Kreislaufsaenderungen auf
die Urinzusammensetzung, Deutsches Arch. f. klin. Med., Leipz., Ixxxiv, 579.
Stewart, J.: Tolerance to Nitroglycerin, J. Am. M. Ass., Chicago, 1905, xliv, 1678.
POTASSIUM IODIDE.
Potain: La clinique medicale de la Charite, Par., 1894.
Miiller, O., and Inada: Zur Kenntniss der lodwirkung bei der Arteriosklerose, Deutsche
med. Wchnschr., Leipz., 1904, xxx, 1751.
Determann. Quoted on page 40.
Koranyi, Loeb and Githens. Quoted on page 189.
POTASSIUM THIOCYANATE.
Pauli, W.: Ueber lonenwirkung und ihre therapeutische Verwendung, Muenchen. med.
Wchnschr., 1903, 1, 153.
Pal, J.: Die Gefasskrisen, Leipz., 1905.
VI.
GYMNASTICS AND HYDROTHERAPY.
GYMNASTICS.
FUNDAMENTAL PRINCIPLES.
During recent years gymnastic exercises have come to play a major
role in the treatment of cardiac diseases. Although this treatment was
introduced empirically, its physiological basis is found in the fact, shown
by Frank and Hirschfelder, that a strain upon the ventricles which does
not exhaust them tends to act as a stimulus which gives rise to more forci-
ble contractions, increases their tonicity, and causes the residual blood
(and hence the dilatation) to decreas'e. The guiding principle is further
given by the experimental evidence produced by these writers, that when
the strain was excessive it had the opposite effect, and caused weakening
of the contractions, diminished tonicity, and dilatation of the heart. (See
Fig. 119, page 136.)
In dealing with normal individuals it is observed that the strengthen-
ing of every normal individual, the training of every athlete or laborer con-
sists in the habituation of the body, and particularly of the heart, to gradu-
ally increasing muscular effort and exercises. (See page 198.) To a great
extent, as has been seen, page 129, this consists in securing a greater increase
in output of blood at each beat without calling upon any of the accessory
nervous mechanism to bring this about. Such exercises have also been
used with great success in the treatment of patients with heart failure. It
stands to reason that they should not be used at once when the patient is
brought in with an acute heart failure; but after a sufficiently long period
of rest, when the acute condition has passed off and he can sit up in bed
without discomfort, a few of the mildest arm movements may be begun
with great advantage. It is often better to train the patient by a few mild
passive or resisted movements while he is still in bed than to subject
him at once to the strain of getting up for an hour or so after his sojourn
in bed. Moreover, many other muscles may be kept in tone, the blood-
vessels in the muscles may be kept dilated, and the resistance to blood
flow may thus be diminished.
SYSTEMS OF EXERCISE.
In accordance with these facts several systems of exercises have been
developed for assisting in the training of the heart. In all of them the cru-
cial point lies in the avoidance of the slightest fatigue, holding of the breath,
or increased breathing. Hence the actual result obtained depends more
upon the vigilance and intelligence of the physician, nurse, or attendant
who supervises the exercises than upon the exercises themselves.
13 193
194 DISEASES OF THE HEART AND AORTA.
In general the exercises may be divided into four classes:
(1) Passive movements.
(2) Contraction of antagonistic muscles.
(3) Resisted movements.
(4) Mechanical gymnastics.
Passive Movements. — These are the mildest possible forms of exercise.
The attendant grasps the patient by the hands or feet and moves these
members gently and slowly about, while the patient makes no effort at
contraction whatever. Such movements have the effect of increasing
the circulation of lymph, the absorption of oedema, and, to a
certain extent also, of increasing the rapidity of blood flow. It is impor-
tant to avoid all exercises in which the arms are raised high above the
head, since this hydrostatically increases the pressure in the vena cava and
may cause momentary dilatation of the heart.
The following exercises or modifications of them may be carried out
while the patient is still in bed, provided the greatest precaution is used
in their execution.
(1) Arms horizontal, to the front and back to the line of the shoulders.
(2) Arms horizontal in line of shoulders, thence down to the sides of the body.
(3) Arms horizontal, describe circles with hands.
(4) Arms vertically, dependent at sides, flex and extend elbows.
(5) Arms dependent at sides, pronate and supinate alternately.
(6) Clinch and open fists.
(7) Legs straight, abduct; then adduct thighs.
(8) Flex and extend knee at side of couch, never raising knee above level of body.
(9) Flex and extend foot at ankle-joint.
(10) Rotate thighs internally and externally.
(11) Execute small circles with feet without raising them more than one foot; legs
straight.
Contraction of Antagonistic Muscles. — Substantially the same exercises
may be carried out by allowing the patient himself slowly and simultane-
ously to contract both the muscles concerned in the movement and those
which antagonize them, — i.e., biceps and triceps, flexors and extensors of
wrist, etc. In this way little movement is made, the pulse-rate is slowed
rather than accelerated, and yet a good deal of energy may be expended.
The blood-pressure is raised, however. If the patient can be trained to
avoid all difficulty in breathing and all discomfort, a good deal of improve-
ment in muscular strength and in cardiac tonicity may be obtained by
this method. Its main drawback lies in the fact that the intensity of the
exercise is controlled not by the attendant but by the patient, and that
the latter is most likely to do more than is beneficial.
RESISTED MOVEMENTS. (SCHOTT MOVEMENTS.)
Probably the most widely used of all the cardiac gymnastics are the
passive movements introduced by August Schott of Nauheim. These are
generally used in connection with the Nauheim baths. This combination
is particularly advantageous and permits at once of all the advantages
of mild exercise, of baths, of rest and stimulation to sleep, of psychic
sedative, and of the psychic suggestion to the patient that a great deal is
being done and a great effort is being made for his welfare.
GYMNASTICS AND HYDROTHERAPY. 195
The Schott movements consist of practically the exercises described
above carried out by the patient himself, but with an attendant who makes
a slight resistance to each movement. The resistance should be just enough
to prevent the movement from being made rapidly, and at no time should
it cause the patient any apparent effort or increase his respirations. Each
day the resistance may be increased slightly, so that in a short time the
patient may be doing a good deal of work without realizing it. In exe-
cuting the resistance the attendant's mind is kept fixed upon the condition
of the patient, and he is consequently more likely to notice over-exertion
in the latter than if he were merely supposed to watch him without doing
anything himself. In carrying out the Schott movements the following
rules are prescribed.1
Precautions for Schott Exercises. — (1) Each movement is to be performed slowly
and at uniform rate.
(2) No movement is to be repeated twice in succession in the same limb or group
of muscles.
(3) Each single or combined movement is to be followed by an interval of rest.
(4) The movements are not to be allowed to accelerate the
patient's breathing, and the operator must watch the face for the slightest
indications of (a) dilatation of the nostrils, (6) drawing of the corners of the mouth, (c)
duskiness or pallor of the cheeks or lips, (d) yawning, (e) sweating, (/) palpitation.
(5) The appearance of any one of the above signs of distress should be the signal
for immediately interrupting the movement in process of execution, and for either sup-
porting the limb which is being moved or allowing it to subside into a state of rest.
(6) The patient must be directed to breathe regularly and
uninterruptedly, and, should he find any difficulty in doing s\>, or for any reason
show a tendency to hold his breath, he must be instructed to continue, counting in a
whisper throughout the progress of each movement.
(7) No limb or portion of the body of the patient is to be so constricted as to compress
the vessels and check the flow of blood.
Schott Exercises. — The following is a list of Schott exercises in the
order in which they are given. The resistance is moderate and steady, the
operator's hand always being applied upon the surface of the extremity
toward which the movement is made, even if that entails gliding around
it gently during the movement. Usually the operator's hand is at one side
of the patient's limb at one phase of the exercise and at the opposite when
the movement is reversed.
1. Arms extended in front, palms facing each other. The operator's palms rest upon
the backs of the patient's hands. Patient's arms carried backward to line of shoulders,
the movement being gently resisted by operator (Fig. 134). The operator's palms are then
rested against those of the patient, and the return of the arms in front of the chest is re-
sisted.
2. One arm at side, elbow-joint flexed upward to shoulder, then extended to original
position.
3. Arms at side, raised outward till thumbs meet over the head, then brought back
to the original position.
4. Hands at level of pelvis in midline, fingers slightly flexed. Arms raised to the
vertex of the head, then back.
5. Arms at sides, then raised forward in parallel planes until they are vertical, then
moved back. The hand of the operator must glide around the wrist so that it is always
applied to antagonize the movement.
1 Quoted from W. Bezly Thome.
196
DISEASES OF THE HEART AND AORTA.
6. Trunk flexed on hips, knees straight; trunk then extended.
7. Trunk rotated without movement of the feet. Operator exerts resistance against
the shoulders.
FIG. 134.— Schott resisted movements. (Modified from W. Bezly Thorne.) The attendant's hands are indi-
cated in black; the direction of the movement made by the patient is indicated by the black arrows.
8. Trunk flexed laterally, first to one side then to the other, the movement being an-
tagonized by resistance applied in the axilla, the operator's other hand resting on the hip.
9. Movement like No. 2; fists clinched.
10. Same, but palmar surface of fist turned outward.
11. Arm extended from side, palm down, raised forwards and upwards describing
a semicircle until it is raised vertically along side of the ear. The movement is then reversed.
GYMNASTICS AND HYDROTHERAPY.
197
12. Arms at sides, palms inward, moved upwards and backwards in parallel planes.
13. Patient rests one hand on chair or table, raises knee to horizontal, flexing at hip
and knee.
14. With one hand resting on table, patient swings extended leg forward and back-
ward from the hip-joint.
15. Resting with both hands on chair in front, raises foot by flexing knee without
movement at hip.
16. Resting one hand on chair at side, patient swings opposite extended leg out-
ward from hip-joint, then returns to normal.
17. Arms rotated outwards and inwards from shoulder-joint, operator grasping the
metacarpal portion of the hand.
18. Wrist-joint flexed and extended.
19. Ankles dorsoflexed and extended alternately.
When these precautions are taken the exercises have an excellent
effect in a considerable number of cases, bringing about relief of the dilata-
tion and more or less immediate improvement (increased tonicity). An
example of this is shown in Fig. 135, illustrating the diminution in the
cardiac shadow under the X-ray after
a very few resisted movements. On
the other hand, there is the greatest
danger that the treatment will be ap-
plied in cases where it could not have
been expected to do good and where
it actually does harm, producing over-
strain and decreased tonicity of the
cardiac muscle.
MECHANOGYMNASTICS.
Movements may also be carried
out by means of the elaborate and
ingenious apparatus devised by Z an -
d e r for regulating them in direction
and intensity. In these exercises the
movements are semi-passive, being
determined to a great extent and car-
ried on by the apparatus. Hence it
becomes more difficult to control
them accurately than is the case with the resistance movements. It is
unquestionable that excellent results have been obtained by this method,
especially in cases where there is mild dilatation but no serious heart
lesion; but it is certain that the limits of the patient's strength are too
readily overstepped; and equally certain that, in the large institutions
where this is carried out, the superintendents usually pay so little atten-
tion to the individual patient that these exercises very frequently do dis-
tinct harm.
FIG. 135. — Orthodiagraphic outline of a
patient with dilated heart, showing the effect of
Schott movements. (After W. Berly Thorne.)
Solid line, outline before treatment; broken line,
outline after resisted movements.
WALKING AND CLIMBING.
The question of walking involves not only an important form of exer-
cise treatment but also the regulation of the convalescent's daily life. As
has been stated above, walking up and down stairs frequently introduces
198 DISEASES OF THE HEART AND AORTA.
the greatest strain upon the patient's heart. It is most important that this
strain should be minimized. This may be done by causing him to rest upon
each step long enough to count five, ten, or twenty, thus insuring him against
hurry and breathlessness (J. O. Hirschfelder) . Another method which has
been found useful was suggested by the writer's wife while climbing moun-
tains in the Sierra Nevadas. She noticed that she could climb quite steadily
up the steepest trails provided she took a deep or normal inspiration each
time the same foot touched the ground. In this way a relation was estab-
lished between speed and respiration, the former was regulated by the
latter, and a certain balance maintained between the rate at which oxygen
was used up and that at which it was supplied. As the pulse-rate is often
some definite multiple of the respiratory rate, this procedure also tends to
regulate the former. This rhythm is one which is very satisfactory for
patients with heart disease. It is readily acquired, and, having once
become habitual, does much, automatically, to keep the patient within his
physiological limits, thus enhancing the beneficial effect of the exercise
while establishing a safeguard against overstrain.
Oertel's Mountain Climbing. — Long walks and mountain climb-
ing were introduced as an after-treatment in cardiac disease by O e r t e 1 .
Oertel found that patients convalescent from heart failure, and especially
those suffering from fatty infiltration of the heart, were much benefited
by long walks taken slowly, interrupted by frequent rests. Walks along
gradually sloping paths in the mountains were most beneficial, and in fact
became a feature of the method. This is designed, however, only to put
the finishing touches upon the treatment, and to fit the patient whose heart
is already in good working order for the more strenuous life to be pursued
after his discharge.
CHOICE OF EXERCISE.
As regards the choice and use of exercise in treatment, the following
general principles may be laid down:
(1) No exercise should be begun until the patient has been under
observation for a few days, so that his general condition is thoroughly
understood.
(2) If the patient is not improving under absolute rest, exercises
would only increase the work imposed upon the heart and would do harm.
(3) If the patient has improved under absolute rest, he may be given
one or two passive movements (each carried out five or ten times) two or
three times a day, and the exercises very carefully increased in number
and intensity each day before allowing him to get out of bed. Even a few
mild resisted arm exercises may be tried, bearing in mind the same princi-
ples, for it must be remembered that the patient may obtain much more
complete and immediate rest after these exercises while in bed than when
out of it, and also that he is not at the same time subjected to the strain
of standing.1
1 The relative mildness of such exercises in patients still bed-ridden is seen in the
fact that their pulse-rate and respiration return at once to normal on cessation of the exer-
cise. Physiologically, to exercise in the horizontal posture increases the systolic output
more and changes the pulse-rate less than in the erect posture (Erlanger and Hooker).
GYMNASTICS AND HYDROTHERAPY. 199
Once out of bed the patient should at first be given a day or two of
complete rest to accommodate himself to the new position. Then he may
be allowed to begin gradually with a few of the resisted movements, if a
competent attendant or physician can supervise them; if this is not avail-
able, he may be allowed to practise a few exercises in contracting antago-
nistic muscles (Selbsthemmungsbewegungen) , at first under the direction
of the physician, later under the observation of a skilled attendant, or of some
reliable member of the family who has been carefully instructed in the pre-
. cautions given above. About this stage the bath treatment may be begun.
(4) Mechanical gymnastics (with the Zander apparatus or modifica-
tions thereof) can be recommended only when supervised by persons of
great experience and excellent judgment.
Training at End of Treatment.— (5) When the patient has recovered
somewhat, but not sufficiently to withstand the wear and tear of daily
life, he should be encouraged to take short walks, gradually lengthening
the space covered, at first about the hospital grounds, later about the
city or country, keeping records of the distance traversed each day. He
may then be allowed to walk up hill. Pari passu with this the resisted
or antagonized movements and the baths should be given. Before dis-
charging the patient, he should be compelled to take some regular gym-
nastic exercises every day and made to do work at least as strenuous as
that which will form the routine of his daily life after passing from under
the physician's care. It is no more fair to the convalescent to put him
directly back from the sedentary life of the bedroom or the hospital to the
deadly struggle for existence outside than it would be to match the average
citizen against a prize-fighter. He must be gradually trained for the effort.
This principle was very well recognized by da Costa during the Civil War.
Before sending his patients back to their regiments where they were subject
to heavy field duty, forced marches, etc., he kept them at lighter duties
about the hospital, upon local guard duty, etc., and from time to time
during this period subjected them to tests of increasing severity (running
races, etc.) until he was quite certain of their ability to stand the strain.
The magnificent results which he reports from his large series of cases
treated under otherwise unfavorable conditions constitute a fitting monu-
ment to one of America's greatest clinicians, and merit the careful study
of all who would learn how cures should be obtained in heart diseases.
Treatment and Occupation. — On the other hand, the training to which
the patient need be subjected should be suited to the life that he leads. It
would be unnecessary to train a clerk in a store up to the point of muscular
strength that is necessary for the ordinary laborer. But it is necessary
that he should not be exhausted by a few hours' standing lest the cardiac
overstrain return. On the other hand, when restitutio ad integrum has not
been possible, the patient's life must not be the same as it was before his
illness. His work must be cut down. This may often be done in the more
well-to-do without changing the business by employing assistants to attend
to all except the more essential affairs. Poorer persons must change their
occupations. It is as much the duty of the physician to see
that this is done after the recovery as it was his duty
during the height of the illness to give correct treat-
200 DISEASES OF THE HEART AND AORTA.
m e n t . Otherwise he has merely prepared the patient for another break-
down. The difficulty in finding suitable occupation and the acumen neces-
sary in meeting changed conditions increase rather than decrease the
responsibility of the physician in this regard. He must see to it that, as
stated by Professor Osier, " the patient must always live within his income
of cardiac energy." His mode of life, and especially the speed of his move-
ments and the intensity of his efforts, should be so regulated that he no
longer feels at any time palpitation, shortness of breath, or precordial pain.
HYDROTHERAPY IN THE TREATMENT OF HEART DISEASES.
Although the healing power of mineral springs and baths was thought
by the older physicians to be well-nigh universal, the scientific application
of hydrotherapy to heart disease is due largely to the studies of a small
group of men at Bad Nauheim, Germany. Benecke, in 1870, noted the
favorable action of baths at this watering-place, but it is to August Schott
that is due the real credit for introducing into cardiac therapy what is
really a very valuable method of treatment.
PHYSIOLOGICAL ACTION OF BATHS.
Physiologically it'has been found, especially by Erlanger and Hooker,
and a little later by Jacob and Strasburger, that all baths given at about
the temperature at which the body neither gives off nor loses heat (92° F.,
33° C.) increase the pulse-pressure and slow the pulse-rate. Strasburger
found this to be particularly true as regards baths of the same composition
as those at Nauheim, or indeed any other baths in which CO2 is effervescing;
and ascribes this action to the dilatation of the vessels in the skin over the
whole body, as well as to the cardiac reflexes from stimulation of the sensory
nerves by the prickling sensation of the CO2. These effects in themselves
would be sufficient upon a priori grounds to indicate a probable value of
such baths in weakened hearts. Schott's treatment has, however, long
antedated these explanations. Schott, Thorne, Schminke, and a host of
other observers have demonstrated that the area of cardiac dulness and
the X-ray shadow of the heart diminished after such a bath (cardiac tonicity
increased) .
An excellent treatise of his results and those obtained by other ob-
servers is given in extenso in English in the monograph of W. Bezly Thorne,
to which the reader is referred for details of the method. Other excellent
accounts are given by Satterthwaite, P. K. Brown, et al.
PRECAUTIONS.
The baths should not be given to patients who are in the extreme
stages of cardiac break-down, nor indeed to any very weak patients, until
they have been prepared for the slight strain which accompanies them by
some course of mild exercises, preferably resistance exercises (see page 195).
They should never be taken less than one or two hours after a light meal
or four to five hours after a heavy one, and, on the other hand, should not
be given upon an absolutely empty stomach.
GYMNASTICS AND HYDROTHERAPY. 201
NATURAL AND ARTIFICIAL NAUHEIM BATHS.
The Nauheim baths are obtained from several mineral springs of different com-
position. A course of baths is begun in the Great Sprudel (composition H2O 1000, NaCl
2.18, KC1 0.5, CaCl2 1.7, MgCl2 0.4, calcium bicarbonate 2.3, CO, 3.17; temperature 31.6° C.,
88.8° F.), most of the CO2 being allowed to escape before immersion of the patient.
The effect of the Nauheim baths can be imitated at home or in the hospital by add-
ing the same salts to the water in the bath-tub. A great variety of such artifi-
cial Nauheim salts are on the market, put up in packages ready for use. The
most satisfactory known to the writer1 contains:
Grammes. Pounds. Per cent.
Sodium chloride 3500 8 2.2
Calcium chloride (magnesium chloride) 900 2 0.53
Sodium bicarbonate 800 1 -J 0.1
Sodium bisulphate yielding CO2 1000 2J 0 . 29
In order to prevent the bisulphate from injuring the tub it is advisable to cover the
walls and floor of the latter with a large sheet of rubber cloth about 6 x 8 ft. in size. The
bath is filled with warm water, 90°-95°F. (a good-sized bath requires 40 to 45 gal. — 150 to
175 litres) and the salts added — first the sodium chloride, then the calcium chloride, then
the sodium bicarbonate, and lastly the acid sulphate (NaHCO3 + NaHSO4 = Na2SO< + CO2 +
H2O). The effervescence continues throughout the bath.
CAUTIONS IN GIVING BATHS.
In preparing the first bath it is better to begin with half
strength of the salts or even less. The patient is allowed to remain in
this bath not longer than fifteen minutes, being watched care-
fully during this time and removed at once if there is the slightest
increase in cyanosis or real discomfort of any kind — flushing,
excitement, or syncope. "The immediate effect of the first few baths is to
produce a sense of oppression at the precordium, under the influence of
which the patient breathes slowly and deeply for two or three minutes.
Respiration then becomes easy and continues slower by from two to four
breaths a minute," after which the symptoms subside. In general the effect
should be similar to that in the following case quoted from Thome :
"A patient, aged 46, whose health had been declining for years, was found to have
a pulse of 80 in the recumbent, and of 88 in the sitting, position. While he stood it varied
from 100 to 104, and if he walked ten paces it rose from 120 to 130. The apex was found
to beat an inch outside the nipple line. Within two minutes of immersion in his first
thermal bath the pulse had fallen to 70, and judged by the finger appeared to have doubled
its volume;2 at the end of four minutes it was 68, in six minutes 66, in eight minutes 68,
and while standing after the bath it was 90. Before he left the bath after an immersion
of ten minutes, the apex beat was found to have receded half an inch in the direction of
the mesial line, and nails and fingers, which had been snow-white up to the junction of
the second with the first phalanx, had assumed a healthy flesh tint. "
This healthy reaction of the skin should be present within a few minutes
after the bath. Its absence indicates that the treatment has been too
1 Put up by R. R. Rogers Chemical Co., San Francisco. This preparation is partic-
ularly useful, owing to the excellent grade of sodium bisulphate prepared and the perma-
nent and convenient form in which it is put up. Moreover, the sodium bisulphate is put up
in lumps the size of a hazel-nut, which allows the CO2 to be generated uniformly through-
out the bath.
2 Probably the pulse-pressure had actually doubled.
202 DISEASES OF THE HEART AND AORTA.
violent, too prolonged, or in other ways unsatisfactory, and unless this can
be obviated after the next bath or two the treatment should be discontinued.
After the bath the patient should be made to lie down and rest, if
possible to sleep, for at least an hour before leaving the building or doing
anything else, and upon this rest as much as anything else depends the
success of the treatment.
BIBLIOGRAPHY.
GYMNASTICS AND HYDROTHERAPY.
Herz, M.: Lehrbuch der Heilgymnastik, Berl. and Vienna, 1903.
Schott, Aug.: Zur Therapie der chronischen Herzkrankheiten, Berl. klin. Wchnschr., 1885.
Thorne, W. B.: The Schott Methods in the Treatment of Chronic Diseases of the Heart.
Nebel : Bewegungskuren mittelst schwedischer Heilgymnastik und Massage mit besonderer
Beriicksichtigung der mechanischen Behandlung des Dr. G. Zander, Wiesbaden, 1889.
Oertel: Ueber Terrainkurorte, Leipz., 1886. Ueber die chronischen Herzmuskelerkrank-
ungen und ihre Behandlung, Verhandl. d. Kong. f. inn. Med., Wiesb., 1888, v, 13.
Allgemeine Therapie der Kreislaufstorungen, 1891, 4th ed.
Beneke, F. W.: Ueber Nauheim's Soolthermen, Marburg, 1859; Weitere Mittheilungen
ueber die Wirkung der Soolthermen Nauheims, Marburg, 1861; Nauheim's Soolther-
men gegen Gelenkrheumatismus mit oder ohne Herzaffection., Berl. klin. Wchnschr.,
1870, 269.
Schott, A.: Die Wirkung der Bader auf das Herz, ibid., 1880, xvii, 357, 372.
Erlanger and Hooker, 1. c.', page 35.
Strasburger, J.: Ueber Blutdruck, Gefasstonus und Herzarbeit bei Wasserbadern ver-
schieder Temperatur und bei Solbadern, Deutsches Arch. f. klin. Med., Leipz., Ixxxii,
459.
Satterthwaite: Nauheim Methods in Chronic Heart Disease with American Adaptations,
Internat. Clin., Phila., 1903, 13 ser., i, 52.
Brown, P. K.: Artificial Nauheim Baths in Chronic Heart Cases, Boston M. and S. J., 1906,
civ, 276.
VII.
HYPERTROPHY AND ATROPHY.
HYPERTROPHY.
To enable the heart to recover from an overstrain and the consequent
dilatation, to maintain the circulation in the presence of a valvular lesion
or dilatation, or to reestablish compensation once broken, it must put forth
an increase in force. The stimulus for this seems to lie in the increase in
residual blood in the ventricle, which acts as an increase in load upon the
heart muscle, and thus tends to increase both irritability and force of con-
traction, as shown by O. Frank (see page 135), and particularly to bring
FIG. 136. — Hypertrophic, normal, and atrophic hearts. (From specimens in the Army Medical Museum,
Washington, D. C.)
about an increase in tonicity. It seems probable that this increase in
tonicity is of primary importance as a predisposing factor to hypertrophy,
and Barcroft and Dixon have shown that increased tonicity is accompanied
by an increased CO2 metabolism in the heart.
PATHOLOGICAL ANATOMY.
Changes in the Fibres. — The main visible change which the heart muscle undergoes
is a swelling of the individual fibres (Tangl, Goldenberg, Dehio, R. M. Pearce) with little
if any multiplication of the muscle-cells. Goldenberg finds that the muscle-cells in the
wall of the hypertrophic heart have a diameter of 17.65 /", in the normal heart 12.85 ft,
and in the atrophic heart 10.84 ^. The striation of the fibres also becomes less distinct,
and vacuoles appear in the sarcoplasm, changes which are similar to what is observed in
203
204
DISEASES OF THE HEART AND AORTA.
a striated muscle as the result of prolonged contraction. Ranke has shown that in skeletal
muscle these changes are due to imbibition or endosmosis of water, which, according to
the beautiful experiments of J. Loeb and his pupil, Miss Cooke, is brought about in the
following way: During the muscular contraction the more complex molecules break down
into several simpler ones, thereby increasing the number of molecules in solution in the
muscle plasma, the osmotic pressure rises, and hence brings about an endosmosis of water
into the fibres. Having once entered, the water molecules remain and the muscle swells.
There can be little doubt that the same process is going on in cardiac muscle, especially
when subjected to overwork, but no observations have actually been made upon this
phase of the subject.1
In cardiac hypertrophy three anatomical changes may be said to take
place simultaneously: (1) an increase in size of the individual muscle-
cells, but apparently no increase in their number; (2) a certain amount of
FIG. 137. — Photomicrographs of atrophic and hypertrophic heart muscle. A. Atrophic heart
muscle, showing small cells. The specimen also shows some oedema and slight mononuclear infiltration
between the muscle cells. B. Hypertrophic heart muscle showing large cells with swollen nuclei.
degeneration is almost always present in some of the muscle-cells; (3) a
proliferation of the strands of connective tissue between the bundles of
muscle-fibres (interfascicular myofibrosis, see page 234).
Dehio and Pearce have shown that each fibre may pass through the
following stages: normal -* hypertrophy -» degeneration, the latter stage
being associated with proliferation of interstitial connective tissue (myo-
fibrosis). Accordingly, we may find the heart-cells in the following con-
ditions :
(1) Normal + hypertrophied (heart somewhat enlarged; as in athletes, also in Kiilbs's
dogs).
(2) Hypertrophied -f degenerated; some proliferation of connective tissue (heart
much enlarged — cor bovinum; still strong).
(3) Degenerated. Marked proliferation of connective tissue. Marked weakness of
the heart. Large failing heart. Hypertrophy + dilatation (digitalis often harmful).
1 Fleischer and Leo Loeb have advanced the same explanation.
HYPERTROPHY AND ATROPHY. 205
Types of Hypertrophy.— Hypertrophy was supposed by Cohnhoim to
assume three types:
(1) General concentric hypertrophy, involving all the
chambers of the heart about equally.
(2) Local concentric hypertrophy, involving the walls
of one or more chambers of the heart which is subjected to extra work.
The fibres are not especially elongated.
(3) Local (excentric) hypertrophy with elongation of
the muscle-fibres, as in aortic insufficiency. The elongation of the fibres is
somewhat out of proportion to the increase in size of the heart.
The existence of these three types of hypertrophy as separate entities
was already disputed by Cruveilhier in 1833. It is probable that the size
of the cavities as found at autopsy bears no constant relation to that pres-
ent during life. Moreover, the ventricular cavities in cases of chronic
nephritis are often quite as large as those in hearts of aortic insufficiency,
though the former typifies the so-called concentric, the latter the excentric
hypertrophy.
Occurrence and Sites of Hypertrophy. — The relative frequency with
which these factors occur in cases of hypertrophy is shown in the following
statistics compiled by W. T. Howard from autopsies made in the Patho-
logical Department of the Johns Hopkins Medical School upon 108 subjects
showing hypertrophy of the heart.
Cases. Per cent.
Arteriosclerosis 65 59
Nephritis 14 13.4
Valvular lesions of the heart 13 12.4
Adherent pericardium 8 7.6
Hard work 4 3.8
Tumors 2 1.9
Aneurism of the heart wall 1 0.95
Haemic plethora 1 0 . 95
Total 108 100
The right ventricle showed hypertrophy in 70 cases (66 per cent.), of
which there were —
Arteriosclerosis (often of pulmonary artery), 52; adhesive pericarditis, 6; valvular
lesions, 8; chronic nephritis, 3; hydraemic plethora, 1.
Hypertrophy of the auricles (atria) was most marked in mitral stenosis
and adhesive pericarditis.
Strain, Exercise, and Hypertrophy. — In normal individuals the weight
of the heart is almost proportional to the weight, not of the entire body,
but of the musculature (W. Miiller, Hirsch), being relatively low in fatty
and relatively high in muscular individuals. The absolute weight of the
heart is about ^ (.0059) of the body weight in men, Ti7 (.00546) in
women. The same general principle applies in animals, the most active
animals having the largest hearts, especially race-horses, hares, etc., as
compared to less active members of the same species.
When, however, the heart is subjected to abnormal strain, especially
as the result of valvular lesion, it hypertrophies and increases in size to
dimensions which are often enormous. It is not very uncommon to find
206 DISEASES OF THE HEART AND AORTA.
hearts of twice or even three times the normal size (500 to 800 Gm., 17 to
26 oz.), and in the Army Medical Museum in Washington there is a speci-
men of one weighing 1000 Gm. (33 oz.). Another heart of 1400 Gm. (46J
oz.) has been reported. Such a heart is usually designated as a beefy
heart or cor bovinum, indicating the animal to which its size would be
proportioned.
Work Hypertrophy. — Whether a true hypertrophy occurs in a per-
fectly healthy heart has been much disputed, many writers taking the
stand with Romberg that, " though the possibility of a ' work hypertrophy '
cannot be denied, more proofs of its existence are necessary."
FIG. 138. — Heart (A) of normal dog and (B) of dog which has run for three months on a tread-mill.
(After Kulbs, Arch. /. exper. Path. u. Pharmacol., Iv.)
Recently, however, absolute proof of a work hypertrophy without myocardial degen-
eration has been brought by the beautiful experiments of Kiilbs. This observer took two
dogs of the same litter and of equal size, kept them in neighboring cages upon the same
diet, but compelled one of them to run upon a tread-mill daily for three to six months,
while the other was kept quiet and used as a control. At the end of this time both dogs
were killed in the same manner.
First set. Second set.
Work doc;. Control. Work dog. Control.
Total weight 15,200 15,000 19,200 20,400
Musculature 5,696 5,342 6,489 6,776
Heart 152 99 172 113
Kulbs's results have been confirmed by Grober and by Joseph.
The increase in size of the heart was not accompanied by any change in the skeletal
musculature, nor were any pathological changes present in the heart or arteries. The
muscle here simply underwent an increase in size, the purest form of hypertrophy. Kulbs's
dogs were simply in training to run on a tread-mill. The process was exactly the same as
the "training" of an athlete, and, clinically, it is often found that athletes have mildly
hypertrophied hearts. Schieffer has demonstrated with the orthodiagraph that the size
of the heart is increased in persons whose occupations require hard work and decreased in
those with sedentary callings. He has also shown that the hearts of the young men doing
military service in the German Army increase in size somewhat during their period of
service. However, these men often indulge in excess of alcohol or tobacco, so that before
they die enough myocardial change has set in to justify the scepticism of men like Krehl
(I.e.) and Romberg (I.e.). Nevertheless, though a true "work hypertrophy" must be
admitted, in these experiments it is noticeable that the increase in weight of the heart
HYPERTROPHY AND ATROPHY. 207
amounted to only 52 per cent, as compared with changes of 100 to 300 per cent, often
observed in man. It is doubtful whether a corresponding degree of hypertrophy would
be noticeable clinically.
ETIOLOGICAL FACTORS.
Hypertrophy in Chronic Nephritis. — The most remarkable and most
important of all these forms of hypertrophy is that taking place in chronic
nephritis. This was first noticed by Richard Bright in his classical descrip-
tion of dropsy in nephritis.
In 1853, Wilkes thought that the lesions of the kidneys and arteries were part of the
same morbid condition; while Gull and Sutton assumed that the general arteriocapillary
fibrosis brought about an increased resistance through narrowing of the arterial bed, and,
as a result of this, high blood-pressure and hypertrophy of the heart. Senator ascribed the
hypertrophy to a "dyscrasic" property of the blood in nephritis, stimulating the heart
to contractions of .abnormal force. Passler and Heineke have recently subjected the
matter to critical experiment. They found that if they cut out pieces of kidney from a
dog bit by bit until renal substance equal to 1^ kidneys had been removed, the heart then
began to hypertrophy and the blood-pressure to rise. If considerably more tissue was
removed, the animal became cachectic, the blood-pressure remained low, and the heart
did not hypertrophy. They ascribed these cardiac changes, as George Johnson had done,
to the presence in the blood of some substance having a digitalis-like action, being either
retained in the circulation in abnormally large quantities as the result of disturbed excre-
tion, or being a true internal secretion from the diseased kidney.1
Numerous other theories of cardiac hypertrophy in renal disease have been advanced.
Chief among these is the theory of J. Cohnheim and Traube that the sclerosis of renal
vessels narrowed the arterial bed in the kidney, thereby introducing an increased resistance
into the general circulation, and that these changes in the renal vessels were enough to
raise the general blood-pressure. It would appear in the light of more modern research
that this cutting off of the blood stream is in itself insufficient. On the other hand, Buhl,
Huchard, and Albrecht have suggested that the hypertrophy is not a true one but simply
a pseudohypertrophy (interfascicular myofibrosis, see page 234), the entire increase in
size of the heart being due to growth of connective tissue and not of the heart muscle, but
histological examinations do not bear out this view.
Hypertrophy from Overdrinking. — Closely allied to this condition is the
tremendous heart hypertrophy which is universally found to result from
drinking large quantities of beer, and, since it does not accompany excess
in any other form of alcohol to the same extent, it is thought to be clue to
the large quantity of fluid ingested. That increase in the fluid in the blood
at once results, not so much in a rise in arterial blood-pressure as in rise in
venous blood-pressure, dilatation of the heart, and increases in the systolic
output, even to the point of doubling or trebling it, can easily be shown
with Henderson's cardiometer, and this no doubt illustrates the mechanism
by which the change is brought about.
Hypertrophy and Arteriosclerosis. — The relation of hypertrophy of the
heart to arteriosclerosis independent of any renal changes is also of funda-
mental importance. The coincidence of the two conditions in the same
individual has long been noted, and both have been brought about experi-
mentally by administration of certain poisons, notably adrenalin (Josue*,
Erb, Pearce, et al.).
1 Tigerstedt and Bergmann (Skand. Arch. f. Physiol., Leipz., 1898, viii, 224) found that
injection of renal extract actually raised the blood-pressure, owing to the presence of a
substance which they named "renin."
208 DISEASES OF THE HEART AND AORTA.
Cardiac and Adrenal Hypertrophy. — A new light has been thrown upon
the subject by the studies of Vaquez and Aubertin (1905), Aubertin and
Clinet, Wiesel, and Gaillard.
Aubertin was able to produce cardiac hypertrophy in rabbits by various means,
and found in every case a simultaneous hyperplasia of the medullary
substance in the adrenals. A similar finding had been made by Vaquez and
Aubertin in cases of chronic nephritis associated with hypertrophy of the left ventricle,
which was confirmed by Wiesel in 1907. In December, 1907, Aubertin and Clunet made
a study of 120 unselected autopsy cases. Of these 18 showed very definite hypertrophy
of the medulla of the adrenals, and 16 of these 18 showed marked hypertrophy of the
heart. On the other hand, but 10 of these hypertrophied hearts were associated with renal
disease: the others occurred in conjunction with valvular lesions, congenital defect in the
septum ventriculorum, aortic sclerosis, etc. Aubertin, however, states very definitely that
besides these groups they encountered cases of cardiac hypertrophy without the existence
of adrenal hyperplasia, so that this association is not invariable; and they conclude that
it is at present impossible to decide whether the cardiac hypertrophy occurs as a result of
oversecretion of adrenalin, or whether the hyperplasia of the adrenals occurs as a result
of slight venous stasis in those organs while the hypertrophy is going on. Arteriosclerosis
was the rule but not invariably in these cases with adrenal hypertrophy.
It must be noted that the action of adrenalin is just that which might be expected
to bring about hypertrophy of the heart, for it causes, (1) a general vasoconstriction ;
(2) a marked increase in the tonicity of the heart; (3) an increase in the force of the beat
and in the systolic output.
However, the results of Cohn, under AschofP s direction, are less favor-
able to this theory. In 12 cases of hypertrophy of the left ventricle with
chronic nephritis, he found hypertrophy of the adrenal cortex in only 3
(25 per cent.), while in 23 cases of chronic nephritis without hypertrophy
of the heart he found hypertrophy of the adrenal cortex in 8 (34 per cent.).
These findings tend to throw considerable doubt upon the theory of Vaquez
and Wiesel.
Hypertrophy and Abdominal Arteriosclerosis. — Hasenfeld has found
that no hypertrophy sets in unless arteriosclerosis is
present in the aorta above the level of the superior
mesenteric artery. Practically all the substances which are known
to bring on arteriosclerosis are vasoconstrictors, and beginning arteriosclero-
sis in man seems usually to be accompanied by vasoconstriction. It is
readily conceivable that any sclerotic obstruction below the mesenteric
would be easily compensated for by dilatation of the abdominal vessels,
and, consequently, would bring about no increased resistance to blood flow,
while at the higher level the presence of sclerosis is more or less equivalent
to clamping the abdominal aorta.1
DIAGNOSIS.
It would appear at first sight to be extremely easy to determine clini-
cally whether in a given case hypertrophy is present or not, and the older
clinicians laid down very definite rules for its detection, most of which were
fallacious. In general, we may agree with Gibson that the most important
signs of hypertrophy of the left ventricle are increase in cardiac dulness to
the left, with a more or less steady, forceful, and "heaving" impulse, and a
1 An excellent discussion of the theoretical and experimental side of the question is
given by R. M. Pearce.
HYPERTROPHY AND ATROPHY.
209
booming first sound of low pitch, and an accentuated second sound at apex
and aortic area. These signs are dependent largely upon the contact of the
heart with the chest wall; and if, as is often the case in an emphysematous
individual, the lung intervenes between the left border of the heart and the
chest wall, all the signs may be diminished beyond recognition. The diag-
nosis may, however, often be made from the history in spite of the clinical
findings. Thus, if an aortic or
mitral insufficiency has persisted
for some time and the heart is
in a condition of moderate vigor
with a normal pulse-rate, it may
be assumed that hypertrophy of
the heart has had to take place
in order to maintain the circula-
tion, in spite of distant heart
sounds and absence of the apex
beat. Prolonged high blood-
pressure is usually associated
with some degree of hypertrophy
of the left heart, but not invari-
ably. In differentiating from
dilatation it may be stated that,
except under unusual conditions
brought on by stimulation of the
vagus, the factors bringing on
dilatation quicken the pulse-
rate, and an enlarged but slowly
beating heart is almost always
hypertrophied. In hypertrophy
of the left ventricle, in contra-
distinction to that of the right,
the maximum impulse is usually
a systolic protrusion, while in
the latter case it is a systolic
retraction. The latter is also
frequently the case when both
ventricles are hypertrophied.
Hypertrophy of the Left Ven-
tricle. — Palpation of the apex
impulse, which many writers,
even as late as Romberg, con-
sider a most important sign of hypertrophy of the left ventricle, need not
be decisive, since, as Katzenstein has shown, the weakest hearts may often
beat the most violently, especially when beating rapidly; the strongest, on
the other hand, may be separated from the chest wall by a layer of lung.
Dulness is, however, increased to tho left.
Hypertrophy of the Right Ventricle.— The hypertrophy of the right
ventricle is not so easy to diagnose. Its presence may be inferred when
the area of cardiac dulness is enlarged and a systolic retraction is
14
FIG. 139. — Areas of pulsation and retraction hyper-
trophy of the right and left ventricles. ^, retraction;
^, pulsation. The light line indicates the area of the
cardiac dulness. A. Hypertrophy of the left ventricle.
B. Hypertrophy of the right ventricle.
210 DISEASES OF THE HEART AND AORTA.
noted at the point of maximal impulse and over the interspaces between
it and the sternum as well as in the epigastrium. The heart need not be
enlarged toward the right, since the right ventricle rarely passes the sternal
margin. Indeed it rather tends to lift the apex and shift it to the left. The
area of cardiac flatness is increased to the right, reaching
to the sternal margin. An increased area of dulness to the right of the ster-
num is due to the right auricle. The second pulmonic sound is intensified
and ringing, but this may also be the case in any condition in which there
is some obstruction to the pulmonary circulation or some insufficiency of
the left heart.
Hypertrophy of the auricles cannot be diagnosed from
objective signs except in mitral stenosis, in which an hypertrophied auricle
gives rise to a loud presystolic murmur. This is not present when the auri-
cle is weak. Hypertrophy of the right auricle is sometimes shown by a
high presystolic wave upon the jugular venous pulse-curve and very rarely
by a presystolic wave upon the liver pulse (Mackenzie) ; but, as a rule, it
shows no signs.
Prognosis. — A certain amount of hypertrophy is necessary whenever
a valvular lesion or ,any other abnormal factor tending to increase the
work of maintaining the circulation is present. Hence failure of the heart
to hypertrophy under these conditions would be regarded as an unfavor-
able condition, and would probably soon be associated with cachexia. On
the other hand, an extreme degree of hypertrophy is evidence that the
heart is doing its maximal work, that the fibres ere long will begin to
degenerate, and the heart must be spared as much as possible.
Hypertrophy in itself does not demand treatment, but 'diminution of
the causal factor as far as is possible is advisable. If this be nephritis or
arteriosclerosis, a quiet life and diet poor in salt and purin bodies should
be resorted to, with occasional courses of potassium iodide. If a valvular
lesion be present and the hypertrophy is slight, little attention need be
paid to it until the patient reaches the latter half of the fourth decade,
when he should begin to spare his heart and arteries as much as possible,
should abstain from alcohol, coffee, and tobacco, and should in every way
avoid those influences leading to the production of high blood-pressure and
arteriosclerosis.
Reserve Force of the Hypertrophied Heart. — One of the most impor-
tant questions that arise in connection with hypertrophied hearts is
whether or not a hypertrophied heart possesses as much reserve force as a
normal one. This question is variously answered in the text-books, most
of them agreeing with Krehl et al. that .the reserve force is lessened; while
the experimental work, especially that of Romberg and Hasenfeld, indi-
cates that the strength of the hypertrophied heart muscle itself is actually
increased. However, a great deal depends upon the stage of hypertrophy
in which the individual heart happens to be. Thus a heart in the first
stage, with fibres normal and hypertrophied, would show an increased
strength (as in athletes' hearts, or in hearts of early hypertrophy after
valvular lesion as compared to the same hearts at the very onset of the
lesion) ; while a heart in the second stage, with fibres partly hypertrophic,
partly atrophic, would in most cases show a marked diminution in
HYPERTROPHY AND ATROPHY.
211
strength and still greater loss in reserve force, and an increased effort would
hasten the degeneration.
Another and really main factor in the apparent weakness of the hyper-
trophied heart is that in practically all hearts the hypertrophy is brought
on by some valvular lesion or by some persistent increase in peripheral
resistance; so that such hearts are continually wasting much of their energy
in overcoming these pathological conditions, besides bestowing the usual
amount of it upon the maintenance of the circulation. In bodily exertion
or other conditions calling upon the reserve force, not only the actual
circulation must be increased, but the abnormal factor
inducing wasting of energy, the valvular lesion, etc., »
becomes more severe as well, and hence the extra call
upon the diseased heart is double the extra call upon the
normal and requires double the reserve force to meet it.
Otherwise the reserve force, though actually more, may
be apparently less than in the normal heart, as shown
diagrammatically in Fig. 140. For practical purposes,
however, it may be regarded as indisputable that, in
every case where a cardiac lesion is present, the hyper-
trophied heart has less available reserve force than
normally, and in some cases (stage 3) less than if it
had not hypertrophied at all.
[NOR
I
MAI ATHUTE
ATROPHY.
Fia. 140.— Diagram
showing power of nor-
mal and hypertrophied
(athlete's) heart at rest
and during exercise, also
that of a diseased heart.
The length of the arrow
indicates the reserve
force. The unshaded
portion indicates the
cardiac energy ex-
pended, but wastedi
owing to the lesion.
Atrophy of the heart is more or less the reverse
process of hypertrophy. Whenever the body diminishes
in weight from cachexia, infectious disease, or starva-
tion, the heart muscle diminishes with it, and according
to Hirsch in about the same ratio. The epicardial fat,
on the other hand, is but little diminished. When the
atrophy is the result of starvation it may be of very
high degree, but the size and condition of the heart may return to normal
when an adequate diet is resumed (Schieffer).
As in the case of hypertrophy, there seems to be little change in the
number of the muscle-cells, but the latter diminish in size (10.84 /* instead
of 12.85 n, Goldenberg), and the removal of substance is marked by the
deposition of brown granules of haematoidin in fusiform arrangement about
the nucleus. These granules are formed when part of the muscle-cell pro-
teid is broken down during the atrophy, the haematoidin portion being
left. Macroscopically they impart a tobacco-brown color to the heart, so
that the condition is often designated as "brown atrophy of the heart."
To a certain extent a diminution in size of any chamber of the heart
may occur if its work is lessened by obstruction to the blood flowing into
it; as, for example, the left ventricle in pure uncomplicated mitral stenosis.
The atrophy is rarely so marked here as in starvation, phthisis, or cachexia,
and is indeed the exception rather than the rule in mitral stenosis, for other
factors, tachycardia, irregularity, or mitral insufficiency, usually contrib-
ute to keep the left ventricle doing an at least normal amount of work.
212 DISEASES OF THE HEART AND AORTA.
Like hypertrophy, cachexial atrophy of the fibres may lead on to growth
of interstitial connective tissue and fibrous myocarditis, but true brown
atrophy is not so common a forerunner of myocarditis as is hypertrophy
of the heart. Functionally, the force of the heart is impaired about propor-
tionally to its diminution in weight. The blood-pressure is usually low
and the muscle easily fatigued. Overstrain readily occurs in such hearts;
and sudden death is not uncommon.
BIBLIOGRAPHY.
HYPERTROPHY.
Thorel, Ch.: Pathologie der Kreislauforgane, Lubarsch-Ostertag's Ergebnisse der Patho-
logie, Wiesb., 1903, ix, Abth. I, 559.
Heinz, R.: Handbuch der experimentellen Pathologie und Pharmakologie, Jena, 1905,
i, iite Halfte.
Gibson, G. A.: Diseases of the Heart and Aorta, Edinb. and London, 1898.
Barcroft, J. L., and Dixon, W. E.: The Gaseous Metabolism of the Mammalian Heart,
J. Physiol., Lond., 1906-7, xxxv, 182.
Tangl: Arch. f. path. Anat., etc., Berl., 1889, cxvi, 432.
Goldenberg, B.: Ueber Atrophie und Hypertrophie der Muskelfasern des Hefzens, Arch.
f. path. Anat., etc., 1886, ciii, 88.
Dehio: Ueber myofibrosis Cordis, Deutsches Arch. f. klin. Med., Leipz., Ixii, 1.
Pearce, R. M.: Experimental Myocarditis; a Study of the Histological Changes following
Intravenous Injections of Adrenalin, J. Exper. Med., N. York and Lancaster, 1906,
viii, 400.
Pearce, R. M.: The Theory of Chemical Correlation as Applied to the Pathology of the
Kidney, Arch. Inter. Med., Chicago, 1908, ii, 77.
Ranke, J.: Tetanus, Eine physiologische Studie, Leipz., 1865.
Loeb, J.: Ueber die Entstehung der Activitatshypertrophie der Muskeln, Arch. f. d. ges
Physiol., Bonn, 1894, Ivi, 270.
Cooke, E.: Experiments upon the Osmotic Properties of the Living Frog's Muscle, J.
Physiol., Camb., 1898, xxiii, 137.
Fleisher, M. S., and Loeb, L.: Experimental Myocarditis, Arch. Inter. Med., Chicago, 1908,
ii, 78.
Muller, W.: Die Massenverhaltnisse des menschlichen Herzens, Berl., 1878.
Hirsch, C. : Ueber die Beziehungen zwischen dem Herzmuskel und der Korpermuslculatur
und ueber sein Verhalten bei Herzhypertrophie, Deutsches Arch. f. klin. Med., Leipz.,
1899, Ixiv, 597.
Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart, 1906.
Krehl, L.: Erkrankungen des Herzmuskels, Nothnagel's Handbuch des speziellen Pathol.
u. Therap., Wien, 1898.
Lewy, B.: Die Arbeit des gesunden und des kranken Herzens, Zeitschr. f. klin. Med.,
Berl., xxi, 321 and 521.
Kiilbs: Experimentelle ueber Herzmuskel und Arbeit, Arch, f . exper. Pathol. u. Pharma-
kol., Leipz., 1906, Iv, 288.
Groeber: Untersuchungen zur Arbeitshypertrophie des Herzens, Deutsches Arch. f. klin.
Med., Leipz., 1907, xci, 502.
Joseph, D. R.: The Ratio between the Heart-weight and Body-weight in Various Animals,
J. Exper. Med., N. York and Lancaster, 1908, x, 521.
Schieffer: Ueber den Einfluss der Berufsarbeit auf die Herzgrosse, Deutsch. Arch. f.
klin. Med., Leipz., 1908, xcii, 383; also, Ueber den Einfluss des Militardienstes auf die
Herzgrosse, ibid., 1908, xcii, 392.
Howard, W. T.: An Analysis of 105 Cases of Heart Hypertrophy (from the Autopsy
Records of the Johns Hopkins Hospital), Johns Hopkins Hosp. Rep., Bait., 1894,
iii, 266.
Wilks, S.: Cases of Bright's Disease, with Remarks, Guy's Hosp. Rep., Lond., 1853, ii
Ser., viii, 232.
HYPERTROPHY AND ATROPHY. 213
Senator, H.: Ueber die Herzhypertrophie bei Nierenkranken, Deutsch. med. Wchnschr.,
Leipz. u. Wien, 1903. Die Erkrankungen der Niere, Nothnagel's Handb. d. speziellen
Pathol. u. Th., Wien.
Passler, H.: Ueber Ursache und Beutung der Herzaffektion Nierenkranker, Volkmann's
Sammlung klin. Vortrage, Leipz., 1906, No. 408.
Johnson, G.: Lectures on Bright's Disease with Especial Reference to Pathology, Diag-
nosis, and Treatment, Lond., 1873.
Cohnheim, J.: Lectures on General Pathology, New Sydenham Society.
Traube, L.: Gesammelte Beitrage zur Pathologic und Physiologic, Berl., 1871-1878.
Buhl: Mitth. a. d. pathol. Inst. Munchen, 1878, 38.
Huchard, H.: Maladies du Coeur, Paris, 1899-1905.
Albrecht, E.: Der Herzmuskel, Berl., 1903.
Josu6 O.: Hypertrophie cardiaque caused per 1'adrenaline, Compt. rend. Soc. de Biol.,
Par., 1907, Ixiii, 285.
Erb, W.: Experimentelle und histologische Studien iiber Arterienerkrankung nach Adre-
nalininjektiorien, Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1905, liii, 173.
Vaquez: Hypertension arterielle, Bull. soc. m6d. d. hop. de Paris, Feb. 5, 1904.
Vaquez and Aubertin: Sur 1'hyperplasie surre"nale des nephrites hypertensives, ibid.,
1905, xxii, 705.
Wiesel: Renale Herzhypertrophie und chromaffines System, Wien. med. WTchnschr., 1907,
Ivii, 673.
Schur, H., and Wiesel, J.: Beitrage zur Physiologic und Pathologic des chromaffinen
Gewebes, Wien. klin. Wchnschr., 1907, xx, 1202. Also, Ueber eine der Adrenalin-
wirkung analoge Wirkung des Blutserums von Nephritikern auf das Froschauge, Wien.
klin. Wchnschr., 1901, xx, 699.
Gaillard. Quoted from Aubertin.
Hasenfeld, A.: Ueber die Entwicklung einer Herzhypertrophie bei der Pyocyaneusendo-
carditis und der dadurch verursachten Allgemeininfection, Deutsch. Arch. f. klin.
Med., Leipz., 1899, Ixiv, 763.
Hasenfeld und Romberg: Ueber die Reservekraft des hypertrophischen Herzmuskels,
u. s. w., Arch. f. exper. Pathol. u. Pharmakol., 1897, xxxix, 333.
Katzpnstein, J.: Dilatation und Hypertrophie des Herzens, Muenchen, 1903.
Aschoff and Cohn: Bemerkungen zu der Schur- Wieselschen Lehre von der Hypertrophie
des Nebernierenmarkes bei chronischen Erkrankungen der Nieren und des Gefass-
apparatus, Verhandl. d. deutsch. path. Gesellsch., Jena, 1908, xii, 131.
VIII.
FATTY DEPOSITS IN AND ABOUT THE HEART.
Fat may be deposited in the heart in two ways: (1) In solid masses
of adipose tissue, especially in the pericardium in fat individuals, particu-
larly in those addicted to alcohol, and very often associated with coronary
sclerosis. This condition is designated as fatty infiltration or obese
FIG. 141. — Distribution of fat in and about the heart. A, normal; B, deposit in an obese heart; C, deposit
in a fatty degenerated heart.
heart (Mastfettherz, Kisch). (2) In fine droplets occurring diffusely
within the heart muscle-cells, especially in anaemia, infectious diseases, in
persons poisoned by phosphorus, arsenic, and numerous other substances,
and in association with other changes in the myocardium. This condition
is called fatty degeneration.
FATTY INFILTRATION OR OBESITY OF THE HEART.
DEPOSITION OF THE FAT.
Harvey, the discoverer of the circulation, describes the hearts of certain
fat persons as covered with a layer of fat so extensive as almost to obscure
the heart muscle from view, and this condition is one of not very infrequent
occurrence. In normal hearts there is a considerable amount of fat (30
to 60 Gm., 1 to 2 ounces) collected just beneath the endothelial layer of the
pericardium, along the auriculoventricular and interventricular grooves
(coronary and longitudinal sulci), at the base of the aorta, and scattered
elsewhere over the heart. As the individual lays on more body fat, more
fat is deposited in the pericardium, at first only at the usual sites along the
sulci; but later it spreads over and into the myocardium, penetrating into
it between the larger strands of muscle, and finally settling beneath the
endocardium, especially about the bases of the papillary muscles.
The weight of adipose tissue may actually exceed the weight of cardiac muscle
(W. Miiller, Hirsch, Kisch), as shown by the following figures determined by W. MiiJler
(for the method see page 4).
214
FATTY DEPOSITS IN AND ABOUT THE HEART.
215
Total weight
of heart.
Heart
muscle.
Fat removable by
dissection.
Per cent,
of fat.
253.6
363.5
327.6
494.3
240.7
326.2
181.3
228.3
12.9
37.3
146.3
266
5.1
10.3
45.6
53.5
Normal male (thin).
Cardiac hypertrophy.
55F"} fatty heart.
Nature of the Fatty Deposit. — Under these circumstances the fat is deposited in
exactly the same manner as elsewhere in the body. The pathological character con-
sists not in the process but in the amount of the deposit. The adipose tissue in this
region does not differ macroscopically or microscopically from the fat elsewhere. Neither
does it differ chemically. It is ordinary "translocation fat" (Rosenfeld, Leick and
A
B
FIG. 142. — Photomicrographs of fat deposits in the heart. A. Heart muscle of an obese indi-
vidual, showing fat cells. B. Heart muscle of a patient who died of pneumonia, showing fat droplets
within the cells (fatty degeneration). (Photomicrograph by Dr. Chas. S. Bond.)
Winckler), derived directly from the food ; for Leick and Winckler have shown that if
dogs be overfed with mutton tallow, the fat deposited in the pericardium has an iodine
absorption coefficient approaching more nearly to what is in the sheep than to that of the
dog. The pericardial fat differs from the fat elsewhere in but one important respect, and
one which is especially to be borne in mind in treating the condition, namely, that it is
relatively poor in lipase, the enzyme which forms and splits fat, and h e n ce is
relatively stable. According to Loevenhart it would appear that lipase is present
in the cells in considerable amounts at the time the fat is deposited, but is then gradually
destroyed; so that if subsequently the fat of the body is reduced from inanition or other
cause, there is no more enzyme remaining in the pericardium to split up what is stored
there and to return it to the general circulation. Accordingly, it is found that in starva-
tion the pericardial and perirenal fat remain after all the rest has
disappeared from the body (Loevenhart, Schieffer). This matter will be re-
ferred to again in connection with treatment.
216
DISEASES OF THE HEART AND AORTA.
CARDIAC CONDITIONS ASSOCIATED WITH OBESITY.
There are three definite conditions which, though in no way part of
the general process of obesity, are often associated with it; and it is
these, rather than the obesity itself, which give rise to
the symptom complex referred to as " fatty heart," or, as
Romberg more properly designates
it, "cardiac insufficiency of fat per-
sons " (Die Herzmuskelinsufficienz
der Fettleibingen) . These are (1)
atrophy of the heart muscle, and
(2) s c 1 e r o s i s of the coronary arte-
ries, (3) a high diaphragm.
1. Atrophy and Cardiosclerosis.
—It is especially worthy of notice
that the increase in size and weight
of the heart may conceal an actual
atrophy of the heart muscle (Hirsch)
(see table above) and a correspond-
ing weakness of the heart. Accord-
ing to most writers, this lies mainly
in the left ventricle, but Hirsch has
shown that not only does the fatty
infiltration penetrate chiefly
the wall of the right ventricle, but
that the symptoms most common
among fat persons are those due to
primary failure of the right
side of the heart. A general cardio-
sclerosis (see page 235) is often asso-
ciated with the deposit of fat. It is a
self-evident fact that smch enormous
deposits of fat increase the work
done by the heart, first by increas-
ing the weight to be moved at each
systole, and secondly by increasing
the total bed of the blood stream.
It might be supposed that this would
in itself bring about hypertrophy, but hypertrophy is rarely demonstrable.
The tendency to obesity usually occurs either in persons whose lives are
sedentary and whose skeletal and cardiac muscles are therefore under-
developed, or else in those addicted to excesses of alcohol or overeating,
factors which in themselves bring on myocardial changes and hypertrophy.
2. Coronary Sclerosis. — The pathological changes and symptoms due
to sclerosis of the coronary arteries do not differ from those arising without
the presence of abnormal fat deposits and will be discussed in a separate
chapter (page 280).
3. High Diaphragm. — V. Frey and Krehl have shown in animals that
pushing up the diaphragm, and thus displacing the heart, greatly inter-
FIG. 143. — An excessive deposit of epicardial
fat. (From a specimen in the Army Medical Mu-
seum, Washington, D. C.)
FATTY DEPOSITS IX AND ABOUT THE HEART. 217
feres with the work of the latter. Myers and Schott found that soldiers
whose diaphragms are pushed up by tight belts about the abdomen exhibit
symptoms of cardiac overstrain much more readily than do normal indi-
viduals. Myers found acute dilatations most common in the British
regiments in which cuirasses and tight belts were worn.
Wenckebach has called attention to the fact that a large amount
of intra-abdominal fat pushes up the diaphragm and thus pushes the
heart into a more transverse position (apex often in the fourth interspace),
thereby hampering its action. This factor must be reckoned with in the
genesis of the cardiac weakness of fat persons.
ETIOLOGY.
Clinically, the cardiac manifestations in fat persons are very variable.
They occur most frequently in association with (1) general obesity, either
hereditary or arising primarily from over-eating; (2) in childhood; (3) after
castration or menopause; (4) overindulgence in alcohol, especially malt
liquors, with or without the presence of gout; (5) diabetes mellitus with
obesity (lipogenous diabetes) ; (6) they are most frequent and most intense
after the age of fifty.
PHYSICAL SIGNS.
Upon physical examination the most striking features are the general
obesity ; the relative weakness of the skeletal muscles ; the groups of dilated
venules, especially the "Bardolphian" "butterfly" area of dilated venules
about nose and cheeks, as well as similar areas along the attachment of
the diaphragm and elsewhere. According to Hirsch, dilatation of the
superficial veins in the subcutaneous fat is a premonitory sign of cardiac
weakening; but this is certainly not the case always. Often there is no
visible apex impulse; the relative cardiac dulness is increased to both left
and right, owing to the transverse position; the cardiac flatness is dimin-
ished. The heart sounds usually have a distant character and may be free
from murmurs. Occasionally there may be slight oedema of the feet and a
small amount of albumin in the urine. In advanced cases of cardiac insuf-
ficiency the patient may become much thinner (owing to diminished absorp-
tion of fat from the intestine, see page 159), but the pericardial fat may
remain undiminished.
TREATMENT.
The treatment of cardiac weakness of fat persons depends entirely upon
the stage at which the patient is seen. If oedema and persistent dyspnoea or
palpitation upon slight exertion are already present, the case must be treated
exactly like one of cardiac overstrain or heart failure from any other cause
manifesting similar symptoms, except that, owing to the frequent atrophy
and infiltration of the heart muscle, drugs of the digitalis group are often
of little use and may even be harmful. The patient should be put upon rest,
restricted diet, with liquids restricted to 1000 c.c., purged freely, and
bled if symptoms of failure of the right heart set in. Amyl nitrite, nitro-
glycerin, and erythrol tetranitrate may be used to relieve attacks of dysp-
noea, and massage, passive movements, and finally resisted movements, and
cold water or Nauheim baths when the patient is able to get out of bed.
218
DISEASES OF THE HEART AND AORTA.
When, as is usually the case, the patient is seen before the stage of
actual heart failure has set in and is suffering only from what may be con-
sidered as the premonitory symptoms of cardiac affection, — palpitation
and shortness of breath on exertion, weakness, and giddiness, — the treat-
ment should then be directed toward the obesity rather than toward the
heart. A main indication is then gradually to restrict the diet to a heat
equivalent of about 1200 to 1700 calories, of which 500 calories (about 120
Gm., 4 oz.) should be proteid (v. Noorden).
(1) Restricted Diet. — Numerous restricted diets have been laid down,
especially by Banting, Oertel, Hirschfeld, Kisch, and Ebstein. The restric-
tion should not take place suddenly, for fear of weakening the patient, but
should take place in several stages, reducing 500 calories each week until
the lower limit is reached.1
(2) Liquids should be restricted to less than 1000 c.c. (1 quart) per
day; this also should be done gradually.2
Sample Diet. — V. Noorden gives the following outline diet, which is very satisfactory
as a basis capable of modification:
.
Prot.
Fat.
Carb.
Cal.
8 A.M.
Breakfast—
80 Gm. cold lean meat
30.5
1.4
\ white roll (25 Gm )
1 8
0 2
14
205
10 A.M.
1 egrsT . .
6 5
6 1
85
12 M
1 cup lean bouillon
0 8
7
( 1 small plate clear soup
0 8
2 0
4
I 150 Gm. (5 oz.) lean meat or fish
57.3
2.8
1 P.M.
<( 100 Gm potatoes .
1 9
180
j Peas, beans, cauliflower, asparagus
[100 Gm fresh fruit
3.0
0 5
10
15
8
583
3 P.M.
Black coffee ... . ...
0
4 P.M.
200 Gm. fresh fruit
6
16
90
6 P.M.
250 c c (1 glass) skim-milk .
6 8
2 0
12
97
8 P.M.
Supper —
125 Gm cold lean meat with pickles
36
3
Red beets, radishes, etc
2
5
30 Gm graham bread
2 0
0 3
12
2-3 teaspoonf uls boiled fruit (no sugar)
0.5
8
299
Total
1556
28.6
112
1087
1 100 Gm. (3 oz.) raw meat (proteid 20 per cent., fat 1.7 per cent.) = 100 cal. 100 Gm.
(3 oz.) cooked lean meat (proteid 37 per cent., fat 2.5 per cent.) = 175 cal. (about 25 per
cent, higher in well-done roasted meatsj. 100 Gm. (3 oz.) cooked meat of stall-fed animals
(no visible fat) (proteid 36 per cent., fat 6 per cent.) =200 cal. 1 egg (6.5 Gm. proteid +
6.2 Gm. fat) =85 cal. Cheese (proteid 28 per cent., fat 30 per cent., carbohydrate 2 per
cent.) =400 cal. Milk (proteid 3.4 per cent., fat 3.0 per cent., sugar 4.5 per cent.) = 60 cal.
per 100 c.c. (20 cal. per ounce). Potatoes 100 Gm. (3 oz.)=80 cal. Bread (proteid 7-9
per cent., carbohydrate 35 to 80 per cent., the latter in zwieback and dry breads) 100 Gm. =
200-350 cal. Sugar 100 Gm. = 400 cal. Butter 100 Gm. = 930 cal.
2 Oertel and Schweninger thought that drinking water is a factor producing fat.
Straub and others have shown that this is by no means the case. The only influence of
the water lies in the fact that when a meal is taken dry the appetite is less than when water
is taken, and consequently less is eaten. However, considerable amounts of fluid increase
the volume of blood and the work of the heart, and hence the limitation of fluid saves
the heart in this way.
FATTY DEPOSITS IN AND ABOUT THE HEART.
219
(3) Increased Exercise. — Increase exercise gradually as much as pos-
sible, especially by walking, either on the level or on gentle gradual ascents,
interrupted by frequent rests before either weariness or shortness of breath
sets in.1 In this way the energy used by the body, and hence also the fat
burned up, can be materially increased.
Weight of patient ....
Walking on Level.
Per mile.
Per hour.
150 Ibs.
60 cal.
75 cal.
200 Ibs.
85 cal.
100 cal.
150 Ibs.
170 cal. (18 Gm. fat)
230 cal. (30 Gm. fat)
200 Ibs.
225 cal. (25 Gm. fat)
310 cal. (40 Gm. fat)
Rate 2.7 miles per" hour. . .
Rate 3.4 miles per hour. . .
In walking up grade the energy used up is equal to elevation X weight of patient
plus the energy expended in traversing the distance; but this is theoretically equalled
by the energy saved in the subsequent descent, and, on the other hand, both are
increased by bringing into play a different group of muscles; these factors can scarcely
even be approximately estimated in the individual case. However, Zuntz gives the fol-
lowing empirical figures: a man, 150 Ibs., climbing 3 kilometres (1.8 miles) in one hour
upon a 10 per cent, grade uses up about 28 Gm. (almost 1 ounce) of fat.
(4) Resisted movements (Schott) carried out under the supervision of
an attendant; or contraction of antagonistic muscles (Herz) (see page 194).
(5) Nauheim baths (see page 201) or daily cold baths as cold as can
be borne by the patient without shock.
(6) Drug Treatment. — Strychnine may be administered to increase
muscular tone, provided this does not also increase the appetite too much.
Thyroid extract and other "antifat" medication should be
scrupulously avoided. Metabolism experiments have shown that the admin-
istration of thyroid substance, though increasing the oxidative processes, causes a split-
ting of proteid to a greater degree than of fat, and hence defeats its own end, namely,
that of burning up the fat without affecting the muscle. It also brings about palpita-
tion, tachycardia, and other distressing symptoms, and tends to increase rather than to
diminish the cardiac features, even though it maybe diminishing the obesity itself.
In the obesity of the menopause, tablets of ovarian extract are
used to increase oxidation, as this effect has been demonstrated in animals,
but clinically the results from its use are rather uncertain.
FATTY DEGENERATION.
PATHOLOGY.
Pathological Anatomy. — In the condition known as "fatty degenera-
tion" the fat is deposited not by an increase of adipose tissue but in the
form of fine droplets within the heart muscle-cells (Figs. 141 and 142).
In some cases these droplets can be seen to almost fill the entire cell,
in others they appear as a few diffusely scattered droplets in the sarcoplasm.
1 It must be borne in mind that sclerosis of the coronary arteries is a frequent con-
comitant of heart weakness in fat people, and hence sudden overexertion or severe exer-
cises are to be avoided, at least until the physician has thoroughly acquainted himself with
the patient's condition and endurance.
220 DISEASES OF THE HEART AND AORTA.
Not all the cells are invaded by the fat, but with the naked eye yellow areas
of fatty degeneration may be seen mingled with normal areas of red-brown
color, which appear normal in structure under the microscope.
As regards distribution, Ribbert recognizes three types: (1) diffuse general
fatty degeneration, in which all the cells are loaded with fat; (2) mottled de-
generation? occurring in the areas which lie midway between or at points
most distant from the larger arteries ; occurring especially in anaemic individuals
and in persons whose blood-pressure is very low, so that the cells which are most distant
from the arteries suffer from ischaemia; (3) mottled periarterial fatty de-
generation produced by the action of poisonous substances in the circulating blood, such
as phosphorus, arsenic, bacterial poisons, etc., in which those cells suffer most which are
brought most closely into contact with the poison, i.e., the cells lying in the vicinity of the
larger arteries, while the areas remote from these vessels are normal or involved to a lesser
degree.
Nature of Fatty Degeneration. — The fatty degeneration may go on
in hearts otherwise healthy in connection with infectious diseases, or in
chronic myocarditis and in valvular heart diseases. The exact nature of
the process is not clear. Virchow termed it a "degeneration," but this
term, although in very general use, does not seem to designate accurately
the process. It appears to be a disturbance of cellular metabolism rather
than a degeneration of cell protoplasm, and it has been suggested that
perhaps this is due to some interference with the oxidizing enzymes such
that the fat cannot be oxidized, just as the sugar fails to be oxidized in
diabetes. But this suggestion is not founded upon any experimental data.
It is therefore most important from the stand-points of both pathology
and prognosis to learn where this fat comes from and how it is formed.
Virchow was the first to teach that there was a true fatty degeneration, that
is that the fat was formed from non-fatty (probably proteid) substances
of the sarcoplasm. It must be borne in mind that the fat might be present
in combination as it is in lecithin without being visible, but that it may
become visible when it is split off from the lecithin molecules and deposited
as highly refractive droplets of true fat.
However, the analyses of numerous observers (Bottcher, Krehl, Rosenfeld) show* a
definite increase in the fat present in the heart muscle in fatty degeneration. Indeed,
according to Rosenfeld, the muscle shows " fatty degeneratio'n " whenever it contains more
than 15-17 per cent, of fat within the muscle-cells (in marked fatty degeneration usually
20-21 per cent.). As he put it, ' 'there is no true fatty degeneration, but
the cell becomes poor in proteid and fat enters it." That this fat is
not derived from the breaking down of cell substance, but is derived either from
the fat of the food or from that transferred from the subcutaneous tissue else-
where in the body, has been shown in many ways. In the first place, Krehl demonstrated
that the lecithin content of the heart muscle was practically constant and quite indepen-
dent of the degree of fatty degeneration, and hence that the fat was not derived from this
source. Secondly, Rosenfeld showed that in a heart whose left ventricle appeared normal,
but whose right ventricle was very yellow in appearance (and showed fatty degeneration
on section), the nature of the fat was identical in both. Thirdly, it was shown also by Rosen-
feld that if dogs were starved until their subcutaneous fat had disappeared and were then
poisoned with phosphorus, the fatty degeneration did not then appear as it did in well-
fed dogs. This fact was further demonstrated by Leick and Winckler, who poisoned their
dogs with phosphorus and then fed them on mutton tallow (iodine absorption coefficient
38.2), and obtained a deposit within the heart muscle not of dog fat (I. A. C. 58.6) but of
mutton tallow. This seems to prove that the "fatty degeneration" of heart muscle is
simply a deposit of fat within the muscle-cell, just as it occurs within the connective-tissue
cell under normal circumstances. The deposition of this fat is not associated with any
FATTY DEPOSITS IN AND ABOUT THE HEART. 221
change in the lipase of the heart muscle nor of the liver, in spite of the apparent increase
in fat metabolism. The author also found that the amount of lipase in the lean areas of
a human liver mottled with fatty degeneration was the same as in the neighboring yellow
areas. It would appear, therefore, that, chemically, the primary change being absent, fatty
degeneration lies not in the heart but elsewhere in the body. This is further borne out by
the fact that in animals poisoned with phosphorus, oil of pulegon, etc., the total amount
of fat in the body is diminished, while that in the heart and liver is increased. The latter
organs seem merely to deposit the fat thrown into the general circulation.
ETIOLOGY.
Fatty degeneration in the human heart occurs most commonly in
association with alcoholism, either acute or chronic, primary and secondary
anaemias, after -hemorrhages, in association with myocarditis, valvular
and other cardiac lesions, in most infectious diseases, in miners, smelters,
and many metal workers, as well as in numerous other industries where
poisonous substances are employed. In a number of cases of death
from chloroform anaesthesia fatty degeneration has been found and is
usually ascribed to the action of the chloroform, but Rosenfeld believes
that in these cases the fatty degeneration is always present before the
chloroform was given, and that this fact accounts for the death of the
patient.
Not infrequently, as in cases of phosphorus poisoning and of infectious
diseases, the same agent which brings about the fatty degeneration also
gives rise to diminished tone of the vasomotor centre. Failure of the cir-
culation may result from the latter factor, but this need scarcely be ascribed
to the fatty change in the heart.
STRENGTH OF HEART WITH FATTY DEGENERATION.
These results of chemical investigation also find their parallel in the
effects upon muscle. Welch, in 1888, was able to show that the hearts of
rabbits rendered fatty by prolonged exposure to high temperatures were
quite normal as regards preservation of blood-pressure, reactions to vagus
stimulation, etc.; while Hasenfeld and Fenyvessy ten years later showed
that animals poisoned with phosphorus withstood the strain from clamping
the abdominal aorta quite as well as did normal animals. On the other
hand, de la Camp compelled his phosphorus dogs to run a tread-mill until
fatigue set in, and found with the X-ray that their hearts had dilated,
whereas those of normal dogs did not dilate under these circumstances.
The tonicity of the cardiac muscle was diminished.
De la Camp's experiments have not been repeated as yet, but they seem
to have been very carefully carried out. It seems certain that, as Kraus
claims, there is a considerable difference between the endurance of normal
hearts and of those with fatty degeneration.
Moreover, patflKts with fatty degeneration of the heart are very sen-
sitive to digitalis and are frequently injured by it. Sudden death from
overdose of digitalis or from acute cardiac overstrain is more common in
patients with fatty degeneration of the heart than in almost any other
condition. The relative frequency with which fatty degeneration is asso-
ciated with spontaneous rupture of the heart is also evidence of weakness
of the walls.
222 DISEASES OF THE HEART AND AORTA.
SYMPTOMS AND SIGNS.
The most characteristic symptoms associated with the condition are
those of general debility and feebleness, more or less languor and somno-
lence, as a rule without marked cardiorespiratory symptoms except short-
ness of breath on exertion. The pulse is usually small, rather collapsing,
and feeble; the blood-pressure is below normal, except when complicated
by chronic myocarditis or valvular lesion (maximal pressure 90 to 115
mm. Hg) ; the pulse-rate is increased. On physical examination the heart
may be either normal or dilated, the sounds either feeble and distant or
short and sharp; the apex impulse may or may not be well marked. The
liver and spleen are often enlarged as part of the general malady of which
the cardiac condition also forms a part. There is sometimes oedema of the
feet and ankles. However, it must be frankly admitted that none of these
is either constant or characteristic; and the diagnosis may have to be
made from inference only.
DIAGNOSIS.
The diagnosis .of fatty degeneration may often be made with more or
less probability from a knowledge of the etiological factors,, but not from
any of the physical signs, so that, as Krehl puts it, there are no clin-
ical signs for the diagnosis of fatty degeneration of
the heart.
TREATMENT.
When the condition is recognized, or rather suspected, the treatment
consists of absolute rest in bed for at least two weeks after the acute dis-
turbance has passed off and until slowed respiration and increased tolerance
to mild but gradually increasing arm exercises show that the heart muscle
has regained its normal condition. Whether it is possible to overcome the
fatty degeneration of a chronically diseased heart is questionable, but in
that, as in other conditions, treatment must be guided by the general
response of the patient, and over-exertion must constantly be shunned.
It must be borne in mind that hearts which are in a state of fatty
degeneration are particularly sensitive to digitalis; so that, when this con-
dition is suspected, digitalis should be either avoided or given in smaller
doses than usual.
PROGNOSIS.
Spontaneous recovery is the rule if too great a burden is not imposed
on the heart; but in spite of the results of animal experiments, especially
those of Welch and Hasenfeld and Fenyvessy, attention must be called
to the fact that sudden death is far from a rare occurrence in hearts with
fatty degeneration. It occurs most frequently after or during exertion.
One can scarcely avoid the suspicion that perhaps the condition which
brings about the change in the fat metabolism is also one which limits the
total metabolism of the heart muscle-cells and consequently their contrac-
tility; so that after a certain limit is passed they suddenly cease their func-
tion, just as is the case in the cellular asphyxia of intermittent claudica-
FATTY DEPOSITS IN AND ABOUT THE HEART. 223
tion and coronary sclerosis (see page 282, Fig. 166), or in toxic myocarditis
from diphtheria. Spontaneous rupture of the heart is par-
ticularly common in cases of fatty degeneration. The latter was present
in 77 per cent, of the cases collected by Hamilton.
BIBLIOGRAPHY.
HEART OF OBESITY.
Kisch, H.: Zur Lehre vom Mastfettherzen, Muenchen. med. Wchnschr., 1902, lii, 546.
Miiller, W.: Die Massenverhaltnisse des menschlichen Herzens, Hamb. u. Leipz., 1883.
Hirsch, K.: Ueber den gegenwartigen Stand der Lehre vom sogenannten Fettherzen,
Muenchen. med. Wchnschr., 1901, xlviii, 1867.
Leick and Winckler: Herkunft des Fettes bei Fettmetamorphose des Herzfleisches, Arch.
f. exper. Pathol. u. Pharmakol., Leipz., 1902, xlviii, 163.
Loevenhart, A. S.: On the Relation of Lipase to Fat Metabolism — Lipogenesis, Am. J.
Physiol., Bost., 1902, vi, 331.
Schieffer: Ueber den Einfluss des Ernahrungszustandes auf die Herzgrosse, Deutsch.
Arch. f. klin. Med., Leipz., 1908, xcii, 54.
Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart,
1906.
V. Noorden, K.: Die Fettsucht, Nothnagel's Spec. Pathol. u. Therap., Vienna, 1900, vol.
vii, 1st half.
Banting, W.: Letter on Corpulence; address to the public, 1863, 1864, 1865, 1868.
Oertel: Kritisch-physiologische Besprechung der Ebstein'schen Behandlung der Fett-
leibigkeit, Leipz., 1885. Obesity, Twentieth Century Practice of Med., N. Y., 1895.
Hirschfeld: Die Behandlung der Fettleibigkeit, Ztschr. f. klin. Med., Berl., 1893, xxii, 142.
Kisch: Das Mastfettherz, Prag, 1894. Zur Insufficienz des Mastfettherzens, Therap. d.
Gegenwart, 1899, xl, 296.
Ebstein, W.: Die Fettliebigkeit und ihre Behandlung, Wiesbaden.
FATTY DEGENERATION OF THE HEART.
Ribbert, H.: Beitrage zur pathologischen Anatomic des Herzens, Arch. f. path. Anat. etc.,
Berl., 1897, cxlvii, 193. •
Krehl, L.: Ueber fettige Degeneration des Herzens, Deutsch. Arch. f. klin. Med., Leipz.,
1893, li, 1, 416.
Rosenfeld, G.: Der Prozess der Verfettung, Berl. klin. Wchnschr., Berl., 1904, xli, 587.
Ueber Herzverfettung beim Menschen., Zentralbl. f. innere Med., Leipz., 1901, xxii, 145.
Leick and Winckler: Herkunft des Fettes bei Fellmetamorphose des Herzfleisches, Arch.
f. exper. Pathol. u. Pharmakol., Leipz., 1902, xlviii, 163.
Rubow: Ueber die Lecithingehalt des Herzens und der Nieren unter normalen Verhalt-
nissen, Hungerzustande und bei der Fettigen Degeneration, -Arch. f. exper. Path. u.
Pharmakol, Leipz., 1904-5, lii, 173.
Welch, W. H.: Cartwright Lectures on the Nature of Fever, Medical News, N. Y., 1888.
Hasenfeld, A., and Fenyvessy, B.: Ueber die leistungsfahigkeit des fettig entarteten Her-
zens, Berl. klin. Wchnschr., 1899, xxxvi, 80, 125, 150.
De la Camp, O. : Quoted on page 145.
Kraus, F.: Die klinische Bedeutung der fettigen Degeneration des Herzmuskels schwer
anaemischer Individuen, Berl. klin. Wchnschr., 1905, xlii, p. 44A.
IX.
AFFECTIONS OF THE MYOCARDIUM.
A certain amount of degeneration in the fibres of the heart muscle
occurs during the course of every acute febrile disease or intoxication. As
has been seen in previous chapters, the heart under these conditions exhibits
signs of overstrain, and the diagnosis of myocarditis, therefore, depends
upon the degree rather than the mere existence of cardiac weakness.
However, in certain cases the signs of cardiac weakness overshadow those
of the original disease and it is in these that acute myocarditis is usually
recognized. The chronic changes, however, which follow long after the
original disease has subsided, present a less complicated picture and there-
fore are more easily recognized.
PATHOLOGICAL ANATOMY.
The lesions of acute and chronic myocarditis are merely different
stages in a process which is more or less continuous. The lesions of chronic
myocarditis are always preceded by the acute lesions, but the degeneration
may not be so severe at any of the earlier periods as to give rise to symp-
toms of cardiac weakness.
In the first stage of acute myocarditis there is injury and degeneration
of the muscle-fibres, with oedema about them, and infiltration of polymorpho-
nuclear or mononuclear cells into the oedematous spaces between the fibres.
Degenerative Changes. — The degenerative changes which take
place in the heart muscle are: (1) parenchymatous degeneration,
(2) fatty degeneration, (3) hyaline and amyloid degenera-
tion, (4) calcareous degeneration, and (5) fragmentation.
Parenchymatous degeneration of the heart muscle was first
described by Virchow and Boettcher. The muscle-fibres swell, lose their
striation, and the plasma contains numerous granules of an albuminous
material, probably altered muscle proteid (myosin). They retain their
contractile power to a certain extent, but its force at this stage is somewhat
impaired, and the cell may subsequently return to normal without under-
going complete necrosis. In the more severely injured cells the nucleus
is destroyed, the sarcoplasm becomes filled with vacuoles, takes on a basic
stain, and is gradually absorbed, leaving only the sarcolemma. Often, but
not always, parenchymatous and fatty degeneration go on in the same
fibre, the fat being deposited as the proteid is removed.
In some cases fibres undergo hyaline or waxy degeneration
(Zenker) and present an absolutely homogeneous appearance, taking up the
acid stains (protoplasmic) with great avidity. In rarer cases there is a
calcareous degeneration with deposit of calcium salts in the muscle-
cells. These cells then take up the basic (or nuclear) stains (description of
224
AFFECTIONS OF THE MYOCARDIUM.
225
a case and discussion of the literature is to be found in the article of E. K.
Cullen). The degeneration is never uniformly distributed throughout the
cells, not all the cells being affected at once or in the same degree.
Occasionally the heart muscle-cells show peculiar splits extending transversely across
the whole or part of the cell. This condition is known as "fragmentation." The
fibres may show no other signs of degeneration, the transverse striations may be clear, and
the longitudinal stria? may be distinct up to the line of the fracture. Fragmentation has
been found after death from a tremendous variety of causes, even in individuals dying from
accident. It does not seem, therefore, to be a sign of specific degeneration. Dietrich's
attempts to prove it an artefact, and either to exclude it when once present or to bring on
fragmentation by allowing the heart to pass through various stages of decomposition, have
been unsuccessful, "and Buhlig in a very careful research seems to have shown that it
is an artefact which is produced when the microtome knife cuts at right angles to the
muscle-fibres. This observation still requires confirmation. Otherwise the consensus of
opinion seems to be that fragmentation is the result of some change in the muscle-fibres
occurring during the death agony, and that it is not to be regarded as a degeneration.
As illustrating the frequency of the several types of myocardial degeneration Romberg
finds the following frequency in 29 cases:
Typhoid fever — 11 coses: Parenchymatous (albuminous) degeneration, moderate or
intense 10: fatty, present 6, absent 5; hyaline or waxy (slight) 2, absent 9.
Scarlet fever — 10 cases: Albuminous degeneration, present 8, absent 1, not noted 1;
fatty, intense 1, moderate 1, absent 8; hyaline or waxy, moderate 3, absent 7.
Diphtheria — 8 cases: Albuminous, intense 1, moderate 4, absent 3; fatty, intense 5,
absent 3; hyaline or waxy, present 2, absent 6.
FIG. 144. — Infiltration along the course of the blow! -vessels in subacute myocarditis. Blood-vessels
injected. A. how power. B. Same, higher power. (Photomicrograph by Dr. C. S. Bond.)
Distribution of Myocardial Changes.— In man, according to Krohl,1
acute myocardial lesionsare particularly common in the
papillary muscles of the left ventricle and in the mus-
1 Examination of Specimens. — In cases in which the state of the myocardium is
of importance, the microscopic structure of the heart muscle should always be examined
by the method of Krehl. Krehl cuts the heart into cubical blocks 1 cm. in size, numbering
them in order so that the exact location of each block can be accurately determined. These
blocks are fixed in Muller's solution and a section or two from each is examined. In this
way a very thorough idea of the extended distribution of lesions may be gained, and a study
of a very few hearts thus reveals more accurate knowledge than can otherwise be gained
from a large number of organs examined less thoroughly.
15
226
DISEASES OF THE HEART AND AORTA.
culature about the left auriculoventricular ring. Pearce
and Fleisher and Loeb have produced in rabbits myocardial lesions having
the same distribution by the injection of adrenalin (Pearce) or adrenalin
with spartein or caffeine (Fleisher and Loeb). Roy and Adami have
shown that oedema occurs most readily in these regions during experi-
mental cardiac overstrain.
In contrast to the lesions upon the valves, the toxic or infective agents
giving rise to lesions of the myocardium do not spread through the walls
from the cavity of the ventricles, but are carried into the heart muscle
through the coronary arteries and distributed through their finer branches.
The foci of inflammation whether of bacterial
or toxic origin usually arise within the lymph
spaces around the arteries, which they
surround in sleeve, cuff, or signet-
ring distribution.
Abscess. — The form which the foci as-
sume depends chiefly upon the nature and
properties of the infective agent. If the
virulence of the germ is great, abscesses may
be produced in the heart muscle (suppurative
myocarditis) as elsewhere in the body. These
abscesses are usually produced by small septic
thrombi which plug the minute branches of
the arteries. Under the influence of the fibrin
ferment secreted by the bacteria, the vessel
soon becomes completely filled with a throm-
bus, an area of ischsemia results in the heart
muscle, which quickly becomes infected and
breaks down to form an abscess. These ab-
scesses vary in size from a submiliary nodule
to a cavity separating the muscle layers in the
entire interventricular septum. They are
usually produced by the pyogenic cocci in
septicaemia or following trauma to the heart (see page 519). The outcome
is usually fatal. Occasionally there is rupture of the ventricle through
the necrotic portions of the wall.
"Rheumatic" Foci. — In the less virulent infections, such as rheuma-
tism, typhoid fever, influenza, the foci do not undergo suppuration, but
the lymph spaces around the arteries and capillaries are filled with cellular
infiltration, polymorphonuclear in most of the acute infectious diseases,
while mononuclear cells predominate in myocarditis from typhoid fever
and subacute rheumatism.
Since rheumatic fever is perhaps the most common cause of myocar-
ditis, the lesions which it produces are of particular interest. Romberg,.
Aschoff, Geipel, and Coombs have called attention to the presence of small
submiliary foci 0.1-0.2 mm. in diameter, which occur with great frequency
in rheumatic patients, especially in the musculature about the mitral ring.
Each focus consists of a hyaline centre formed by agglutinative thrombosis
within a capillary. About this there is a zone of giant cells each containing
FIG. 145. — Septic myocarditis with
multiple abscesses in the heart wall.
The arrows point to the abscesses.
AFFECTIONS OF THE MYOCARDIUM. 227
2-4 nuclei, and these in turn are surrounded by a wider zone of mononuclear
cells interspersed with eosinophiles. The writers mentioned regard these
foci as pathognomonic of rheumatism, although they may bear only the
general features of a subacute inflammation about an area of hyaline throm-
bosis. Indeed the most typical specimen of these found in the Johns
Hopkins Pathological Museum was seen in a case of non-rheumatic myocar-
ditis. On the other hand, Freund has reported a case of acute rheumatic
myocarditis in which the infiltration was mainly polymorphonuclear.
Bracht and Wachter have recently produced arthritis, endocarditis, and myocarditis
with lymphocytic infiltrations in animals by injection of cultures of diplococci obtained
from two cases of acute articular rheumatism. These infiltrations contrast sharply with
the polymorphonuclear infiltrations usually produced by pyogenic streptococci.
FIG. 146. — Photomicrograph showing an abscess in the heart muscle. A. Low power. B. Same, higher power.
Subsidence of Lesions. — The changes which occur in the myocardium
when the patient recovers from the acute infection or intoxication, which
is the causal factor, vary both with duration and intensity of the disease
and the rapidity and completeness of the recovery. If the causal factor
completely disappears and its sojourn in the body has been a short one, no
permanent changes may have taken place. The oedema of the fibres disap-
pears, the cellular exudate may be absorbed in toto, and the myocardium
may resume its normal appearance. If areas of fibres have been destroyed
their place may be taken by scar tissue. But if the duration of the process
has been so long that connective tissue has begun to be formed in the
exudate, the traces are no longer obliterated and a chronic myocarditis
has set in.
PATHOLOGICAL PHYSIOLOGY.
As has been seen in previous chapters, hearts whose muscle
is injured become dilated upon comparatively slight
exertion, while healthy hearts resist dilatation in spite of tremendous
228 DISEASES OF THE HEART AND AORTA.
exertion. Moritz and Dietlen, whose X-ray studies have demonstrated
that the normal heart becomes smaller in severe exercise, have shown that,
on the contrary, the heart whose muscle is diseased undergoes tremendous
dilatation. Nevertheless it may maintain a normal or even heightened
blood-pressure without apparent effort, and except for the dilatation may
present no other signs of abnormality. It is more common in conditions
of acute myocardial change to have a low blood-pressure, but this is due
to the fact that the toxic substances which injure the heart muscle also
depress the vasomotor centre. The low blood-pressure is due to the latter
influence and not to the weakness of the heart.
These facts were brought out by very interesting studies of the physiology of the
heart muscle after injections of diphtheria toxin which were made by Roily and later by
v. Stejskal. Roily used a dose of toxin which just killed his rabbits in twenty-four hours,
and then began his experiments about twenty-two hours after the injection. He found
that at this time the blood -pressure arid pulse-rate of the animal
were still quite normal, and that the heart was still able to respond well to
increased work thrown upon it by compressing the abdominal aorta, etc., and that the blood-
pressure increased considerably. About half an hour before death, however, the blood-
pressure began to fall, owing to loss of vasomotor tone, as had been shown by Romberg.
Even at this time the heart was still strong enough to respond by a second rise of blood-
pressure upon clamping the abdominal aorta. Very soon after this, however, within a
few minutes, the rate became irregular and the heart weak-
ened completely. V. Stejskal's results were similar. The action of the diphtheria
toxin had not been immediate, but it had required several hours to combine with the heart
muscle, after which its weakness was manifest.
The conclusion reached by Roily and v. Stejskal is that the heart
remains competent in spite of muscular weakness until
a certain degree of strain is imposed upon it, when it
suddenly crosses the threshold that leads to failure, dilatation, and even
death. The threshold of cardiac overstrain in the healthy heart is at a
much higher level.
Arrhythmia in Acute Myocarditis. — Irregularity of the pulse cannot be
brought about by injuring the myocardium by injection of alcohol, iodine,
or even KCN, but often occurs in man as a result of myocardial lesions,
especially after exercise and overstrain. Gerhardt, Miiller, and Schonberg
have called attention to the association of irregularity with structural
changes and paralyses of the right auricle. In mitral disease it is probable
that irregularity arises in the left auricle rather than in the right, since the
latter is then not the seat of pathological conditions.1
Bradycardia is met with in the late forms of diphtheric, influenzal,
and pneumonic myocarditis and occasionally during the febrile stage. It
is often vagal in origin, but is sometimes due to depressed conductivity
of the auriculoventricular bundle, the ventricle responding only to alter-
nate contractions of the auricle (2 : 1 rhythm) . It is probable that under
these conditions toxic myocardial changes have taken place in the bun-
dle (Mackenzie). It is not unlikely that some of the sudden deaths
during convalescence from diphtheria may be due to this cause (Dunn,
see page 478).
1 More fully discussed in chapter on Mitral Stenosis.
AFFECTIONS OF THE MYOCARDIUM. 229
SIGNS AND SYMPTOMS.
The most characteristic sign of myocardial weak-
ness is dilatation of the heart (see page 227) . The heart
is usually, but by no means always, rapid, the sounds may be clear but are
usually short and sharp; they may be embryocardiac in rapid hearts; a
g a*l 1 o p rhythm, especially of the presystolic type, may be present,
or the sounds. may be definitely split (reduplicated). It is also very com-
mon to hear soft systolic murmurs over the apex or the tri-
cuspid area, due to functional insufficiencies at the auriculoventricular
orifices (see page 140), or to hear the "accidental" systolic murmur in
the pulmonary area. The second pulmonic sound is usually ac-
centuated from stasis in the pulmonary vessels.
Clinically, uncomplicated myocarditis is met with in the course of the
febrile diseases and the intoxications, especially alcohol-
ism, phosphorus poisoning, and ptomaine poisoning. It is present
also in a certain degree in almost every case of acute endocarditis or peri-
carditis, where it is but part of the general "carditis."
Its manifestations are simply those of acute heart failure or of cardiac
overstrain occurring while at rest or upon very slight exertion. The symp-
toms are, therefore, sometimes those of broken pulmonary
compensation (failure of the left ventricle, page 139), sometimes
those of broken systemic compensation (failure of the
right ventricle), according as the left ventricle or the right is the one most
affected. In many cases there are attacks of precordial pain
amounting almost to angina pectoris, coming on when the heart is acutely
dilated after excitement or exertion.
ACUTE MYOCARDITIS IN RHEUMATIC FEVER.
Although weakening of the» heart is one of the most important factors
in- general asthenia that accompanies or follows tonsillitis or rheumatic
fever, it does not often kill the patient and hence is not often a striking fea-
ture at the autopsy table.
The following history illustrates the course in fatal cases, showing (1)
the gradual insidious onset, (2) shortness of breath, extreme weakness,
and finally ascending oedema, (3) dilatation of the heart, with oedema and
degenerative changes in the heart muscle, without either hypertrophy,
fibrous changes, or valvular lesion.
CASE OF ACUTE RHEUMATIC MYOCARDITIS.
Annie Jones, female, colored, 48, admitted July 5, 1904, complaining of " rheu-
matism,'' of which she has had attacks for many years, especially marked during the
last two years. The knees and shoulders have been the joints most frequently
affected. She has had no other infectious diseases and the previous history is otherwise
negative. No shortness of breath nor palpitation. During past four weeks has been com-
pelled to sleep upright in a Morris chair, and has had incontinence of faeces.
PHYSICAL EXAMINATION. — Patient is a very stout colored woman, lying quietly
on her back in bed. Pupils equal and react to light and accommodation. Chest clear.
Heart. — Impulse is not visible. Relative cardiac dulness extends 13
cm. to left of midline in fourth interspace, 30 cm. to the right. First sound at apex
230
DISEASES OF THE HEART AND AORTA.
is very loud and not perfectly clear, though there is no definite murmur. Second sound
resembles the first in quality but is clear. Pulse regular, of good volume, rather high
tension, 100 per minute. Vessel wall somewhat thickened.
Abdomen is extremely large and swollen; there is dulness in dependent portion.
Liver is not enlarged. Legs are extremely swollen and indurated; do not even pit on
pressure. Knee- and ankle-joints much swollen and stiff. A round perforating ulcer is
present at left heel. No disturbance of sensation anywhere.
Temperature 99°; red blood-corpuscles 4,046,000; haemoglobin 55 per cent.; leuco-
cytes 3800.
Ordered rest in bed; soft diet; diuretin 1 Gm. (gr. xv) q. 4 h.; ulcer of foot to be
irrigated with sol. potass, permang. 1:20000 b. d. On July 7, ordered tinctura dig-
italis 1 c.c. (Nlxv) q. 4 h., ad dos. viii; this was then repeated and continued throughout
the course of disease. Spts. glycerylis nitrat. gtt. ii, q. 4 h., alternating with sod. nitrit.
0.3 Gm. (gr. v) q. 4 h.; rnorphin. sulph. 0.008 Gm. (J gr.) p!r.n.
July 12. Heart's action irregular; first sound reduplicated over tricuspid area; no
murmurs. July 15. There is a large perforating ulcer just below coccyx. This was irri-
gated with potass, permanganate 1 : 20000 and packed with iodoform gauze. July 16.
Temperature 106°; percussion note impaired at left base behind, where breath sounds are
absent. A few rales have previously been heard in this area. Ordered strychnine sulph.
0.003 Gm. (aV gr.) and digitalin 0.003 Grn. (^ gr.) hypo. q. 4 h. At 7.30 P.M., respiration
shallow with expiratory grunt. At 11.00 became unconscious, and died at 12.45.
AUTOPSY showed about 1 litre of fluid in peritoneal cavity; congestion of lower lobe
of lungs.
Heart . — Several opaque white patches over epicardium, one with a diameter of
3 cm. Coronary arteries soft and smooth. Heart muscle soft, flabby,
and of yellowish -brown color, studded with numerous small
opaque white areas. The muscle bundles are widely separated nuclei. Under the
microscope the muscle-fibres are seen to be
swollen ; little new growth of interstitial connective
tissue. Heart weighs 250 Gm. Slight sclerosis about
base of aorta, none elsewhere. Kidneys normal in size,
pale and cloudy. Liver shows some fatty degeneration.
DIPHTHERIC AND INFLUENZAL MYOCARDITIS.
Acute myocarditis is the chief cause of death
in diphtheria and influenza. In these conditions
it may manifest itself either, (1) as an early form
during the course of the fever, or (2) as a late form
which becomes manifest after the temperature
has fallen. The cases of diphtheric myocarditis
have been most carefully studied by Hibbard
in 800 cases with 119 deaths (15 per cent.) at
the Boston City Hospital. In spite of the high
average mortality, the mortality was less than
5 per cent, in those cases in which the pulse-
rate was below 130 per minute, increasing as the pulse-rate increased
above that figure. Death was especially frequent in those cases in which
a gallop rhythm was noted. Bradycardia (under 60 per minute) was not
a severe sign in adults (14 cases without a death; only 2 with cardiac
symptoms), whereas in cases under 7 years it was a very grave sign
(6 cases, 5 deaths). In all Hibbard's fatal cases there were both acute
myocardial change and degeneration of the fibres of the vagus.
Sudden death is not uncommon in cases of diphtheric myocar-
ditis; in Dunn's case, from the onset, heart-block (Adams-Stokes syndrome)
FIG. 147. — Orthodiagraphic out-
lines of the heart of a child during
the course of a severe diphtheria.
(After Dietlen, Munchen med.
Wchnschr., 1905, lii.) + + + ++,
outline on fifth day (MR. = 3.0
cm., ML. = 6.0 cm., L. = 9.1 cm.);
, outline on seventh day
(MR. = 3.5 cm., ML. = 8.1 cm., L.
= 12.4 cm.); , outline on
twenty-sixth day (MR. = 2.0 cm.,
ML. = 6.5cm., L. = 9.3cm.).
AFFECTIONS OF THE MYOCARDIUM. 231
was the result of myocardial change in the vicinity of the auriculoventricular
bundle. The slow pulse also is often due to partial heart-block, 2 : 1
rhythm, though this may be due to overstimulation of the vagus as well
as to injury of the bundle.
Just as diphtheria affects the myocardium in the very young, influenza
affects it in the aged. Indeed myocarditis constitutes one of the gravest
effects of this disease, and is especially to be feared after the sixth decade.
The following case serves as an example :
CASE OF INFLUENZAL MYOCARDITIS.
Patient, aged 75, of sedentary habits, rather stout, but free from all cardiac symp-
toms. Pulse had always been of good volume and regular. Had a severe attack of
influenza in March, 1903, confining her to bed for a month. No special car-
diac features. After a short convalescence she was again able to be up and about. A few
days later, just after retiring, she had a severe attack of cardiac asthma,
breathlessness, orthopnoea, and slight precordial pain. No true
angina. Moderate degree of cyanosis. Pulse small, rapid, irregular. Cardiac dulness
slightly enlarged. Soft systolic murmur heard over the entire heart. The attack lasted
half an hour, symptoms being much relieved by inhalations of amyl nitrite.
Patient was given complete rest in bed for a few days, with fluidextract of digitalis
ttlv (0.3 c.c.) three times a day and soft diet, and was then kept at rest in a large arm-chair.
Gradual convalescence. Soon became free from symptoms, but pulse remained 70 and
irregular and she was compelled to refrain from every effort except one daily trip up and
down stairs, during which she rested at each step long enough to count twenty. In June
and July, 1904, she had several similar attacks, and though she improved somewhat her
pulse remained permanently irregular. Died suddenly a year and a half later, death fol-
lowing six weeks after a severe cellulitis of the leg.
CASE OF SUBACUTE ALCOHOLIC MYOCARDITIS.
B. C. S., reporter, married, aged 36, admitted to the service of Prof. J. O. Hirsch-
felder, City and County Hospital of San Francisco, January 23, 1905, complaining of
shortness of breath and swelling of feet. Father and brother are subject to rheumatism,
and patient himself had swelling of joints four years ago, about the time of a gonorrhoea!
infection. He had measles, whooping-cough, and scarlet fever as a child, and typhoid
fever seven years ago. Denies syphilis. Married, but has had no children. Uses tobacco
in moderation, but drinks whiskey in excess, as a probable result of which he has fallen
from the best to the lowest strata of society.
PRESENT ILLNESS. — Four weeks ago while in the midst of a series of debauches he
noticed that his shoes became tight, and in a few days his legs became so swollen
that he could not put on his drawers. He had pain in the legs on walking, owing to the
oedema. He also felt very weak and became exhausted easily. Has had shortness
of breath on exertion.
PHYSICAL EXAMINATION. — Well-nourished man of good color. Tongue and uvula
deviate slightly to the right. General glandular enlargement. Epitrochlears palpable.
Chest negative except for a few moist rales over right .axilla and base.
Heart . — Cardiac impulse not visible. Relative cardiac dulness extends to 12.5
cm. from midline in fifth interspace (3 cm. outside mammillary line), 4 cm. to
right of midline and above to the third rib. Sounds are very rapid, the first sound every-
where replaced by a systolic murmur which is loudest at the apex; not transmitted to the
axilla; pulmonic second accentuated.. Pulse 108, regular in force and rhythm, low tension,
fairly good volume. Radial artery not palpable.
Liver just palpable. No scar on genitalia. Lower extremities are covered
with pediculi and raw scratch marks. Marked oedema of both legs. Urine nega-
tive, sp. gr. 1028.
Ordered liquid diet; fluidextract digitalis 0.3 c.c. ("lv) q. 4 h.; spir. glycerylis nitratis
1 gtt. q. 4 h.; sol. magnes. sulphat. sat. 30 c.c. (3i); ung. zinci oxid. to legs.
232 DISEASES OF THE HEART AND AORTA.
Jan. 30. Pulse slow and somewhat irregular, venous tracing show-
ing that some of the auricular impulses did not reach the ventricle (2 : 1 heart -block).
Given atropine 0.0015 Gm. (1 gr.) at 12.45 P.M. At 2.00P.M., max. pr. 135, min. 75-
80. Pulse-pressure 60 X pulse-rate 60 = 3600. Pulse-rate absolutely regular, as
shown in the brachial artery tracing taken at 1.45 P.M. Digitalis was now
discontinued.
Feb. 2. (Edema gone. Soft systolic murmur still present at apex. Pulse-rate 72, abso-
lutely regular, responding to all impulses from the auricle. It never again became irregular.
Feb. 11. Feels quite strong. Up and about. Heart has been regular and all mur-
murs gone.
March 2. Has had slight swelling of feet. Was again put to bed. The swelling
disappeared within 24 hours.
In a few days the patient was again up and about, and in a week or ten days later was
allowed to continue his work in the pantry. Was discharged apparently cured about
May 15.
DIAGNOSIS.
As has been seen, the diagnosis of acute myocarditis in many cases is
made more by inference than by definite signs. The presence of symptoms
of cardiac weakness in an infectious disease, out of proportion to the
severity of the latter or to the apparent seventy of the endocardial lesion,
is presumptive evidence of severe myocardial involvement. The symptom-
complex of restlessness or marked dulness, constriction over the chest, and
precordial pain, vomiting, cyanosis, and increase in the area of cardiac
dulness, during or after an attack of an infectious disease or of delirium
tremens, is practically pathognomonic. The presence of a systolic murmur
at the apex and over the body of the heart, which may even be transmitted
to the axilla but which disappears during convalescence, added to the other
symptoms above mentioned, would indicate myocarditis rather than endo-
carditis. It must be borne in mind, moreover, that the presence of true
endocarditis or pericarditis is evidence in favor rather than against the
presence of an additional myocarditis, and that in the acute form the symp-
toms are quite as liable to be due to the insufficiency of the muscle as to
the valves. On the other hand, just as a most acute nephritis may be pres-
ent without the presence of albumin or casts in the urine, so acute myo-
cardial changes may be present without definite signs of cardiac weakness
other than a tendency to fatigue. In view of the observations of de la
Camp, Moritz, Dietlen, and Hornung, myocardial changes may be diag-
nosed in cases in which the heart undergoes transitory dilatation (with
or without transitory valvular insufficiencies) upon comparatively slight
exertion. The cardiac area under such conditions must be most carefully
outlined, if possible with the orthodiagraph. In the absence of the latter
careful percussion may often; suffice. The changes must be 1 cm. or more
before they should be considered as definite.
TREATMENT.
The management of a case of acute myocarditis differs essentially from
that of the chronic form, owing to the fact that in the former the changes
in the muscle may be of a temporary character, while in the latter the
changes are permanent. Accordingly, in the acute form the aim
is to allow the muscle to return to its normal state,
AFFECTIONS OF THE MYOCARDIUM. 233
while in the chronic form this cannot be hoped for,
and the treatment is directed toward obtaining the best functional result
possible in the changed muscle that is left. The one aims at bringing
about subsidence, the other at inducing hypertrophy.
Accordingly, even in the mildest form of acute myocarditis rest is all-
important— c omplete rest in bed until the degenerative
changes rn the muscle have subsided. This is especially
important, since cardiac overstrain sets in very easily in such hearts, and
it is probable that this, in even the slightest degree, increases the injury
to the muscle-fibres as well as the extent of the interstitial ccdema and
infiltration. The patient should be kept in bed at least two weeks after
any indications of myocardial weakness have subsided, and if possible
until the pulse-rate has again become slow. An easily digestible diet equiva-
lent to about 1000-1500 calories should be enforced (see page 167), frequent
feeding of small quantities being resorted to in the place of three compara-
tively large meals.
An ice-bag should frequently be applied to the precordium, since it
tends to slow the heart-rate. Some writers, especially Caton, strongly
favor the application of small blisters to the precordium and the administra-
tion of small doses (0.3 Gm. or 5 gr.) of potassium iodide, but it is extremely
doubtful whether this has any effect upon the course of the disease.
If ansemia arises, iron should be ordered in some form, usually as
Blaud's pills, — ferri carbonas saccharatus (0.25 Gm., 4 gr.), — or Vallet's
mass (same as Blaud's pills with honey instead of sugar but more perma-
nent), or elixir ferri, quininaeet strychnine phosphatum (4 c.c., 1 fluidrachm).
If constipation or other digestive disturbances result, hipmatin or some
other "organic" iron preparation, that is, where the iron is combined with
proteid. The patient's bowels should be kept freely moving without effort,
best by means of Rochelle salts, sodium phosphate, Epsom salts, or Seidlitz
powders. The effervescent citrate of magnesia usually causes greater
abdominal distention than is desirable, owing to the upward displacement
of the diaphragm.
Hypersensibility to Digitalis. — The usefulness of digitalis in acute
myocarditis is a debatable question. Digitalis acts as a spur to the heart
and raises the strength of the contraction until it enables the fibres to draw
on their reserve force at each contraction, but it does not raise the limit
strength. When that limit is already approached it spurs them too far,
and drives them to overstrain and even to death.
Whether, in any individual case, digitalis will do good or harm will
depend, therefore, upon the degree to which degenerative changes have
progressed and the amount of reserve force that is left. Thus, in the case
of B. C. S., the myocardial degeneration was slight and the beneficial action
of digitalis was marked. With A. J., however, the case was different.
Degeneration had reached too advanced a stage and the drug was useless,
perhaps even harmful.
Even the heart of B. C. S., however, manifested the abnormal suscepti-
bility of such hearts to digitalis, since it produced partial block and extra-
systoles with doses which barely sufficed to slow the heart of the average
patient.
234
DISEASES OF THE HEART AND AORTA.
Moreover, in acute myocarditis the heart is hypersensitive to digitalis.
For example, in the case of B. C. S., a normal dose produced an abnormally
intense reaction with signs of the first stage of digitalis poisoning — partial
heart-block and extrasystoles. Fortunately in this case the good effects
outweighed the bad, but it belonged to the group of cases which prove con-
clusively that in acute myocarditis digitalis should always be given in
smaller doses than would be used for a heart with a valvular lesion which
showed the same degree of heart failure.
Strychnine. — As regards strychnine, both its beneficial and its harmful
effects are less marked than those of digitalis. It is therefore less liable to
overstep the limit of tolerance. In ordinary doses it tends to increase the
cardiac tonicity, as well as to stimulate the cardiac nerves, the respiratory
and vasomotor centres, so that it becomes a valuable drug in such conditions.
CHRONIC MYOCARDITIS.
PATHOLOGICAL ANATOMY.
Pathologically the chronic inflammatory changes in the myocardium
may be divided into three groups:
1. Cicatricial patches or scars arising from the healing of isolated areas of inflam-
mation (abscess or focal infiltrations) or from the organization of areas of infarction.
2. Thickening of the septa that separate the muscle strands (interfascicular myo-
fibrosis, Dehio) occurring when the heart muscle hypertrophies.
3. Diffuse degeneration of the muscle-fibres with invasion of the fibre bundles by
strands of connective tissue (cardiosclerosis, Huchard; interstitial myofibrosis, Dehio).
FIG. 148. — Specimen showing a cardiac aneurism
covered with pericardial adhesions.
FIG. 149. — Chronic myocarditis (cardiosclerosis).
Cardiac Cicatrices. — The areas of cardiac cicatrices are quite common
in coronary sclerosis, in which they represent the site of healed infarcts
in the area supplied by the affected artery. The fibrous tissue composing
the scar, relatively poor in elastic fibres, is weaker than the rest of the
heart wall, presenting the condition termed by Ziegler myomalacia cordis,
and it may bulge out to form an aneurism of the heart (Fig. 148).
AFFECTIONS OF THE MYOCARDIUM.
235
Spontaneous rupture occurs in such areas, and death occurs from hemor-
rhage into the pericardium, though, according to Hamilton, this is not as
frequent a cause of spontaneous rupture as is fatty degeneration.
On the other hand, the smaller areas of cicatrization may represent
complete obliteration.
Interfascicular Connective-tissue Proliferation. — Interfascicular myo-
fibrosis or hyperplasia of the septa between the bundles is to be regarded
as a concomitant of cardiac hypertrophy, and represents a strengthening
rather than a weakening of the heart.
FIG. 150. — Specimens showing chronic myocarditis. (Photomicrographs by Dr. Chas. S. Bond.)
A. Intrafascicular myofibrosis, penetrating into the bundles of muscle-fibres. Hypertrophy of some fibres;
atrophy of others. B. Coarse strands of connective tissue penetrating between the bundles of muscle-
fibres (interfascicular myofibrosis).
Cardiosclerosis. — The most important form of lesion in chronic myo-
carditis is the interstitial myofibrosis or cardiosclerosis. This
form is met with in senile hearts and in most cases of chronic heart failure.
According to Dehio, it occurs only in those hearts which have been sub-
jected to long-continued dilatation, frequently in hearts in which hyper-
trophy has preceded the dilatation. The heart muscle is oedematous.
The fibres are found in all stages of change — normal fibres, large healthy
hypertrophic fibres, large vacuolated degenerating fibres, and small ones
in the various stages of atrophy — in a single microscopic field. Many of
them are undergoing fatty degeneration. In response to the well-known
biological law that wherever the parenchyma of an organ is gradually
•destroyed hyperplasia of the interstitial tissue takes its place (Weigert,
Dehio), fine strands of connective tissue are seen everywhere winding
their way between the muscle-fibres and gradually taking their places.
RELATION OF SITE OF MYOCARDIAL LESION AND DISTURBANCE OF FUNCTION.
Lesions in the Ventricles. — Attempts have been made by numerous
investigators to demonstrate a definite connection between the exact site
of the myocardial lesions and the disturbance of function met with.
Krehl, who under Ludwiii-'s inspiration was the pioneer in this field, inau-
236
DISEASES OF THE HEART AND AORTA.
gurated the method of studying sections from every part of the heart, and
found that the papillary muscles and the musculature about the mitral
ring were affected with great frequency; but he was unable to establish more
definite relations. Albrecht's attempt to do this for the various muscle
layers discovered by Krehl and J. B. MacCallum has
called forth a vigorous contradiction from Ascttoff
and Tawara, who have made a most careful study
of 150 pathological hearts by KrehFs method.
On the other hand, His, Erlanger, Stengel,
Schmoll, and a host of others have demonstrated that
lesions in the auriculoventricular bundle give rise to
heart-block, while Aschoff, Tawara, Saigo, Barker,
and Hirschfelder have shown that lesions affecting
one branch of this bundle do not affect the contrac-
tion of either ventricle. Very recently, however, H. E.
Hering has revived interest in these questions by
showing upon the excised heart that if the strand of
Purkinje fibres (conduction system) to one papillary
muscle is cut or injured, that papillary ceases to con-
tract, although the rest of the heart continues to do so.
Lesions in the Auricles.— Studies of lesions in
the auricles, though fewer, have been still more
remunerative. Dehio and his pupil, Radasewsky,
demonstrated that in chronically dilated hearts the
myocardial changes in the auricles were much more
marked than those in the ventricles; and Schonberg,
under D. Gerhardt's direction, has shown that per-
manent arrhythmia with auricular paralysis is asso-
ciated with infiltrations of the intervenous area which correspond to the
embryonic sinus, the spot at which the cardiac impulse probably originates.
FIG. 151. — Hypertrophy
of some muscle bundles in
the auricle with atrophy
(transparency) of other
areas. (From a specimen
in the Army Medical Mu-
seum, Washington, D. C.)
PATHOLOGICAL PHYSIOLOGY.
The chief physiological features of chronic myocarditis are:
(1) Chronic weakness of the heart, with tendency to undergo dilatation and overstrain.
(2) Frequency of extrasystolic or absolute irregularities.
Compensation in Myocarditis. — The course and characteristics of myo-
cardial weakness have been fully discussed under the pathological physiol-
ogy of cardiac overstrain (page 134). Indeed, the persistence of a primary
overstrain with the concomitant oedema of the heart muscle may be an
important factor in instituting chronic myocardial changes or in rendering
the heart especially susceptible to alcohol, toxins, tobacco, or other influ-
ences that would otherwise not affect it. The changes in the myocardium,
the lowered tonicity, the persistent oedema, the reduction in the number
of efficiently contracting muscle-fibres, all tend to lower the threshold of
exertion at which overstrain is ushered in. Whether the overstrain mani-
fests itself as a broken pulmonary or a broken systemic compensation, or
as both together, depends upon the relative and absolute strength of the
two ventricles as well as the nature of the exertion.
AFFECTIONS OF THE MYOCARDIUM.
237
Blood=pressure. — The occurrence of such overstrain is, however, quite
consistent with the maintenance of a normal or, especially, a high blood-
pressure. This high blood-pressure, strange to say, is in itself the result
of the chronic cardiac insufficiency and the slowing of the circulation. With
the slowing of the circulation there comes asphyxia of the med-
ullary centres, which stimulates them and brings on an intense
vasoconstriction. The vasoconstriction narrows the arterial bed so much
the arterial pressure must be raised until the blood flows through the medul-
lary centres at the proper rate. The weakened heart must thus rise to the
occasion and sacrifice itself to save the medullary centres. The more it
fails the more work these inexorable centres demand from it, the more
they throttle the arteries in their struggle to get blood from the flagging
heart. The more the arteries are throttled the greater the constriction,
the smaller the arterial bed, and the less the systolic output necessary to
overfill the arteries, the greater the force necessary to drive it. The heart
may therefore empty itself incompletely but at high pressure against this
high peripheral resistance, while the increase in residual blood within the
ventricles leads to dilatation and stasis. This condition of stasis with high
pressure, both resulting from chronic cardiac weakness, is
usually termed "high pressure stasis'1 (Hochdruckstauung) .
Its factors actually constitute a vicious circle :
Cardiac weakening
* t I
Increased cardiac effort Slowed circulation
High blood-pressure through medulla
t I
Vasoconstriction
Fio. 152. — Curve of blood-pressure in a case of chronic myocarditis, showing the high blood-pressure per-
Msting until shortly before death. (IIigh-pP->.-ur»- stasis.)
This accounts for the fact that under such circumstances venesec-
tion may rlTi s e , digitalis may lower the blood-pressure, and,
on the other hand, the blood-pressure may rise rather than fall as death
approaches (Fig. 152).
Arrhythmia. — In many cases of chronic myocarditis the heart is
irregular in both force and rhythm, especially in the later stages.
238 DISEASES OF THE HEART AND AORTA.
The chief types of arrhythmia observed are :
(1) Extrasy stoles of auricular or more frequently of ventricular
origin.
(2) Perpetual absolute arrhythmia.
The extrasystoles seem to result from the overloading of the
chambers in which they arise; the perpetual arrhythmia both
from the overloading of the auricle and the presence of chronic myocardial
changes in the muscle strands of the intervenous area (embryonic sinus
reuniens). (The mechanism and significance and diagnosis of these ar-
rhythmias have been discussed on page 75.) This irregularity in itself
also exerts an unfavorable action upon the circulation. When the site at
which the impulse arises is diseased, it may be impossible for this area to
generate cardiac impulses in rapid succession, and hence the pulse and the
circulation may remain slow in spite of the needs of the body for increased
aeration.
SYMPTOMS AND SIGNS.
From the above cited cases it will be seen that the symptoms of chronic
myocarditis are usually those of gradually developing cardiac weakness,
progressively increasing weakness and dyspnoea, at first on exertion, later
when at rest, and finally reaching the stage of orthopnoea. Palpitation is
a frequent symptom; sometimes there is precordial pain, usually behind
the sternum, associated with sudden dilatation of the heart. Swelling of
the abdomen and often pain in the right hypochondrium are associated
with the stretching of the capsule of the liver as the latter enlarges.
(Edema ascending from the feet and legs, diminution in the amount of
urine, at first during the day, with frequent and increased micturition at
night, and later marked diminution in total urine secretion mark the later
stages of broken systemic compensation.
Physical signs are : cyanosis; dilatation of the venules, especially
over the face; general engorgement of the larger veins, often
with disappearance of the "double" venous pulse, and either total absence
of the pulsation in the jugular veins or appearance of a "single" venous
pulse ; often irregularity of the arterial pulse, usually with presence of marked
arteriosclerosis; increase in area of cardiac dulness to right or felt; occasion-
ally a catarrhal jaundice is a marked sign of the hepatic engorgement.
The blood count often shows polycythsemia and high haemoglobin,
without change in leucocytes. Blood-pressure may or may not be elevated ;
but in most cases it is not decreased. Pulse tracings from the radial and
carotid arteries and jugular veins often show persistent absolute arrhyth-
mia, with paralysis of the auricles, with absence of signs of organic valvular
lesion. There may be a more or less transitory soft systolic murmur
present at apex due to functional mitral insufficiency, but this is rarely
transmitted to the axilla and often passes off during treatment. The same
applies to the systolic murmur, which may be loudest over the tricuspid
area. There is usually absence of diastolic murmurs except in cases in
which functional pulmonary or aortic insufficiencies are suspected.
A mild bronchitis with rales and some oedema is common, espe-
cially at right base. Enlargement of the liver, with either systolic impulse
AFFECTIONS OF THE MYOCARDIUM. 239
(tricuspid insufficiency) or systolic retraction (tumultuous action of the
right ventricle), occurs in the later stages.
The urinary findings, cardiac symptoms, and clinical course in such
cases may be very similar to those of cases which are primarily renal in origin.
CASE OF CHRONIC MYOCARDITIS.
George G., a laborer, aged 56, was admitted to Prof. J. O. Hirschfelder's wards of
the City and County Hospital, San Francisco, on April 21, 1905, complaining of
asthma. His father had died of dropsy. The patient had had rheumatism in 18S7
and 1895, and has had to pass water during the night for some years.
Except for occasional shortness of breath he was well until two weeks before admis-
sion. Ha has had shortness of breath for the past two years; weakness and oedema of the
feet for the past two weeks.
PHYSICAL EXAMINATION. — Patient is a fairly nourished man ; face flushed and
venules dilated. No marked respiratory distress. Head is of peculiar shape. Pupils equal
and react to light and accommodation. No jaundice. Definite congenital external stra-
bismus of right eye. Eyes move well in all directions. Tongue coated. Throat clear;
tonsils not enlarged; no tracheal tug. No enlargement of lymph-glands. Thorax
barrel-shaped. Vocal fremitus equal except below level of tenth dorsal vertebra on right
side, where it is increased. Percussion note everywhere clear except over this area, where
breath sounds are distant and a few rales are heard. A few moist rales are also heard over
the apices. Heart . — Diffuse but feeble impulses in sixth left interspace 15
cm. from midline, from which point cardiac dulness extends above to the upper
border of the third rib and 6 cm. to the right of the midline in the fourth interspace. Heart
sounds feeble and accompanied by a soft systolic murmur. Neither sound
at base specially accentuated. Pulse very feeble, rapid, and irregular. There is no auricu-
lar wave upon the tracing of the venous pulse, and the arrhythmia is devoid of any
regularity in sequence. Radial arteries are very sclerotic. No cedema of feet or legs.
Patient has some cough, raising mucopurulent sputum, with large numbers of strepto-
cocci but no influenza or tubercle bacilli. Urine negative; sp. gr. 1010; no albumen,
casts, or sugar.
Ordered: Soft diet. Pil. cathart. co., ii, q. n.; sol. magnesii sulphatis sat., 30 c.c.
(,fi) q. A.M.; fluidextract digitalis, 0.3 c.c. (fi\,v) q- 4 h.; spir. glycerylis nitratis, q. £ h.,
commencing with 1 gtt. and increasing 1 gtt. at each third dose until patient feels throb-
bing of the head or flushing of face, after which next dose is to be omitted, and subsequent
doses of 1 gtt. less than the last are to be then given. Morphin. sulph., 0.008 Gm. (£ gr.)
p. r. n. (for extreme dyspnoea).
April 25, 7.00 P.M. No change in condition. No urgent dyspnoea. Haemoglobin
110 per cent. (Dare). Cyanosis still marked. No auricular wave in venous pulse. Heart's
action still weak and irregular.
1100 c.c. of blood were then removed from right arm, after which
haemoglobin fell to 65 per cent. The right border of cardiac dulness retreated
1cm. toward midline; upper border receded .5 cm.; left border unchanged. No change
in cardiac sounds nor in pulse tracing. No auricular wave in venous tracing. Blood-
press ure: before venesection, 7.00 P.M., maximal 107, minima)
87, pulse-pressure 20, pulse-rate 116, pulse-pressure X pulse-rate = 2320; after vene-
section 8.30P.M., maximal 112, minimal 92, pulse-pressure 20, pulse-
rate 112, pulse-pressure X pulse- rate = 2240 (see chart, page 176). Cyanosis has, however,
been replaced by a healthy color, and patient feels decidedly better. The improvement
in this case is due entirely to relief of the over-distended right heart, partly by diminution
of fluid, partly by diminution in the viscosity of the blood from the removal of so many
blood-corpuscles.
The patient passed a comfortable night and for several days felt somewhat better.
The course of symptoms and their relation, medication, and blood-pressure changes are
shown in the chart (Fig. 130). He was bled (350 c.c.) again on May 14, with
considerable benefit, and from that time his condition steadily improved.
240
DISEASES OF. THE HEART AND AORTA.
PARALLELISM BETWEEN MANIFESTATIONS OF PRIMARY MYOCARDITIS AND
PRIMARY NEPHRITIS.
The cases of chronic myocarditis with arteriosclerosis and secondary
renal involvement often very closely resemble those of primary renal
involvement with secondary myocarditis, since there are both cardiac and
renal failure in both conditions.
The following abstracts show the close parallelism between the symptoms and signs
of two such cases which in the early stages were almost exactly similar:
Chronic myocarditis (C. B.). (Diagnosis on
first admission " chronic nephritis " ).
Chronic nephritis (J. B.).
Illness..
Signs..
Urine.
Autopsy. . .
Shortness of breath, palpitation, cough,
swelling of abdomen and legs. Voids
during night.
Pale pasty color. Moist rales in chest.
Heart dilated to left (15 cm.); rapid
regular pulse 120; sclerotic radials.
Maximal blood-pressure. 180 mm.
Hg. Later, two attacks of angina
pectoris, with death in the second.
Varying from 2000-3000 c.c. per day,
with sp. gr. 1007, trace of albumen
and a few hyaline casts, to less than
1700 c.c., with sp. gr. 1020, large
amount of albumen, and numerous
hyaline casts.
Heart hypertrophied 650 Grn., auri-
cles dilated; intense cardiosclerosis,
with some hypertrophy. Both coro-
nary arteries diseased, left descend-
ing branch almost obliterated.
Kidneys large, purple, with a few
depressed scars and retention cysts;
cortex thicker than normal; no in-
crease in interstitial tissue; no
marked nephritic changes.
Adrenals — fatty degeneration of
cortical cells; no hypertrophy.
Shortness of breath, orthopnoea, swell-
ing of legs.
Pale pasty color. Moist rales in chest.
Heart dilated to left (14 cm.) and
right (5 cm.). Pulse rapid and
regular. Maximal blood-pressure
200 mm. Hg; later ranged from
130 to 170 mm. Hg. Fundi oculo-
rum normal. Later, Cheyne-Stokes
breathing. Delirium; headache; dul-
ness.
Urine varied from 400 c.c., with sp.
gr. 1022, 2.5 Gm. albumen per litre,
and numerous hyaline and granular
casts, to 2500 c.c., sp. gr. 1007, trace
of albumen, and few casts.
Heart dilated 350 Gm.; pale pink
walls, with slight fibrosis. Coronary
arteries sclerotic.
Kidneys small, scarred, cortex thin;
extensive epithelial degeneration
with corresponding proliferation of
connective tissue. Many glomeruli
have undergone fibrosis.
It may be almost impossible to establish differential diagnosis between
two such cases early in the disease. The course of the two cases, however,
showed clearly the divergence, the one toward the type of coronary sclerosis,
dilated heart, precordial pain, paroxysmal dyspnoea, the other toward
the ursemic, with progressive dulness, oliguria. Albuminuric retinitis did
not develop in the case cited, or the diagnosis might have been simplified.
Catalase Test. — Recent studies of M. C. Winternitz indicate that in
many cases at least the diagnosis may be made by a simple chemical test.
AFFECTIONS OF THE MYOCARDIUM. 241
He has found that in chronic nephritis the catalase of the blood is destroyed,
so that, when placed in contact with hydrogen peroxide, no oxygen is
liberated; while the blood of patients with cardiac weakness splits peroxide
as before. By this test he has made correct diagnosis in a number of doubt-
ful cases. However, this difference in the catalase manifests itself only in
the ursemic and preuramic states and is of value only in distinguishing
between these conditions and cases of myocardial weakness with drowsiness.
DIAGNOSIS.
In making the diagnosis it is most important to differentiate chronic
myocarditis from the following conditions: (1) organic valvular heart
lesions, (2) obesity, (3) primary cardiac overstrain, (4) primary chronic
nephritis, (5) chronic polycythsemia (erythraemia) with enlarged spleen, (6)
neurasthenia and psychasthenia, (7) chronic nephritis.
In cases of chronic myocarditis it may be extremely difficult to exclude an
organic valvular disease. This is especially true of mitral insufficiency, for
there is frequently a functional mitral insufficiency present with systolic murmur and
horizontal dilatation of the heart to the left. While it is true that the murmur of a func-
tional mitral insufficiency is rarely as rough as those of organic origin may become, and is
as a rule not as well transmitted into the axilla, nevertheless in individual cases these
differences may not be striking. Much more striking are the changes in the character of
the murmur as the patient's condition improves. In organic lesions the murmur will
become louder as improvement sets in, because the heart has become stronger. In
functional cases, though it may become louder at first, it will vary greatly in character
and in intensity, especially if the patient is made to exercise slightly. It may show a ten-
dency to disappear altogether during recovery.
The presence of a large, slow, heaving apex beat with slow pulse and systolic mur-
mur as well as a large slow pulse speaks in favor of organic mitral insufficiency (marked
hypertrophy of the left ventricle), though a functional papillary insufficiency might per-
sist from localized myocarditis of one of the papillary muscles in spite of the hypertrophy.
From other valvular diseases the diagnosis is comparatively easy. In
occasional cases the beat of the auricle becomes audible, suggesting the presystolic rumble
of mitral stenosis (Sewall); and occasionally blowing diastolic murmurs at the sternal
margin suggest organic aortic or pulmonic insufficiency. But such dilatations of the aortic
ring and conus arteriosus or cardiopulmonary murmurs are rather rare and are usually
transitory.
A functional tri cuspid insufficiency results so constantly from weak-
ening of the right ventricle that it is a lesion to be included under rather than excluded
from the picture of chronic myocarditis.
Primary cardiac overstrain may be excluded through the history, the
trouble in the latter condition coming on suddenly in a previously healthy individual
during or immediately after a severe strain, while in chronic myocarditis there is usually
a more gradual onset of symptoms, frequently traceable to febrile disease or intoxication.
Obesity is diagnosed from the general appearance of the patient, concomitant
chronic myocarditis being excluded when the trouble seems to bear a relation to too good
health rather than to disease. However, myocardial changes may be very hard to rule out.
The differentiation from chronic nephritis has been discussed above.
Chronic polycythaemia (erythnemia) with enlarged spleen may present
a picture very similar to primary chronic myocarditis, and in the later stages a consider-
able grade of myocarditis may be present. The size and hardness of the spleen, the color,
and the high blood count are the features upon which the diagnosis is made.
Neurasthenia, cardiac neuroses, or pseudocardiac visceral disease,
must be carefully excluded (see page 593). In the former the weakness \\hen self-
conscious and the strength when the mind is distracted are totally disproportionate;
while the myocarditic is reminded of his weakness by the stern hunger for air.
242 DISEASES OF THE HEART AND AORTA.
A careful general examination should always be made to exclude cardiac weakness
from enteroptosis and similar disorders that may reflexly give rise to a true cardiac
weakness.
The venous pulse helps somewhat, the presence of a visible " single venous
pulse" of auricular paralysis or extrasystoles suggesting myocardial change. However,
these may not be conclusive. For the past year the writer has had under observation a
young athlete with permanently irregular pulse and auricular paralysis and symptoms of
slight cardiac weakness on exertion. There are, however, no infectious diseases nor indis-
cretions to account for the production of a myocarditis, and, though the writer inclines
toward the diagnosis of the latter condition, it seems difficult in so healthy a young person
to exclude a neurotic basis.
TREATMENT.
The treatment of chronic myocarditis in the main should follow the
general scheme laid down in detail in Chapters IV., V., and VI. : re s t in bed
during the severer stages of failure, purgation, light diet, digitalis or
strophanthus in severe cases, graduated resistance exercises and Nauheim
baths during convalescence, gradually increasing walks and moderate
exercise before returning to every-day life. However, certain exceptions
must be noted, especially in the severer forms of myocarditis. For example,
digitalis only occasionally corrects an irregularity which has become
relatively permanent; though it is very useful in curing the milder forms
of irregularity, such as a continual bigeminal pulse or occasional ventricular
extrasystoles. It is less, indeed rarely, efficient in removing the irregulari-
ties arising at the auricles. On the other hand, in dealing with the advanced
grades of permanent arrhythmia with paralysis of the auricles, where there
is usually advanced myofibrosis and only a few of the heart muscle-cells
have survived the general atrophy, it is found that these often respond
well to small doses (about half the normal), whereas a normal dose
may give rise to symptoms of definite digitalis poi-
soning and often hasten death. This is not always to be avoided by the
apparently mild routine of administering the drug in "courses," since the
initial dose may be too large for the individual case. Each case must be
considered for itself, with these facts constantly borne in mind. The moder-
ate-sized initial dose or two followed by prolonged administration of very
small doses, suggested by Frankel (see page 179), seems to be the safest and
surest method in these cases, in order to prevent cumulative effects.
The recent introduction of single doses of strophanthin intra-
venously, which does not increase peripheral resistance, gives promise
of great results in the future, especially in this group of cases, although its
use has not yet become general enough to warrant a verdict.
As to graduated exercises, these are useful in many cases,
but are distinctly contraindicated after myofibrosis has set in and dyspnoea
persists while the patient is at rest. Mere arrhythmia, even with paralysis
of the atria, does not contraindicate their use, but points a warning, and
in many cases shows that the practitioner is treading on dangerous ground.
This applies also to Nauheim and other baths. Coronary sclerosis,
on the other hand, stenocardia, and severe pains down the arms furnish
distinct contraindications to all exercises except such as are necessary.
Even those of Schott must be carried out with the utmost precaution, and
the bending exercises may well be eliminated. The walks, etc., which
AFFECTIONS OF THE MYOCARDIUM. 243
terminate the treatment must be taken slowly and with the greatest pre-
caution in avoiding fatigue.
For the stenocardiac attacks and paroxysmal dyspnoea the greatest
relief is given by a pearl or two ofamyl nitrite followed by n i t r o -
glycerin and sodium nitrite. Indeed, these drugs furnish a
good deal of relief where the arteriosclerotic element is prominent.
When the blood-pressure is elevated above 140 mm. the salt in the
food should be reduced as low as possible (see page 168).
Venesection may be of the greatest value in tiding over periods
of acute dilatation, as shown in the case of G. G., even when, as in that case,
it produces no change in maximal or minimal blood-pressure or pulse-rate.
This case also exemplifies the fact that the venesection may often be of
great benefit before acute signs of cardiac overfilling set in, and then it is
to be regarded as " a stitch in time," the relief of the over-distention enabling
the heart to right itself. This may be owing to the fact that the over-
stretched fibres are allowed to gain their optimum length, or, on the other
hand, to the removal of a large number of red corpuscles from the circulatory
system, thus decreasing the viscosity. It is easier to pass than to seize the
moment at which a venesection would do most good.
In this every one some day or other receives his lesson. For example, the writer
had a patient under his care in San Francisco who one night had a moderate degree of
dyspnoea and cyanosis, though scarcely enough to cause alarm, and immediate venesec-
tion was considered. The right heart was not markedly enlarged and none of the objec-
tive signs seemed urgent. It was decided to do the venesection the next day, and the
patient was given fifteen milligrams (a quarter grain) of morphine, after which he fell
into a quiet sleep almost immediately. A couple of hours later he became restless and
sank gradually within an hour. We had let the right moment for the venesection pass,
and had masked the symptoms by the morphine.
Dangers from Morphine. — Another danger due to morphine lies
in the danger of habituation (see page 149), and the further danger that
in order to get it the patient will simulate a paroxysm of dyspnoea and
actually make himself sick or even endanger his life by the effort entailed
in doing so. Several patients whom the writer has gradually broken of
their morphine habit confessed to having done so, even though they knew
at the time that the simulation of dyspnoea made them feel worse.
THROMBI IN THE CARDIAC CHAMBERS.
When the circulation is slowed, and especially when one of the cardiac
chambers empties itself insufficiently, large clots are liable to form along
its wall (mural thrombi). This occurs especially in those portions which
are away from the axial stream, such as the recesses between the trabeculse
carnese and behind the papillary muscles, and also out in the tip of the auric-
ular appendages.
Thrombosis within the left auricle occurs quite frequently in mitral stenosis,
especially when the blood stagnates there during periods of overstrain. These thrombi
if fresh sometimes break loose to form emboli (page 151). Sometimes the clot loosened
from the auricular appendix is so large that it cannot pass through the auriculoventricular
orifice, but plugs the latter entirely, producing sudden death. When the clot remains
adherent to the wall for some time, more or less organization goes on. Thrombi which
244 DISEASES OF THE HEART AND AORTA.
adhere to the wall by a few strands of newly formed connective tissue are of every-day
occurrence, and constitute the classical sign for differentiation between intra-vitam and
post-mortem thrombi. In older thrombi the organization is more complete, so that a
thrombus mass may adhere to the cardiac wall by a pedicle of fibrous tissue. It is quite
possible that in some cases these thrombi vibrate to and fro and cause extrasystoles by
striking against the walls of the heart, just as occurred in Cameron's air-bubble experi-
ment (quoted on page 71). In several cases such masses have been known to act as a
ball-valve at the mitral orifice, giving rise to signs of mitral stenosis.
The symptoms and signs given by such thrombi are, however, very obscure. The
fact that they usually arise during the course of a cardiac failure adds to the complexity
of the clinical picture, and the diagnosis can rarely be made until embolism sets in.
In one case of mitral stenosis recently seen by the writer, in which the whole descending
abdominal aorta was suddenly plugged by an embolus and gangrene of both lower extremi-
ties set in, the diagnosis of a clot within the heart was warrantable. Such cases are, how-
ever, rare, and the diagnosis is then made after the harm has been done.
TUBERCULOSIS OF THE HEART.
In spite of the great frequency with which tuberculosis affects the lungs, pleura, and
pericardium, independent affection of the myocardium, endocardium, and valves is quite
infrequent.1 Thus Willigk found only 2 cases of tubercle of the myocardium in 1845
autopsies on persons with tuberculosis. Other observers confirm this view of its rarity.
Pathologically the lesions in tuberculosis of the myocardium resemble those of tuber-
cles elsewhere; they are somewhat more common in acute miliary tuberculosis than in
the chronic form, but in the latter are larger in size. The most common cardiac lesion of
tuberculosis is, however, neither miliary nor large solitary tubercles, but a fatty degener-
ation of the myocardium, due in part to the anaemia and in part to the toxins secreted
by the bacilli.
The effect of the tuberculous lesions upon the circulation is usually masked by the
general cardiac weakness due to the intoxication and anaemia, and, as v. Leyden states,
does not present any characteristic features. It is almost impossible to diagnose clinically,
for the symptoms and signs are quite independent of the tubercle. Often, as in Pollak's
case, a man of 65 who had a large tubercle in the wall of the auricle, there are no signs what-
ever, even of cardiac weakness. V. Tabora and Tilp report a case in which a systolic mur-
mur was heard over the apex, but this, of course, presents nothing characteristic and might
well have been due to the accompanying weakness of the myocardium or papillary muscles.
Indeed, as Romberg states, tuberculosis of the myocardium interests the pathologist rather
than the clinician.
SYPHILIS OF THE MYOCARDIUM.
Syphilitic affection of the heart is more frequent and presents a somewhat more
definite picture than tuberculosis. The most common form in which syphilis affects the
heart is the sclerotic lesion of the aortic valves (see page 361), though
in this case the pathological process originates in the aorta rather than in the myocardium.
Grassmann has called attention to the frequency with which signs of severe cardiac
weakness occur during the secondary stage of syphilis, accidental or functional
systolic murmurs being present in 40 per cent, of his cases. Dilatation, especially of the
right heart, was common, as well as alterations of rhythm, — sometimes arrhythmia,
sometimes bradycardia, sometimes tachycardia. Precordial pain and anginal
attacks were frequent. The blood-pressure was usually low, as was also the haemoglobin.
It is not impossible that the major role in many of these cardiac manifestations is played
by the anaemia and the fever rather than by spirochaete pallida within the heart muscle;
but the presence of tertiary myocardial lesions demonstrates that the latter play an im-
portant part. The diagnosis is based upon the above-mentioned symptoms arising
during the secondary stage. Treatment should, of course, be vigorous, and as a precau-
tionary measure the patient should be kept in bed until all cardiac weakness has passed.
If the symptoms do not rapidly subside, a few doses of digitalis or strophanthus may be
tuberculous endocarditis is discussed on page 303.
AFFECTIONS OF THE MYOCARDIUM. 245
given. Indeed, a few small doses of one of these drugs may well be given to relieve promptly
the dilatation and thus to forestall the danger that may lurk in an oedematous heart muscle
(see page 235)."
Cardiac lesions are rather common in congenital syphilis, though this is
not true of typical gummata. Thus Mracek found myocardial changes (acute myocarditis
with patches of perivascular infiltration of mononuclear cells) present in 24 out of 150
autopsies upon syphilitic foundlings, but gummata in only 4. The non-gummatous
changes are well described by I. Adler as infiltrations of mononuclear cells about the
blood-vessels and in the connective-tissue septa between the muscle-fibres. The striking
feature is early typical chronic endarteritis with thickening of the intima, destruction of
the elastica interna. This is often accompanied by hemorrhages into and about the vessel
wall. Clinically hereditary lues of the myocardium probably cooperates with the other
syphilitic lesions in bringing about the death of the child, but the importance of its role
cannot be judged, since it is rarely if ever the only luetic lesion present.
The tertiary myocardial lesions of adults are fairly common. The lesions
in 60 cases collected by Mracek showed the following distribution: gummatous myocar-
ditis, 10; fibrous myocarditis, 9; gummatous and fibrous, 8; endocarditis, 2; coronary
arteries alone, 3; pericardium alone, 1; myocardium and pericardium, 15; pericardium,
myocardium, and endocardium, 1; myocardium and coronary arteries, 1; all parts of the
heart, 6; cardiac ganglia, 4.
Judging by the number of cases of Adams -Stokes syndrome due to
lues (see page 471), the intraventricular septum seems to be a rather frequent site for
the lesions. Excepting such lesions as are so situated that they give rise to heart-block
or to the Adams-Stokes syndrome, the syphilitic lesions of the myocardium rarely give
distinct manifestations. A general myocardial weakness, shortness of breath, dilatation
with or without exertion in persons who have had lues (especially with other visceral
involvement) is suggestive evidence of fibrous luetic myocarditis with or without gumma.
The latter can rarely if ever be diagnosed. Huchard and Fiessinger report a case in which
dyspnoea set in suddenly 15 days before death, due to the growth of a gumma involving
the tricuspid valve, but even in such a case the data are too uncertain to permit a definite
clinical diagnosis. A positive Wassermann reaction, which Collins and
Sachs and W. Longcope have found so useful in the diagnosis of luetic aortic insufficiency,
is of less value in the diagnosis of luetic myocarditis, since the evidences of myocarditis
are in themselves less definite. However, in cases of chronic myocardial weakness in which
lues is suspected, the presence of a positive Wassermann reaction renders a vigorous ad-
ministration of mercurial inunctions or hypodermic injection of mercurial salts, as well
as vigorous doses of potassium iodide, highly advisable. In occasional cases it may be
possible to secure a considerable and permanent improvement by vigorous antiluetic
treatment, even when the Adams-Stokes syndrome is present; but it must not be forgotten
that the cardiac infiltrations are among the most stubborn of all luetic lesions.
TUMORS OF THE HEART.
Primary tumors of the heart are so rare that in 3000 consecutive autopsies at Niirn-
burg Thorel did not encounter a single one, and Hektoen, who reported three cases in 1893,
states that reports of only 110 cases of cardiac tumors were to be found in the Index Cata-
logue of the Surgeon-General's Library, and most of these were secondary.
Primary Tumors. — Bertheson was able to collect 28 primary tumors of the following
types: sarcoma 9; myxoma 7; fibroma 6; carcinoma 3; lipoma 2; cystoma 1. Link
(1909) has recently collected the data of 91 cases; 61 of these were as follows: carcinoma
7; fibroma 7; myoma 5; lipoma 8; sarcoma 13; myxoma 18; rhabdomyoma 1; tera-
toma 1; papilloma 1. In addition to these Knox and Schorer and Wolbach have collected
12 cases of rhabdomyoma; 6 of which were associated with other malformations, especially
cerebr.-il M-l<-r«sis and hydrocephalus.
Hektoen calls attention to the fact that the heart, and hence also its primary tumors,
are of mesoblastic origin; which accounts for the relative rarity of primary car-
cinomata and the preponderance of sarcomata. Thorel believes that many of the fibro-
mata found represent merely old organized thrombi clinging to the heart wall, and believes
that many of the (relatively frequent) myxomata represent merely degenerating forms of
246 DISEASES OF THE HEART AND AORTA.
such thrombi. The lipomata he regards merely as abnormally large pockets of epicardial
or intramural fat rather than as true tumors.
As Regards site, Link found in right auricle 10; left auricle 24; right ventricle 14;
left ventricle 8; valves 16; interauricular septum 2.
Metastatic Involvement of the Heart—Secondary neoplasms affecting the heart are
somewhat more common, and scarcely any pathologist of experience has failed to meet
with them, especially in cases with multiple metastasis. Of the metastatic neoplasms
carcinomata are the most frequent. Thorel encountered 6 instances in his 3000 autopsies,
the primary sites being uterus 2, rectum 1, gall-bladder 1, kidney 1, lung 1.
Geipel stated that in a series of 16 cases of carcinoma of the oesophagus 6 gave metas-
tases to the heart; but this is an unusually high percentage, and Thorel from his experi-
ence does not regard such oesophageal tumors as especially liable to cardiac metastases.
Clinically the presence of a tumor in the heart in itself exerts little influence, unless,
as in Luce's case of sarcoma, it presses upon the auriculoventricular bundle and produces
heart-block, or it is so situated as to produce either stenosis or regurgitation at a valvular
orifice. The benign tumors exert little or no effect upon the force or rhythm of the heart;
the malignant tumors give rise merely to signs of cachexia in which the cardiac weakness
seems incidental rather than primary. In cases of generalized carcinosis and sarcomatosis,
those in which the metastatic nodules are most common, the cachectic myocardial weak-
ness is still more intense whether the tumors affect the heart or not. The accidental finding
of a loud harsh murmur suddenly developing and progressing with the metastasis elsewhere
in the body is very suggestive; but this is rarely encountered.
In some cases in which the tumors are superficial, pericarditis may set in. Effu-
sion, especially blood-stained, is rather common under these conditions
and the signs of the latter may be the first and only sign of the condition.
In 1905 the writer aspirated a pericardial exudate which contained 10 per cent, of
haemoglobin and some methsemoglobin. The patient died the next day, and autopsy
revealed carcinomatous masses in the myocardium wall and pericardium, which were
metastases from a very small primary carcinoma of the bronchus quite unsuspected during
life. The finding of tumor cells in such an exudate would, of course, give the diagnosis.
Tumors of the heart, even if diagnosed, would, of course, be inoperable.
BIBLIOGRAPHY.
MYOCARDITIS.
Sobernheim: Praktische Diagnostik der innere Krankheiten, Berl., 1837.
Boettcher, A., and Zenker. Quoted from Krehl.
Cullen, E. K.: So-called Spontaneous Focal Myocarditis and the Occurrence of Calcifi-
cation of the Degenerate Muscle Fibres, Bull. Johns Hospkin Hosp., Bait., 1906, xvii,
267.
Dietrich: Die Querlinien des Herzmuskels, Verh. d. Deutsch. pathol. Gesellsch., Jena,
1906, x, 40.
Buhlig, W. H. : A Preliminary Note upon Certain Mechanical Microtechnical Factors
Concerned in the Production of the Segmentation and Fragmentation of the Myo-
cardium, J. Med. Research, Bost., 1902, ii, 428.
Krehl, L.: Beitrag zur Pathologic der Herzklappenfehler, Deutsch. Arch. f. klin. Med.,
Leipz., 1890, xlvi, 454. Beitrag zur Kenntniss der idiopathischen Herzmuskeler-
krankungen, ibid., 1891, xlviii,.414. Clinical pathology (transl. by A. W. Hewlett),
Phila., 1905.
Romberg, E.: Ueber die Erkrankungen des Herzmuskels bei Typhus abdominalis, Schar-
lach und Diphtheric, Deutsch. Arch. f. klin. Med., Leipz., 1891, xlviii, 369.
Aschoff, L.: Zur Myokarditisfrage, Verh. d. Deutsch. pathol. Gesellsch., 1904, viii, 46.
Geipel, P.: Untersuchungen ueber rheumatische Myokarditis, Deutsch. Arch. f. klin. Med.,
Leipz., 1906, Ixxxv, 75.
Coombs, C.: The Myocardial Lesions of Acute Rheumatic Infection, Brit. M. J., Lond.,
1907, ii, 1513. Rheumatic Myocarditis, Quart. J. Med., Oxford, 1908-9, ii, 26.
Bracht, E., and Wachter: Beitrage zur Aetiologie und pathologischen Anatomic der Myo-
carditis rheumatica, Deutsch. Arch. f. klin. Med., Leipz., 1909, xcvi, 493.
Cole, R. L, 1. c., p. 320.
AFFECTIONS OF THE MYOCARDIUM. 247
Freund, G.: Zur Kenntniss der acuten diffusen Myocarditis, Berl. klin. Wchnschr., Berl.,
1898, xxv, 1077.
Pearce, R. M.: Experimental Myocarditis; a Study of the Histological Changes following
Intravenous Injections of Adrenalin, J. Exper. Med., N. York and Lancaster, 1906,
viii, 400.
Fleischer, M. S., and Loeb, Leo: Experimental Myocarditis, Arch. Intern. M., Chicago,
1909, ii, 78.
De la Camp, Moritz, Dietlen, Hornung. See Chapter on the Physiology of Cardiac Over-
strain.
Roily, F.: Ueber die Wirkung des Diphtheriegiftes auf das Herz, Arch. f. exper. Pathol. u.
Pharmakol., Leipz., 1899, xlii, 283.
V. Stejskal, K. Ritter : Kritsch-experimentelle Untersuchungen ueber den Herztod in
Fogle von Diphtherietoxin, Part I, Ztschr. f. klin. Med., Berl., 1902, xliv, 367; Part
II, ibid., 1904, li, 129.
Mackenzie, J.: New Methods in the Study of Affections of the Heart, Brit. M. J., Lond.,
1905, i, 521.
Hibbard, C. M.: Heart Complications in Diphtheria, M. and S. Rep., Bost. City Hosp.,
Bost., 1898.
Forster, Fr.: Ueber Myokarditis und Gefasserkrankungen im Kindesalter insbesondere
nach akuten Infektionskrankheiten, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxv,
35.
Hallwachs: Ueber die Myocarditis bei Diphtheric, Deutsch. Arch. f. klin. Med., Leipz.,
1899, Ixiv, 770.
Ziegler, E.: Lehrbuch der Pathologic und der pathologischen Anatomic, 9th ed., Jena,
1898.
Huchard, H.: Etude clinique de la cardio-sclerose,. Rev. de me"d., Par., 1892, xii, 421.
Dehio, K.: Myofibrosis cordis, Deutsch. Arch. f. klin. Med., Leipz., 1899, Ixii, 1.
Radasewsky: Ueber die Muskelerkrankungen der Vorhofe des Herzens, Ztschr. f. klin.
Med., Berl., 1895, xxvii, 529.
Albrecht, E.: Der Herzmuskel und seine Bedeutung fiir die pathologische Physiologic
und Klinik der Herzens, Berl., 1903.
Aschoff, L., and Tawara, S.: Die heutige Lehre von den pathologisch-anatomischen
Gnmdlagen der Herzschwache, Jena, 1906.
Mackenzie, Keith, Wenckebach, Schonberg. Qpoted on p. 15.
Saigo: Purkinjeschen Muskelfasern bei Erkrankungen des Myokards. Verhandl. d. deutsch.
path. Gesellsch., Jena, 1908, xii, 165.
Hering, H. E.: Ueber kontinuerliche Herzbigeminie, Deutsch. Arch. f. klin. Med., Leipz.,
1904, Ixxix, 175.
Marey, E. J.: La circulation du sang a 1'gtat physiologique et dans les maladies, Paris,
1881.
Knoll, Ph.: Ueber die Veranderungen des Herzschlages bei reflectiorischer Errazung des
vasomotischen Nervensystems; sowie bei Stiegerung des intracardial Drucks ueber-
haupt, Sitzungsber. d. k. Akad. d. Wissensch., Wien, Abth. Ill (Physiol. Anat. u.
Med.), 1872, Ixv-lxvi, 195.
Hering, H. E.: Ueber die haufige Kombination von Kammervenenpuls mit Pulsus irreg-
ularis perpetuus, Deutsch. med. Wchnsch., Leipz., 1906, xxxii, 1.
Gerhardt, D.: Arhythmia perpetua des Pulses, Deutsch. med. Wchnschr., 1907, xxxiii,
448.
Theopold, J.: Ein Beitrag zur Lehre von der Arkythmia perpetua, Deutsch. Arch. f. klin.
Med., Leipz., 1907, xc, 77.
Hewlett, A. W.: The Interpretation of the Positive Venous Pulse, J. Med. Research,
Bost., 1907, xvii, 119.
Mackenzie, James, and Gibson, G. A. Quoted on p. 78.
TUBERCULOSIS OF THE MYOCARDIUM.
Pollak, S.: Ueber Tuberculose des Herzmuskels, Ztschr. f. klin. Med., Berl., 1892, xxi, 185.
Brosch, A.: Ein Fall von Herztuberkulose mit typischen Weilschen Symptomenkomplex,
Wien. med. Pr., 1896, xxxvii, 985.
248 DISEASES OF THE HEART AND AORTA.
V. Leyden, E.: Ueber die Affection des Herzens mit Tuberculose, Deutsche med. Wchn-
schr., Leipz., 1896, xxii, 1.
V. Tabora and Tilp: Zur Kasuistik der Herztuberkulose, ibid., 1908, xxxiv, Vereinsbeil 805.
CARDIAC SYPHILIS.
Grassmann: Ueber acquerirte Syphilis des Herzens, Miinchen. med. Wchnschr., 1897,
xliv, 473, 506, 522. Klinische Untersuchungen an den Kreislauforganen im Fruh-
stadium des Syphilis, Deutsches Arch. f. klin. Med., Leipz., 1900, Ixix, 58, 264.
Mracek, F.: Die Syphilis des Herzens bei erworbener und ererbter Lues, Arch. f. Dermatol.
u. Syph., Wien and Leipz., 1893, xxv (Erganzungshefte), p. 279.
Adler, I.: Observations on Cardiac Syphilis, Trans. Assoc. Am. Phys., Phila.. 1898, xiii,
73; and N. York M. J., 1898, Ixviii, 577.
Sacharjin: Die Lues des Herzen von der klinischen Seite betrachtet, Deutsches Arch. f.
klin. Med., Leipz., 1889, xlvi, 388.
Le Count, E. R.: Gummata of the Heart in a Case of Congenital Syphilis, J. Am. M. Assoc. ,
Chicago, 1898, xxx, 181.
Huchard, H., and Fiessinger: Syphilis gommeuse du coeur, Rev. de Med., Par., 1907, xxvii.
TUMORS OF THE HEART.
Thorel, C.: Pathologic der Kreislaufsorgane, Ergebn. d. allg. Path. u. path. Anat. d. Mensch.
u. d. Tiere, herausg. v. Lubarsch u. Ostertag., Wiesb., 1903, ix, 1 Part; and 1907,
xi, Pt. 2. With excellent bibliography.
Hektoen, L.: Three Specimens of Tumors of the Heart, etc., Med. News, Phila., 1893,
Ixiii, 571.
Berthenson, L.: Zur Frage von der Diagnose primarer Neoplasmen des Herzens, Myxom
des linken Vorhofs, Arch. f. path. Anat., etc., Berl., 1893, cxxxii, 390.
Link R.: Klinik der primarer Neubildungen des Herzens, Ztschr. f. klin. Med., Berl.,
1909, Ivii, 272.
Knox, J. H. M., and Schorer, E.: A Multiple Rhabdomyoma of the Heart Muscle, Arch.
Ped., N. York, 1906.
Wolbach, S. B.: Congenital Rhabdomyoma of the Heart, J. Med. Research, Bost., 1907,
xvi, 495.
Geipel. Quoted from Thorel.
Luce. Quoted on p. 478.
X.
ARTERIOSCLEROSIS.
NORMAL CHANGES IN THE ARTERIES DURING LIFE.
A certain degree of progressive change in the walls of the arteries
occurs normally throughout life, and is therefore not to be considered
pathological. The condition of the arteries normal to a man of thirty
would be thoroughly abnormal in a child, and those normal for a man of
seventy would in turn be regarded as abnormal in a man of forty.
Thus, Thayer and Fabyan state that "at birth the artery (radial) is delicate,
translucent, extremely thin, and collapsing. The surface on opening is perfectly smooth.
The i n t i m a consists of a single endothelial layer lying directly on the surface of a deeply
undulating elastica interna. The media, which consists of transversely arranged smooth
muscle-fibres with rather large vesicular nuclei, has a depth of seven to eight layers of cells.
Connective tissue, if present in the intima and media, is extremely scanty, none being
revealed by the Mallory or Van Gieson stains. There is, however, a relatively large amount
of elastic tissue which appears on cross section as very thin, parallel, slightly wavy lines.
The elastica externa is neither as coarse nor as deeply undulating as the interna.
" The adventitia, considerably thicker than the media, consists of compact con-
nective-tissue fibres with relatively large nuclei. The elastic fibres are fairly numerous.
" By the middle of the first decade, the intima has become thicker owing to the appear-
ance of a fresh layer of elastica interna, while more muscle-fibres appear in the media.
"10-20 years. Walls of the vessel become thicker but still collapsed. Intima
and media thicker, the elastic tissue being relatively less marked.
"21-40 years. Slight further general thickening of intima and media. A sec-
ond elastic layer appears in the intima. In the media the connective tissue begins
to be demonstrable by Van Gieson's stain.
"41-50 years. Decided change. Lumen cf the vessel remains open. Areas of
calcification in the deep layers of the intima are frequent. The media reaches its
maximum thickness. There is a good deal of connective tissue.
"After the fifth decade there is a progressive increase in the thickness of the intima
.... and a diffuse connective-tissue thickening becomes the common type The
media after the fifth decade becomes on the whole rather thinner; there is a marked
increase in the connective tissue.
"Calcification in the deep layers of the intima becomes more common with
age, four out of five cases in the eighth and ninth decade showing this change."
PATHOLOGICAL ANATOMY.
Theoretical Considerations. — Pathologically, arteriosclerosis is char-
acterized by the occurrence of changes in and thickening of the intima,
which was supposed by Rokitansky to be due to the' depositing of cells
directly from the blood stream; by Virchow to be a true inflammatory
hyperplasia as the result of some "formative s t i in u 1 u s " ; and by
Thoma to be a compensatory thickening of the wall in order to
diminish the lumen of the vessel after the stretching which occurred under
the increased blood-pressure with which it was usually associated. Jores, on
the other hand, regards this as a true hyperplasia resulting from
249
250 DISEASES OF THE HEART AND AORTA.
the high blood-pressure but independent of the lumen of the vessel, return-
ing to a certain degree to the view of Virchow. These observers con-
sidered the' changes in the intima as primary, and
tended rather to neglect the second important change which characterizes
arteriosclerosis, namely inflammatory changes within the media.
On the other hand, Koster and his pupils called attention to the im-
portance of degenerative and calcareous changes in
the media. and adventitia as well as in the intima. Koster
studied the inflammatory process very carefully by means of serial sections
and injected specimens, and claimed that the arteriosclerotic lesion always
took its origin in the adventitia as an infiltration surrounding
the vasa vasorum like a sleeve. This infiltration followed the
vasa vasorum into the media. Koster found that in the normal artery
the vasa vasorum do not pass deeper than the outer third of the media,
though in certain arteries (notably those of the brain and the lungs) there
was a fine capillary network penetrating the deeper layers of the media as
well and spreading along the medial surface of the elastica interna.
Changes in Vasa Vasorum. — This view is confirmed by v. Ebner
(in Kolliker's Handbuch der Gewebelehre) , who states that "the media
of the larger arteries and veins, according to the consensus of opinion
of many authors, contains blood-vessels, though in small numbers and only
in the external layers ; whereas the inner layers of the media and the intima
seem to be always free from vessels (in the ox the wall of the vena cava is
richly supplied with vessels even down to the intima) .
The infiltration about the vasa vasorum follows these paths, setting up areas of
infiltration, necrosis, and calcification in the smooth muscle and elastic fibres of the media.
When it penetrates to the elastica interna a small area of this is first injured, the inflamma-
tion acts as a stimulus, and hyperplasia of the intima sets in. The intima becomes thick-
ened until its cells undergo spontaneous fatty degeneration, after which they either calcify
or the capillary network penetrates through the elastica interna and a true process of organ-
ization and proliferation of connective tissue goes on.
Koster admits that it is possible that the degenerative and hyperplastic changes in
the intima may go on without the entrance of blood-vessels, as do those seen in inflamma-
tions of the cornea; but he states that if the lesions are followed in serial sections there
is almost always a demonstrable continuity between the patches of endarteritis, mesar-
teritis, and periarteritis.
The number and size of the vasa vasorum and the richness of the capil-
lary network are always increased in arteriosclerosis and in phlebosclerosis.
He states that endarteritis occurs only in .arteries that have vasa vasorum,
that is, in the larger arteries and in the smaller arteries of the brain and
the lungs.
Koster's version is extremely fascinating, especially since it presents a
simple explanation of a complex picture, and, on the other hand, presents
a clear analogy with the processes involved in myocarditis, endocarditis,
and other lesions. As far as the media and adventitia are concerned his
findings have been confirmed by Ophiils, whose careful study constitutes
one of the most important and clearest of the recent contributions to the
subject. Ophiils, however, was unable to demonstrate any constant rela-
tion between lesions in the media and those in the intima, and believes that
they are produced independently though from the same general cause.
ARTERIOSCLEROSIS. 251
He states that " anatomically arteriosclerosis of the aorta is a unit. It is
a chronic inflammatory process of the vessel wall which attacks all the coats
simultaneously, which as a rule first produces changes in the intima and
adventitia." He believes therefore that, as Koster suggested, the changes
in the intima begin as parenchymatous changes without the presence of
blood-vessels, like the inflammations within the cornea.
CLASSIFICATION OF ARTERIOSCLEROTIC LESIONS.
Following this view in adopting a pathological classification, one might
distinguish the following groups of arteriosclerotic lesions, dependent upon
the arterial coat most affected and the distribution of the lesions within
that coat.
ANEURISM raiAnnmraiooo*
THROMBCWOT150BUTEIW6 INOAKT[3ITI5 06UTERAN5 WDARTERITI5 ^&zr^ ME5ARTERITI5
FIG. 153. — Various types of arteriosclerotic lesions. (Schematic.)
I. Adventitia chiefly affected (no weakening of arterial wall).
1. Localized or nodular infiltrations (periarteritis nodosa).
2. Diffuse infiltrations about the vasa vasorum (causing uniformly thick-
ened arteries which give the sensation of thick rubber tubing).
II. Lesions in the media predominate (with .weakening of the arterial wall),
especially common in syphilis.
1. Localized necrosis of elastic tissue with calcification
(atheroma) (pipe-stem or "goose-neck" arteries, Monckeberg's arterio-
sclerosis, experimental toxic arteriosclerosis).
2. Diffuse or patchy medial f i b r o s i s with more or less calcifica-
tion, often leading to aneurism.
III. Changes in the intima predominate (with no weakening of arterial wall).
1. Hyperplasia of intima with fatty degeneration at its centre (acute aortitis),
(a) without, (b) with calcification of the areas of fatty degeneration (athero-
matous placjue or "ulcer," "endarteritis deformans," Longcope).
2. Simple hyperplasia of intima (diffuse endarteritis) with increase of
elastic fibres, finally leading to
3. Obliterative endarteritis, in which the process is still more
chronic and intense and capillaries enter from the vasa vasorum.
According to Weiss and v. Winivvarter, and later Buerger, this last is to be sharply
differentiated from thromboangitis obliterans, in which intravascular co-
agulation precedes or is independent of the change in the intima, in which the lumen of
the vessel finally becomes obliterated by secondarily forming granulation tissue devoid
of elastic fibres and arising from about the newly formed ends of the vasa vasorum.
Periarteritis nodosa (Kussmaul and Maier) (supra-arterial fibroid
nodules) , one of the rarer forms of arteriosclerosis, is produced by the for-
mation of small areas of nodular infiltrations in the adventitia, and gives
the vessel a nodular appearance and consistency. It is almost always
closely associated with inflammatory changes in the media and a local pro-
liferative endarteritis (Ziegler).
252
DISEASES OF THE HEART AND AORTA.
Diffuse Periarteritis. — The diffuse thickening of the adventitia (periar-
teritis) is more common, occurring about the arteries of the brain, about
the coronary arteries in myocarditis, and in many other organs in subacute
inflammatory processes. In the radial and other large arteries it seems to
be quite common. The uniformly thickened arteries of leathery consistency
which are so commonly met with in young or middle-aged persons who do
hard work seem to be of this type, though the fact has not yet been settled
with definiteness. Whether such changes may be transitory or are always
permanent has not been definitely settled. The boy of six cited below
(page 259) may perhaps represent such a case.
FIG. 154. — Cross section of a radial artery showing arteriosclerotic changes in the media. (Photo-
micrographs by Dr. C. S. Bond.) A. Cross section of the entire artery (low power). B. Lower left-
hand corner of the same specimen (highly magnified) showing destruction of the elastica interna and
thickening of the intima. C. Orcein specimen showing destruction of the elastic fibres (E) of the media
with proliferation of white fibrous tissue (F) and blood-vessels (BL). (Kindness of Prof. W. Ophiils.)
Medial Changes (Mesarteritis) . — The rigid "pipe-stem" or "goose-
neck" radial arteries often met with in very old persons are formed by the
presence of areas of degeneration and calcification within the tunica media.
This condition occurring without any changes in the intima has been de-
scribed in man by Monckeberg, and represents the type of arteriosclerosis
or arterionecrosis produced experimentally in animals with bacterial
toxins, acids, adrenalin, and alkaloids.
Calcification. — According to Klotz, Wells, and Baldauf, the process of calcification
seems to go on in the following way: As a result of the inflammatory changes, the muscle
cells degenerate and the lecithins become split up into fatty acids, glycerophosphic acid,
and cholin, causing the appearance of a fatty degeneration. The calcium and magnesium
in the serum then enter into combination with the phosphoric acid and are precipitated to
ARTERIOSCLEROSIS.
253
form calcareous plaques and granules in the media. Klotz believes from histo-chemical
evidence that there is intermediate or concomitant formation of calcium soaps, but Wells
and Baldauf have not found soaps on chemical analyses. Baldauf and also Selig find that
most of the calcium is in the form of phosphate and sulphate, little as carbonate. The ash
from arteriosclerotic plaques contained CaO 53.384 per cent., Fe2O3 0.25 per cent., Na.,0
0.72 per cent., K only traces, P,O5 40.19 per cent., SO3 0.43 per cent., Cl trace, F negative,
CO, traces (Selig).
Klotz finds that the calcium is by no means always deposited in the patches of athe-
roma, but exists also as rows of fine granules between the muscle-fibres. In this condi-
tion it gives no macroscopic evidence of its presence, and merely causes a slight increase in
the rigidity of the artery. When the necrosis of the arterial
wall proceeds more slowly, the phosphoric acid or glycero-
phosphoric acid derived from the lecithin is removed by the
blood-vessels (capillaries of the vasa vasorum) which enter the
diseased area of the media, and the injured elastic tissue is
replaced by fibrous tissue without the deposition of calcium.
Whether the calcium is deposited or not, the
area of diseased media constitutes a weak-
ened portion of the wall and is the lesion which
in the large arteries is particularly responsible for
aneurism formation (see also page 521). It has
been claimed by some writers (Heiberg, Heller,
and others) that this lesion was confined to luetic
cases, but both clinical and experimental data
show that it is due to non-luetic lesions about
as frequently as are any of the other lesions of
arteriosclerosis (Ophiils).
Intimal Thickening. — The lesion which Vir-
chow, Thoma, and many writers have regarded
as the fundamental one in arteriosclerosis is thick-
ening of the intima. Virchow believed that it arose
as an inflammatory hyperplasia resulting from some
"formative stimulus" within the blood stream.
Thoma believed that this stimulus was the me-
chanical factor of high blood-pressure, and that
the thickening of the intima represented a com-
pensatory hypertrophy to prevent aneurismal dila-
tation; but Ophiils has shown that, in marked
contrast to the area of medial disease, there are no
bulgings of aortic wall at the areas of intimal
atheroma, even when the artery is distended under
a pressure of 160 mm. Hg.
The "formative stimulus" is probably not mechanical but
chemical, perhaps the same as those which have been shown experimentally
to give rise to arterionecrosis in small animals. Under the influence of these
stimuli the intimal layers undergo hyperplasia, with increase of both fibrous
tissue and elastic fibres (Fig. 156). Since, as Koster has shown, there are
no blood-vessels, but only lymph spaces or lacunae, the hyperplasia soon
reaches its limit, and under the further influence of the toxic agent the
cells at the centre undergo "fatty degeneration" from ischasmia. ^udi
areas present at first a translucent appearance and are known as areas of
Fio. 155. — Arteriosclerosis
of the descending aorta, show-
ing atheromatous plaques.
254 DISEASES OF THE HEART AND AORTA.
"acute aortitis." Later calcium salts are usually deposited (as described
above), and they become converted into calcined plaques of atheroma or
atheromatous ulcers. When the process is more chronic there is usually
a wandering in of capillaries from the media after the manner described
by Koster, and under the influence of the improved nutrition the intimal
hyperplasia may go on at an increased rate even to the obliteration of the
lumen (endarteritis obliterans). Thromboangitis obliterans will be con-
sidered in Chapter IX.
Unity of Arteriosclerotic Processes. — Although a large number of
writers attempt to put each case into one or the other of these groups,
Ophiils has shown, by a careful complete study of seventy consecutive
unselected cases, that such divisions are based upon unessential differences
FIG. 156. — Atheromatous plaque, showing the changes in the intima. (Photomicrograph by Dr.
Charles S. Bond.)
and that, as a matter of fact, any or most of the forms may arise in the
same case. This division was attempted especially by Heiberg, Heller,
and his pupils, who believed that mesarteritis, particularly when it attacked
the first part of the aorta and the ascending arch, was characteristic of
syphilitic disease. While it is quite true that syphilis may give rise to a
mesarteritis, and occasionally even to the formation of miliary gummata
in the adventitia,1 nevertheless these lesions are far from characteristic,
and very similar non-luetic structures occur about thrombosed vasa vasorum.
Moreover, Ophiils was unable to find any difference in the distribution of
luetic and non-luetic arteriosclerotic lesions in the seventy cases of his
series.
ETIOLOGY.
The most important etiological factors in the production of arterio-
sclerosis in man are age, hard work, alcohol, syphilis, and the more acute
1 Some writers claim to have found the spirochaete pallida in these lesions by means
of the rather questionable Levaditi's silver nitrate method, though Ritter, Buerger, and
many others have failed in spite of painstaking search in many cases. However, Collins
and Sachs, Longcope, and Clough and Guthrie at the Johns Hopkins Hospital have been
able to diagnose luetic arteriosclerosis during life by the Wassermann reaction.
ARTERIOSCLEROSIS. 255
infectious diseases, especially typhoid fever. The relative frequency of
these causal factors, as indicated by the palpability of the radial artery in
4000 consecutive cases admitted to the Johns Hopkins Hospital, has been
made the subject of a careful study by Thayer and Brush.
These observers found palpable arteries in the following percentage of the patients
under fifty years who had been subject to various etiological factors:
After scarlatina, radials palpable in 16.4 per cent.
No causal factor, radials palpable in 16. 5 per cent.
Pneumonia, radials palpable in 17 per cent-
Diphtheria, radials palpable in 17 per cent.
Malaria, radials palpable in 20 per cent.
Typhoid fever, radials palpable in 26 per cent.
Rheumatism, radials palpable in 34 per cent.
Alcohol, radials palpable in 46.8 per cent.
Hard work, radials palpable in 57 . 5 per cent.
Richard Cabot takes exception to these 'findings of the high frequency of arteriosclerosis
after alcohol, basing his conclusions upon autopsies of dipsomaniacs under fifty in whom
he says arteriosclerosis was not present in more than twenty per cent. His exceptions to
Thayer's findings are, however, somewhat against the general consensus of opinion, as well
as against the experimental evidence of Aubertin, who produced arteriosclerosis and cardiac
hypertrophy in rabbits by the injection of alcohol. On the other hand, Cabot is supported
by Fahr, who performed 309 autopsies on habitual drunkards dying at the Harbor Hospital
of Hamburg and found arteriosclerotic changes no more common than in abstemious indi-
viduals, occurring in 95 cases, 82 of whom were over 40 years of age. Only 7 drunkards in
his series died before 40 from causes referable to arteriosclerosis. Similar changes existed in
only six other patients under 40. Unlike Aubertin, Fahr was unable to produce arterio-
sclerosis in rabbits by administration of alcohol for over two years. From this it would
appear that the evil effects of alcohol have been considerably exaggerated, at least as far
as the arteries are concerned. It must be borne in mind that indulgence in a certain
amount of alcohol is almost universal, especially in those persons who do hard work, hence
it is extremely difficult to segregate these factors in any large number of cases. If, for
example, a patient has had typhoid fever, has used alcohol, and has done hard work, it is
not logical to enter his name into each of the three columns, for it is not possible to deter-
mine which of th^ factors is the most important.
Fortunately, however, for the decision of these doubtful points, the experiments of
Pic and Bonnamour (1. c.) upon experimental adrenalin arteriosclerosis have shown that
where two factors are actin.g together, arteriosclerosis may be produced
in conditions in which it could not be brought about by one of them alone. Thus, tuber-
culosis + adrenalin yielded arteriosclerosis in young rabbits which would not have shown
arteriosclerosis after adrenalin alone, and there is no doubt that the same is true in man.
Syphilis is a most important factor, especially in the arteriosclerosis
which occurs below the age of thirty-five. As stated above, it was supposed
by Heiberg, Heller, and their pupils that luetic arteritis assumed a definite
type, the media, the adventitia, and especially the vasa vasorum showing
considerable small round-celled infiltration; but, although it is possible
that the media and adventitia are attacked more constantly than in other
forms, this form is not to be regarded as specific. The tendency to form
lesions above the semilunar valves and along the ascending aorta is by no
means confined to arteritis of luetic origin (Ophuls), though extremely
frequent in the latter (Osier, Collins and Sachs, Longcope). A positive
Wassermann reaction is often obtained in cases of
luetic aortitis in which there are no other active
luetic processes.
256 DISEASES OF THE HEART AND AORTA.
Lead poisoning (especially chronic plumbism) and gout are
important etiological factors, as is also chronic nephritis. Overeating
is thought to play an important role, especially when the diet is rich in
meats, sweetbreads, livers, kidneys, etc., — in other words, in purin bodies
and in kreatin. The exact role of these substances has not been carefully
studied, although Croftan found that long-continued injection of 0.5 to
5.0 mg. xanthin into rabbits caused a rise of forty millimetres in blood-
pressure, as well as sclerotic changes at least in the renal arteries. (He does
not describe the condition of the other arteries.) From the stand-point
of both blood-pressure and gaseous metabolism it has been shown that the
digestion of large meals materially increased the work of the body, pro-
ducing thereby an effect not dissimilar to that of hard physical exercise
(increase in pulse-pressure, increase in pulse-rate, increase in CO2 output)
(effect of large meal, after Erlanger and Hooker). It is therefore quite nat-
ural that overeating should rank with hard work as a main cause of arte-
riosclerosis, but the exact extent of its occurrence is more difficult to deter-
mine in a large series of cases than in an individual case in private practice.
Lastly, and still more important in the etiology of arteriosclerosis, are
age and heredity (Israel) .
Thus, Osier states that "entire families sometimes show this tendency to early
arteriosclerosis, a tendency which cannot be explained in any other way than that in the
make-up of the machine bad material was used for the tubing." This is especially true as
regards alcoholism, as has been shown in a recent statistical study by Emerson, who found
that this factor was of more importance than the drinking of alcohol by the individual
himself in determining arteriosclerosis and longevity, and that an alcoholic ancestry was
very frequently followed by a generation with a tendency to early arteriosclerosis.
Experimental Arterionecrosis in Animals. — A most interesting side
light upon the genesis of arteriosclerosis has been thrown by attempts to
produce it experimentally in animals, especially in rabbits and guinea-
pigs. The lesions which have been produced cannot be termed true arterio-
sclerosis like that seen in man, but are confined to the media and adventitia,
the intima always remaining clear. The reason for this is not evident.
Even the possibility that in these small animals the blood supply of the
arterial wall is different from that in man, and that owing to this difference
lesions occur most readily in the media, does not hold, since Ophiils has
demonstrated the occurrence of spontaneous endarteritis in rabbits. The
experimental and clinical conditions seem to be closely analogous, but it
is not possible to draw an absolute parallelism between them.
Gilbert and Lion have been able to produce arteriosclerosis experimentally in ani-
mals by the injection of bacterial toxins, and this has been confirmed by Klotz.
This fact is of great importance, not only from the stand-point of experimental arterio-
sclerosis, but also because it establishes the importance of bacterial disease in the etiology
of arteriosclerosis met with clinically.
The earliest observation of arteriosclerosis brought about by toxic action of organic
compounds, and one which establishes beyond doubt the deleterious action of tobacco
upon the arteries, is that of Isaac Adler, demonstrating sclerosis in the smaller peripheral
arteries of rabbits as a result of feeding them with infusions of tobacco. Boveri confirmed
these results by giving infusion of tobacco by stomach-tube, and obtained atheromatous
plaques or thickening at the base of the aorta in ten out of sixteen rabbits, while Baylac
obtained sclerosis in each of eight rabbits into which tobacco infusion was injected either
intravenously or subcutaneously. Jebrowsky and later W. E. Lee have produced it in
rabbits made to inhale tobacco smoke. From Baylac's experiments it would appear that
ARTERIOSCLEROSIS. 257
in general the liability to occurrence bears some relation to the channel by which it enters
the body. This may explain the very marked action of tobacco inhaled and entering the
heart directly from the pulmonary circulation in smokers, as compared with the somewhat
milder effects of chewing tobacco, under which condition the nicotine passes through and
is perhaps somewhat attenuated in the liver before entering the systemic circulation,
and has still to pass through the venae cavae, right heart, and pulmonary circulation before
reaching the coronary circulation. In smoking, however, the nicotine enters through
the lungs and strikes its first blow at the coronary arteries and base of the aorta, where the
elastic fibres are under the greatest tension and hence most liable to degeneration. It is,
therefore, easy to understand why smoking of heavy cigars should be one of the most
potent factors in the etiology of arteriosclerosis and coronary sclerosis.
An almost new era in the study of arteriosclerosis was, however, introduced by the
discovery of Josue" that the repeated intravenous injection of adrenalin
into rabbits brought about sclerosis and calcification in the aorta within a few weeks.
This was very soon confirmed by W. Erb, Jr., who produced the lesions in a large number
of animals, and demonstrated the considerable uniformity with which such lesions fol-
lowed the injections. Similar results have been obtained in rabbits by Fischer by the
intravenous injection of a very large number of substances, — h ydrochloric acid,
phosphoric acid, lactic acid, calcium phosphate, chloralamide,
mercuric chloride, trypsin, diuretin, and physiological salt solu-
tion, so that the effect can scarcely be considered as specific for adrenalin.1
On the other hand, Pic and Bonnamour, as well as Adler and Hensel, have called
attention to the fact that in none of the series of experiments published did more than a
certain number of the animals injected show lesions, and in a very large series the latter
showed that it was practically impossible to produce arteriosclerosis in rabbits by these
poisons until they had attained a certain age. After that age arteriosclerosis occa-
sionally occurred spontaneously, but could be brought on with considerable frequency by
the injection of toxic substances. As stated above, Pic and Bonnamour have, however,
been able to produce it in young animals whose vitality was diminished by tuberculosis,
etc., indicating that disease may be an accessory factor in diminishing the resistance of
the arteries to toxic influences which ordinarily leave no traces. This carries the clinical
corollary that persons liable to arteriosclerotic changes should particularly avoid all con-
tributing factors (alcohol, tobacco, hard work, etc.) for some time after infectious diseases.
It is quite remarkable that Pearce and Baldauf, as well as other investigators, report
that they have been able to produce arteriosclerosis, and that Josue" claims to have
produced permanent elevation of blood-pressure in rabbits by a single injection of adren-
alin, since Fleisher and Loeb failed to do so in a large series of experiments in which such
injections did produce severe myocarditis.
Mechanism Producing Experimental Arteriosclerosis. — The mechanism by which
arteriosclerosis is produced has been the object of considerable study. In the case of
adrenalin at least, Erb believes that a spasm of the vasa vasorum takes
place, bringing about an insufficient blood supply to the coats of the vessels, and thereby
ischsemic degeneration of the latter, especially of the tunica media. This view was also
shared by Pearce and Stanton and other observers, but Fleisher and Loeb have shown
that considerable areas of aorta may be kept ischaemic by com-
pression without producing arteriosclerosis. The factor must , therefore,
be toxic. It is possible that in some cases with high blood-pressure actual rupture of the
weakened elastic fibres takes place, which serves as a centre for areas of necrosis. W. H.
Harvey has shown that if bits of excised aorta are filled with agar under various pressures
and then transplanted into subcutaneous tissue, those under tension degen-
erate more rapidly. The same is probably true of the fibres within the artery.
Moreover, Josue" has shown that repeated injections of adrenalin in the rabbit are followed
by permanent rise in blood-pressure. An increase in blood-pressure is indeed the rule in
arteriosclerosis, although, as Hasenfeld has pointed out, it occurs only in persons whose scle-
rosis involves the splanchnic arteries. Neither increase in blood-pressure nor hypertrophy
of the heart necessarily occurs in patients where these vessels are not involved. The
1 A summary of the recent literature upon this point will be found in the papers of
Saltykow, Adler, and Benda.
17
258
DISEASES OF THE HEART AND AORTA.
reason for this may be that the cutting down of the circulation of so large an area as
the splanchnic region in itself increases the resistance to blood flow and thereby raises
pressure. There is also no doubt that, besides the single artery involved in the sclerosis,
the latter is often the result of prolonged vasomotor spasm in the femoral artery, etc.
On the other hand, such spasm may be transitory and be accompanied by temporary
rise of blood-pressure and sensory phenomena which cause the syndromes described by
Pal as vasomotor crises (see page 270). Aubertin, Vaques, Wiesel, and others have found
hyperplasia of the adrenals present in many experimental and clinical conditions in
which hypertrophy of the heart and high blood-pressure are present. It therefore seems
quite possible, in the light of these findings, that hypertrophy of the heart and arterio-
sclerosis may often be the result of a hypersecretion of adrenalin, perhaps
also of some other internal secretions. Why this should be associated with splanchnic
arteriosclerosis is easy to see. The latter condition tends to diminish the circulation through
the abdominal viscera, and more blood is thus shunted through the adrenal arteries which
lie just above the mesenteries, thus bringing about an increase in adrenal secretion.
It may be added that Bayer, in Krehl's clinic, has shown that some-
times the high blood-pressure is, in part at least, dependent upon the
amount of salt in the food, being low on salt-free and high on diet rich in
salt, though this is by no means the rule.
DISTRIBUTION OF ARTERIOSCLEROTIC LESIONS.
As regards the distribution of arteriosclerotic lesions and its relations
to etiology, Harlow Brooks has given the following statistical summary
based upon notes of autopsies on 400 cases:
Artery.
Cases.
Etiological factors.
Aorta
400
301
Alcohol 149, among laborers 118, nephritis 51, syph-
ilis 38, old age 38. Males 275, females 125.
Visceral trunks
Coronary arteries
Brain
368
270
132
Alcohol 107, nephritis 35, syphilis 27, excessive
tobacco 9.
Alcohol 48, nephritis 21 syphilis 19
Renal
Pancreas
81
74
Alcohol 43, nephritis 10, syphilis 10.
Alcohol 19, syphilis 9 senility 9
Hepatic
Splenic
43
35
Alcohol 12, nephritis 8, syphilis 6, senility 3.
Alcohol 9 syphilis 7 nephritis 4 endocarditis 2
Lungs
senility 2, tuberculosis 2.
Syphilis 5, senility 5, alcohol 4, tuberculosis 4
Creliac axis and branches. .
Spinal vessels
19
20
nephritis 2.
Most of them with alcoholism. Sclerosis of mesen-
teric, all cases with adiposis.
Alcoholic 4, syphilitic 4, most of the rest in primary
spinal diseases.
ARTERIOSCLEROSIS IN THE YOUNG.
Arteriosclerosis in infants, children, and young persons while rare is
not extremely so.
According to Fremont Smith, who has given an excellent review of the subject,
congenital syphilis is the cause in about forty per cent, of the cases, and diphtheria, scarlet
fever, and typhoid fever, as well as infections in the mother during pregnancy, are impor-
tant factors. The blood-pressure is not usually elevated, often being as low as 70 mm.
ARTERIOSCLEROSIS. 259
Hg. The writer has seen one case of a boy aged six suffering from acute nephritis, com-
plicated by lobar pneumonia, large bacillus coli abscess of the buttocks, cystitis caused by
the same germ, who in spite of continuously low blood-pressure developed tortuous and
apparently thickened temporal and thickened radial arteries. After a few months these
arteries were no longer palpable. It is possible that these changes may have been merely
mononuclear infiltration about the vessels of the adventitia.
CLINICAL MANIFESTATIONS OF ARTERIOSCLEROSIS.
Clinically, the symptoms due to arteriosclerosis usually express
themselves in several groups dependent upon the arteries most affected.
(1) Cardiac, associated with myocarditis and coronary sclerosis;
often with renal symptoms (see Chapter IX). As shown by Fleisher and
Loeb, the myocarditis may be produced by the same cause and may be
more severe than the arteriosclerosis itself.
(2) Simple coronary sclerosis, paroxysmal dyspncea, angina
pectoris, Adams-Stokes syndrome, paroxysmal tachycardia, sudden death.
(3) Cerebral symptoms.
(4) Aneurism.
(5) Intermittent claudication.
(6) Vasomotor crises (Pal):
(a) Abdominal pain from vasoconstriction;
(6) Raynaud's disease;
(c) Pain down arms and legs.
The clinical characteristics of the cardiac and renal cases have been
discussed in Chapter IX under the head of the myocarditis which
invariably accompanies them. They may be briefly summarized as
shortness of breath, especially on exertion, often asthmatic or
paroxysmal in character; palpitation; weakness; occasionally a
considerable degree of nervousness, loss of memory, and insomnia.
In advanced cases with some sclerosis of cerebral arteries there may be more
or less transient irrationality, especially at night or on awakening.
There may be pains over the precordium, in the shoulders, or down
the arms, or in the abdomen or legs, which may be definitely associated
with periods of high blood-pressure (the vasomotor crises of Pal) ; there
may be sudden pain and sudden paralysis of a leg, disap-
pearing on rest, reappearing after a few steps are taken (intermittent
claudication, Charcot, Erb) ; or there may be severe precordial pain with
a feeling of weight and constriction over the sternum and an utterable
fear of impending death (angina pectoris). On the other hand, the hand
or foot may become cold or numb, the pulsation disappear from
the arteries, intense pain set in (Raynaud's disease), or finally be followed
by gangrene (thromboangitis obliterans). Still further the patient may
suffer from all the signs and symptoms of aneurism.
On physical examination the radial arteries may or may not be
found to be thickened or beaded (atheromatous) , dependent partly
upon the distribution of the sclerosis, since the radial artery may be spared.
Some writers state, however, that in men who do hard manual labor the
radial arteries are the first attacked, while in those who lead a sedentary
life sclerosis may appear very early about the base of the aorta, and the
radial, nevertheless, may be perfectly normal.
260
DISEASES OF THE HEART AND AORTA.
The artery in which the sclerosis is next most readily observed is the
temporal, which usually stands out like a cord or is very tortuous, and when
pressed against the bone feels thickened and leathery. This tortuosity
may also be present in the brachials and even in the abdominal aorta, and
is probably brought about by the stress of the arterial tension exerted upon
the walls, which are in some places weaker and less elastic than in others;
so that we have a force (blood-pressure) which is exerted equally on all
sides against walls which interpose a greater resistance on one side than on
the other, hence the curvature results. As might be expected, the tortu-
ousness is therefore greater when the disturbing
force is high (high blood-pressure) and less when
it is low, as shown in the figure (Fig. 157).
Other superficial arteries which may be felt
are the brachials, axillaries, facials, popliteals, and
dorsalis pedis.
Changes in the Retinal Vessels. — Hirschberg
in 1882 called attention to the fact that changes
in the retinal vessels constitute an early sign of
arteriosclerosis, and later demonstrated that this
change was normal in old persons and usually began
in the fifth decade. Friedenwald and Preston exam-
ined twenty-three persons suffering from general
arteriosclerosis, and found only seven normal reti-
nas among them.
De Schweinitz gives the following criteria for sclerosis of
the retinal vessels:
(1) Suggestive Signs. — Uneven caliber and undue tortu-
Ousness of the retinal arteries (corkscrew form), increased dis-
tinctness of the central light streak, an unusually light color of
the artery, and alterations in the course and caliber of the veins.
(2) Pathognomonic Signs. — Changes in si/e and breadth
of the arteries, loss of translucency, lesions in the arterial walls
consisting of white stripes in the form of perivasculitis, inden-
tation of the veins by the stiffened arteries, tortuousness of
veins and white stripes or varicosities along their courses, oedema of the retina in the
form of gray opacity around the disk or following the course of the vessels, hemorrhages
as linear extravasations or roundish infiltrations. Sometimes very sudden changes in
the caliber of the retinal arteries may be seen accompanying vasomotor crises.
X-ray Examination. — Absolute proof of arteriosclerosis is also given
by the X-ray, by which calcified plaques along the course of deeply situated
arteries (popliteals, femorals, abdominal aorta, etc.) may be discerned as
distinct shadows ranged along the course of the artery. These may be
brought out more distinctly by using two stereoscopic pictures instead of
Orie. Unfortunately, it has not been possible to discern sclerosis of the
coronary arteries in this way.
Sclerosis of the Abdominal Aorta. — Arteriosclerosis of the abdominal
aorta and splanchnic vessels is very common, as has been shown by Hasen-
feld, Bond, Brooks, Ortner, and Gilbride. In fact, it may almost be diagnosed
with certainty when the blood-pressure is elevated. Occasionally the course
of the abdominal aorta may be felt to be tortuous. Sclerosis of the abdom-
FIG. 157. — Tortuous radial
artery. (After Pal.) Solid line,
course of the radial artery at
200 mm. Hg blood -pressure.
Broken line, course of the ar-
tery at 95 mm. blood-pressure,
after amyl nitrite.
r ir ^
i ir J~^~ ^1
Fio. 158. — Retinal changes in arteriosclerosis. A, Normal fundus. B to F, successive changes
occurring in arteriosclerosis, including pallid arteries (B), later assuming a silver-wire appearance (C);
indented veins (B, C), afterward showing ampulliform enlargements (D, E); corkscrew capillaries (C, D);
corkscrew arteries and veins (D, E); perivasculitis (C. D); sclerosis of vessels (F); oedema of disk
(B, C, D, E). hemorrhages (C F).— D. (After de SchweiniU.)
ARTERIOSCLEROSIS.
261
inal vessels is not infrequently accompanied by crises of severe abdominal
pain not unlike those of tabes (abdominal vasomotor crises), but these may
also be present from simple pulsation of the abdominal aorta when tugging
upon loose peritoneal moorings. Sclerosis of the pancreatic artery is often
accompanied by diabetes mellitus.
BLOOD-PRESSURE AND PULSE.
In arteriosclerosis the mechanical factors affecting blood-pressure
tend to approach those in a system of rigid tubes, — a high pressure through-
out systole, a low pressure in diastole. In such a system we should have,
as a rule, a greater difference between pressure in systole and in diastole
than when the normal elasticity tends to keep up the diastolic pressure,
so that the pulse-pressure is often more than 50 to 60 mm. rather than being
nearer 30 or 40 mm. as in the normal individual.
FIG. 159. — Effect of arteriosclerosis upon the circulation. I, normal. II, arteriosclerosis, with
high peripheral resistance and anacrotic form of pulse wave; the arrow points to a rise in maximal and
minimal pressure and increased pulse-pressure. Ill, arteriosclerosis with low peripheral resistance,
showing low blood -pressure and increased pulse-pressure and collapsing pulse.
Pulse. — The pulse may assume any form whatever, from collapsing
and almost water-hammer in character to an anacrotic plateau, or even
in rare cases to a pulsus tardus. These depend upon the relation between
strength and size of beat and outflow through the arterioles. Thus, if the
peripheral arteries or any large areas of blood-channels are dilated and
lacking in elasticity, there will be a momentary rise in pressure at the begin-
ning until the pressure wave is transmitted from the aorta to the periphery.
When it reaches this point there is a sudden outflow through those vessels
and a sudden fall or collapse, which is greater than it would be in a more
elastic system (see Fig. 159). On the other hand, if the peripheral outflow
is small, the pressure in the non-elastic system quickly rises higher than
in an elastic system and remains so throughout systole, forming a systolic
plateau (anacrotic pulse) with a large rapid rise and plateau reaching to
the end of systole, then a gradual fall during diastole. The pulse form
accordingly gives us the information in arteriosclerosis as in other condi-
tions (see page 44), — namely, indicates low peripheral resistance when
it is collapsing and high peripheral resistance when it is anacrotic or sus-
262
DISEASES OF THE HEART AND AORTA.
tained. The pulse may either be quite large or very small, dependent upon
the degree either of vasoconstriction or of endarteritis. Its character may
be very variable; it may be quite quick and collapsing, corresponding to a
general rigidity of the whole vascular system, or the vessel may fill rapidly,
remain well sustained with long systolic plateau, and may then decline
either rapidly or slowly. However, the lumen of the radial artery may
have decreased so much from an endarteritis that the filling of the artery
is slow and the up-stroke on the pulse-tracing very oblique, just as would
be typical of aortic stenosis. This is not extremely common, and the very
quick up-stroke is the form most frequently seen. On the other hand, in
rarer cases when, as Romberg and also Hasenfeld have pointed out, the
splanchnic vessels are not involved, the maximal blood-pressure may be
quite normal (110-120 mm.) and the minimal also (90 mm.).
Blood=pressure. — The blood-pressure is often high. Thayer found
in his studies of post-typhoid arteriosclerosis that the maximal blood-
pressure was usually 20-30 mm. higher than for normal individuals of
corresponding age.
Romberg and Sawada, on the other hand, found that this occurred in only
12.5 per cent, of all arteriosclerotics, while Groedel found hypertension in only 37
per cent, of 446 cases of arteriosclerosis free from chronic nephritis. Dunin found
similar results. Israel, however, found hypertension — over 140 mm. Hg or 180 cm.
H2O (v. Recklinghausen apparatus) — in 64.4 per cent, of 45 cases of arteriosclerosis. The
minimal pressure was also increased, but less than the maximal. Israel gives the
following average figures:
Max.
Min.
Mean.
Pulse- pressure
(amplitude).
Normal —
cm. H2O
170
110
140
60
mm. Hg
125
81
103
44
Arteriosclerosis —
cm. H2O
240
140
190
100
mm. Hg
177
103
140
74
Average increase —
mm. Hg . ...
52
23
37
30
Israel's figures accord well with the writer's experience (using the Erlanger ap-
paratus). The highest of these blood-pressures are seen in cases with chronic nephritis
(Israel, Janeway, Horner). The writer has often found a maximal pressure of 220 mm.
Hg with a minimal of 160, though usually in association with nephritis.
As has been seen under cardiac overstrain, the presence of arterio-
sclerosis has a marked effect in impairing the bodily strength and the ability
to withstand strain. The diminution in arterial bed increases the total
work of the heart, and the patches of arterial fibrosis prevent the arteries
from dilating under functional activity. On the other hand, the loss of
arterial elasticity removes a factor which tends to propel the blood during
diastole and thus to maintain the blood flow at the least expenditure of
energy by the heart. As a result of this factor, the heart is compelled to
increase its systolic output (increased pulse-pressure) under normal condi-
ARTERIOSCLEROSIS. 263
tions and hence has little ability for further increase in reserve. Muscular
effort therefore gives rise to signs of greater strain than in normal individ-
uals, greater increase in blood-pressure, and greater fatigue.
The intensity of vasomotor reactions varies considerably in different
cases of arteriosclerosis. In some cases, as Romberg has shown, the vaso-
motor reaction of the arm vessels to cold may entirely disappear; while in
others (vasomotor crises) the reactions are so intense as to produce ischaemia
of the parts.
The Second Aortic Sound. — Corresponding to the high blood-pressure
there is also accentuation of the second aortic sound, which on the one hand
may be due to the heightened blood-pressure and the greater tension of the
aortic valves, or, on the other, to the thickening and partial calcification
of the valves themselves, which gives rise to a louder sound than usual
when the valves strike together, even under the usual pressure. A marked
accentuation of the aortic second sound therefore always leads to the
suspicion of arteriosclerosis, even in the absence of thickening in the walls
of the superficial vessels. However, it is not pathognomonic, since it may
often be heard in cases where no special sclerosis is present, especially at
times when the heart is acting strongly and probably giving forth a larger
output into the aorta at each systole, as in typhoids with dicrotic pulse
or in perfectly healthy young persons during attacks of palpitation. In
such cases the accentuation of the second sound is transitory.
BLOOD COUNT IN ARTERIOSCLEROSIS.
The blood count may vary considerably, first on account of the great
variety of diseases associated with arteriosclerosis, and secondly, because
the latter is sometimes accompanied by polycythaemia or erythrscmia.
There are no blood changes which in themselves can be said to be defi-
nitely associated with arteriosclerosis.
AORTIC SCLEROSIS.
When the aortitis near the base of the aorta is marked, and especially
if calcified plaques are present, the first sound as well as the second may be
changed and may be accompanied by a loud murmur which is usually trans-
mitted to the carotid and brachial arteries, resembling that heard in aortic
stenosis but less intense. Since the condition is much more common than
the latter, this murmur is also more commonly due to this cause, but in
the absence of the characteristic pulse it is quite indistinguishable from
that of aortic stenosis, for both arise at the same site at the same time and
are transmitted in the same way. The murmur is often accompanied by
a marked thrill having the same distribution and is followed by a distinct
diastolic shock.
As regards sclerosis of the aorta alone, Bittorf ha^ found that it frequently occurs at
an average age of fifty-five (forty-five in syphilitics) as a result of the usual factors; some-
times a single trauma to the chest may seem to be the important moment in the etiology.
It is especially common in syphilitics and fat persons, and is frequently associated with
pale, ashy-gray color, very high blood-pressure (170 to 220 mm.), occasionally difference
in size of the pupils, pains over the chest and down the arms, oedema over the sternum,
264 DISEASES OF THE HEART AND AORTA.
unilateral dilatation of veins in second and third interspaces, ringing aortic second sound
without diastolic murmur, hypertrophy of the heart, often pulsus celer, rarely pulsus
tardus or pulsus paradoxus. Cardiac pain may be present, often felt just after percus-
sion, and described as something boring through the sternum, sometimes with a feeling of
constriction, sometimes radiating to the arms and neck. Occasionally spells of weakness
in the arms may be felt not unlike intermittent claudication.
The differential diagnosis from aortic stenosis is made by the gradual
up-stroke on the pulse tracing in the latter case, as contrasted with the sudden up-stroke
and plateau in the former; from aortic insufficiency by the diastolic murmur and high
pulse-pressure; from aneurism by the percussion and fluoroscopic findings. Nevertheless,
it must be admitted that many doubtful cases arise.
SCLEROSIS OF THE PULMONARY ARTERY.
Primary sclerosis of the pulmonary artery is not extremely rare, but is difficult or
impossible to diagnose with certainty; but the presence of very loud sounds in the pul-
monic area or of a rough systolic murmur heard loudest at the pulmonic and
transmitted upward towards the left clavicle arouses the suspicion of a pulmonary
sclerosis, especially if signs of congenital lesion are absent and the murmur is not heard
over the carotid. However, sclerosis of the pulmonary artery is often secondary to
mitral stenosis and emphysema.
CASE OF PRIMARY PULMONARY SCLEROSIS.
Romberg reports the case of a man, aged 24, who had had no infectious diseases
except measles as a child and a recent slight muscular rheumatism, three months after
which he began to have gradually increasing shortness of breath, epigastric
pressure, occasional headaches and giddiness, and his color became very blue. On ex-
amination he showed marked cyanosis over the face, body, and limbs.
There was a pulsation due to the right ventricle in the fourth interspace 4 cm. inside the
mammillary line and thence inward to the sternum, also a smaller pulsation (left ventricle)
in the fifth interspace mammillary line, cardiac dulness 7 cm. to right, 15 cm. to left. Both
pulmonic sounds were louder than the aortic. Pulse small, regular, 116. Liver enlarged;
spleen enlarged. No oedema; no swelling of vessels of neck.
Probable diagnosis (Curschmann) , congenital heart lesion. Patient gradually became
worse; digitalis was without effect. Died one month after adniission.
Autopsy showed enlarged heart; right ventricle hypertrophied and
forms the entire apex, and the conus arteriosus and right auricle are espe-
cially hypertrophied. All the valves intact and normal; aorta free from sclerosis,
but unusually small. Ductus arteriosus closed. Tremendous sclerosis and
atheroma of the pulmonary artery and all its branches.1
The murmur may be distinguished over the abdominal aorta and the
femoral artery, though the thrill is rarely transmitted so far. There is no
Duroziez double murmur unless aortic insufficiency is also present.
Sanders has recently collected similar cases from the literature.
TREATMENT.
The general treatment of arteriosclerosis is mainly prophylactic,
hygienic, and dietetic, and actual specific treatment is of far less value.
Diet. — Carefully selected diet is a most important factor, restriction
being in both quality and quantity. The general diet given in
heart cases (see page 167) is of great benefit here, or equivalent diets with
1 Notes of a case of pulmonary arteriosclerosis (O. A. K.) secondary to mitral stenosis
are given on p. 354.
ARTERIOSCLEROSIS. 265
this as a basis. However, in simple arteriosclerosis the quantity taken at
a time need not be so greatly restricted; but the total quantity in twenty-
four hours should not exceed twenty-five hundred calories, and should
always be near the lower level for proteids, and as free as possible of purin
bodies (nitrogenous extractives such as are found in meat), creatinin, etc.,
and also of salt. The more recent studies quoted above seem to indicate
that excess in salt is almost as injurious as are excesses in alcohol, and that
the salt mackerel of Boston is as dangerous as the beer of Milwaukee. For
the sclerotic danger probably lurks in the Smithfield ham or the cold smoked
tongue as well as in the Baltimore rye or the Martini cocktail (Beyer, Baric",
Hadfield). The patient's safety lies in milk, eggs, potatoes, bread, other
carbohydrates, butter, and the simpler fruits.
Restriction of Liquids. — On the other hand, the liquid intake also
should not be excessive, since drinking large amounts either of water or
of beer seems to favor sclerosis (Krehl), but the amount ingested should
remain in the vicinity of fifteen hundred cubic centimetres a day, some
persons thriving best at five hundred cubic centimetres above, some at
five hundred cubic centimetres below this level.
Tobacco and alcohol should be dispensed with entirely if possible ;
if the patient insists on taking small quantities, one or two light dry cigars,
as thin as possible (Lee), or "stogies," a day are perhaps the mildest that
one may prescribe. Cigarette smoke is usually inhaled and pipes are very
heavy. Thick Havana cigars should be entirely prohibited.
As to alcohol, if the patient insists upon taking a small quantity,
this should be limited to an occasional glass of claret or white wine, or
perhaps a single glass of beer at rare intervals. The latter in large quan-
tities is especially undesirable, both on account of the large amounts of
liquid taken and because it contains both alcohol and proteid and purin
substances extracted from the yeast. Gin is perhaps more dangerous
than whiskey.
Coffee and tea should be taken in only small quantities, since
the vasoconstrictor action of the caffeine favors the onset of spasmodic
vasoconstriction (vasomotor crises), and, on the other hand, the increase of
blood-pressure itself brought on by caffeine is damaging to the arteries.
However, it must be stated that, in contrast to nicotine, lead, adrenalin,
etc., injections of caffeine into animals have thus far failed to bring on
arteriosclerosis and that perhaps the deleterious effect of caffeine may be
overestimated.
Hydrotherapy. — Systematic hydrotherapy is of considerable value in
arteriosclerosis, especially the use of warm baths, warm douches
(Brieger), or alternating warm and cold douches (Riley) applied both locally
and generally. They owe their efficacy to the vasodilatation which they
bring about, and hence must be classed in effect with the drugs of the nitrite
group. In most cases the effect of a good warm douche or warm bath is
more marked and more lasting than that of any of these drugs, and it is
further devoid of that certain residuum of deleterious effect which all
drugs leave behind them. So that, while one cannot agree with Brieger
that arteriosclerosis can be entirely cured symptomatically by proper
hydrotherapy, nevertheless warm baths and warm showers
266 DISEASES OF THE HEART AND AORTA.
once or twice a day should be an indispensable part
of the treatment of every arteriosclerotic. Cold baths
should be avoided, since they precipitate vasomotor reactions, which in
the arteriosclerotic may amount to vasoconstrictor spasm.
Drugs. — Potassium Iodide. — As to drugs, universal experience points
to the efficacy of potassium iodide in doses ascending from 0.3
Gm. (gr. v) t.i.d., p.c., to as high as 4 Gm. (5i) ; some clinicians favor-
ing the smaller, some the larger doses. In the writer's experience doses
under 1 Gm. (gr. xv) seem to have some effect in alleviating symptoms;
and when there is a suspicion of lues the dose should be increased still
further. (The therapeutic action and its limitations are discussed in
Chapter V.)
It has been attempted to settle the question experimentally by deter-
mining the effect of potassium iodide upon the course of adrenalin atheroma
in rabbits. Koranyi, Boveri, and Cummins and Stout, who were the first
to undertake these investigations, all reported that potassium iodide or
iodipin, when injected during the time that adrenalin was being injected,
inhibited the production of atheroma. However, it must be borne in mind
that Biland, Loeb and Githens, Adler and Hensel found that large doses
of potassium iodide seemed to increase rather than inhibit the atheromatous
changes. It is at present impossible to tell exactly what quantity repre-
sents the optimum dose for human beings, and whether therapeutic doses
ever reach the stage of harmfulness.
While sclerosis of the pulmonary artery secondary to the pulmonary
stasis of mitral stenosis is relatively common, primary sclerosis of this
artery is rather rare. •
Nitrites. — Next to the iodides in general use is the group of nitrites, —
amyl nitrite, nitroglycerin, sodium nitrite, erythrol tetranitrate. These
drugs are of value for symptomatic treatment, to relieve pain or discomfort
for the time being, but they exercise no inhibitory influences upon the prog-
ress of the arteriosclerosis, as has been shown for adrenalin arteriosclerosis.
On the other hand, their effect upon the symptoms due to arteriosclerosis,
the pain of intermittent claudication, of angina pectoris, of the abdominal
and peripheral vascular crises, is most remarkable, and in this regard they
are invaluable (Lauder Brunton). However, in their administration it
must be borne in mind that persons with arteriosclerosis seem to have
considerable tolerance for nitrites (page 188), and to bring about vasodila-
tation and fall in blood-pressure much larger doses must be given than is
necessary to produce the effect in normal individuals. Accordingly, as
indicated in Chapter V, the drug should be administered in increasing
doses until the physiological effect (flushing, throbbing in head, ringing
of the ears) is obtained, and then continued in a dose just a little smaller
than this. One need not be surprised, however, to find that this dose for
a person with arteriosclerosis, particularly a colored person, may be ten
or even twenty times the average dose for a normal individual. When
such is the case the blood-pressure is probably a beneficial compensatory
phenomenon, and the nitrites should be discontinued.
In the chronic hypertension of arteriosclerosis venesection is
not only useless but often harmful.
ARTERIOSCLEROSIS. 267
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nificance, Internat. Clinics, Phila., 1907, 17th Ser., vol. i, 177.
Romberg and Hasenfeld. Quoted on p. 213.
Thayer, W. S.: On the Late Effects of Typhoid Fever on the Heart and Vessels, Am.
J. M. Sc., Phila. and N. York, 1904, cxxvii, 391.
Romberg, E.: Ueber Arteriosklerose. Verh. d. Kong. f. innere Med., Wiesb., 1904, xxi, 60.
Sawada: Blutdruckmessung bei Arteriosklerose, Deutsch. med. Wchnschr., 1904, xxx, 425.
Groedel: Ueber den Wert der Blutdruckmessung fur die Behandlung der Arteriosklerose,
Verhandl. d. Kong. f. inn. Med., Wiesb., 1904, xxi, 113.
Israel, A.: Klinische Beobachtungen ueber das Symptom der Hypertension, Samml.
klin. Vertr., Leipz., 1907. Innere Med., No. 135-136.
Janeway and Homer. Quoted on p. 35.
Bittorf, A.: Zur Symptomatologie der Aortensklerose, Deutsch. Arch. f. klin. Med.,
Leipz., 1904, Ixxxi, 65.
Romberg, E.: Ueber Sklerose der Lungenarterie, Deutsch. Arch. f. klin. Med., Leipz.,
1891, xlviii, 197.
Sanders, W. E,: Primary Pulmonary Arteriosclerosis with Hypertrophy of the Right
Ventricle, Arch. Int. Med., Chicago, 1909, iii, 257.
Rogers, L.: Extensive Atheroma and Dilatation of the Pulmonary Arteries, without
marked Valvular Lesions, as a not very Rare Cause of Cardiac Disease in Bengal,
Quart. J. Med., Oxford, 1908-9, ii, 1.
Brieger, L.: Clinical Lectures at the Hydrotherapeutische Anstalt der Kgl. Poliklinik,
Berlin, 1906.
ARTERIOSCLEROSIS. 269
Riley: Blatter f. klin. Hydrotherap., 1898; cited from Buxbaum, B., Lehrbuch der Hydro-
therapie, Leipz., 1903.
Senator, H.: Ueber die Arterioskelerose und ihre Behandlung, Therap. d. Begenw., Berl.,
1907, xlviii, 97.
Koranyi, V.: Ueber die Wirkung des lods auf die -durch Adrenalin erzeugte Arterione-
krose, Deutsch. med. Wchnschr., Leipz., 1908, xxxii, 679.
Boveri, P.: Contribute allo studio degli ateromi aortici sperimentali, Clin. med. ital.,
Milano, 1906, xlv, 41.
Cummins, W. T., and Stout, P. S.: Experimental Arteriosclerosis by Adrenalin Inocula-
tions and the Effect of Potassium Iodide, Univ. Penn. M. Bull., Phila., 1906-7, xix, 101.
Biland, J. Ueber die durch Nebennierenpraparate gesetzten Gefass- und Organverander-
ungen, Deutsch. Arch. f. klin. Med., Leipi., 1906, Ixxxvii, 413.
Loeb, L., and Githens, T. C.: The Effect of Experimental Conditions on the Vascular
Lesions produced by Adrenalin, Am. J. M. Sc., Phila. and N. York, 1905, cxxx, 658.
Loeb, L., and Fleisher, M. S.: Influence of Iodine Preparations on the Vascular Lesions
Produced by Adrenalin, ibid., 1907, cxxxiii, 903.
XI.
VASOMOTOR CRISES AND THE ANGIONEUROTIC LESIONS.
VASOMOTOR CRISES.
GENERAL CONSIDERATIONS.
The general clinical manifestations of arteriosclerosis bear a close
relation to the condition described by Pal as "vasomotor crises/' under
which he includes all conditions which are associated with more or less
sudden constriction or dilatation of the arteries, and whose symptoms and
signs disappear or markedly diminish as soon as this paroxysmal change in
the blood-vessels passes off. There are accordingly
(1) Vasoconstrictor crises, usually associated with hypertension.
(2) Vasodilator (hypotension) crises.
The vasoconstrictor crises Pal divided into
(1) Abdominal type. (2) Pectoral type. (3) Cerebral type. (4) Crises in the ex-
tremities. (5) Crises in the large arteries.
The vasodilator crises according to Pal include
(1) Ordinary syncope. (2) Surgical shock. (3) Collapse after infectious disease
or most poisonings. (4) Erythromelalgia and many other "trophic" skin disease.1 (5)
Occasional cases of tabes with lancinating pains and low blood-pressure. (6) Various
attacks of weakness in Addison's disease.
Probably no unit cause exists for the crises themselves; the visceral
crises and lancinating pain in tabes, the painter's colic, the ursemic con-
vulsion, the delirium of the cerebral sclerotic, the pain of angina pectoris,
and the attack of cardiac asthma seem to have little etiology in common
except their relation to the sympathetic nerves. However, all manifest
high blood-pressure, and, according to Pal, all are relieved by artificial
depression of blood-pressure. It is, therefore, not unlikely that; however
diverse the ultimate causes of the condition, the cause of the symptoms
is high blood-pressure with localized vasoconstriction. The variation in
the areas of constriction in regions whose arteries are already sclerotic
accounts for the occurrence of the different symptom complexes.
As to treatment, the statements of Pal would lead one to believe that
they are all relieved by vasodilators, especially nitro-
glycerin and the nitrites, occasionally by sodium thiocyanate,
and that marked improvement results while the blood-pressure is lowered.
The symptoms return if the blood-pressure again rises. (Pal, also Heitz,
and Norrero.) However, Prof. Barker's experience at the Johns Hopkins
Hospital does not warrant such sweeping conclusions.
1 Buerger's studies indicate that there are organic lesions in some of these cases.
270
VASOMOTOR CRISES.
271
CASE OF ABDOMINAL VASOMOTOR CRISES. (QUOTED FROM PAL.)
P. V., sausage maker, aged 57, had rheumatism 14 years ago, and for the past year
pain and pressure in the epigastrium, especially on taking a deep breath. Has occa-
sional paroxysms of extreme dyspnoea and palpitation of the heart, but
always has some shortness of breath. He was formerly a heavy drinker, now drinks two
or three litres of beer a day as well as a half litre of wine and some whiskey! He also
smokes in moderation.
On admission, April 7, 1904, he was found to be a well-nourished man, slightly cyanotic.
Lungs clear, respiration 34. Heart. Maximum impulse in sixth interspace two ringers'
breadth beyond mammillary line. Dulness extends to third rib above and two fingers'
breadth beyond the right margin of the sternum. Sounds quite clear at apex and base,
second aortic sound not accentuated. Pulse
68; radial walls stiff; blood-pressure 225.
Liver enlarged; spleen not palpable. Slight
oedema of feet and legs. Urine 2600 c.c.; sp.
gr. 1010; albumin 1.5 Gm. per litre.
Patient was given 0.5 Gm. (gr. viii) so-
dium thiocyanate t.i.d. to diminish his blood-
pressure.
April 21. Patient delirious; blood-pres-
sure 110. Thiocyanate discontinued, where-
upon delirium disappears. The chart in Fig.
160 shows the course of the blood-pressure,
pulse-rate, and respiration. The patient was
free from other exceptional symptoms from
April 7 to May 1. May 1, 8.00-11.30 A.M.
Feels hot and cold. 11.30. Sudden attack
of severe pain and great feeling of pressure
in epigastrium. 11.35. Pains in back and
third to seventh vertebrae. Cries out with
pain, and also cries "I am choking." Lungs
clear. Cardiac dulness only to right sternal
margin and to two fingers' breadth within
left mammillary line. 11.40. Symptoms
diminish but pressure in epigastrium still
present. 11.41. Symptoms reappear. 11.42. A second severe attack as before. 11.55.
Diminution of symptoms, pains less. After a few minutes patient has a third momentary
attack with blood-pressure over 200 mm. Hg, which then subsides. 12.10.
Feels better. 12.55. Still better. Free from attacks until May 3, during which time he
receives 0.5 Gm. (gr. vii) diuretin t.i.d. On May 18, sodium thiocyanate wa»
again given, which lowered blood-pressure but caused delirium.
From that time until discharged frequent attacks of pain and hypertension.
Pal reports similar hypertensive crises in association with the colic of
lead poisoning and also with the visceral crises of tabes,1 the pain being
always relieved when the blood-pressure is brought down by amyl nitrite
or nitroglycerin; as, for example, in the following case.
CASE OF ABDOMINAL CRISIS IN LEAD POISONING.
N. J., painter, aged 31, has had lead colic twice before. Was free from it
on change of occupation, but it returned when he again worked in lead. Drinks little;
denies lues. He has had abdominal pain for three weeks. During past few days has
—BLOOD PRESSURE -PULSE RATE RESPIRATION
FIG. 160. — Blood-pressure chart of P. V. Typical
vasomotor crisis.
1 The claim of Pal that a similar association of pain with high blood-pressure exists
with the lancinating pains of limbs cannot be maintained, since the pains in his own cases
are sometimes associated with hypotension, sometimes with hypertension.
272
DISEASES OF THE HEART AND AORTA.
had continuous cramps, loss of appetite, and no stool. He is pale and has a
marked lead line. Pupils react readily. Lungs clear. Heart normal; pulse rather hard.
Abdominal walls tense, tender on both sides. Spleen just palpable.
July 23. 8.30 P.M. B. P. 130. Slight pain.
9.10 P.M. P. 68. B. P. 170. Increased pain.
9.13P.M. Amyl nitrite inhalation.
9.15P.M. B. P. 105. No pain.
9.17 P.M. B. P. 165. Pain again, lasting then over one-half hour with same B. P.
9.45P.M. B. P. 95. After amyl nitrite, which again gave relief.
9.48 P.M. B. P. 140. Pains return.
12 M. 160. Further increase of pain.
4.20A.M. B. P. 135. Pains diminish under amyl nitrite.
They return again, but
6.30A.M. B. P. 85. Pains disappear under amyl nitrite.
After July 25, blood-pressure was always under 130 (during last four days under
110), the patient was free from pain, and bowels were regular.
CASE ILLUSTRATING THE CEREBRAL CRISES.
The following case, illustrating what Pal terms the cerebral type of vascular crisis,
was under the writer's care at the Johns Hopkins Hospital:
J. M. C., grocer, aged 52, who had suffered repeatedly with myocarditis,
hypertrophied heart, irregular pulse, and general anasarca, entered the Johns
Hopkins Hospital in September, 1903.
Oct. 24. Restless at night. Left pupil
larger than right; both react normally.
Nov. 2. Very weak. Pulse weak and irregu-
lar. Liver enlarged.
Nov. 5. At 12.30 P.M. began to complain
of general discomfort with numbness in legs;
complained of nervousness and restlessness.
At 12.45 P.M. the restlessness became
150
FIG. 161. — Blood -pressure chart showing a vascu-
lar crisis of the cerebral type.
very marked; he began to strike out with
his hands and to try to get out of bed. Was
at this time conscious and able to understand
questions. (Blood-pressure curve shown in
Fig. 161.) No aphasia. Pupils equal and
dilated. Head and eyes drawn to right and
rigid. There was some twitching of muscles
of both arms and hands. Reflexes of right
arm slightly exaggerated. Soon became cya-
notic and vessels of neck stood out. Be-
came unconscious. Respiration stertorous.
Blood-pressure 270 mm. Hg. After
600 c.c. of blood had been withdrawn from left arm, cyanosis slowly subsided, respira-
tion becoming less stertorous and blood-pressure falling to 180 mm. Hg.
Becomes conscious after catheterization at 7.30 P.M. Still picking at bedclothes,
which continued until next morning. He was then mentally clear by 11 A.M. and pupils
reacted to light.
Nov. 6. 9 P.M. Remained clear and recalled hallucinations of previous night,
realizing them as hallucinations. Blood-pressure 160.
Had no further attacks of this kind and blood-pressure remained below 190.
Died March 28, 1904. Autopsy showed chronic myocarditis (heart 1000 Gm.), chronic
adhesive pericarditis, coronary sclerosis, hydronephrpsis, and stone in right kidney.1
1 It is possible that this attack may have been due to transitory cerebral oedema
like that described by H. Cushing and James Bordley (Subtemporal Decompression in a
Case of Chronic Nephritis with Uremia; with Especial Consideration of the Neuro retinal
Lesion, Am. J. M. Sc., 1908, cxxxvi, 484).
VASOMOTOR CRISES. 273
INTERMITTENT CLAUDICATION.
This condition is always associated with sclerosis of the femoral,
popliteal, or one of the other arteries of the leg which are usually pipe-stem
in character. Often the atheromatous changes are readily demonstrable
by the X-ray. Owing to the narrowed lumen of the artery, the amount
of blood that can flow through it is limited,
but this is sufficient to supply the muscle when
at rest. During slow walking the CO2 pro-
duced by the muscle and the oxygen needed
by it increase greatly. If the arterial flow is
sufficient, no symptoms appear; but when
rapid walking or running is begun, there is a
sudden increase in the oxidation in the muscle,
and, since the blood supply cannot keep pace
with it, asphyxia of both the muscle and its
nerve endings sets in, accompanied by paralysis solid line indicates co* formation
FIG. 162.— Diagram to illustrate
of the limb and often intense pain arising from dB±fn ^X^ent tL
stimulation of the sensory fibres by the CO2. of c°2 elimination. * indicates the
mi .. , . ni^iij T^« ii degree of CO* accumulation at which
The patient is compelled to halt. During the pain sensations set in.
rest the CO2 production falls, and the slow cir-
culation is able to carry off the excess and to supply fresh oxygen to the
tissues. With the renewed aeration, function returns. The patient is able
to walk again until local asphyxia sets in; and, since this will be brought
about by the same amount of CO2 as before, his walking will be limited to
the same distance. He must travel in stages. (Fig. 162.)
CASE OF INTERMITTENT CLAUDICATION.
H. E., carpenter, aged 74, complains of pain in right foot, drinks beer and whiskey
in moderation, smokes very little, and has always been healthy. In October toe was red
and ached. For the past ten or fifteen years patient has been at-
tacked by severe pains in both feet, causing him to stop in his
walks. Knees never gave way. The attacks came on oftenest during exercise. On
examination, thorax is emphysematous; heart slightly enlarged to left. Blowing systolic
murmur heard over the tricuspid area, becoming musical over the apex, well heard in the
axilla, but faint and blowing in the pulmonary area, where the second sound is accentuated.
Pulse slightly irregular. Right radial more sclerotic than left. Blood-pressure 165 mm.
General reddening from tarsometatarsal joints to the toes of right foot, where pulsa-
tion of dorsalis pedis is not felt. Both tibials are palpable, but pulsation
is well felt. Left foot normal, artery pulsating well. Both popliteals are very sclerotic.
Given nitroglycerin mg. 1 (gr. 55) t.i.d., alternating with sodium nitrite 0.2 Gm.
(gr. iii) t.i.d. He was somewhat improved by treatment, but left the hospital a few
days later.
Prognosis. — Since the claudication is simply part of the general arterio-
sclerosis, the prognosis is bad, for the coronary arteries, aorta, and cerebral
arteries may be involved. Sometimes, however, the arterial change is
confined to the limbs, occurring simply as degeneration of the media with
atheroma, exactly as is found in experimental adrenalin arteriosclerosis.
In that case the prognosis as to life is, of course, better.'
274 DISEASES OF THE HEART AND AORTA.
HYPOTENSIVE VASOMOTOR CRISES.
The so-called " hypotensive " crises seem to bear no relation to arterio-
sclerosis, but rather to trauma, action of toxic substances, and perhaps
to cutaneous diseases. They are in the main associated with depression
of the vasomotor system and have been discussed elsewhere. The one
condition with paroxysmal depression of the blood-pressure which may
owe its origin to arteriosclerosis is paroxysmal tachycardia (see page
560).
ANGEIONEUROSES.
Maurice Raynaud in 1862 described many cases of this group, espe-
cially of the condition which bears his name. He showed that the three
phenomena manifested in these conditions are:
1. Local syncope, i.e., blanching from absence or diminution
of blood in the arteries of the part affected; — Raynaud's disease a spas-
modic vasoconstriction. This is usually symmetrical in its distribution,
affecting the ends of the extremities, i.e., toes, hands or feet, arms or legs.
The trouble in one extremity is frequently more intense than in the other.
Often it leads to formation of bullse, ulceration, and to symmetrical gangrene
(Raynaud's disease).
2. Local asphyxia, i.e., presence of a venous blood, that is to
say of a blood insufficiently oxygenated, causing blueness of the part (now
designated as acrocyanosis) with a distribution corresponding to that of
Raynaud's disease.
3. Local hyperaemia, giving rise to redness (as in the condi-
tion termed erythromelalgia by Weir Mitchell).
Later investigations have enabled Cassirer as well as Barker and
Sladen to epitomize the symptoms of vasomotor disease as follows :
The vasomotor symptoms include (1) hyperaBmia, (2) syncope, and (3)
asphyxia; the sensory, (1) pain, (2) hyperaasthesia, (3) anaesthesia, (4)
parsesthesia; the trophic, (1) ulceration, (2) gangrene, (3) dystrophies
of the skin (Barker and Sladen). They affect the fingers and particularly
the toes. The chief types of disease are acrocyanosis (Cassirer), erythro-
melalgia (Weir Mitchell), and Raynaud's disease.
The symptoms may be arranged as follows in ascending scale (Barker
and Sladen) :
1. Acrocyanosis.
Vasomotor symptoms — venous stagnation and hyperaemia in fingers and
toes with cyanosis; sensory and trophic disturbances absent.
2. Acroparsesthesia.
Acrocyanosis — sensory symptoms (parsesthesia), numbness, pain, and tingling.
3. Erythromelalgia.
Vasomotor — hyperaemia (arterial). Sensory — pain.
4. Raynaud's disease (all the symptoms).
Vasomotor — hyperaemia, syncope, and asphyxia. Sensory — pain, anaesthesia,
paraesthesia. Trophic — gangrene and scleroderma.
As might be expected, there are many cases with symptoms inter-
mediate between these groups and many transitions from one to the other
(Sachs).
ANGEIONEUROSES. 275
Pathology. — Raynaud realized that the gangrene in the disease which
bears his name differed from ordinary gangrene and directed his first inves-
tigations to the state of the arteries. He found that, though the
pulse became very small or impalpable during the
attacks of blanching, it returned to normal volume
between attacks. He made very careful pathological studies of
the extremities in a number of cases, and finding the arteries clear con-
cluded that the trouble was of vasomotor origin, a view which he supported
by demonstrating transitory changes of caliber in the radial, popliteal,
and retinal arteries, associated with the attacks. In accordance with these
studies of Raynaud the vasodilation of erythromelalgia corresponds to a
period of paralysis of the vasoconstrictor nerves (sympathetic paralysis)
quite similar to the active hypersemia which Claude Bernard produced in
the rabbit's ear by cutting the cervical sympathetic. Just such a local
paralysis of the vasomotors produced by the overheating of a hand or foot
benumbed by cold gives rise to the condition of " chilblains." The latter
condition is always associated with overheating after exposure to cold
and often with formation of blebs, while attacks of erythromelalgia may
occur spontaneously from slight emotional or nervous disturbances or from
slight exposure to cold without overheating. There is rarely bleb forma-
tion. An attack of chilblains induced by overheating may thus be con-
tinued in spontaneous attacks of erythromelalgia.
Ray n a ud's disease, on the other hand, corresponds
to an extreme vasoconstriction, like that produced
in ergotism. Raynaud himself was so much impressed with this
similarity that he made searching inquiries in all his cases regarding the
character of rye bread taken, and conducted an extensive series of experi-
ments upon ergotism in various animals. He was forced to discard the ergot
hypothesis by the absence of any obtainable evidence of ergot ingestion,
but the parallelism between the two conditions remains.
CASE OF MILD RAYNAUD'S DISEASE.
A. S., a trained nurse, aged 30, was always healthy until the age of nineteen, when
during her period of training she was compelled to have a small ovarian cyst and one
ovary removed. For some years she suffered considerable pain from adhesions, so that
three years ago these were broken up by a second operation. She bore the operation
well, but during convalescence three weeks later had a fainting spell, since when she
suffers from severe palpitation. For the past two years she has found that in cold weather
both her hands and forearms become absolutely white, cold, and numb. This condition is
soon relieved by rubbing or by laying them in a basin of warm water, but is sufficiently
severe to prevent her from accepting a very desirable appointment in a colder climate.
Between attacks the patient seems perfectly healthy, has a good color. All the arteries
are soft. They appear to be of normal caliber and pulsate normally. The heart is normal
in size but moves 7 cm. from left to right as the patient turns from one side to the other.
The right kidney is also palpable and very movable. The rest of the abdomen and the
lungs are clear. The blanching of the-hands occurs less frequently and less intensely when
the patient's health is good, but it occurs much more frequently when the patient is excited.
Nitrites, belladonna, digitalis, bromides, and a large number of cardiac stimulants
have been tried by the patient without marked effect.
276
DISEASES OF THE HEART AND AORTA.
THROMBOANGITIS OBLITERANS.
In recent years Weiss and v. Winiwarter, and especially L. Buerger,
have discovered a group of cases in which symptoms at times simulating
those of the vasomotor trophoneuroses are produced by complete occlu-
sion of the arteries or veins with spontaneous thrombosis (thromboangitis
or thrombophlebitis obliterans). In such cases the largest artery and
sometimes both artery and vein become occluded by a thrombotic process
of considerable extent. After a short time the fresh red thrombi within
the vessels undergo organization, usually with permanent obliteration of
the lumen by white fibrous tissue. There is no proliferation of new elastic
fibres encroaching on the lumen as is the case in arteriosclerosis
(Fig. 163), though a few elastic fibres are found in the newly formed blood-
vessels.
FIG. 163. — Thromboangitis obliterans (A) and endarteritis obliterans (B). (After Buerger.) The
elastic fibres (stained black) are absent from the organized thrombus in A but present in large numbers in
the arterioscleriotic lesion B.
This was the condition first sought for by Raynaud to explain the
origin of symmetrical gangrene, and described by him under the head of
senile gangrene. In Buerger's experience of over 70 cases, however, it is
most frequent in Russian and Polish male Hebrews between twenty and
thirty-five or forty, and hence is usually a "presenile" gangrene. In
such cases the local syncope and ulceration are due to arterial occlusion.
The red blush is due to compensatory capillary dilatation (termed eryth-
romelia by Buerger, in contrast to erythromelalgia) . Cyanosis of the limb
occurs when the venous circulation is slowed from any cause.
The sensory disturbances found in the trophoneuroses are also found
in thromboangitis obliterans.
The clinical picture produced by thromboangitis obliterans is some-
times so similar to that of Raynaud's disease (spasmodic vasoconstriction)
that Buerger has found some undoubted cases of the former condition
reported in the literature as cases of the latter.
Differentiation between Thromboangitis Obliterans and Angeioneuroses. — Dr. Buerger
has informed the writer that he finds the following points useful for clinical differentiation:
1. There is always at least one vessel which remains permanently
pulseless, while in Raynaud 's disease the pulse soon returns to normal.
THROMBOANGITIS OBLITERANS.
277
2. Intermittent clandication is present in most of the cases.
3. Usually one limb is affected a considerable time before the other, and
the disease usually attacks the lower extremities.
4. There are exacerbations, but they come on and subside rather
gradually and are not paroxysmal like Raynaud's disease.
5. Limbs which are red (erythromelia) or blue in the dependent position become
blanched and ischaemic when elevated.
6. Migrating phlebitis is not infrequently associated with thromboangitis obliterans.
7. He has seen over 70 cases in Russian and Polish male Hebrews, but never in a
female. Raynaud's disease occurs more often in females.
8. Onset is usually gradual, while it is sudden in Raynaud's disease.
9. The circulatory phenomena are for the most part not of "vasomotor" origin,
but are due to occlusion of vessels. They therefore bear the stamp of permanency.
Nevertheless, Dr. Buerger has found a number of cases in which the
clinical differentiation from Raynaud's disease was very difficult. Dr.
Bernard Sachs, on the other hand, believes that the vasomotor neuroses
manifest themselves in diseased blood-vessels as well as in healthy ones,
and that the pathological diagnosis of endarteritis or thromboangitis does
not exclude the clinical diag-
nosis of erythromelalgia or
Raynaud's disease. Indeed it
is readily conceivable that
thrombosis should occur more
readily in somewhat diseased
arteries than in normal ones.
Even Dr. Buerger has found
some intimal changes in his
cases. Vasoconstriction may
also favor thrombosis. More-
over vasoconstriction, arterial
disease, and the formation of
agglutinative thrombi may, as
is seen in ergot poisoning, all
be produced by the action of a
single toxic agent.
CASE OF THROMBOANGITIS
OBLITERANS.
The following is the history of
a case which, though at the time
diagnosed as Raynaud's disease and
manifesting many symptoms of the
latter, in the light of Buerger's in-
vestigations appears to be one of
thromboangitis obliterans.
H. F., tailor, aged 32, admitted April 14, 1903, complaining of sore toes and
sore fingers. Had rheumatism -at 12 years; otherwise well. Smokes ten cigarettes
daily. In December, 1899, cold began to cause a burning sensation in big toe of
right foot. In March, 1900, pus collected under the base of nail. The nail was
removed, and four months later the entire toe. Wound did not heal well. After this,
tingling in other toes when out of doors, never when indoors. In April,
1902, the fingers and thumb of the right hand began to tingle and become painful, and a
little later on those of the left hand. In January, 1903, the left big toe began to become
gangrenous.
Fio. 164. — Hands and feet of a patient with thrombo-
angitis obliterans, Hhowing gangrenous ulcers and the
stumps of amputated toes. The arrows point to the gan-
grenous ulcers.
278 DISEASES OF THE HEART AND AORTA.
Physicial examination on entrance, negative except for the extremities. Both
hands are flushed, not blue, not tender, but there is some deformation of the
second phalanx of the middle fingers. Right big toe missing; sloughs between third and
fourth digits. Left great toe necrotic; tenderness and pain over both first metatarsais.
Patient complains of paroxysms of intense pain during the night, lasting
five to ten minutes. Elevation of the limb, warm dressings, massage, were a.l without
effect. Condition became worse in spite of hot HgCl2 compresses, etc., and the left great
toe had to be removed. The stump did not heal for several months. There
was never pulsation in either popliteal; very little in either
femoral. Patient discharged in February, 1904, unimproved.
During this time blood count: red blood-corpuscles 5;000,000-5,500,000. Hemo-
globin 100 per cent. Urine normal. Blood-pressure 100 to 130 mm. Hg. Pulse 80.
The following history represents a more typical case of thromboan-
gitis obliterans (quoted from Buerger).
M. K., 44 years, Russian Hebrew, father of three healthy children, was admitted to
Mt. Sinai Hospital on December 8, 1908. His limbs never troubled him until about a year
ago, when he felt the presence of tender spots on the inner side of the right foot. Soon other
hard "lumps" and "cords" appeared; some of these in the neighborhood of the ankle,
others higher up on the leg. After two months these disappeared, only to recur after a very
short interval. Since then he has never been absolutely free from peculiar "painful spots,"
and now, on admission, he still has signs of some of them. About three months after the
onset of these symptoms he experienced pain in the big toe, especially on walking. This
has become gradually worse, so that he has been unable to get about properly for almost
two months. Of late he has often had cramps in the calf and instep of the right leg after
walking for a short distance. His chief complaint, however, is the painful condition of the
inner side of his right leg.
Physical examination showed evidences of circulatory disturbance in the right lower
extremity. Both the dorsalis pedis artery and the posterior tibial were pulseless, although
pulsation of both the femoral and posterior tibial artery could be easily detected.
Over the inner border of the right foot there is a red streak about one-half inch in
length. This corresponds to a tender indurated mass which thins out and is lost as it is
traced upward. A short distance below the middle of the leg the upper end of a hard cord
can be palpated. This extends down behind the border of the tibia for more than two
inches, is adherent to the skin, somewhat nodulated, and marks the centre of an area of
hypersensitive, swollen, turgid skin. There are no trophic disturbances. Diagnosis :
thromboangitis and thrombophlebitis of the interned saphenous and some of its tributaries.
On December 15, 1908, a portion of the thrombosed saphenous was removed for
pathological examination.
On December 26, 1908, the physical examination was recorded as follows: In the
horizontal position, the right foot has a light shade of red; this is most marked over the
big toe and fades off towards the ankle. In the web between the third and fourth toes
there is a superficial ulcer. On the inner side of the foot almost two inches from the internal
malleolus there is a hard, cord-like nodule which is adherent to the skin. Behind the tibia
there is the scar left after removal of a portion of the saphenous vein. The saphenous can
no longer be felt.
On elevation of the foot blanching sets in rapidly and pain becomes intense. The
pendent foot turns very red (marked erythromelia) .
FURTHER COURSE. — February 15, 1909, the pain in the foot has been getting steadily
worse, and the fourth toe is beginning to turn black. On the 23d of February amputation
at the knee was done, at the request of the patient, for early gangrene of the fourth toe.
TREATMENT.
In the light of Buerger's pathological studies, treatment should be
directed toward keeping up a rapid circulation through the part and dimin-
ishing the tendency to coagulate. To bring about the former the vasodilator
drugs, especially the nitrites, should be freely used, but most of all the
THROMBOANGITIS OBLITERANS. 279
mechanical methods of inducing arterial hyperaemia, — hot poultices,
mustard foot or hand baths, or the Bier's hyperaBmia by suction in vacuo
(not Bier's stagnation hypersemia). Exsanguination of the arm or leg
with the Esmarch bandage, which has been advocated by some writers,
has given but little clinical encouragement; and in the light of the recent
pathological studies seems to be the worst possible procedure, since it
provokes the stagnation it intends to cure, at least long enough to induce
further thrombosis.
It is possible that the administration of sodium citrate by mouth, in
doses sufficient to slow the coagulation time of the blood, might aid in
diminishing the tendency to intravascular coagulation, but, since the fibrin-
ferment is supplied on the spot from the cells of the intima, it is probable
that this would not be of much avail.
To keep up arterial hyperaemia until the thromboangitis has been
repaired is the only hope in therapy.
From the time of Raynaud to the present excellent results have been
reported from the use of warm (but not too hot) poultices.
BIBLIOGRAPHY.
VASOMOTOR CRISES AND ANGIONEUROSES.
Pal, J.: Die Gefasskrisen, Leipz., 1905.
Charcot, J. M.: Sur la claudication intermittente observed dans un cas d'obliteration com-
plete de lune des arteres iliaques primitives, Compt. rend. Soc. de Biol., Paris, 1857,
2 se"rie, xii, 225. Sur la claudication intermittente par obliteration arterielle, Progres
MeU, Paris, 1887.
Erb, W.: Ueber das " intermittirende Hinken" und andere nervose Storungen infolge von
Gefiiss erkrankungen, Deutsch. Ztschr. f. Nervenheilk., xiii, 1. Ueber Dysbasia angio-
sclerotica, Muenchen. med. Wchnschr., 1904, li, 905.
Barker, L. F., and Sladen, F. J.: On Acrocyanosis Chronica Anaesthetica with Gangrene,
etc., J. Nerv. and Ment. Dis., N. York, 1907, xxxiv, 745.
Cassirer, R.: Die Vasomotorische Trophoneurosen, Berl., 1901.
Mitchell, S. Weir: Phila. M. Times, 1872; quoted from Sachs. Mitchell, S. W., and Spiller,
W. G.: A Case of Erythromelalgia with Microscopical Examination of the Tissue
from an Amputated Toe, Am. J. M. Sc., Phila., 1899, N. S. cxvii, 1.
Raynaud, A. G. M.: De 1'asphyxie locale et de la gangrene syme"trique des extre"mit£s,
Par., 1862; also, On Local Asphyxia and Symmetrical Gangrene of the Extremities,
Transl. by T. Barlow, Lond., 1888.
Buerger, L.: Thromboangiitis Obliterans; a Study of the Vascular Lesions leading to
Presenile Gangrene, Am. J. M. Sc., Phila. and N. York, 1908, cxxxvi, 567. The Veins
in Thromboangiitis Obliterans, with Particular Reference to Arteriovenous Anas-
tomosis as a Cure for the Condition, J. Am. M. Asso., Chicago, 1909, Hi, 1319.
Sachs, B.: Raynaud's Disease, Erythromelalgia, and the Allied Conditions, in their
Relation to Vascular Disease of the Extremities, Am. J. M. Sc., Phila. and N. York,
1908, cxxxvi, 560.
Also, Strauss, H.: Ueber angiospastische Gangran (Raynaud'sche Krankheit), Arch. f.
Psychiat., Berl., 1905, xxxix, 109.
XII.
SCLEROSIS OF THE CORONARY ARTERIES, AND ANGINA
PECTORIS.
PHYSIOLOGY OF THE CORONARY CIRCULATION.
The coronary arteries have usually been considered to be terminal arteries in the
sense of Cohnheim; that is, that their branches did not anastomose with one another suffi-
ciently to maintain an adequate circulation, and infarction follows their occlusion. This
is correct under most clinical conditions; and Porter has found experimentally that the
infarction is proportional to the size of the ligated branch. In many cases ligation of a coro-
nary gives rise to fibrillary contractions and sudden death (Porter, Magrath and Kennedy,
Kronecker) ; in others death may follow within a few minutes (Cohnheim and v. Schulthess-
Rechberg), within an hour (Panum), or the animal may live several weeks or more
(Baumgarten) if the operation is done aseptically. Death even then often occurs suddenly.
FIG. 165. — Effect of ligation of a large coronary artery upon the blood-pressure.
Schulthess-Rechberg.) Coronary artery ligated at a.
(After Cohnheim and v.
Distribution of the Coronary Arteries. — Walter Baumgarten in Porter's laboratory
was able to ligate the various coronary branches of cats and dogs under aseptic precau-
tions and produced infarcts in the corresponding areas of the myocardium. He found
the following effects by ligating the various branches:
Ramus descendens: Anterior wall of left ventricle, anterior papillary mus-
cle, left half of the thickness of the interventricular septum.
Ramus circumflexus: Posterior wall of left ventricle, apex, posterior papil-
lary muscle, a certain extent of the right ventricle, posterior wall of left atrium, posterior
third of the septum.
Ramus septi: This is given off in the dog near the origin of the ramus descen-
dens or independently of it. Ligature produces a triangular infarction with the apex of the
triangle towards the ligature.
Right coronary: Greater part of right ventricle, posterior portion of the
appendix atrii. (The smaller branches of the atria are not caught in the ligature.)
Baumgarten also excised the anemic area and perfused it with defibrinated blood,
and found this region was able to resume contractions when the cir-
culation was renewed within six to eleven hours after the artery had been ligated. The
region of the centre of the infarct lost its contractility before that near the periphery,
indicating that a certain degree of collateral circulation, perhaps through the vessels of
Thebesius, had taken place. This work explains why it is that a certain time elapsed
between the obstruction of the artery and the sudden cessation of beat in the experi-
280
SCLEROSIS OF THE CORONARY ARTERIES. 281
ments of Panum and of Cohnheim and v. Schulthess-Rechberg. The greater number of
Baumgarten's dogs and cats survived the operation well and showed no change in heart
action beyond a transitory arrhythmia lasting twenty-four to thirty-six hours. The
sounds were normal in every respect and possessed no undue valvular quality.
Only two animals showed signs of sudden cardiac failure, one dying in the midst
of violent exertion and the other soon after it, exactly as occurs in man (see
page 284).
Hirsch and Spalteholz found that, though infarcts weTe produced by ligation of the
coronary artery, the infarcts were smaller than the area supplied anatomically by the
artery, and there was a not inconsiderable amount of anastomosis, especially between the
branches near the surface of the heart. In man Chiari has found complete occlusion of
the right coronary artery without infarction, and Pagenstecher has ligated that artery
in an operation without evil result. These are the main facts regarding the coronary circu-
lation which throw light upon the clinical conditions observed.
Pratt has shown that the excised mammalian heart can be nourished
through the veins of Thebesius sufficiently to carry out forcible contrac-
tions for a considerable time, though this probably is not the case in the
living animal.
It has long been a matter of debate whether the heart muscle was
nourished with blood during the systolic or during the dias-
tolic period; the earliest contention being that of Scaramucci (1689) that the coro-
nary vessels are squeezed empty by the contraction of the heart muscle-fibres during systole
and fill from the larger and more superficial coronary vessels during diastole. After a long
controversy, during which Rabatel showed that the curve of coronary blood-pressure and
apparently also the curve of blood velocity were exactly similar to the curve in the aorta,
the question was definitely settled upon the excised heart by Porter and his pupils
in favor of the old view of Scaramucci. They also found that the blood in the coronary
veins is squeezed out in diastole.
The existence of vasomotor nerves for the coronaries has been proved
by Maass, who found that the vagus exerted a vasoconstrictor, the accel-
erator a vasodilator action upon these vessels.
This was confirmed by O. Langendorff and Wiggers, who found also that adrenalin
exerted a vasodilator action upon the coronary arteries of the excised heart instead of its
usual vasoconstrictor action. Both Wiggers and G. S. Bond have found that the outflow
through the coronary veins of the dog's heart in situ is increased by the administration
of adrenalin. Bond investigated the effects of a large number of other drugs as well, and
found that the coronary outflow always followed the curve of general blood-pressure; so
that, under the experimental conditions, he was unable to demonstrate any specific action
upon the coronary vessels, even from doses far larger than would be administered in thera-
peutics. However, the operation is so severe that the animals are always in profound
shock.
Ida Hyde in Porter's laboratory found that the coronary blood flow was diminished
by distention of the heart, a fact which may account for the weaker contraction of over-
dilated hearts.
SCLEROSIS OF THE CORONARY ARTERIES.
PATHOLOGICAL ANATOMY.
While the sclerosis of the coronary arteries does not differ in its pathol-
ogy from the sclerosis of arteries elsewhere, nevertheless the action upon
the heart gives rise to clinical and to secondary pathological conditions
which are quite different from those of general arteriosclerosis, and which
therefore deserve special consideration.
282
DISEASES OF THE HEART AND AORTA.
Another important condition which is very common is arterioscle-
rotic or atheromatous change arising in the aorta with or without associated
involvement of the coronaries themselves, but spreading so as to involve
the mouths of the coronaries as they arise from the aorta, and strangu-
lating these vessels as they pass through the aortic wall (see Fig. 166).
This has the same effect as a metal band constricting an artery would have ;
namely, of diminishing the blood-pressure and the velocity of flow in the
artery beyond it, of allowing the walls of the artery to contract down and
hence of producing a further permanent secondary narrowing of the lumen,
with progressive diminution in the blood supply to the part (Halsted).
The course of the artery may show patches of hardening with indentations
and widenings, collar-like constrictions, or uniform widenings; or, on the
other hand, the arteries may be converted into uniform tubes whose walls
may give the sensation of rubber
tubes on the one hand (uniform
fibrous sclerosis), or of absolute
pipe-stems (complete calcification)
on the other. This condition is, of
course, particularly common in
arteriosclerosis affecting the base
of the aorta and in the arterio-
Fio. 166. — Sclerosis of a coronary artery, producing an area of infarction near the apex. A. Show-
ing the entire specimen. B. The sclerotic coronary artery, camera brought closer; a wire has been passed
through the mouth of the coronary artery.
sclerotic form of aortic insufficiency, and may account for many of the
symptoms to be discussed later (see page 284).
Since the heart muscle requires much more blood when it is beating
forcibly and rapidly than when it is beating slowly and quietly, it is easily
seen that this collateral circulation may be sometimes adequate and some-
times not. Also, since in different individuals of the same species there are
variations both in the structure and disposition of the minute arteries and
in the needs of the muscle-fibres for nourishment, it is but natural that the
results of coronary disease should vary greatly.
CLINICAL MANIFESTATIONS.
The clinical pictures associated with coronary sclerosis are character-
ized by some or all of the following features: pain over the precordium
or down the arms, feelings of suffocation or of impending death,
SCLEROSIS OF THE CORONARY ARTERIES. 283
paroxysms of most intense dyspnoea with palpitation, enlargement
and pulsation of the liver, general weakness, sudden death.
A considerable grade of arteriosclerosis may be present in both young
and old individuals without giving any symptoms whatever, as shown in
the case of J. L. (page 467). Another example of this was a colored boy
under the writer's care who after very vigorous life died at the age of nine-
teen in the fifth week of typhoid fever. Neither before nor during the fever
had he had any cardiac symptoms. However, his coronary arteries were
found to be very sclerotic.
Sudden Death. — S udden death is frequently the first manifesta-
tion of the condition, and examples are almost daily in the newspapers of
persons, usually men past middle life, who drop dead without warning and
with no previous illness, due to sudden thrombosis of the sclerotic coro-
nary arteries, or perhaps merely to the fact that, though the sclerotic
process has been going on gradually, the instant has passed at which the
cardiac nutrition becomes insufficient and ischaemia sets in with sudden
functional insufficiency, just as occurs in the leg in intermittent claudka-
tion. This must be the case in many hearts in which no actual thrombosis
or embolism can be found post mortem.
Paroxysms of dyspnoea such as those described on page 148, the so-
called cardiac asthma, are also extremely common in coronary sclerosis,
especially when combined with aortic insufficiency (vide page 366), in
which case they are no doubt due to the dilatation and weakening of the
left heart and the consequent accumulation of CO2 in the blood. It has
been suggested by Drs. C. M. Cooper and E. O. Jellinek of San Francisco
that this was always an accompaniment of sclerosis of the right coronary
artery and dilatation of the right heart, but in autopsies of two cases under
the writer's care who had suffered from such attacks the right coronary
was absolutely free from sclerosis.
Sensations of pain in the precordium, and especially behind the sternum,
as well as pains and tenderness over various interspaces and radiating down
the arms, are especially common in coronary sclerosis.
Paroxysmal Tachycardia. — Attacks of tachycardia beginning with
sudden doubling of the pulse-rate and ending in sudden halving of the latter,
just as is present in essential paroxysmal tachycardia, have been described
by Romberg as manifestations of coronary sclerosis, and Krehl also cites
similar findings.
In Romberg's case the pulse-rate rose suddenly from 100 to 200, while the respira-
tion remained at 20. The attack lasted two days and then the pulse-rate dropped sud-
denly to 100. Later an aortic stenosis developed gradually and the patient died of heart
failure, the autopsy showing aortic stenosis and sclerosis and marked coronary sclerosis.
Dr. Barker informs the writer that he also has seen a couple of cases in which such
attacks were associated with coronary sclerosis.
Quite recently similar attacks have been produced by T. Lewis upon ligating the
coronary arteries in cats even after the cardiac nerves had been sectioned.
Painful sensations about the heart are particularly common in asso-
ciation with coronary sclerosis, but on the one hand they are by no means
confined to this condition, and on the other hand most extensive coronary
sclerosis may be present without the occurrence of cardiac pain. The most
marked form of cardiac pain, the so-called "angina pectoris" (pronounced
284 DISEASES OF THE HEART AND AORTA.
an'gina, not angl'na) to be discussed below, is in its most typical form
usually associated with a certain degree of coronary sclerosis.
ANGINA PECTORIS.
In 1768 both Heberden and Rougnon described attacks of pain in the
chest. Tne former recognized the condition the more clearly and described
it in the following words:
"But there is a disorder of the breast marked with strong and peculiar symptoms,
considerable for the kind of danger belonging to it, and lot extremely rare, which deserves
to be mentioned here at length. The seat of it, and sense of strangling and anxiety with
which it is attended, may make it not improperly be called angina pectoris.
" They who are afflicted with it are seized while they are walking (more espe-
cially if it be up-hill and soon after eating) with a painful and most disagreeable
sensation in the breast, which seems as if it would extinguish life if it were to increase or
to continue; but the moment they stand still all this uneasiness vanishes.
"In all other respects the patients are, at the beginning of the disorder, perfectly
well, and in particular have no shortness of breath, from which it is totally
different. The pain is sometimes situated in the upper part, some-
times in the middle, sometimes at the bottom of the os sterni,
and often more inclined to the left than to the' right side. It like-
wise very frequently extends from the breast to the middle of the arm. The pulse is,
at least sometimes, not disturbed by this pain, as I have had opportunities of
observing by feeling the pulse during the paroxysm. Males are most liable to this
disease, especially such as have passed their fiftieth year. After it has con-
tinued a year or more, it will not cease as instantaneously upon standing still, and it will
come on not only when the persons are walking but when they are-lying
down, especially if they lie on the left side, and oblige them to rise out of their beds.
In some inveterate cases it has been brought on by the motion of a horse or a carriage
and even by swallowing, coughing, going to stool, speaking, or
any disturbance of mind.
"Such is the usual appearance of this disease, but some varieties may be met with.
Some have been seized while they were standing still or sitting, also upon first waking out
of sleep, and the pain sometimes reaches down the right arm as well
as the left and even down to the hands, but this is uncommon; in a
very few persons the arm has at the same time been numbed and swelled. In one or two
persons the pain has lasted some hours or even days, but this has happened when the com-
plaint has been of long standing and thoroughly rooted in the constitution; once only the
very first attack continued the whole night.
" I have seen nearly a hundred people under this disorder, of which num-
ber there have been three women and one boy two years old. All the rest
were men near or past the fiftieth year of their age.
" Persons who have persevered in walking till the pain has returned four or five times
have then sometimes vomited. .... The termination of angina pectoris is remarkable.
For if no accident intervene but the disease go on to its height, the patients all
suddenly fall down and perish almost immediately. The angina
pectoris, as far as I have been able to investigate, belongs to the class of spasmodics, not
of inflammatory complaints. For,
" In the first place, the access and the recess of the fit is sudden.
"Secondly, there are long intervals of perfect health.
"Thirdly, wine and spirituous liquors and opium afford considerable relief.
"Fourthly, it is increased by disturbance of mind.
"Fifthly, it continues many years without any other injury to the health.
"Sixthly, in the beginning it is not brought on by riding on horseback or in a car-
riage, as is usual in diseases arising from scirrhus or inflammation.
"Seventhly, during the fit the pulse is not quickened.
"Lastly, its attacks are often after the first sleep, which is a circumstance common
to many spasmodic disorders.
ANGINA PECTORIS. 285
"With respect to the treatment of this complaint, I have little or nothing to advance.
. . . . Quiet, warmth, and spirituous liquors help to restore patients
who are nearly exhausted and to dispel the effects of a fit which does not soon go off.
Opium taken at bedtime will prevent the attacks at night."
Heberden's contemporary, the great John Hunter, suffered from this
disease, and described his attacks most vividly.
The modern aspects of the whole subject have been discussed in a
masterly way by Sir W. Gairdner as well as in the more recent monographs
of W. Osier and G. A. Gibson.
k
CHARACTER OF THE PRECORDIAL PAIN AND CLINICAL SUMMARY.
In Heberden's description we have epitomized almost all the clinical
features. (1) The sudden attacks of oppression in the chest, with a feeling
of strangling, and, as Hunter puts it, "as though the sternum was being
drawn back to the spine," or, in the words of Matthew Arnold, as "though
there were a mountain upon my chest/' (2) The mental anguish (termed
by Gairdner angor animi), with the fear of impending death, especially pro-
nounced in John Hunter. (3) The intense pain, situated sometimes in the
lower sometimes in upper part of the sternum, more frequently to the left
than to the right (although occasionally to the latter), and very often
radiating to the arm, especially the left. (4) Some of the disturbances
of sensation; even Heberden speaks of numbness of the arm. (5) Changes
in the pulse in some cases: intermissions; extrasy stoles in some cases
(Hunter) ; alternating pulse in others (Mackenzie). (6) The extreme pallor
and constriction of peripheral arteries during the attack. (7) The sudden
death. (8) The main factors in bringing on attacks, — walking up-hill,
flatulence and digestive disorders, bending down in undressing, mental
excitement or anxiety, and especially anger; but none of the more gentle
emotions, such as pity, sorrow, etc., even when felt intensely. (The effect
of exposure to cold does not seem to be mentioned by these writers.) (9)
The association of the condition with sclerosis of the coronary arteries. (10)
Its frequent association with abnormal fatty deposits about the heart
(cf. Jenner and also page 214). (11) The relief of symptoms by means of
opium, warm applications, hot drinks (vasodilator mechanisms), and
counter-irritation (Heberden). (12) Its incurability, owing to the seat of
the trouble.
To these points clinical observations since Jenner have added: (1)
The existence of anginoid attacks with several conditions other than those
of coronary sclerosis, particularly with over-indulgence in tobacco, with
hysteria, with hyperthyroidism, and with other purely vasomotor phe-
nomena, as well as with practically all the valvular diseases of the heart.
(2) The frequent association of angina pectoris with certain definite areas
of tenderness which represent spinal segments corresponding to the referred
pain. (3) The occurrence of rise in blood-pressure with each attack. (4)
The relief of the attacks by inhalations of amyl nitrite and other vasodilator
drugs.
Sir William Gairdner has called attention to the occurrence of certain
cases resembling Heberden's angina pectoris in every way except in the
absence of pain as a symptom (an<;in:t sine dolore).
286
DISEASES OF THE HEART AND AORTA.
Paths Traversed by the Pain Sensations. — The afferent impulses from
the heart have been traced by Ludwig and Cyon through the depressor
fibres of the vagus. It has been shown by Eyster and Hooker that the
afferent impulses from the aorta and coronary arteries do not take this
same path but pass upward in the main bundle of the vagus. There is no
evidence from animal experiment that afferent impulses pass in any other
way; but Henry Head, as a result of his most extensive studies upon pain
in visceral disease, states that this "produces impulses which pass into
the spinal cord by the white rami. The segment on which they
infringe is excited and pain is produced. At the same time all potentially
painful influences passing into this segment from the afferent nerves are
exaggerated, and ultimately the body wall may become tender."
These sensations of referred pain follow the same path as has been described by
Bayliss for the vasodilator fibres with which protopathic sensation seems to be closely
associated, as shown in herpes zoster, etc. Protopathic sensations are referred back to the
distribution of the corresponding nerve segments without close reference to the points
at which they arise.
Insensibility of the Heart to Touch. — The heart itself seems to be devoid of tactile
sensation, for Harvey gives the following description of the condition in the nineteen-year-
old son of Viscount Montgomery, who had a fistulous opening in the chest wall over the
heart following fracture of the rib in early childhood. " I found a large open space in the
chest into which I could introduce three of my
fingers and my thumb ... I saw that I was
handling the apex of the heart ! covered over with
a layer of fungous flesh by way of external de-
fence, as commonly happens in old foul ulcers.
. . . The youth never knew when we touched
his heart except by the sight or the sensation he
had through the external integument."
Palpitation and Anginal Sensations
Compared. — The sensations which may be
felt from the heart itself may be either
rhythmic and felt as a distinct sensation
accompanying each systole of the heart,
such as the feeling of palpitation, or the
pain felt at each beat in some cases of
pericarditis, especially those associated
with pneumonia. The sensation in the
latter condition may, however, arise in
the parietal pericardium, and may have
nothing to do with the heart itself.
Sensations of palpitation may be
very distressing, partly on account of the
feelings of suffocation which accompany
them, partly on account of the mechan-
ical shock of the heart beating forcibly against the chest wall like a bird
in a cage. But, however intense and distressing, the sensation of palpi-
tation is always a pressure sensation and never one of pain. On the other
hand, the real cardiac pain is never intermittent, never felt as a distinct
sensation with each beat of the heart, but, whether dull and aching or
sharp and stabbing, it has no throbbing quality about it. It is, therefore,
FIG. 167. — Distribution of pain in attacks
of angina pectoris. (Schematic, after Head
and Mackenzie.) ASCAO, area correspond-
ing to the ascending aorta; TR,AO, area cor-
responding to the transverse aorta; L.A,R.A,
area corresponding to left and right auricles.
ANGINA PECTORIS.
287
not at all homologous with the sensation of palpitation and must belong
to a quite different category. Hirschfelder has added some evidence for
this view by observing that in some cases of palpitation the sensation
was referred definitely to the root of the aorta, and was exactly similar
in character to other sensations of throbbing in the radial artery alone,
which were sharply localized along its course and not spreading like a pro-
topathic sensation.
Referred Pains in Angina Pectoris. — James Mackenzie and Henry
Head have called attention to the commonness of referred pain and tender-
ness in angina pectoris. Mackenzie showed that there is often tenderness
in the areas supplied by the second
and third cervical segments, whose
fibres along with some from the
spinal accessory run down to the
heart through the vagus. This would
account for the occipital headaches
and tenderness of the sternocleido-
mastoid and trapezius muscles which
are frequently present. The muscu-
lar tenderness is elicited by squeez-
ing gently between the thumb and
forefinger.
The distribution of the pain and
hypersesthesia, according to Head,
bears a close relation to the chamber most affected, and particularly to
the somatic segment of the embryo to which it corresponds.
FIG. 168. — Distribution of attacks of pain and
sensory disturbances in a case of angina pectoris.
(After Head, with permission of the publishers of
Brain.)
Correspond embryo-
logical ly to
Nerve supply
Associated phenomena and
pain referred to
Auricles. .
5, 6, 7, 8 thoracic
Ventricles 2,3,4,5,6 thoracic
Ascending aorta. . .
3 and 4 cervical.
5, 6, 7, 8 segments
2-6 thoracic seg-
ments
3 and 4 cervical
segments
I
Transverse arch ... C. IV C. IV..
Descending aorta. . Thoracic segments 2-12, esp. 4-12
corresponding
2-12
Pulmonary artery. C. V-VIII
Lower axilla and shoulder-
blades.
Chest wall from 2d-7th rib,
ulnar surface of forearm
to wrist, and inner aspect
of upper arm.
These segments also to 3 and 4
c. and 1 thor. Tenderness
in neck of sternomastoid and
trapezius muscles. Tender-
ness and pain at back of
neck. (Dilatation of pupil?)
Laryngeal areas of neck (4th
branchial bar).
Back or front of chest, espe-
cially below nipple; abdo-
men.
Outer two-thirds of arm and
hand; ami muscles.
Thus, the auricles (atria), which are the hindmost in the development of the cardiac
tube, receive their innervation from and refer their pain to the fifth, sixth, seventh, and
i-iirhth thoracic segments. The ventricles, the next chambers lu-adward, correspond to
288
DISEASES OF THE HEART AND AORTA.
the second to the sixth thoracic; the ascending aorta from the semilunar valves to the
origin of the ductus arteriosus corresponds to the primitive aorta with the third and fourth
branchial artery, and the pain is referred to these segments (but an aneurism, etc., involv-
ing this in adult life will also involve the neighboring nerves and the pain will be referred
to the first, second, and third thoracic segments as well). The fifth to the eighth cervical
segments, corresponding to the pulmonary artery, will not be involved, and pain may not
be referred over these areas.1 (There are many notable exceptions to this rule even among
Head's cases; but there is usually overlapping of these areas.)
Sudden Death and Motor Disturbances. — The phenomena thus far
considered are purely sensory; and the question arises, what are, if any,
the motor disturbances connected with angina pectoris? It is evident that
the cessation of the heart-beat in sudden death that occasionally occurs
may be due either to the occlusion
of the artery or to a sudden onset
of complete heart-block as in the
Adams-Stokes syndrome. The lat-
ter condition is sometimes associ-
ated with angina pectoris and very
frequently with coronary sclerosis
(see page 472), though this is rare,
and more frequently the pulse be-
comes regular after a short time, or
sudden death from heart-failure sets
in just as in the experiments of Cohn-
heim and v. Schulthess-Rechberg.
During the attacks of angina
pectoris the blood-pressure is often
high, though Mackenzie states that in many cases there is no change
whatever. This seems to be due to a true pectoral vasomotor crisis in the
sense of Pal, rising sharply with and falling sharply after the attack, as
shown in Fig. 169.
FIG. 169. — Blood -pressure curve showing crises of
hypertension during attacks of angina pectoris.
ETIOLOGY AND VARIETIES OF ANGINA PECTORIS.
The idea that sclerosis of the coronary arteries was the lesion which
caused angina pectoris seems to have originated not with Heberden but
with Edward Jenner, the discoverer of vaccination, who was so certain of
its pathology that before doing an autopsy upon a case he made a bet
with a friend that he would find thickening of the coronary arteries. He
won the bet.
This indeed seems to be correct for almost all cases of fatal angina,
since Huchard found coronary sclerosis present in 128 out of 145 autopsies
recorded in the literature, and most of the others were in cases of adherent
pericardium or valvular disease. A few cases of death have occurred in
attacks of angina due to tobacco or in post-febrile conditions where the
coronary arteries were clear, but in these the possibility of obscure myo-
cardial change must be borne in mind (Osier).
1 His own cases 56, 57, and 58, as well as cases of many other writers, show tenderness
during and after attacks due to aneurism involving the ascending aorta.
ANGINA PECTORIS. 289
Angina Pectoris without Coronary Sclerosis. — However, in 1812, J.
Latham reported a number of cases which, in spite of the occurrence of
intense anginal symptoms, did not run the usual course ending in sudden
death, and to these he gave the name of "pseudo-angina" (angina
notha).
Bean, Stokes, and Graves also described reflex and toxic forms of
angina, but a much clearer light was thrown upon the subject by Noth-
nagel's article entitled "Angina pectoris vasomotoria." He says, "We
must interpret this symptom-complex to indicate that we are not dealing
with a disease which arises primarily in the heart, but that the symptoms
of stenocardia are of secondary origin and are brought on by a very general
spasm of the arteries."
The term "pseudo-angina" has been severely criticised by Balfour
and Gibson, since "angina" is a symptom, not a disease, and in all cases it
is a very real one. Nothnagel's term, "vasomotor angina," or Huchard's
"reflex angina," seems to the writer to be preferable.
Theories as to Causation of Anginal Pain. — Many theories have been
advanced to explain the causation of pain in anginal attacks. These may
be classified as follows:
(1) Ischaemia \om Coronary Stenosis. — The original view of Jenner was later supple-
mented by Allan Burns, that the attack may be brought on by asphyxia of the heart muscle
when there was a disproportion between the amount of blood flowing to it and the amount
of blood which it needed. Potain, in 1870, was the first to introduce the theory that
angina pectoris is due to "the intermittent claudication of the heart"; but Allan Burns
had already completely demonstrated this causal factor in 1809 and had described his
observations in the following words: "If we call into vigorous action a limb round which
we have with a moderate degree of tightness applied a ligature, we find that the member
can only support its action for a very short time, for now its supply of energy and its expen-
diture do not balance each other ... we witness an induction of an extreme degree
of debility and we have the patient complaining of an unusual painful feeling in the limb,
but still all its muscles are in a state of inactivity. ... If a person with the arteries
of the heart diseased in such a way as to impede the progress of the blood along them
attempt to do the same (ascend a steep or mount a pair of stairs), he finds that the heart
is sooner fatigued than the other parts are," and the same pain results.
(2) Ischaemia from vasoconstrictor spasm of the coronary arteries, which reduces
the functional condition to the same state as described by Allan Burns for the coronary
sclerosis. This seems to apply to the vasomotor and toxic anginas and often consti-
tutes a factor superimposed upon the coronary sclerosis in the angina vera. Such an
action of drugs upon the coronary vessels has been demonstrated on the excised heart by
O. Loeb, Langendorff, and Wiggers (see page 281).
(3) Acute dilatation of the heart, producing a pain similar to that of in-
testinal colic. This theory particularly has been adhered to by many writers. The
similarity between the anginal pain and that of renal, biliary, pancreatic, and intestinal
colic suggests that it belongs to the common form by which the visceral nerves give
expression to overdistention. Some dilatation usually accompanies the attack, and
seems to be a primary cause of the pain in cardiac overstrain and in many cases of val-
vular lesion.
(4) Neuritis. — It may at times be due to neuritis of the cardiac nerves, or, on
the other hand, to a neuritis primary in the brachial nerves and referred to the heart.
Lesions of the cardiac plexus have been described by Lancereaux, Grocco, and Benenati. but
Herard and others have failed to find them. Nevertheless it is quite possible that sub-
stances like tobacco (nicotine), which stimulate sensory nerves in the heart and which have
a specially toxic action upon the ganglion cells, may produce toxic neuritis of these nerves.
(5) Neuralgia of the cardiac nerves.
(6) Action of other constitutional diseases like gout, diabetes, and chronic nephritis.
19
290 DISEASES OF THE HEART AND AORTA.
But it is most probable that the effects are due to the other above-mentioned factors which
accompany these diseases, — arteriosclerosis and the presence of vasoconstrictor substances
either as retention products or internal secretions.
ASSOCIATED CLINICAL CONDITIONS.
The various conditions with which angina is associated most commonly
might be classified as follows:
I. Organic Lesions.
A. Sclerosis of coronary arteries.
B. Aneurism, especially of first part of ascending aorta.
C. Valvular lesions, especially aortic insufficiency. (This constitutes a very
common group.)
D. Aortic aneurism, especially of the sinuses of Valsalva and the ascending
arch.
E. Adherent pericardium. (The most frequent form which is seen in
children.)
II. Vasomotor anginas.
A. Hysterical type, most common in women, associated with other vaso-
motor disturbances and stigmata of hysteria.
B. Toxic, due to the action of various poisons, especially (a) tobacco, (6)
caffeine, taken both as tea and as coffee.
C. Associated with hyperthyrodism and exophthalmic goitre.
III. Attacks of more or less anginoid pain occur in the cases of acute dilatation of
healthy hearts, due to primary cardiac overstrain.
Angina Pectoris in Valvular Diseases. — The attacks of angina pectoris
associated with coronary sclerosis, which represent the original form de-
scribed by Heberden, are usually designated as angina vera. These are
very often associated with valvular lesions, especially with aortic insuffi-
ciency in which the coronary lesions are usually continuous with those of
the aorta, but they are also common in association with other valvular
lesions, since it is rare to find a case of chronic valvular disease without
some disease of the coronary arteries. The presence of valvular disease,
therefore, rather favors than excludes the diagnosis of coronary sclerosis.
In spite of the frequency with which these two conditions are asso-
ciated, occasionally one encounters cases of angina with valvular disease,
especially aortic insufficiency, without any disease of the coronary vessels
whatever, as was well exemplified by a patient with a ruptured aortic valve
who was for five years under observation at the Johns Hopkins Hospital.
During this time he suffered from very frequent attacks of typical angina
pectoris. He died suddenly while at stool. Autopsy showed rupture of
aortic leaflet. The coronary arteries were soft and the walls were not
thickened anywhere.
Angina Pectoris in Acute Dilatation. — It is possible: (1) that under
these conditions acute dilatations of the heart, due to momentary diminu-
tion in tone of the heart muscle, might be the immediate cause of the pain,
which would thus be of primary cardiac rather than vascular origin. (2)
That in such dilatation, etc., centripetal stimuli may arise in the heart
which may cause a general vasoconstriction. (This is contrary to the usual
depressor effect of stimuli arising in the heart, but it is not at all certain
that in the presence of such a pathological condition as angina pectoris
the paths of least resistance in the central nervous system may not be quite
ANGINA PECTORIS. 291
different from what they are in the normal individual.) (3) Miss Hyde in
Porter's laboratory has shown that dilatation of the heart in itself caused
diminution in the flow through the coronary arteries, and it is possible
that the circulation may thus be diminished to a point at which relative
ischsemia of the heart may set in and cardiac pains result.
Angina Pectoris in Aneurism. — Attacks of angina pectoris are very
common in cases of aneurism involving the ascending arch, and especially
in early small aneurisms near the sinuses of Valsalva. This has long been
known, but is the subject of an especially interesting article by Dr. Osier
upon "Angina pectoris as an early symptom of aneurism."
The anginoid pains in this condition are probably simply reflex, not the result of
primary peripheral vasoconstriction, cardiac ischsemia, etc., but simply the occurrence of
pain sensation arising in the aortic walls from overstretching of the aorta under pressure
heightened from any cause whatever, or from increased excursion of the aortic wall as a
result of increased systolic output, etc., as is so frequently seen in the abdomen in nervous
women with epigastric pain due to a throbbing of the abdominal aorta. In the later stages
of the aneurism, the symptoms may be less intense, due perhaps to the fact that by erosion,
etc., pressure upon the aneurism has diminished, perhaps to the fact that after a time
endings of the sensory nerves have been permanently injured or rendered less sensitive
by the progressive change in the aortic wall.
Anginal Attacks in Children. — Angina pectoris also occurs in children, especially in
association with mitral stenosis, as illustrated by the following case: The patient was
a boy aged 8 who had had rheumatism in the right hip two years previously, and since
then "had attacks of pain over the heart, especially after exercise. The pain was so
severe that it compelled him to stand perfectly still until it passed off; his cheeks became
blue and pale. He sometimes felt as though held in a vise, but never had any feeling of
fear. He also had at times pain on the right side over about the sixth rib, which was
sometimes present with that on the left side, but often present without it. Exercise seemed
to bring on both. Examination showed a very slightly enlarged heart with systolic retrac-
tion over the fourth left interspace, none about origin of diaphragm (Broadbent's sign
absent). Area of cardiac flatness changes with respiration. The first sound at the apex
was snapping in character and was preceded by a well-defined rumble. Second sound was
clear, accentuated over the pulmonic area. Pulse 92 per minute, of good volume, regular
in force and rhythm."
Such attacks are quite definite angina vera in the sense of Heberden, and indeed the
latter includes a similar case in his list. In children the association is, however, much
more commonly with valvular lesions than with coronary sclerosis, and perhaps most
frequently of all with
Adherent Pericardium. — This is an extremely common concomitant and cause of
anginal attacks, especially in children and adolescents. The pains are, perhaps, simply
reflex aches from the ordinary tugs upon the pericardium, perhaps brought about by the
stretching of the pericardial fibres which occurs when the heart becomes dilated.
VASOMOTOR ANGINA.
The second great group of cases with anginal symptoms are those in
which the anginal symptoms are of purely vagomotor origin (Raynaud's
disease of the heart) and are not associated $with organic lesions, — the
angina pectoris vasomotoria of Nothnagel (angina pectoris spuria of Latham,
angines de poitrine reflexes of Huchard). The characteristic phenomenon
in this group is the occurrence of general or local vasocon-
striction ushering in the attack; that is, there are usually
coldness, numbness, often tingling, weakness, and heaviness in the left
arm, pallor of the latter, with marked diminution in size and caliber of
the left radial, often also of the right radial artery, sometimes of the vessels
292 DISEASES OF THE HEART AND AORTA.
of the leg, trunk, and head. The patient may become pale and blue or the
lips ashen, and the course of the attacks may exactly simulate those of
coronary sclerosis. Death in such attacks is, however, extremely rare.
It has occurred in several cases in which no coronary sclerosis nor other
lesion was present to account for the death. However, Dr. Osier suggests
that in these cases there may have been myocardial changes demonstrable
only by the method of Krehl.
Hysterical Angina. — The most common form of vasomotor angina is
the neurotic or hysterical type, which is most common in young women
and is associated with the other stigmata of hysteria, — exaggerated emo-
tional response with marked histrionic tendencies, transitory vasomotor
disturbances, shifting areas of anaesthesia and hyperaBsthesia, characteristic
epileptiform seizures, and the existence of hysteriogenic zones where pres-
sure calls forth the above-mentioned symptoms.
Clinical Groups with Anginal Symptoms and their Characteristic Features
(modified from Huchard) .
Coronary Angina. — Site of disturbance. — Stenosis or obliteration of the
coronary arteries. (In some cases valvular lesion or aneurism only). Age.
— Age of arteriosclerosis after 40. Factors bringing on attack. — Effort of
some sort, mental or physical. Rarely spontaneous, sometimes nocturnal.
Not associated with any other form of neurosis. Nature of pain. — Ag-
onizing sensation of pressure. Usually felt most acutely behind sternum.
Referred pain down arm, especially left arm, and over chest, neck, etc.
Duration. — 2 to 15 minutes, stopping soon after standing still. Attitude.
— Silent, immobile. Prognosis. — Grave; almost always fatal. Treatment.
—Vasodilators.
Hysterical Angina. — -Site of disturbance. — Central nervous system acting
through the vasomotor nerve and cardiac plexus. Age. — At all ages, even
childhood; sometimes at menopause. Most frequent in women. Factors
bringing on attack. — Usually spontaneous onset without effort, often recur-
ring at fixed hours and associated with other neurotic symptoms. Nature
of pain. — Pain less agonizing, with feeling that the heart is distended — felt
most intensely at the apex. Duration. — 1 to 2 hours, not diminished by
standing still, not increased by walking. Attitude. — Agitated; walking about.
Prognosis. — Mild ; never fatal. Treatment. — Antineurotics and antineuralgics.
Gastrointestinal . — Site of disturbance. — Distention or neuralgia due to
gastric troubles. Age. — At all ages, especially among women. Factors
bringing on attack. — Not brought on by effort. Nature of pain. — Precordial,
not substernal pain; with fulness of chest and distention of heart but less
radiation. Signs of dilatation of right heart; increase of inverse diameter
to right. Duration. — 1 to 2 hours. Prognosis. — Death rare. Treatment.—
Antidyspeptic remedies.
Tobacco. — Site of disturbance. — Spasm of coronary arteries. Factors
bringing on attack. — Angina associated with toxic disturbances, vertigo,
gastric and respiratory troubles. Onset spontaneous. Nature of pain.—
Attacks associated with bradycardia, intermittent pulse, arrhythmia, pal-
pitations. Attacks longer than those of angina vera. Prognosis. — Death
ANGINA PECTORIS. 293
rare. Attacks often disappear rapidly on giving up tobacco. Treatment.—
Stopping tobacco, tea, and coffee. Rest and mental quiet. Light diet.
(Anginas due to tea, coffee, etc., brought about by the same cause.)
Acute Cardiac Overstrain (with or without Valvular). — Site of disturbance.
— Sudden dilatation of the heart. Age. — At any age, but most common in
young athletes, soldiers, anaemic girls. Factors bringing on attack. — Comes
on in the midst of some unusual effort, such as a mountain climb, boat race,
a charge, or a dance. Nature of pain. — In the heart itself, usually retro-
sternal. Associated with signs of dilatation to right and left, extreme
dyspnoea, often systolic murmur and arrhythmia. Duration. — In maxi-
mum intensity a few minutes, after cessation of attack, the pains often
continuing or recurring as less intense pain, tachycardia or arrhythmia
usually persisting some time after attack. Attitude. — Immobile. May
throw himself to the ground in the midst of the effort. Prognosis. — Death
rare. Permanent weakening of the heart if the over-exertion is soon and
frequently repeated. Treatment. — Prolonged rest and general cardiac
therapy until cardiac dilatation has passed off; gradual resumption of
active life.
Angina Pectoris in Hyperthyroidism. — Very closely resembling the
neurotic group are the cases of angina associated with exophthalmic goitre,
in which the attacks are sometimes more like those of neurotic, sometimes
more like those of the coronary type. The crucial point in the diagnosis
is the detection of hyperthyroidism by the application of the numerous
tests for Graves's disease, etc.
A case which has been for the past year and a half and still is under
the writer's care will serve as type of this condition (see page 586).
Treatment is the same as for the Graves's disease which is the primary
condition (see Part IV, Chapter II). The attacks themselves may be
treated symptomatically with amyl nitrite, etc., but the important factor
is the treatment of the underlying disease.
Tobacco Angina. — Anginal attacks due to tobacco are not uncommon,
both in young persons beginning their first excesses in tobacco and in older
persons whose over-indulgence is adding itself to a beginning or advancing
coronary sclerosis. In both the symptoms disappear soon after the tobacco
is absolutely given up, persistence of the attacks more than a few days
after this being evidence that some damage to the coronaries has occurred.
The attacks themselves may very closely resemble those of true angina, but
very frequently precordial pains not of an anginal character may be felt
by smokers between or for some time before such attacks.
The main factor in the effect of tobacco smoke, as shown by Ratner and Lee, is the
nicotine, although small amounts of HCN, CO, and pyridine bases are present in the
smoke. Moreover, it is probable that the action of smoked tobacco is exerted especially
upon the coronary arteries, because it enters the heart directly from the pulmonary vein
without preliminary dilution in the peripheral circulation.
Nicotine seems to have the effect of (1) stimulating the vagus, (2) producing vaso-
constriction, (3) thereby of raising the blood-pressure. In most cases this leads gradually
to hypertrophy of the heart, but in some, especially weaker individuals, it tends to facili-
tate dilatation, thus facilitating angina. Moreover, Jackson and Matthews have recently
shown for aconite, which in many ways is a similar drug, that much of its action is exerted
through stimulation of the sensory endings of the depressor nerve. It is possible that nico-
tine angina is due in part to similar sensory stimulation.
294 DISEASES OF THE HEART AND AORTA.
Angina in Acute Dilatation. — The attacks of pain and precordial dis-
comfort during acute cardiac overstrain and dilatation may reach anginoid
intensity, as was noted by da Costa among the soldiers of the Civil War.
He not infrequently encountered patients who had suffered so intensely in
the midst of a charge that they could endure it no longer and had thrown
themselves to the ground, exposed to almost certain death from the point-
blank fire of the enemy, rather than continue to bear the torment within
(page 124). These pains are usually retrosternal, often with numbness of
the arms and tingling in the fingers, and associated with feeling of compres-
sion and with palpitation. Although they occur in the midst of extreme
effort and would scarcely be confounded with angina pectoris vera, yet,
since angina pectoris is a symptom and not a disease, these cases must be
classed along with it.
DIAGNOSIS.
The actual differentiation of the various groups is not always easy in
the individual cases, as one frequently has a coronary sclerosis with a
tobacco angina superinduced upon it, a gastric etiology where there are
already attacks of angina vera, etc., and since it is a safe rule never to diag-
nose the milder conditions until the more serious can be ruled out with
reasonable probability. These cases may cause the physician anxiety,
since he remains uncertain whether to expect sudden death or whether
he is dealing with a comparatively mild condition.
CASE ILLUSTRATING DOUBTFUL DIAGNOSIS.
E. W., widow, aged 65, has had, since her menopause at 54, occasional attacks of
precordial pain, most intense just behind the sternum and especially about the level
of the third costal cartilage. She feels as though some one were bor-
ing through from sternum to spine with a sharp instrument. The pain is
also felt over the left side of the chest and down the left arm, which sometimes
becomes numb, cold, weak, and heavy. During the attack she feels as "though the
end has come." These attacks come on apparently spontaneously without definite asso-
ciation with either emotional disturbance, exposure to cold, or muscular effort. They
last an hour or two and are relieved by amyl nitrite or nitroglycerin. She feels
weak for a day or so after an attack, but at other times is extremely active for her age
and rarely short of breath. The patient is not at all neurotic. She has used coffee and
beer in moderation all her life. It must be added that near the end of the menopause
and before the first cardiac attack, she had a severe spell of grippe which kept her
in bed for four weeks and left her very much prostrated.
On physical examination the patient is well nourished. Slightly emphysematous,
but lungs otherwise normal. Heart not enlarged; action regular in force and rhythm;
sounds clear, neither second sound especially accentuated. Pulse between attacks is of
good large volume and quality, apparently about normal tension; vessel wall not specially
thickened. No ascites. Liver not enlarged. Feet always swollen from varicose veins,
not especially so during or after attacks.
In this case the question of crucial importance is whether
the angina is due to the occurrence of the menopause and is
neurotic, or to the influenza which she contracted about the
same timeand which may have brought on a coronary sclerosis.
The attacks themselves resemble angina vera, although their duration is longer than
usual. The age of the patient and the history of severe influenza also are in favor of coro-
nary sclerosis. On the other hand, the fact that ordinary 'exertion does not seem to bring
them on, but that they occur when the patient is moderately quiet, Is in favor of the neu-
rotic. It must, however, be borne in mind that the patient's statements in this regard
ANGINA PECTORIS. 295
may be inaccurate, and, further, that in occasional cases, where the diagnosis of functional
angina seemed quite well established, autopsy has shown definite coronary sclerosis.
It seems impossible to establish a definite diagnosis here, and the management of the case
is therefore directed toward the severer form, ordering as quiet a life as the patient will
carry out (since potassium iodide is not well borne), vigorous use of amyl nitrite and
nitroglycerin at the time of the attacks, and erythrol tetranitrate thereafter. A diet
of small quantities of food low in purin bodies and salt is insisted on.
Since these measures have been instituted she has remained entirely free from
anginal attacks for over two years, in spite of another attack of influenza. These facts
are in favor of a reflex origin of the condition.
Differentiation from Abdominal Diseases. — Angina pectoris is, as a
rule, easily differentiated from other diseases, though occasionally an attack
of biliary, pancreatic, or left renal colic referred to the shoulders or even
intestinal colic high in the epigastrium may closely simulate it: Careful
physical examination and location of the areas of tenderness over the af-
fected viscus should rule out this elror.
TREATMENT.
General Therapeutic Measures. — The old treatment of Heberden men-
tioned above, — "quiet, warmth," and hot drinks, even if spir-
ituous, also " o pi u m , ' ' best in the form of morphine, 15 mg. ({ gr.) hypo-
dermically or by the mouth, during the attack, and repeated if necessary.
As Heberden stated, it is well to bring on perspiration (and hence vasodila-
tation) in any way possible.1
Nitrites. — The most important means for the relief of the attack is,
however, the inhalation of amyl nitrite.
In 1867, Lauder Brunton tried the effect of inhalations of this substance upon patients
suffering from an acute attack of angina pectoris, and demonstrated that it produced very
marked, almost instantaneous relief. He was led to investigate this substance by the
realization that the attack was accompanied by vasoconstriction and high blood-pressure,
and by the knowledge that the newly investigated amyl nitrite had been found to have
a vasodilator action. Lauder Brunton 's observations have been generally confirmed, and
this drug has become the classical remedy for relief of the attack. Its action should be
supplemented at once by hypodermic or oral administration of one or two drops of spirits
of nitroglycerin (or more if the patient has been found resistant to it), and this may be
followed by erythrol tetranitrate by the mouth, since this drug exerts a slower action
lasting over three to six hours. Erythrol tetranitrate should be continued for some time
after the attack.
Potassium Iodide. — Between attacks potassium iodide in moderate
doses — 0.3 Gm. (gr. v) to 4 Gm. (3i) t.i.d. — should be given, as it seems to
diminish the frequency and severity of attacks.
Dr. G. S. Bond in the writer's laboratory has found that practically all the drugs
which he has investigated affected the outflow from the coronary veins in the dog's heart
exactly as they affected the general blood-pressure. Amyl nitrite and nitroglycerin were no
exceptions to this rule. They lowered the general blood-pressure and decreased the outflow
through the coronaries. The effect was the same whether the heart was dilated or not,
and seemed also to be independent of the strength of the heart. In view of these findings,
it must be borne in mind that Hewlett has found that a rise in blood-pressure fol-
lows quite uniformly within one minute after the inhalation of amyl nitrite is begun.
Whether it is the fall of blood-pressure or the rise of blood-pressure which is accompanied
l'\ increased flow through the coronary vessels after the inhalation cannot be regarded as
1 Perhaps this may bring with it a dilatation of the coronary arteries.
296 DISEASES OF THE HEART AND AORTA.
certain. It must be admitted, however, that in Bond's experiments the coronary arteries
were not in a state of vasomotor spasm, and therefore the analogy is not an absolute one.
It is also probable that the mere lowering of the general blood-pressure, independently
of any action upon the coronaries, tends in itself to relieve the cardiac dilatation by dimin-
ishing the work of the heart.
Caffeine, Theobromine, and Theophylline. — Caffeine and especially
theobromine and theophylline preparations — especially acettheobromine
sodium ("agurin") and acettheophylline — have been highly recommended,
from the clinical stand-point, by Askanasy, Kaufmann and Pauli, R. Breuer,
Buch, Pineles, v. Leyden, and others, to relieve and to ward off the attacks
of stenocardia.
Oswald Loeb has given an experimental basis to these observations by demonstrat-
ing on the excised heart that these drugs increase the blood flow through the coronary
vessels as well as increase the systolic output and the force of the heart-beat.1 Theobromine
and theophylline are to be preferred to caffeine, since they do not increase peripheral
resistance and have little action upon the higher nervous centres, but, on the other hand,
a more marked action on the coronary arteries. On the other hand, they are not very
certain in producing their effect. They may be helpful in some cases and may absolutely
fail in others, and, while they are worthy of a trial in almost every case, they cannot as
yet be expected to supplant the nitrites and iodides.
Diet. — Diet is all-important. It should be chiefly lactovege-
t a r i a n in character. The meals should be small in amount, to
prevent overloading and distention of the stomach and hence the pushing
up of the diaphragm. Gastric fermentation should be prevented
by removing from the diet any articles, such as soft hot breads, heavy and
greasy pastry, etc., which may be found to produce flatulence, and by
general treatment of the gastric condition. Air-swallowing should
be carefully looked for and treated (see page 604). Meat and soups
should be reduced to small quantities, since they contain considerable
quantities of purin bodies which have a vasoconstrictor action and which
also act injuriously upon the kidneys. The vegetable and cereal foods
should make up the bulk of the diet. Salt should be reduced for the same
reason. Liquids should be restricted to about 1500 c.c. a day.
Milk may be a staple article in the diet, unless, as in many persons,
it tends to flatulence. This is sometimes obviated by adding a very little
weak tea or coffee, but very often it must be dispensed with altogether.
Tobacco should be absolutely excluded in both organic and func-
tional cases.
Tea and coffee in small amounts (one cup a day, very weak) probably
have very little effect upon the average individual who has been accustomed
to them, but may be quite important factors in bringing on the attacks
in persons whose sensitiveness is a little above normal and in whom there
is a tendency to angina. It is best for them to be given up.
Local Treatment of the Chest Wall. — Vigorous counter-irritation to
the chest wall, by blistering, etc., is also of value, and Hasselbach and
Jacobaeus report very marked improvements, lasting a year or so, from
1 Dr. G. S. Bond, in the writer's laboratory, has been unable to produce any appre-
ciable change in the outflow from the coronary veins of the dog's heart in situ; and with
the amyl nitrite and nitroglycerin observed a marked decrease in the outflow, even when
the animal's heart was dilated.
ANGINA PECTORIS. 297
exposure of the precordium to the Finsen light for an hour a day until a
marked cutaneous reaction or even blistering has set in.
Electrical Treatment. — J. O. Hirschfelder states that in five cases he
has obtained striking relief of the symptoms by treatment with the
galvanic current, applying the anode (a pad 4 cm. in diameter)
to the neck over the course of the vagus, and the cathode (6-12 cm.
in dianeter) to the precordium, and passing a current of 20 milliam-
p e r e s for five minutes to each side of the neck. One patient remained
free from attacks until his death two years after the treatment ; another has
remained free for several years. In the other three the relief was less
permanent, but still very gratifying.
In other cases the use of electric baths, and especially with the
sinusoidal current, may be of value (Rumpf), but the effect is
readily overdone. The alternating current is certainly much less soothing
than the sinusoidal.
BIBLIOGRAPHY.
Porter, W. T.: On the Results of Ligation of the Coronary Arteries, J. Physiol., Camb.,
1893, xv, 121.
Magrath, G. B., and Kennedy, H.: On the Relation of the Volume of the Coronary Circula-
tion to the Frequency and Force of the Ventricular Contraction in the Isolated Heart
of the Cat, J. Exp. Med., N. Y., 1897, ii, 13.
Cohnheim, J., and v. Schulthess Rechberg, A.: Ueber die Folgen der Kranzarterienver-
schliessung fur das Herz., Arch. f. path. Anat., etc., Berl., 1881, Ixxxv, .503.
Panum: Experimentelle Beitrage zur Lehre von der Embolie, ibid., 1862, xxv, 308 and 433.
Baumgarten, W.: Infarction in the Heart, Am. J. Physiol., Bost., 1899, ii, 243.
Hirsch, C., and Spalteholz, W.: Coronarterien und Herzmuskel, Deutsch. med. Wochen-
schr., Berl., 1907, xxxiii, 790.
Pratt, F. H. : The Nutrition of the Heart through the Vessels of Thebesius and the Coronary
Veins, Am. J. Physiol., Bost., 1898, i, 86.
Porter, W. T.: The Influence of the Heart-beat on the Flow of Blood through the Walls of
the Heart, ibid., 1898, i, 145.
Maass, P.: Experimentelle Untersuchungen iiber die Innervation der Kranzarterienge-
fiisse des Siiugethierherzens, Arch. f. d. ges. Physiol., Bonn, 1899, Ixxiv, 281.
Langendorff, O.: Ueber die Innervation der Koronargefasse, Zentralbl. f. Physiol., Leipz.
u. Wien, 1907, xxi, 551.
Hyde, I.: The Effect of Distention of the Ventricle on the Flow of Blood through the
Walls of the Heart, Am. J. Physiol., Bost., 1898, i, 215.
Halsted, W. S. : The Results of the Complete and Incomplete Occlusion of the Abdominal
and Thoracic Aortas by Metal Bands, J. Am. M. Ass., Chicago, 1906, xlvii, 2147.
The Partial Occlusion of Blood-vessels, Especially of the Abdominal Aorta, Johns
Hopkins Hosp. Bull., Baltimore, 1905, xvi, 346.
Also Miller, J. L., and Matthews, S. A.: Effect on the Heart of Experimental Obstruction
of the Left Coronary Artery, Arch. Int. Med., Chicago, 1909, iii, 476.
Romberg, E.: Lehrbuch der Krankheiten des Herzens, Stuttgart, 1906, 115.
Lewis, T.: Paroxysmal Tachycardia, Heart, Lond., 1909, i, 42.
Jellinek, E. O., and Cooper, C. M.: Cardiac Asthma and Sclerosis of the Right Coronary
Artery, J. Am. M. Asso., Chicago, 1908, 1, 689.
ANGINA PECTORIS.
Heberden, Wm.: Commentaries on the History and Cures of Disease, Philadelphia, 1845.
Home, Everard: Life of Hunter, prefixed to the "Treatise on Inflammation," 1794, p. 45.
Quoted from Sir W. T. Gairdner's article on "Angina Pectoris and Allied States"
in Reynolds's System of Medicine, Philadelphia, 1877, iv, 534.
Baron: Life of Jenner, London, 1827. Quoted from W. Osier's " Angina Pectoris and Allied
States," N. York, 1897.
298 DISEASES OF THE HEART AND AORTA.
Gairdner, W. T.: Angina Pectoris and Allied States, in "A System of Medicine," edited
by J. Russell Reynolds, Phila., 1877, iv, 534.
Osier, W.: Lectures on Angina Pectoris and Allied States, N. York, 1897.
Gibson, G. A.: The Nervous Affections of the Heart, Edinb. and Lond., 1905.
Ludwig and Cyon: Ber. d. k. Sachs Gesellsch. d. Wissensch. math. phys. CL, Leipz., 1886,
307. Quoted from Shafer's Physiology.
Eyster, J. A. E., and Hooker, D. R.: Vagushemmung bei des Blutdruckes, Zentralbl. f.
Physiol., Leipz., 1908, xxi.
Mackenzie, James: Heart Pain and Sensory Disorders associated with Heart Failure,
Lancet, Lond., 1895, i, 16.
Head, H.: Pain in Visceral Disease, Brain, Lond., 1893, xvi, 1; 1894, xvii, 339; 1896,
xix, 153.
Head, H., Rives, W., and Sherren, Jr.: The Afferent Nervous System from a New Aspect,
ibid., 1905, xxviii, 99. Sherren, J. : Some Surgical Observations on Referred and
Reflected Pain, Clin. J., Lond., 1905, xxxvi, 168. Abstracted in editorial, J. Am. M.
Ass., Chicago, 1909, Hi.
Head, H., and Thompson, Th.: The Grouping of Afferent Impulses within the Spinal Cord,
ibid., 1906, xxix, 536.
Harvey, Wm. : The Works of Wm. Harvey, trans, by R. Willis. Printed for the Sydenham
Soc., Lond., 1847, 382.
Hirschfelder, A. D.: Observations on a Case of Palpitation of the Heart, Bull. Johns
Hopkins Hosp., Baltimore, 1906, xvii, 299.
Huchard, H.: Traite clinique des maladies du coeur et de 1'aorte, 3d edit., Paris, 1899,
ii, p. 1 et seq.
Ratner, Lee. Quoted on p. 613.
Jackson, D. E., and Matthews, S. A.: The Sensory Nerves of the Heart and Blood-vessels
as a Factor in Determining the Action of Drugs, Am. J. Physiol., Bost., 1908, xxv, 255.
Lancereaux: De 1'alteration de 1'aorte et du plexus cardiaque dans 1'angine de poitrine,
Compt. rend. Soc. de biol., Par., 1864, 4 s., i, 15.
Grocco, P.: Sull angina di petto, Settimana Med. di Sperimentale, Firenze, 1896, i, 1, 13,
109, 169, 181.
Benenati, IL: Sull' origine nevritica dell' angina pectoris da aortite sifilitica, Riforma
Med., Roma, 1902, xviii, 326, 339, 351.
Mott, F. W. Quoted from Oliver, Th.: A Lecture on Angina Pectoris and Allied Con-
ditions, Lancet, Lond., 1905, ii, 812.
Herard : Angine de poitrine caracterisee anatomiquement par un retrecissement considera-
ble des deux arteres coronaires a leur origine sans lesions des plexus cardiaques, Bull.
Acad. de Med., Par., 1883, 2 ser., xii, 1522.
Latham, J.: Med. Trans. Roy. Coll. Phys., Lond., 1812. Quoted from Gibson.
Nothnagel, H.: Angina pectoris vasomotoria, Deutsch. Arch. f. klin. Med., Leipz., 1867,
iii, 309.
Osier, W.: Angina Pectoris as an Early Sign in Aneurism of the Aorta, Med. Chron., Man-
chester, 1906, Ixiv, 69.
Lauder-Brunton, T.: On the Use of Nitrite of Amyl in Angina Pectoris, Lancet, Lond.,
1867, ii, 97.
Askanazy: Klinisches ueber Diuretin, Deutsch. Arch. f. klin. Med., Leipz., Ivi, 209.
Kaufmann and Pauli: Zur Symptomatologie des stenokardischen Anfalles, Wlen. klin.
Wchnschr., 1902, xv, 1160.
Breuer, R.: Zur Therapie und Pathogenese der Stenokardie und verwandter Zustande,
Munchen. med. Wchnschr., 1902.
Pineles, Fr.: Theocinbehandlung stenokardischer Anfalle, Mitth. d. Gesellsch. f. inn. Med.,
Wien, 1903-1904. (Quoted from Pal.)
Leyden, E. v.: Funfzig Jahre innerer Therapie, Therap. d. Gegenw., Berl., 1909, 1, 1.
Hasselbach, H. A., and Jacobaeus, H.: Ueber die Behandlung von Angina Pectoris mittelst
starken Kohlbogenlichtbadern, Berl. klin. Wchnschr., Berl., 1907, xliv, 1247.
Hirschfelder, J. O.: Personal communication.
Rumpf: Zur Einwirkung oszillierender Strome auf das Herz, Zentralbl. f. innere Med.,
Leipz., 1907, xxviii, 441.
PART III.
i.
ENDOCARDITIS.
IN spite of the greater frequency of arteriosclerosis and myocarditis,
the clinical pictures of valvular diseases are so much more definite as to
render them the most striking of all diseases of the heart. They constitute
indeed a large percentage of all diseases seen by the physician, numbering
1781 (7.6 per cent.) of the 23,200 cases admitted to the medical service
of the Johns Hopkins Hospital from 1889 to 1908.
HISTORICAL.
Vieussens in 1715 described lesions of the valves occurring in the form of warty or
cauliflower excrescences or vegetations, which prevented the closure of the valves. Vir-
chow called attention to the fact that as a rule these vegetations were not situated at the
margins of the cusps, but at a little distance from the margin, at the line of closure where
the cusps struck together, at the point where injury to the endothelial cells was most likely
to occur. That this injury was usually due to the action of bactei ia was shown when Winge
and Heiberg and Virchow in 1869 demonstrated microscopically the presence of minute
granules within the vegetations. In 1883 Weichselbaum
cultivated staphylococci and streptococci from endocardial
vegetations, and his pupil Wyssokowitch, as well as Orth
and Ribbert, produced them experimentally in animals by
the injection of bacteria into the blood.
PATHOLOGICAL ANATOMY.
Development of the Lesions. — Mechanical or
toxic injury is an important factor in bringing
about these lesions upon the valves. Indeed
Wyssokowitch found that his experiments suc-
ceeded only after he had punctured or injured
the valves with probes; while Ribbert supplied
the mechanical factor by injecting emulsions
of potato cultures which contained small masses
of potato that hurled themselves against the
valves. Prudden, on the other hand, found
that infection of the valves took place in much
the same way if the valves had been injured with chemical substances.
The fibrinous exudate is exudated rapidly after the injury, and is whipped
into strands by the action of the current, so that within one hour after
mechanical injury of the aortic valve a mass of fibrin having the cauliflower
shape of a vegetation may be found filling the hole in the valve (Hirschfelder) .
299
FIG. 170. — Fibrinous deposit
upon an aortic cusp one hour after
mechanically injuring the valve,
showing how the cauliflower-
shaped mass of fibrin tends to plug
the hole in the valve. (Kindness
of the .I"l i n- Hopkins Hospital
Bulletin.)
300
DISEASES OF THE HEART AND AORTA.
Ulcerative Endocarditis. — The fate of this fibrinous exudate and the
type of the lesion varies with the virulence of the germ. If the virulence
is high the lesion is often large and may involve the walls of the auricle
or ventricle (mural endocarditis) as well as the cusps of the valve (valvu-
litis) . The necrosis spreads into the deeper tissues of the valve or even
penetrates through it, and the vegetation consists of a mass of degenerated
fibrin, clumps of bacteria, and necrotic tissue (Fig. 174) rich in polymor-
phonuclear leucocytes. Under the influence of the ferments which these
secrete, the masses become partly liquefied, so that their attachment to
the cusps is loosened and they may be readily swept off as emboli by the
force of the blood stream only to cause infarction and abscesses in dis-
tant tissues. Such emboli naturally
vary in size from a small bit of fibrin
barely capable of plugging a capillary
to a mass almost the size of the
FIG. 171. — Mitral endocarditis showing large
vegetations. A, mural portion of the vegetations;
B, vegetations along line of closure.
FIG. 172. — Injection of chronically inflamed valves.
(After v. Langer.)
valve itself. However, they rarely reach the tremendous size attained by
the non-septic emboli which arise from intra-vitam thrombi in the auricles.
Chronic Endocarditis. — When the bacteria upon the valves are less
virulent or the immunity of the patient develops, a different process occurs.
The areas of necrosis are smaller and are walled off with leucocytes. Later
these give place to the fibroblasts and plasma cells of chronic inflammation,
which in turn are replaced by strands of newly formed connective tissue,
which push out into the exudate and finally replace it altogether, leaving
a solid vegetation composed entirely of fibrous tissue. With the ingrowth
of connective tissue blood-vessels penetrate into the vegetation, entering
it from the subendocardial layers of myocardium just as they enter scle-
rotic patches in arteriosclerosis (Koester, v. Langer, Darier, Ribbert), Fig.
172. As healing becomes complete the endothelial layer of the intima
slowly grows in from the periphery and gradually covers the entire vegeta-
ENDOCARDITIS.
301
tion. This relining of the vegetation with endothelium is, from a prog-
nostic stand-point, a most important step in the healing, for, as Wyssoko-
witch has shown, infection occurs most readily when the surface" of the
valve is injured, and clinical experience shows that a valve once injured
is particularly liable to rein-
fection. Thus, it is common to
find a fresh ulcerative endo-
carditis occurring upon a valve
which is already the subject of
a chronic endocarditis, several
different stages appearing upon
the same specimen.
Muscular tissue
Fibre-
elastic
tissue of
valve-
leaflet'
INFECTIVE AGENTS.
Chord re
tendineie
The most important infec- Endo-
tive agents in the causation of
endocarditis are the micro-
coccus of rheumatic fever,
the pyogenic cocci, the
pneumococcus. the gono-
coccus, the bacillus influ-
enzse, and the spirochaete
p a 1 1 i d a (triponema pallidum)
of syphilis.
Rheumatism. — By far the
most frequent cause of heart
disease is rheumatism, which
gave rise to 62.6 per cent, of
Border's cases of malignant
endocarditis, and occurs in
about the same percentage in
the milder forms. However,
the exact causal factor of rheu-
matism itself is not yet settled.
Sahli in 1893 isolated what he
thought to be a staphylococcus
from joints, endocardium, and Fic"
the heart's blood of patients
dying of acute non-suppurative arthritis, and then stated that he
garded acute articular rheumatism as an infectious
Papillary muscle
173. — Structure of
valve.
the normal auiiculoventncular
(After Piersol.)
1 re-
dis-
ease due to the action of attenuated pyogenic cocci."
Recently Menzer and Rufus Cole have revived this view, and the latter has produced
non-suppurative arthritis and endocarditis in rabbits by the injection of streptococci from
various sources, showing also that in the joints these assume the diplococcus arrangement.
Triboulet, Wassermann, Westphal and Malkoff, and Poynton and Paine, however,
regard the micrococcus (diplococcus) which they have obtained in cases of the rheumatic
1 " . . . Auffassung des Gelenk rheumatismus als einer auf der Wirkung abge-
schwachter pyogenen Kokkenberulienden Infektionskrankheit."
302
DISEASES OF THE HEART AND AORTA.
cycle as a specific organism or at least a specific strain, though Walker has shown that its-
cultural characteristics are by no means sharply defined. The micrococcus (rheumaticus)
of Poynton and Paine assumes the diplococcus form in the joints but becomes a strep-
tococcus in culture media, just as Cole found for many ordinary streptococci. Beattie and
Longcope also have isolated what they believe to be the micrococcus of Poynton and Paine
from cases of arthritis with endocarditis and have produced both conditions in animals.
Poynton has obtained the same germ from the cerebral cortex in simple chorea and from
the tonsils. Meakins, on the other hand, has found large foci of streptococci in the tonsils
which have been removed from patients having rheumatism, but these germs do not show
FIG. 174. — Photomicrograph of a specimen showing acute and subacute endocarditic lesions upon
the mitral valve. A. Entire specimen (low power). B. Outline sketch showing the portions from which
C, D, and E are taken. C. Margin of the area of acute endocarditis (high power). D. Ulcerating area,
showing masses of necrotic tissue and exudate. E. Area where the process is more chronic, showing
strands of newly-formed fibrous tissue entering the vegetation.
any uniformity which would permit them to be identified with the strain of Poynton and
Paine. These points tend to favor the original view of Sahli that rheumatism is not due
to a single strain but to a variety of attenuated cocci, and is therefore to be regarded as
a clinical group of diseases rather than as a single disease.
The Pyogenic Cocci. — The pyogenic cocci of puerperal fever, abscess,
and septicaemia are also very common causes of endocarditis. They are
identified with special frequency in the malignant forms, owing to the readi-
ness with which they are then cultivated, but there seems little doubt that
less virulent strains are responsible for cases of chronic endocarditis as well.
ENDOCARDITIS.
303
Pneumococcus. — Wells found that the pneumococcus caused endo-
carditis in 4 per cent, of his 517 autopsies upon cases dying of pneumonia,
and hence the latter disease is a relatively frequent cause of endocarditis.
Lenhartz states that the endocarditis often arises as a recrudescence after
the fever from the original pneumonia has subsided (13th to loth day),
and that it is often malignant and accompanied by meningitis.
Gonococcus. — The importance of the gonococcus in producing endo-
carditis as well as rheumatism is growing from year to year.
CHOREA
TONSILLITIS'
ARTHRITIS
FIQ. 175. — Portals of infection in endocarditis. (Schematic.)1
The clinical association of endocarditis and urethritis was recognized by Ricord in
1847 and by Brandes in 1854. V. Leyden in 1893 demonstrated upon the valves cocci
which decolorized by Gram's method, but the first positive cultures of the gono-
coccus from the blood during life were made at the Johns Hopkins Hospital by Thayer
and Blumer in 1895. Since then the condition has been found frequently, and should
always be sought for in cases of gonorrhoeal rheumatism.
Miscellaneous Infections. — Occasionally endocarditis arises during or
after diphtheria, scarlet fever, and smallpox, though in these cases, as in
tuberculosis, the lesion is probably most frequently produced by strepto-
cocci which are present as a mixed infection. True tuberculous endocarditis
is rare (Marshall), though it has been produced experimentally in animals
(Michaelis and Blum).
The bacillus of influenza is also an important factor (Austin), though
less frequent in endocarditis than in myocarditis.
1 The term micrococcus rheumaticus is used for convenience, but with all reservations
as to possible specificity.
304 DISEASES OF THE HEART AND AORTA.
Syphilis. — Whether true valvular lesions are produced by the spiro-
chsete pallida of syphilis has not been absolutely proved, but recently
Collins and Sachs and Longcope have obtained a positive Wassermann
reaction in a large percentage of cases of aortic insufficiency in which the
valves were puckered, shrunken, and calcified. In these cases it is not the
intima but the middle nbro-elastic layer of the valves in which the change
goes on, exactly analogous and usually coincident with similar changes in
the deeper layers of the intima and media of the aorta.
Sclerotic and Atheromatous Lesions of the Endocardium. — Besides
these forms of endocarditis there seems to be a certain number of cases,
especially of lesions about the aorta, in which sclerosis and calcification
take place in the nbro-elastic layer of the valves exactly as in the luetic
lesion, but in which the patient has never had a luetic infection (as in the
case of J. L.; page 467). The similarity here is exactly like that between
luetic and non-luetic arteritis, as shown by Ophiils, and needs no further
comment.
PATHOLOGICAL PHYSIOLOGY.
The disturbances in heart action due to endocarditis may depend
upon three immediate causes:
(1) The mechanical effects due to leaks or obstructions at any of the valvular orifices.
(This will be discussed in detail in connection with each of the chronic valvular lesions.)
(2) The weakening of the heart muscle due to the acute myocarditis and the fatty
and parenchymatous changes in the muscle cells, resulting from the direct invasion of the
muscle by the cocci, from effect of their toxins upon it, and from the anaemia which fre-
quently accompanies the infection.
(3) The weakening of the heart which, as in other febrile and infectious diseases,
results from lowering of vasomotor tone, and which is brought about by a relative empti-
ness of the blood-vessels. This is accompanied by low blood-pressure and rapid pulse.
In the chronic forms of carditis the first is the most important factor;
while in the simple acute and the malignant forms the two latter frequently
outweigh it, so that there may be few symptoms referable to the local
mechanical effects upon the circulation.
Effects on the Circulation. — The physical signs will be discussed par-
ticularly in the case of individual valvular lesions; but in general it may
be said that a leak at an orifice necessitates an increase in
the output of the chamber in order to compensate for the
amount regurgitating or an increase in force of contraction of the cham-
ber behind it. Thus, in mitral insufficiency,
Ventricular systolic output = Output into aorta + Backflow
into auricle;
while in aortic insufficiency
Ventricular systolic output = Output into aorta = Outflow
through peripheral vessels + Backflow into ventricle.
In either of these cases the circulation may be maintained either by increasing this output
per beat or by increasing the heart-rate; and in neither of these cases is the pulse-pressure
proportional to the systolic output of the ventricle.
On the other hand, when a valvular orifice is narrowed it may have little or no effect
until the narrowing reaches a certain point; for, though it slows the inflow or the outflow,
as the case may be, yet the duration of systole or of diastole may be sufficiently great to
ENDOCARDITIS.
305
permit of complete filling or emptying during the time available; but beyond this greater
driving power is needed and the chamber behind the stenosis must undergo hypertrophy.
Regurgitations usually cause dilatation of the chambers into which the
leak occurs, unless a great increase in tonicity of the muscle has caused the cavity
actually to decrease in size (Stewart, Cameron, Hirschfelder, Cloetta).
CLINICAL GROUPING.
Clinically, endocarditis (or carditis1) has been divided by Osier into
three groups:
(1) The malignant type, in which septic and highly febrile symp-
toms, with symptoms also due to septic embolism in various parts of the
body, dominate the clinical picture, and in which the cardiac lesions may
spread rapidly and involve almost all the valves. This is usually fatal
during the acute attack.
FIG. 170. — Temperature curve from a case of malignant endocarditis.
FIG. 177. — Temperature curve from a case of simple acute endocarditis.
(2) The simple acute type, in which one or two valves (the
mitral and aortic) are affected, but where the lesions remain confined to
them. The salient features of the disease are not those due to high fever
and embolism, although these may at times be present, but those usually
produced by the infective agent; and in addition there are weakness, an-
orexia, and anemia, some respiratory distress, and syncope on exertion.
1 Carditis = inflammation affecting endocardium, myocardium, and pericardium
simultaneously.
20
306 DISEASES OF THE HEART AND AORTA.
Occasionally there are oedema, enlargement of the liver, ascites, precordial
pain, and palpitation, but these are often absent.
(3) Chronic endocarditis usually follows after an attack of
simple acute endocarditis, although it may set in insidiously as a result of
progressive sclerotic changes in the valves, especially in association with
arteriosclerosis, syphilis, and chronic anaemias. The original characteristics
of an infectious disease have subsided, and the picture is entirely due
to the mechanical effects of leaking valves and weakened heart muscle;
in short, to slowing of the circulation, dyspnoea, cough, oedema, digestive
disturbances, palpitation, precordial and referred pains.
MALIGNANT ENDOCARDITIS.
PATHOGENESIS.
Most commonly an attack of malignant carditis is not the first heart
disease from which the patient has suffered, but it is found that the acute
process involves a valve which already shows marks of a chronic endocardi-
tis. This is not at all surprising, since Rosenbach, Wyssokowitsch, Hasen-
feld, and others have shown that valves once injured become the seat of
inflammatory processes much more readily than when intact. If the
original lesion is a very chronic one and the vegetation well supplied with
blood-vessels (Ribbert), organization of the exudate may go on even more
readily than in an intact valve; but if the older exudate is still fibrinous
or fresh, the tendency to soften and ulcerate is greater than if it were rest-
ing upon a base of relatively healthy tissue.
Often the second and malignant infection may be due to an organism
quite different from that producing the first; so that one frequently finds
a malignant endocarditis, due to the streptococcus, the pneumococcus, or
the gonococcus, attacking vegetations originally of rheumatic origin.
In the chronic forms of valvular lesion the symptoms of an acute
febrile disease have disappeared, and are replaced by clinical pictures with
characteristic forms of hypertrophy, stasis, and murmurs.
Occurrence and Distribution. — The relative rarity of malignant endocarditis is shown
by the fact that only 45 cases have occurred among 23,200 admitted to the Johns Hopkins
Hospital (0.19 per cent.), as compared with 1781 (7.6 per cent.) of chronic valvular disease;
also by the statistics of Horder, who encountered 150 cases among 19,904 patients admitted
to St. Bartholomew's Hospital (0.75 per cent.). The occurrence of Border's 150 cases as
regards age was as follows: Under 5, 2 cases; 5 to 10 years, 5; 10-15 years, 9; 15-20
years, 29; 20-30 years, 39; 30-40 years, 31; 40-50 years, 23; 50-60 years, 8; over 60, 4.
The involvement of the valves was: Mitral, 38; aortic, 22; mitral and aortic, 63;
tricuspid and mitral, 14; pulmonary and mitral, 7.. There were mural auricular lesions
in 43; mural ventricular in 8; congenital heart lesions in 8.
Other signs and complications were: Enlarged spleen, 47; heart failure, 66; haBma-
turia (sometimes only microscopic), 46; petechiae, 43 (on legs only in 10); brain symp-
toms in 22 (choreiform movements in 7; retinal hemorrhages noted in 5, though certainly
more frequent); embolic aneurisms, 20.
TYPES OF MALIGNANT ENDOCARDITIS.
Osier in his masterly lectures has divided the cases of malignant
endocarditis into three clinical groups, which may present both acute
and chronic forms.
ENDOCARDITIS. 307
1. The septicaemic, in which the symptoms are primarily those of septicaemia.
2. The typhoidal type, which closely resembles severe typhoid fever or acute
miliary tuberculosis, — continuous high fever, enlarged spleen, and absence of other local-
ized symptoms.
3. The cerebral type, dominated by embolism of the brain, coma, meningitis,
Septicaemic Type. — The septicsemic type is the most common and
typical, usually following abscess, puerperal fever, operation, wounds,
occasionally tonsillitis or quinsy, or some other definite infection, and is
characterized by prostration, anorexia, malaise, frequently headaches, and
shaking chills. In Herder's 150 cases the fever was continued in
12, irregular and intermittent in 37, quotidian in 40, absent in 5. The
temperature sometimes fell for a period before death. The complexion
has the sallow yellowish color of haematogenous jaundice, there is rapidly
progressing increasing anaemia, and the eyes are dull. There is sometimes
acute purulent conjunctivitis, sometimes disturbances of vision or even
blindness due to the presence of minute emboli or hemorrhages upon the
retina. The cheeks are sunken; the skin is usually dry except during the
rigor (in contrast to the drenching sweats of rheumatic fever) ; the tongue
is dry and furred; the lungs may be clear or septic bronchopneumonia may
be present. Respiration is usually rapid. The signs over the heart are
variable. In some cases there are no abnormalities in heart sounds, cardiac
area, or in pulsations, except for a rapid pulse-rate, and then the diagnosis
may long remain obscure; or, on the other hand, the loudest murmurs may
be present both in systole and in diastole, and these have a distribution
corresponding to almost any of the valvular lesions, or more usually to
several lesions combined. These signs often change markedly
from day to day, corresponding to the progression of the lesion
from valve to valve, the growth of the individual vegetations, or the dis-
appearance of the latter as they slough off into the blood stream. The
pulse is small and collapsing, but usually too rapid for dicrotism, and the
blood-pressure is low (maximal 85 to 110 mm., minimal 60 to 90). It
becomes larger and more typically water-hammer in character, and the
diastolic pressure falls to 40-50 mm. if a leak sets in at the aortic valve.
The loud systolic murmur over the tricuspid area, corresponding to tricuspid
insufficiency either functional or organic, is among the most common in
malignant endocarditis, for this valve bears the brunt of both the increasing
organic lesions and the progressive weakening of the heart muscle. Accom-
panying this there is also systolic pulsation in the jugular vein. A diastolic
murmur may be present to either left or right of the sternum, and may
correspond to. either aortic or pulmonic insufficiency, the distribution in
the latter case being somewhat different from the former. A pericardia!
friction, associated with the onset of fibrinous or purulent pericarditis, is
not uncommon.
The liver is frequently enlarged, either from cardiac weakness or
from a definite suppurative hepatitis and cholangitis. When associated
with triscupid insufficiency it may pulsate with systole.
The spleen is often enlarged, from the presence of infarctions of
greater or less extent. The abdomen may be otherwise normal or may
be tense, and there may be local tenderness and muscle spasm from
308 DISEASES OF THE HEART AND AORTA.
localized infection or general peritonitis; not infrequently these areas
correspond to the uterus (especially in puerperal endocarditis) or to
the kidney, owing to infarction, in which case there are also albuminuria
and hsematuria.
There is sometimes oedema of the extremities. Arthritis is
frequent, often accompanied by injury to the epiphyses as well as
the joints, and occasionally by spontaneous fractures. The skin may show
very numerous small purple petechiae or large areas of ecchymosis;
or, on the other hand, there may be numerous subcutaneous abscesses of
varying size.
The blood count is usually low, especially the haemoglobin, cor-
responding to the type of a secondary anaemia. Sometimes 500,000 ery-
throcytes are destroyed each day. There is almost always a polymorpho-
nuclear leucocytosis (20,000-30,000). As has been seen blood cultures are
positive in about 90 per cent, of the cases, — colonies of the infective agent,
usually 20-40 per cubic centimetre of blood.
The urine is of variable amount, and specific gravity usually
high. It generally contains albumen and casts, and often there is definite
haematuria due to infarction of the kidney. Sometimes the blood can be
seen only with the microscope. Not infrequently there is cystitis with
cocci in the urine in considerable quantities.
Typhoidal Type. — The cases of the typhoidal type are characterized
also by asthenia, by high fever (103° to 106°), which is more or less continu-
ous, frequently flushed face, dry tongue, sometimes coma vigil and picking
at bedclothes, enlarged spleen, but otherwise no definite localizing symp-
toms. There may be a slight bronchitis or small foci of bronchopneumonia.
The cardiac signs may be indefinite, or may be thought to be remnants of
old valvular lesions. The differentiation from typhoid fever on the one
hand and acute miliary tuberculosis on the other may be impossible by
the simple methods of physical diagnosis, and the diagnosis must rest with
the blood culture. Occasionally the presence of petechise in the skin may
suggest typhus fever. Examination of the eye-grounds may show small
white spots of retinal exudation and occasional hemorrhages, but the pic-
ture may be difficult to distinguish from typhoid lymphomata or miliary
tubercles. The presence of leucocytosis is suggestive, but not decisive,
while the absence of Widal reaction is of value only as negative evidence.
The only decisive evidence is given by the blood culture.
Cerebral Type. — In the third or cerebral type the symptoms due to
embolism of the brain and usually of the left middle cerebral artery domi-
nate the picture. There is a history of onset with fever, weakness, and
perhaps chills, perhaps a shower of petechiae over the body, and haematuria,
and then a sudden onset of hemiplegia, with, or more usually without, con-
vulsions, and perhaps relapse into unconsciousness. The patient is then
left with unconsciousness, hemiplegia (usually right-sided), and usually
aphasia, more or less disturbance of vision, and choked disk. The septic
infarct may also give rise to purulent meningitis, so that there may be
unconsciousness, rigidity of the neck, and Kernig's sign as well, and the
cerebrospinal fluid obtained from lumbar puncture may be under high
tension, cloudy, rich in albumen and in cocci.
ENDOCARDITIS. 309
These lesions are produced by septic emboli of varying sizes carried
off the necrotic surfaces of the infected valves. In Border's series they
occurred in 14.6 per cent, of the cases. The symptoms vary in character
and severity, according to the location and extent of the lesion, from a few
choreiform movements to paralyses, convulsions, and coma. Aphasia is,
of course, relatively common.
The diagnosis of the primary condition may depend upon the varying
heart signs and the positive blood culture.
CHRONIC INFECTIVE ENDOCARDITIS (OSLER).
Osier has called attention to the existence of a chronic form of
malignant endocarditis, which may last from four to fourteen
months. It is characterized by an asthenic condition, with remittent or
intermittent fever rising to a maximum of 102°-103°, chills and sweats,
in about 60 per cent, of the cases, petechiae, especially upon the shins,
enlarged spleen, and heart signs, which vary as the process extends from
valve to valve, or the valve substance sloughs. There is usually a progres-
sive anaemia. The leucocytes are almost always increased (10,000 to
15,000 per c.mm.), though not so greatly as in the acute forms, and the
blood culture is usually positive. However, in this condition more than in
any other, it may occur that a single blood culture may be negative,
whereas a subsequent attempt may give a good growth, for the germs are
apt to pass into the blood in showers.
In Osier's experience the disease was always fatal, but Horder reports
one case with recovery.
DIAGNOSIS.
The diagnosis of malignant endocarditis often presents considerable
difficulty. The differentiation from pneumonia may be especially difficult,
since there are usually small areas of septic bronchopneumonia present.
On the other hand, as Rosenow has shown, the blood culture in pneu-
monia often yields large numbers of pneumococci, and this germ is not
infrequently the cause of malignant endocarditis.
Thompson has also called attention to the fact that acute hyperthyroidism (Base-
dow's disease, exophthalmic goitre) may present a clinical picture of fever, chills, sweats,
tachycardia, dilated heart with systolic murmurs, which closely simulates that of malig-
nant endocarditis. The thyroid in these cases is enlarged and tender and the ocular signs
are usually pronounced.
The crucial points in the differential diagnosis of malignant endocar-
ditis are, therefore, given in the following table:
From penumonia — petechiae, signs of valvular lesions.
From typhoid fever — by leucocytosis, absence of Widal reaction, blood culture.
From rheumatic fever — by enlarged spleen, petechiae, chills, blood culture.
From malaria — by absence of plasmodia, leucocytosis, heart signs, positive blood
culture.
From miliary tuberculosis — by leucocytosis, heart signs, absence of tubercle bacilli,
positive blood culture.
From cerebrospinal meningitis — by absence of intracellular diplococci in cerebro-
spinal fluid, positive blood culture yielding other germs.
From acute Basedow's disease — by positive blood culture, absence of oculomotor
signs of Basedow's disease, polymorphonuclear leucocytosis.
310 DISEASES OF THE HEART AND AORTA.
CASE OF MALIGNANT ENDOCARDITIS.
Margaret P., aged 12, factory worker. Previously healthy except for scarlatina at
5 years and measles at 7. Never had rheumatism or chorea. Two weeks before admission
she had a shaking chill, followed by fever and sweats. She has felt
weak, nauseated, has vomited every day, and is irrational on the day of her admission.
Has had no headache nor epistaxis.
At the time of her examination by Dr. Cole she was irrational, chilly, and shivering.
Her color was a dusky pallor with slight cyanosis. Slight enlargement of glands;
lungs clear except for a few mucous rales.
Heart. — Apex impulse cannot be seen or felt. Dulness extends 7 cm. to the
left and 2 cm. to the right of the midline, and above to the second rib. At the apex
there is a well-marked systolic murmur, transmitted as far as the anterior axil-
lary line. Pulse is regular, of fair volume, 108 per minute.
The border of spleen is just felt. Liver dulness extends to the costal margin.
Reflexes: Knee-jerks active; no Kernig's sign. Rectal examination negative. Vaginal
smear shows no intracellular diplococci. Blood count, Nov. 4. Red blood-
corpuscles 4,352,000. Haemoglobin 80 per cent. Leucocytes 31,460.
The maximal blood-pressure ranged between 80 and 105 mm. Hg; the
pulse-rate between 120 and 210. Differential count showed polymorphonuclear
9 6 . 4 per cent.; large mononuclears 1.2 per cent.; small lymphocytes 2.2 per cent. No
malaria parasites in the blood. Widal and blood cultures persistently negative.
The patient's general condition remained about the same. On Nov. 6 a few e c -
chymoses appeared on the back and abdomen. By Nov. 7 the systolic murmur was
well heard in the axilla. Lumbar puncture gave a clear sterile fluid under pressure
of 280 mm. (slightly elevated). Nov. 12. A few pin-point vesicles appeared on the
abdomen, along with new petechiae on abdomen and face. Nov. 14. Patient
better and temperature lower. Nov. 22. Had a severe shaking chill; slight epistaxis.
Nov. 26. Felt faint while in the tub. Nov. 28. Haemoglobin 65 per cent. Nov.
29. Cardiac dulness has increased, extending 9.5 cm. to the left and 4 cm.
to the right; above to the second left interspace. The murmur is about as before; the pulse
large and collapsing. Dec. 1. Anaemia has increased. Red blood-corpuscles
3,800,000; haemoglobin 60 per cent.; leucocytes 27,000. Dec. 4. A well-marked p re-
systolic thrill is felt at the apex. In the afternoon she complained of pain in the
feet and loss of sensation in feet and legs. She cannot feel touch below the
knees. The feet are warm; no discoloration; knee-jerks are present. Dec. 5. Red blood-
corpuscles 2,300,000; haemoglobin 50 per cent.; leucocytes 31,000. The pa-
tient's condition became worse and crops of petechiae appeared. The pulse became irreg-
ular in force and rhythm. She died on Dec. 16.
Autopsy by Dr. MacCallum showed acute vegetative endocarditis
of the mitral valve, cardiac hypertrophy, oedema of the lungs, acute splenic tumor
with anaemic infarction, acute diffuse nephritis with anaemic infarction, embolic occlusion
of the aorta at its bifurcation. A motile coccus (micrococcus rubescens) was found in
the heart; micrococcus albus and bacillus pseudodiphtheriae in the vegetations; and in the
kidney an unidentified actinomyces, sarcina flava, and micrococcus albus.
TREATMENT.
The treatment of malignant endocarditis is the treatment of
any form of general septicaemia, — absolute rest, very light, soft or milk
diet amounting to as near 3000 calories per day as possible, and avoidance
of excit'ement. Drugs are of little value. Strychnine may be given in
doses of 2-3 mg. (-^ to ^V gr.) every four hours, or digitalis also, with a view
of increasing the activity of the vasomotor centre and the tonicity of the
heart; but little is accomplished by their use, and in some cases the heart
muscle is already so much injured by the infection that further stimu-
lation is actually harmful. Salt infusions may be given, but they serve to
ENDOCARDITIS. 311
swell the volume of blood, to dilate the heart, and to increase its work,
and, although they may perhaps "wash out the toxic substances through
the kidneys," it is doubtful whether they are at all effectual.
Intravenous Injections. — Intravenous infusions of collargol and other metallic com-
pounds have been tried and some apparently favorable results reported, but these have
invariably been shown to be overestimated when the work was repeated by more careful
observers. The antistreptococcus serum of Marmorek has been used in cases of malignant
streptococcic endocarditis, but this also has no value.
Inoculations with Bacterial Vaccines. — More recently A. E. Wright has instituted
the method of inoculating the patient with small doses of killed cultures of the germ, caus-
ing the infection in the hope of thereby increasing the production of protective substances.
Though this is the most promising of all the methods, it has failed to give satisfactory
results in the hands of careful observers such as Rosenow and Horder.
SIMPLE ACUTE ENDOCARDITIS.
The malignant forms of carditis described in the foregoing chapter
are relatively infrequent (0.19 per cent, of admissions to the Johns Hopkins
Hospital). Much more common are the milder infections which assume
the form of simple acute or subacute endocarditis, and in which the symp-
toms are often referable mainly to a mild subacute fever and anaemia, and
with comparatively less frequency stamped with the typical features of heart
disease, so that the latter may become evident only on physical examination.
Rheumatism. — Like the malignant form, which is usually of pyogenic
origin, the simple endocarditis is far more frequently rheumatic (Bouillaud,
1835), manifesting itself in association with other manifestations of the
"rheumatic cycle," — tonsillitis, rheumatic arthritis, chorea, pleurisy, or
the rheumatic erythemata; rheumatism being the etiological factor in 65.6
per cent, of all cases of endocarditis in the Medical Clinic at Zurich, in 36.7
per cent, at Jena, and in 58 per cent, at Leipzig.
Similar figures appear from the clinics of Great Britain and America, the statistics
of the Johns Hopkins Hospital being quite according to the rule.
A much higher percentage of the cases of rheumatism acquire endocarditis than is
true of any other disease. It was present in 61.3 per cent, of all cases of this disease in
children in West's series, in 66 per cent, of Fuller's cases and in 80 per cent, of the cases
reported by Cadet de Gassicourt.
Gibson states that the likelihood of endocardial infec-
tion is proportional to the severity of the rheuma-
t i c af f e c tion .
The same relative frequency applies also to chorea, the other important member of
the rheumatic cycle. Stephen Mackenzie finds 60.6 per cent., Donkin 40 per cent., Osier
51.4 per cent., affected with carditis, although the arthritic history is often absent.
Other Infections. — Other diseases, though occasional causes, are much less frequently
followed by endocarditis. Thus, Osier found it twelve times in 216 autopsies upon cases
of phthisis, five times in 100 pneumonia cases, twice in 80 autopsies upon
typhoid fever; and he states that it is not uncommon in scarlet fever.
In most of these cases the secondary infection with streptococcus is probably responsible
for the condition. Influenza, smallpox, measles, and diphtheria also
are occasional etiological factors. In all these diseases any overwork or
other overstrain upon the heart during the course of the in-
fection increases its susceptibility and enhances the liability to affection
of the endocardium, just as, according to Poynton, fright (or hard study at school) pre-
disposes to affection of the brain, namely chorea.
312
DISEASES OF THE HEART AND AORTA.
Age. — As to age it may be said, that, in contrast to both the malignant
and the chronic forms of endocarditis, the simple acute carditis which repre-
sents the usual beginning of the process presents itself most frequently in
children, especially in the second decade of life, and that the age of maxi-
mum frequency is the age of the greatest expo-
sure, the second and third decades.
The frequency is due merely to the fact that rheu-
matism is then more frequent, although when contracted
in childhood it appears to be followed by a greater per-
centage of cardiac complications than in older persons,
and pericarditis (especially adherent pericardium) and
myocarditis are more severe. Of 145 cases under 15
years of age Holt and Crondall found under 5 years 14
cases, 5-10 years 71 cases, and 10-14 years 60 cases,
38 per cent, being males and 52 per cent, females. It
is especially noteworthy that of these 145 cases almost
90 per cent, were brought about by diseases of the rheu-
matic cycle, in contrast to 60-65 per cent, in older persons.
Indeed, the earlier in life the rheumatic infection is con-
tracted, the more it assumes the type of a general carditis
and the less severely are the joints involved. As many
writers have stated, rheumatic fever in children usually assumes the form of a tonsillitis,
with carditis and chorea, and is frequently devoid of any arthritic symptoms whatever.
The myocarditis has been discussed in Part II, Chapter IX, and is an important fea-
ture. The weakness of the heart muscle which results leads to dilatation and overfilling
of the chambers, and this in turn increases the leaks due to the lesions upon the valves.
AGE
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-29
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-69
BerMille
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FIG. 178. — Diagram showing
relative frequency of the most im-
portant valvular lesions at various
ages. (Modified from Gillespie.)
Solid line, mitral insufficiency; bro-
ken line, mitral stenosis; dotted line,
aortic insufficiency. The figures in-
dicate the decades. Under 9 years,
—9; 10-19,— 19; 20-29,— 29; etc.
••CASES J.H.H
E=3 AUTOPSIES -BERL.
FIG. 179. — Diagram showing the relative frequency of the various valvular lesions in 1781 cases of
valvular heart disease admitted to the Medical Service of the Johns Hopkins Hospital from 1889 to
1908, as well as those found by Sperling in 300 autopsies in Berlin. Small space, 5 per cent.; Berl., Berlin;
J. H. H., Johns Hopkins Hospital.
Sex. — Many authors, among them Osier, state that men are more fre-
quently affected than women; though v. Jurgensen states that valvular
disease occurs with practically the same frequency in both sexes.
INVOLVEMENT OF INDIVIDUAL VALVES.
The relative frequency with which the valves are involved is shown
by the analysis of 1781 cases of endocarditis admitted in the Johns Hopkins
Hospital from 1889 to 1908, represented diagrammatically in Fig. 179.
The figures show a general correspondence to those of v. Jurgensen in 2470
cases in the German clinics.
KXDOCARDITIS. 313
PATHOLOGICAL PHYSIOLOGY.
The pathological physiology of simple acute endocarditis presents the
condition due to the individual valvular lesion (to be considered in detail
in the appropriate chapters dealing with the chronic endocarditis), modi-
fied or added to by an element of diminished vasomotor tone due to the
acute febrile condition. As the result of this vasodilatation, especially in
the abdominal area, the blood collects in the dilated veins and capillaries,
the blood-pressure may be low, and the symptom complex of arterial
anaemia or low blood-pressure sets in. Moreover, there is usually a certain
degree of actual anaemia added to the lesion, and this often increases the
difficulty in breathing; although it does not, as a rule, bring on the red and
purple hue of chronic cyanosis. Still further the increase in the leakage
causes damming back and secondary dilatation of the chambers behind
it, oedema in the walls of the ventricles and in the valve cusps, and
increased susceptibility to infection.
PATHOLOGICAL ANATOMY.
The endocarditis itself is less severe than in the malignant form. Fewer
bacteria are deposited upon the valves, and these show less tendency to
multiply, so that the process of organization, as a rule, outraces necrosis,
and consequently the separation of emboli is rare. The valves thus show
an injured surface covered by a more or less thick or exuberant layer of
fibrin, with active organization proceeding upward from its base. This
may be seen in any stage of advancement, from fresh fibrin in the early
stage to completely organized firm young connective tissue, covered by
intact endothelium, when healing has become complete.
Pathologically, the difference between the malignant and the simple
endocarditis is merely the usual difference between a mild and a virulent
infection of any tissue. There may be no actual difference in etiology, and
the malignant form may represent only a very virulent strain of the same
organism which would ordinarily produce a milder infection ; or, on the
other hand, micro-organisms of the same virulence may produce different
types of lesion in persons with different powers of resistance.
SYMPTOMS.
It is particularly noticeable that in these cases during the first attack
the symptoms due to distinct heart failure are largely absent, and the
main symptoms are those of accompanying rheu-
matic disease, along with the weakness, pallor, and anaemia (usually about
60 per cent, haemoglobin) , such as might be due to any mild fever, though
occasionally, as in the case of J. A. (page 316), the onset of aortic insuffi-
ciency is attended by pain and .sudden collapse. The temperature rarely
attains 101° unless an acute arthritis or acute pneumonia is present. The
pulse is usually rapid and regular. Its quality depends upon the nature
of the lesion, being large and collapsing in the presence of aortic insuffi-
ciency, small in mitral stenosis, and of moderate size in mitral insufficiency.
The blood-pressure is sometimes above, sometimes below normal.
314 DISEASES OF THE HEART AND AORTA.
PHYSICAL SIGNS.
As a rule, the patient does not seem very ill, he has sometimes an
anxious expression, is usually pale and sallow, in contrast to the
older cases of mitral disease, who usually show a flushed and cyanotic hue.
Occasionally choreic movements are present. It is very common for the
tonsils to be enlarged, since these are the usual portals of entry for the
rheumatic infection, and there is frequently a yellow exudate in the crypts
or a membrane over their surfaces. In almost all rheumatic cases there
are foci of cocci (streptococcus or micrococcus rheumaticus ?) in the deeper
tissue of the tonsil. Along with this infection the so-called torisillar lymph
gland just below the angle of the jaw and often the submaxillary and
anterior cervical lymph glands are enlarged. The chest shows no special
peculiarity except that precordial bulging is often present, espe-
cially marked in children (see page 88), even in the first attack of endo-
carditis. The cardiac signs are the same as for the chronic valvular lesions,
though usually less marked. They will be discussed in detail under the
special chapters.
The liver is usually not enlarged unless there is marked heart fail-
ure. Occasionally the spleen is palpable and even hard, tender, and
painful, as a result of a fresh or old infarct, and this condition may persist
unchanged for years.
A few months ago the writer saw in the Johns Hopkins Dispensary a young girl in
whom a large, very hard spleen had been present for several years, first appearing during
a rather severe attack of simple acute mitral endocarditis.
There is often slight oedema of feet and ankles, though very many
cases come to treatment before this has set in. The presence of cedema
in an early acute endocarditis is a rather grave sign, since it indicates the
failure of the heart to respond promptly to the added load.
The urine is usually of high specific gravity and contains a small
amount of albumen and a few coarsely or finely granular casts, — a typical
febrile albuminuria.
The blood examination usually shows a slight grade of secondary
anaemia.
SUBSEQUENT COURSE.
As in the cases cited on page 316, there is usually gradual improve-
ment under any treatment in which the main factor is sufficient rest,
during which the infection subsides (the bacteria dying, or more commonly
becoming latent), the vegetations undergo gradual organization and more
or less thickening or shrinkage, and fever passes off, as does the acute myo-
cardial weakness. The patients almost always recover from the first attack.
Recurrence is especially common, and is the danger against which especial
precaution must be taken, the more so as the second attack often spreads
to another valve or even to two more. It is the liability to repeated attacks
which keeps the pathological process ever fresh and increasing. There is
then usually a little area of incompletely organized fibrin always present
to give soil to any stray micrococcus that may be carried by the blood
stream, and thus produce a new outbreak of fresh endocarditis with exacer-
bation and perpetuation of the old symptoms. After a single attack,
ENDOCARDITIS. 315
especially when one only is involved, complete organization of the vegeta-
tion may set in, the acute myocardial changes subside, and the heart muscle
may soon regain its normal function.
Compensation. — A slight leak (see page 322) may remain at the site
of the vegetation, just enough to produce a murmur and perhaps even
bring about slight hypertrophy, but without really impairing the function
of the heart; and the individual who suffers from no further acute endo-
cardial changes may go on for thirty or forty years, until the age of sclerosis
sets in and the leak is widened by sclerotic shrinkage, without the appear-
ance of any further symptoms. On the other hand, as da Costa has shown,
persons with old perfectly compensated valvular lesions are much more
susceptible to cardiac overstrain and acute dilatation than are normal
individuals. With the dilatation there comes a functional insufficiency
of the valves, which adds its effect to that of the organic lesion; and finally,
as Roy and Adami have shown, stasis brings about oedema and cellular
infiltration in the cusps. This infiltration is followed by further valvular
sclerosis and shrinking, and thus the cardiac overstrain in itself tends to
increase permanently the original lesion.
When hypertrophy and compensation are good and the individual
either lives a quiet life or has developed his muscles gradually to meet the
strain of his surroundings, he may escape overstrains entirely, and the
lesion may either be stationary or may shrink by gradual sclerosis. It is
a rather common occurrence to find perfectly healthy young adults or even
active men in middle age who have had well-compensated mitral insuffi-
ciency persent since childhood. The same is also true of aortic insuffici-
ency except that this usually again makes itself felt about the age of arterio-
sclerosis, i.e. about the age of forty. Even then, with good care, general
hygiene, avoidance of muscular overstrain, nervous excitement, and over-
eating, great moderation in the use of alcohol and tobacco, and especially
personal prophylactic measures against infectious diseases, a long life
may be attained by the patient.
Reinfection. — On the other hand, when the patient is still subject to
recurrence of his rheumatism or tonsillitis, or to repeated attacks of pneu-
monia, bronchitis, or influenza, the probability that the cardiac lesion will
remain quiescent is a small one, and it becomes more likely that both valve
and muscle will suffer further changes whose limit it is impossible to pre-
dict. It is therefore most important not to give a definite prognosis to the
family or friends of the patient until he has been under observation for about
a year after the attack of endocarditis has subsided, so that all these factors
may be carefully watched and taken into account, prophylactic measures
be instituted, and the recuperative power of the heart muscle be gauged.
Complications. — Another factor even more important than the endo-
cardial lesion is the involvement of the pericardium and
especially the production of adherent pericardium, so common
in the first and second decades. This condition perhaps more than any
other leads to early heart failure, since it imposes the greatest strain of all
upon the heart; and, as it develops insidiously and frequently reaches its
maximum only after the first acute attack has passed off, it should be
watched for with great care.
316 DISEASES OF THE HEART AND AORTA.
SIMPLE ACUTE ENDOCARDITIS.
J. A., male, cannery worker, aged 15, entered the hospital complaining of rheu-
matism. He has been a rather delicate boy, having had erysipelas, measles, whooping-
cough, and chicken-pox when a child, and attacks of definite articular rheumatism at nine
and ten years. He has done soldering in a cannery for the past two years.
About five weeks before admission he began to complain of p a i n in h i s
ankles and knees, for which he was put to bed. At this time his physician found
a temperature of 104°, and he had chilly sensations, but no shaking chills.
About two weeks later while lying down he felt an intense pain in his heart and be-
gan to get white in the face and blue at the lips. Since then, though he has been
losing weight and strength, he has had no more pain. He has had occasional headaches
during the illness.
Examination shows a well-nourished boy of sallow color, with injected pharynx,
enlarged tonsils, and enlarged posterior cervical and axillary lymph-glands. Chest
is well formed and lungs are negative but for a few moist rales over the left apex.
Heart . — There is marked precordial bulging. The apex beat is seen in
the 4th left interspace 9 cm. from the midline. Dulness extends 4 cm. to the
right of the midline and above to the second rib. There are no thrills. The first
sound at the apex is preceded by a short rumble (Flint murmur) and replaced
by a soft blowing systolic murmur. The second sound is clear at the apex,
but at and near the sternum is followed by a blowing diastolic murmur,
maximum over the insertion of the third right rib. The pulse is 124 per minute,
small but definitely collapsing, and there are well-marked capillary
pulsation and throbbing of the carotids. Blood-pressure: maximal 115-125 mm. Hg.
Joints. — There are swelling of right elbow and left ankle and
soreness of elbows, knees, and right hip; slight wasting of interossei of hands and feet.
Genitalia and reflexes are normal.
There is no oedema. Red blood-corpuscles 5,000,000; haemoglobin 75 per cent.;
leucocytes 11,000. Urine. — Lemon yellow. Specific gravity 1015; alkaline; no
sugar; a trace of albumen; a considerable number of coarsely granular casts.
Oct. 31. Dulness extends 7.5 cm. to the left of the midline and 2.5 cm. to
the right. Nov. 13. Red blood-corpuscles 5,000,000; haemoglobin 80 per cent.; leuco-
cytes 6,600. General condition is excellent. Pulse continues rapid. The joints are clear.
Jan. 5. There has been gradual progressive improvement. Red blood-corpuscles 4,700,000;
hemoglobin 90 per cent.; leucocytes 11,000. There has been a gradual rise in the maximal
pressure to 150-160 mm. Hg, as the patient's improvement has continued in spite of the
rapid pulse. The patient was discharged quite well on Jan. 17, but had a second more
severe attack several years later.
TREATMENT.
The treatment of the acute attack of endocarditis partakes in general
of the treatment of a mild febrile disease or a secondary anaemia on the
one hand, and of the particular valvular disease on the other. Rest in
bed until a couple of weeks after the subsidence of all febrile symptoms
is therefore an absolute necessity, also light and easily digestible diet, at
first of 800-1000 calories, later 2500.
Digitalis and Strychnine. — As a rule, digitalis is not absolutely
necessary, and is dispensed with by most Anglo-American practitioners.
However, Cloetta has shown that the hearts of animals in which aortic insufficiency
has been produced experimentally recover much better, undergo much less dilatation, and
acquire much greater strength if digitalis treatment is begun at once and is continued over
long periods (about a year) than if this treatment is omitted. Cloetta claims equally good
results in man, but his cases are too few to warrant conclusions. Nevertheless, the results
are sufficiently definite to warrant the prolonged use of digitalis in small doses (0.3 to 0.6
c.c.; TTVv to x of the tincture) in cases of acute endocarditis with cardiac dilatation.
ENDOCARDITIS. 317
In cases in which digitalis is not used strychnine should be given
in doses of 2 to 3 mg. (^V to yV gr-) three or four times a day.
The salicylate preparations, sodium salicylate, salol, salipy-
rin, aspirin, etc., should be given for the rheumatism; but, although they
certainly relieve the pain, and it has been shown that they are excreted
into the joint cavity, the duration of the fever and arthritis does not seem
to be much affected by them, and certainly the frequency of cardiac
involvement is unchanged. On the other hand, the salicylates, especially
in large doses, have a depressant effect upon the heart, and the use of
these drugs should therefore be as restricted as is consistent with relief of
arthritic pain.
According to many authorities, the salicylates seem to be more effective when in-
jected directly into the joint or into the tissues immediately surrounding it. The writer's
experience with this method is limited and in the cases tried its results were not striking,
but it is sometimes worthy of trial. Oil of wintergreen (Oleum gaultheriae, methyl sali-
cylate) applied to the skin over the joint also seems to cause great relief of pain, but it is
possible that the rubbing may also cause more of the micrococci to be thrown out in the
blood stream than might otherwise be the case. Hot compresses of saturated aqueous
solutions of oil of wintergreen to the joint may suffice to allay pain.
Other Therapeutic Measures. — It is most important to relieve anaemia,
which is usually present and which is always a contributing factor to the
fatty degeneration and weakness of the myocardium. Rest, full diet
especially rich in eggs, milk, and green vegetables, and administration of
iron usually relieve this symptom.
The iron may be administered as Pil. ferri carbonatis (Blaud's pills), 0.2 to 0.3 G.
{gr. iii to gr. v) t.i.d., p.c.; or Massa ferri carbonatis (Vallet's mass, a more stable prepa-
ration containing honey instead of sugar); Elixir ferri, cjuininae et strychninae, 8 c.c. (oii)
t.i.d., a.c.; or as Syrup, ferri iodid., 1 c.c. (n\, xv) t.i.d., p.c.
If the anaemia is severe or does not yield to iron alone, arsenic should
be given as well, since it has been shown that iron and arsenic together
accelerate formation of red corpuscles and haemoglobin more than does
either drug alone.
Arsenic is usually given in the form of Liquor potassii arsenitis (Fowler's solution),
beginning in doses of 0.2 c.c. (n\,iii) t.i.d., p.c., and increasing one drop at each dose until
1 c.c. (n\,xv) is reached or puffy eyelids and albuminous urine show that the physiological
limit has been reached.
Prophylactic Treatment. — One of the most important factors in hasten-
ing the healing of a fresh vegetation is to keep it from being reinfected by
bacteria floating in the blood stream. Every focus of infection is a store-
house from which a few bacteria are given off from time to time, and hence
is a source of danger. Accordingly in a number of clinics, and particularly
in the medical clinic of the Johns Hopkins Hospital, under Prof. Barker's
direction, an effort is being made to stamp out every focus of infection to be
found anywhere in the body. Carious teeth, paronyohias, and ischiorectal
abscesses are removed. Particular attention is given to the tonsils. These
organs are the main portals of entry for the rheumatic infection. In persons
who are subject to recurrent tonsillitis there are almost always small ab-
scesses containing cocci persisting in the depths of the tonsillar tissue, even
when there is no inflammation visible upon the surface. These are perma-
318 DISEASES OF THE HEART AND AORTA.
nent portals of infection. Dr. Barker therefore insists upon the removal
of enlarged tonsils in most cases of rheumatic heart disease. This
should be done between but not during the attacks, since
there is danger of throwing more cocci into the blood. The improvement
which follows removal is sometimes immediate and striking. The patient's
color improves within a few days. He feels better. His expression is
brighter, and he appears more robust. Improvement is more rapid and,
since reinfection is less frequent, it is more permanent.
It is naturally of great importance that all the tonsillar tissue should be removed,
since a small amount left in place may again undergo hypertrophy and become reinfected.
Such complete removal is impossible with the guillotine, the snare, and the electro-cautery,
and is extremely difficult by even the ordinary intracapsular dissection. The most satis-
factory method known to the writer is the extracapsular dissection as performed by Bordley.
Pallative Treatment of the Tonsils. — By way of palliative or prophy-
lactic treatment various antiseptic gargles may be used. Gargles which
contain hydrogen peroxide are to be preferred, because the pus-cells con-
tain a catalase which sets free the oxygen. The nascent oxygen is a power-
ful antiseptic, and the excess collects in bubbles which mechanically loosen
and sweep off the exudate. The hydrogen peroxide should not be stronger
than 2 volume per cent, (one part commercial hydrogen peroxide to four
parts of water).
Other gargles that may be used are DobelPs solution, dilute Lugol's
solution, and dilute potassium chlorate solution (especially with equal
parts of dilute hydrogen peroxide.)
BIBLIOGRAPHY.
ENDOCARDITIS.
Bouillaud: Traite" des maladies du coeur, Paris, 1835, ii. Quoted from Nothnagel's System,
"Diseases of the Heart," transl. by G. Dock, Phila., 1908.
Lenhartz, H. : Die septische Erkrankungen, Nothnagel's Handb. d. spec. Pathol. u. Therap.,
iii, 2te Theil, Wien, 1904.
Vieussens. Quoted from C. Hilton Fagge, "Diseases of the Valves of the Heart," Rey-
nolds's System of Medicine, vol. iv, Phila., 1877; from which the subsequent references
are quoted.
Hunter, John: Catalogue of Pathological Specimens, iii, 197.
Meckel: Mem. de 1'Acad. Roy. des Sciences, Berl., 1756. Quoted from Friedreich, "Krank-
heiten des Herzens," Virchow's Handb. d. spez. Pathoh u. Therap., 1867.
De Senac, J.: Traite de la structure du coeur, de son action et de ses maladies, Par., 1749.
Corvisart: Essai sur les maladies et les lesions organique du coeur et des Gros Vaisseaux,
Paris, 1806.
Burns, Allan: Observations on some of the Most Frequent and Important Diseases of the
Heart, Edinb., 1809.
Kreysig: Die Krankheiten des Herzens, Berlin, 1815.
Virchow, R.: Ueber die Chlorose und die damit zusammenhangenden Anomalien im
Gefass-Apparate insbesondere ueber Endocarditis puerperalis, Berl., 1872.
Luschka: Sitzungsber. d. k. Akad. d. Wissensch., Wien, 1859. Quoted from Ribbert.
V. Langer, L.: Ueber die Blutgefasse in den Herzklappen bei Endocarditis valvularis,
Arch. f. path. Anat., etc., Berl., 1887, cix, 465.
Darier, J.: Les vaisseaux des valvules du coeur chez 1'homme a 1'etat normale et a 1'etat
pathologique, Arch, de physiol. norm, et path., Par., 1888, 4 se"r., ii, 35, 151.
Winge. Quoted by H. Heiberg, Ein Fall von Endocarditis ulcerosa puerperalis mit Pilz-
bildungen im Herzen (Mycosis Endocardii), Arch. f. path. Anat., etc., Berl., 1872,
Ivi, 407.
ENDOCARDITIS. 319
Weichselbaum : Zue ^Etiologie der akuten Endocarditis, Centralb. f. Bakteriol. u. Para-
sitenk, Jena, 1887, ii, 209.
Osier, W.: On Malignant Endocarditis, Brit. M. J., Lond., 1885, i, 467, 522, 577, 607.
Philipowicz: Ueber das Auftreten pathogener Mikroorganismen im Harne, Wien Med.
Bl., 1885, viii, 673, 710.
Rosenbach, O.: Ueber artifizielle Herzklappenfehler, Arch. f. exper. Pathol. u. Pharmak.,
Leipz., 1878, ix, 1; and Lehrb. d. Herzkrankheiten, Berl.
Wyssokowitsch : Beitrage zur Lehre von der Endocarditis, Arch. f. path. Anat., etc., Berl.,
1886, ciii, 333.
Orth, J. : Ueber die JEtiologie der experimentellen mycotischen Endocarditis Nachschrift
zur vorstehenden Mittheilung des Dr. Wyssokowitsch, ibid., p. 332.
Ribbert, H.: Ueber experimentelle Myo- und Endocarditis, Deutsch. med. Wchnschr.,
Leipz., 1885, and Fortschr. d. Med., Berl., 1886, iv, 1.
Koester: Die embolische Endokarditis, Arch. f. path. Anat., etc., Berl., 1878, Ixxii, 257.
Wyler, M.: Ueber einen Fall von Endokarditis recurrens, Inn. Diss., Zurich, 1897.
Prudden, T. M.: Experimental Mycotic or Malignant Ulcerative Endocarditis, Trans.
Ass. Am. Physicians, Phila., 1886, i, 207.
Hirschfelder, A. D.: The Rapid Formation of Endocarditic "Vegetations," Bull. Johns
Hopkins Hosp., Baltimore, 1907, xviii.
Rosenow: Immunological and Experimental Studies on Pneumococcus and Staphylococcus
Endocarditis, J. Infect. Dis., Chicago, 1909, vi, 245.
V. Jiirgensen, Th., v. Schroetter, L., and Krehl, L.: "Diseases of the Heart," Nothnagel's
Practice, transl. by G. Dock, Phila., 1908.
Ricord: French translation of the works of John Hunter, 1847. Quoted from Lenhartz.
Brandes: Arch. ge"n. de M<kL, Paris, 1854.
V. Leyden, E.: Ueber Endocarditis gonorrhoica, Deutsch. med. Wchnschr., Leipz., 1893.
xix, 909; also, Michaelis, M.: Zur Endocarditis gonorrhoica, ibid., 1893, xix, 1123.
Thayer, W. S., and Blumer, G.: Endocardite ulce>euse blenorrhagique septice"mie d'origine
blenorrhagique, Arch, de Me"d. exper. et d' Anatomic pathol., Paris, vii, 701, and Johns
Hopkins Hosp. Bull., Bait., 1896, vii, 57.
Thayer, W. S.: Gonorrhceal Endocarditis and Septicaemia, Compt. rend. cong. internat.
de Me*d., 1899, iii, 5 sec. 350.
Thayer, W. S., and Lazear, J. M.: A Second Case of Gonorrhoeal Septicaemia and Ulcera-
tive Endocarditis, with Observations upon the Cardiac Complications of Gonorrhoea,
J. Exper. M., N. Y., 1899, iv, 81.
Thayer, W. S.: On Gonorrhoeal Septicaemia and Endocarditis, Trans. Ass. Am. Phys.,
Phila., 1905, xx, 391.
Lartigau, A. J.: Study of a Case of Gonorrhoeal Ulcerative Endocarditis, with Cultivation
of the Gonococcus, Am. J. M. Sci., Phila., 1901.
V. Hofmann, K. Ritter, Gonorrhoische allgemein Infektion und Metastasen, Centralb.
f. d. Grenzgeb. d. Med. u. Chir., 1903, vi, 308. (Complete review of the literature up
to that date.)
Fraenkel, and Gutmann, P., and Netter. Quoted from v. Hofmann.
Horder, T. J.: Infective Endocarditis, Quart. M. J., Oxford, 1909, ii, 289.
Sahli, H.: Zur ^tiologie des acuten Gelenkrheumatismus, Deutsch. Arch. f. klin. Med.,
1893, Ii, 451.
Dana: Microbic Origin of Chorea, Am. J. M. Sci., Phila., 1894, cvii, 31.
Triboulet: Des rheumatismes chroniques d'infection; £tiologie; pathogenic, Rev. de
me*d., Par., 1898, xviii, 189.
Westphal, Wassermann, and Malkoff: Ueber den infectiosen charakter und den Zusam-
menhang von acuten Gelenkrheumatismus und chorea, Berl. klin. Wchnschr., 1899,
xxxvi, 638.
Poynton, F. J., and Paine, A.: The Etiology of Rheumatic Fever, Lancet, Lond., 1900,
ii, 861. Also Some Further Observations upon Rheumatic Fever, ibid., 1901, i, 1260.
The Present Position of the Bacteriology of Rheumatic Fever, Brit. M. J., Lond.,
1901, ii, 779. The Pathology of Rheumatism, Practitioner, Lond., 1901, Ixvi, 22.
Arthritis: A Comment upon and Review of some Recent Literature upon the Subject,
ibid., 1903, Ixxi, 128.
Poynton, F. J.: The Parallelism between Clinical Symptoms and Pathological Lesions of
Acute Rheumatic Fever, International Clin., Phila., 1904, ser. xiii, vol. iv, 95. Re-
320 DISEASES OF THE HEART AND AORTA.
marks on the Infective Nature of Rheumatic Fever, Brit. M. J., Lond., 1904, i, 1117.
A Review and Study of some Recent Writings upon Arthritis and Kindred Disorders,
Practitioner, Lond., 1904, Ixxii, 864. A Lecture on Combined Aortic and Mitral
Disease in Rheumatic Children, Brit. M. J., Lond., 1905, ii, 837. Observations upon
Arthritis in Young Children, Edinb. M. J., 1907, xxii, 226.
Meyer, F.: Zur Bakteriologie des akuten Gelenkrheumatismus, Deutsch. med. Wchnschr.,
Leip/., 1901, xxvii, 81.
Singer, G.: Weitere Erfahrungen ueber die JStiologie des acuten Gelenkrheumatismus,
Wien. klin. Wchnschr., 1901, xiv, 482.
Philipp, C.: Zur ^Etiologie des acuten Gelenkrheumatismus, Deutsch. Arch. f. klin. Med.,
Leipz., 1903, Ixxvi, 150.
Walker, E. W. A.: On the Micrococcus of Acute Rheumatism, Practitioner, Lond., 1903,
Ixx, 185.
Beaton, R. M., and Walker, E. W. A.: The Etiology of Acute Rheumatism and Allied
Conditions, Brit. M. J.. Lond., 1903, i, 237.
Shaw, W. V.: Acute Rheumatic Fever and its Etiology, J. Pathol. and Bact., Edinb. and
Lond., 1903-04, ix, 158.
Beattie, J. M.: Acute Rheumatism caused by the Diplococcus Rheumaticus, ibid., 1904,
ix, 272.
Menzer: Die ^Etiologie des akuten Gelenkrheumatismus, Berl., 1902.
Cole, Rufus I.: Experimental Streptococcus Arthritis in Relation to the Etiology of Acute
Articular Rheumatism, J. Infect. Dis., Chicago, 1904, i, 714. The Etiology of Acute
Articular Rheumatism, N. York and Phila. M. J., N. York, 1906, Ixxxiii, 534.
Longcope, W. T.: Experimental Arthritis and Endocarditis produced by a Streptococcus
Isolated from the Blood of a Case of Rheumatism, Endocarditis, and Chorea, Am.
J. M. Sc., Phila., 1904, cxxviii, 601.
Austin, Mabel F. : Endocarditis due to a Minute Organism, probably the Bacillus Influenzse,
Johns Hopkins Hosp. Bull., Bait., 1899, x, 194.
Marshall, H. T.: Endocarditis in Tuberculosis, Johns Hopkins Hosp. Bull., 1905, xvi, 303.
Michaelis, L., and Blum, S.: Ueber experimentelle Erzeugung von Endocarditis tuber-
culosa, Deutsch. med. Wchnschr., Leipz., 1898, xxiv, 550.
Stewart, H. A.: Experimental and Clinical Investigations of the Blood-pressure Changes
in Aortic Insufficiency, Arch. Int. Med., Chicago, 1907, i, 102.
Cameron, P. D.: Physiological and Pharmacological Studies upon Cardiac Tonicity in
Mammals, Thesis, Edinb., 1908.
Hirschfelder, A. D.: Recent Studies upon the Circulation and their Importance to the
Practice of Medicine, J. Am. M. Ass., Chicago, 1908, li, 473.
Hasenfeld, A.: Ueber die Entwicklung einer Herzhypertrophie bei der Pyocyaneus-
Endocarditis und der dadurch verursachten Allgemeininfection, Deutsches Arch. f.
klin. Med., Leipz., 1899, Ixiv, 763.
Osier, W.: Chronic Infective Endocarditis, Quart. J. M., 1909, ii, 219.
Rosenow, E. C.: Phagocytic Immunity and the Therapeutic Injection of Dead Bacteria
in Endocarditis, J. Am. M. Ass., Chicago, 1908, li, 1571.
Holt and Crondall. Quoted from Horder.
Barker, L. F.: Clinical Lectures at the Johns Hopkins Hospital. (Unpublished.)
II.
^MITRAL INSUFFICIENCY.
OCCURRENCE.
Of all the valvular lesions those involving the mitral valve are the
most common, especially those which lead to the production of a leak at
that orifice (mitral insufficiency, mitral regurgitation, incompetency of the
mitral valve).
Involvement of the mitral valve alone was found to be present in 51 per cent, of 1781
cases of valvular disease admitted to the Johns Hopkins Hospital between 1889 and 1908,
and in 54 per cent, of Sperling's 300 autopsies on similar cases in Virchow's Pathological
Institute in Berlin. (Fig. 179.) Mitral insufficiency, both alone and in association with
other lesions, was present in 64 per cent, of the Johns Hopkins cases, occurring alone in
29 per cent, (see the Table, Fig. 179).
As regards age, Gillespie (Fig. 178) has found from a study of 816
cases that its frequency is about uniform between ten and fifty years, after
which it diminishes. This is in sharp contrast to the cases of mitral ste-
nosis, which are most frequent before the age of thirty and become much
rarer after thirty. In youth women are slightly more often affected; in old
age the affection is a little more common among men. The mortality from
mitral insufficiency becomes greater as age progresses.
PATHOLOGICAL ANATOMY.
Pathologically, cases of mitral insufficiency may be divided into two
groups:
1. Organic, due to vegetations, cicatrizations, or atheromatous plaques,
thickening of the edges of the valves, or ulceration upon the valve itself.
2. Functional (or relative), in which the valves are intact, but closure
becomes imperfect through relaxation of the muscle into which the cusps
are inserted, or through stretching of the chordae tendineae.
Organic Mitral Insufficiency. — The pathogenesis of organic insuffi-
ciency is simple. The lesions arise during the course of an acute or
subacute endocarditis, and frequently result from the accumulation of
inflammatory exudates from several successive infections. These are
cemented into permanent structures by organization and calcification.
Occasionally a perforation of the valve occurs from ulceration. As in
acute endocarditis, infection in the rheumatic cycle is the most common
cause of chronic mitral disease, though other infections may represent not
only primary but exacerbating factors.
The vegetation, once formed, gives rise to the leak by holding apart
the neighboring portions of the cusps so that regurgitant streams occur
about its serrations (Fig. 180, a, A).
21 321
322
DISEASES OF THE HEART AND AORTA.
Tests for Sufficiency of Mitral Valve. — It is easy to demonstrate by the method of
Gad (see page 10) and Meigs that when the vegetation is not extensive the mitral cusps
may adapt themselves perfectly to its contour and prevent a leak altogether; but when,
as is usually the case, their flexibility is altered by a line of vegetation, atheroma, or infil-
tration, this apposition is prevented. The amount of blood actually regurgitating, and
hence the functional importance of the lesion, depends largely upon these factors, as well
as upon the concomitant affection of the cardiac muscle.
At the autopsy table the mitral valves may be tested for leakage in either of the
following ways:
(1) Water may be forced into the ventricle through a cannula attached to the water
faucet. The valve usually holds against leakage. (T. W. King, 1837, G. A. Gibson, Meigs.)
(2) A slit is made in the ventricle wall near the apex. The heart is turned upside
down, the slit at the apex is held open with the fingers and water poured in from above.
The normal valve would show no leakage (Bleichroeder).
B
C
FIG. 180. — Regurgitant streams in organic and functional mitral insufficiencies. A, organic mitral
insufficiency; B, functional insufficiency of the papillary type; C, relative mitral insufficiency; a, view
from above the valves ; b, coronary section through the heart. The arrows indicate the points and direc-
tion of regurgitations.
Coexistence of Organic and Functional Insufficiency. — As has been
stated above (page 226), Koester, Krehl, Geipel, and others have shown that
the occurrence of vegetations upon the valves is often, perhaps usually,
accompanied by foci of myocarditis in the papilla ry mus-
cles and in the ring of musculature about the mitral orifice. It is the
weakening of these muscle-fibres especially which gives rise to the func-
tional insufficiencies, and it is therefore probable that in
many cases of organic mitral insufficiency the ele-
ment of superadded muscular insufficiency is a very
important one. Indeed one often meets with persons who, in spite
of medium-sized vegetations, suffer little or no discomfort as long as the
heart muscle is in good condition, but in whom cardiac symptoms
occur as soon as overstrain, anaemia, or febrile disease weakens the myo-
MITRAL INSUFFICIENCY. 323
cardium. In the periods of apparent health, the leak is confined to the
streams about the edges of the vegetation. In the added functional insuf-
ficiency it also takes place at other points along the line of closure. How-
ever, it is impossible to differentiate clinically between the organic and the
functional elements, and their relative importance in a given case cannot
be accurately estimated.
Atheroma of the Mitral Valve. — Atheromatous and calcified patches along the face
and edges of the cusps of the valves are also not uncommon (see Fig. 275, page 469).
These changes are particularly frequent along the line of closure, where, as shown by Roy
and Adami, mechanical injury, hemorrhages, and exudates are most frequent. Patho-
logically, they are brought about by processes similar to those occurring in the walls of the
arteries during arteriosclerosis, and the condition is frequently associated with extensive
sclerosis of the coronary arteries. Calcified plaques may also be present in the myocardium
(case of J. L., Fig. 275). The mechanical effect of such thickenings and areas of rigidity
is to prevent the cusps from accommodating themselves to one another, giving rise to leaks
which are undistinguishable clinically from those due to vegetations.
Hemorrhage in the Mitral Valve.— Occasionally hemorrhages occur in the cusps of
the mitral valve, especially after trauma to the chest (Kiilbs) or labor (Weber and
Deguy), and in new-born infants (Fahr). It is probable that the organization of the clot
initiates a fibrosis which leads to mitral stenosis.
Functional Mitral Insufficiency. — When the heart muscle attains a
certain degree of weakness, leaks at the mitral orifice may take place.
They may occur as the direct result of acute cardiac dilatation from a pri-
mary cardiac overstrain, though they arise more frequently in hearts whose
myocardium has already undergone degenerative or fibrous changes but
whose valves are still intact. This functional insufficiency is often seen in
cases of myocarditis. On the other hand, functional insufficiency of the
mitral valve may arise as a secondary manifestation in organic disease of the
aortic valves. This occurs especially when the leak attains a severe grade or
the work of the heart is too much increased, the walls of the ventricle and
the papillary muscles becoming overstretched during diastole. This phe-
nomenon will be further discussed in the chapter upon aortic insufficiency.
Types of Functional Insufficiency. — The leaks occurring at the mitral
valve as the result of muscular weakness may be divided into two groups:
1. PAPILLARY INSUFFICIENCY. — Leaks occurring at one or more points along the
valve (Fig. 180, B, b) when the weakness of a papillary muscle or stretching of a chorda
tendinea allows the corresponding portion of the valve to be lifted a little, and a small
regurgitant stream to emerge at one of the points of pouting and puckering along the line
of closure. This may be termed the type of papillary insufficiency, and
like many cases of uncomplicated organic insufficiency may correspond to the escape of
only a small quantity of blood. This papillary insufficiency represents the mildest form of
functional regurgitation. The mitral valve is pushed upward during systole, like a sail,
impelled by the full force of the entire ventricular wall. This is antagonized by the pull
of the relatively bmall papillary muscles. It is evident that fibre for fibre the papillary
muscles incur a much greater strain than the fibres in the ventricular wall, and consequently
they are often the first to weaken. When they weaken apposition of the cusps is impaired
and regurgitation sets in. Moreover, since T. W. King and Gibson have shown that the
normal mitral valve usually holds unless dilatation sets in, it is evident that the papillary
type of insufficiency is the only form of functional insufficiency that can occur in a heart
that is not greatly dilated.
2. RELATIVE INSUFFICIENCY. — The second type of functional insufficiency is met with
when the left ventricle is dilated to such an extent that the mitral
orifice becomes larger than the available area of valve surface,
and what may be correctly termed a relative insufficiency results. Under
324
DISEASES OF THE HEART AND AORTA.
these conditions the leak occurs not at a single point but all along the line of closure (Fig.
180, C). The amount of blood which regurgitates under these conditions may be very large.
PATHOGENESIS OF THESE TYPES. — The mode of occurrence of these types of in-
sufficiency may be readily demonstrated by the method of Gad and Meigs, though care
must be taken that the heart used for the experiment is not in a condition of rigor mortis.
If water is forced into the ventricles at various pressures, it will be seen that, as shown by G.
A. Gibson, leakage will occur at a relatively slight pressure. This regurgitation will be
small in amount, and will be seen to be of the papillary type; but if the pressure is suffi-
ciently increased and the ventricle dilated, the cusps of the valve stand apart, the true
relative insufficiency (type 2) is produced, and a large amount of fluid regurgitates. The
role which stretching of the muscle plays in this regurgitation may be shown by boiling the
heart and thereby shortening the fibres in heat rigor, after which the leak that was present
disappears and does not recur until much greater pressures are resorted to. Gibson has
caused the leak to disappear by tightening a ligature about the mitral muscular ring. It is
therefore evident that the tonicity of the cardiac muscle is an important element in deter-
mining the occurrence and the degree of leak both in functional and in organic mitral insuffi-
ciency. This point is of the greatest importance in therapeutic considerations, and will be
referred to later.
Occurrence of Functional Insufficiency. — Functional insufficiency of
the mitral valve occurs in primary cardiac overstrain, in anaemias, during
the course of and convalescence from infectious diseases, and in many
cases of aortic disease. A certain percentage of the cases in which aortic
and mitral insufficiencies are found simultaneously belongs to this group.
Lian, in Franc. ois-Franck's laboratory, has shown that the contraction
of the ring of muscle about the mitral valve (mitro-aortic ring) narrows
the diameter of the orifice during systole. He demonstrated that when
contraction is weakened the valves may not remain in perfect apposition.
MECHANICS OF THE CIRCULATION IN MITRAL INSUFFICIENCY.
It is almost axiomatic to state that the systolic regurgitation of blood
from left ventricle to left auricle in mitral insufficiency is accompanied by
a fall of pressure in the former and a rise of pressure in the latter.
COMPENSATED
BROKEN PULMONARY COMPENSATION
FIG. 181. — Diagram showing the volume and pressure curves under these conditions. (Schematic.)
Upper curve (A), interauricular pressure; solid black line, volume' curve of the left auricle; lower curve
(V), intraventricular pressure.
The regurgitation of blood into the left auricle causes a systolic rise of
pressure to take place in this chamber, replacing the systolic fall of pressure
which is present under normal conditions (Fig. 181). The pressure curve
within this chamber in mitral insufficiency thus resembles that seen in the
right auricle in tricuspid insufficiency — a rise throughout ventricular systole
with a fall during diastole, and a small rise when systole of the auricle
takes place.
MITRAL INSUFFICIENCY.
325
The pressure conditions within the pulmonary circulation are of the
greatest importance, and in this both the force-pump and the suction-
pump actions of the ventricle show themselves.
Effect of Mitral Insufficiency without Increase in the Strength of the
Ventricle. — If the force of the left ventricle remains unaltered after the
production of the insufficiency, it stands to reason that less blood will reach
the arteries and pass on to the capillaries and systemic veins than did so
before. The arterial blood-pressure will fall. Consequently less blood will
enter the right side of the heart from the venae cavse, and the pressure in the
latter will be lowered. The systolic output of the right ventricle will thus
be diminished and the pressure in the pulmonary artery will fall. On the
other hand, the regurgitated blood in the left auricle and pulmonary veins
added to that coming on from the pulmonary artery will cause the pres-
sure in the left auricle, the pulmonary veins, and the capillaries of the lungs
to rise (Fig. 183, III).
FIG. 182. — Curve of intraventricular pressure in mitral insufficiency produced on a mechanical
model. (After Marey.) P. V., intraventricular pressure; P. R., arterial pressure. The horizontal line
denotes the production of insufficiency. O, notch due to the auricular systole; e, summit of the curve
during systole of the ventricle.
Pulmonary Stasis. — As v. Basch and his pupils have shown, conges-
tion of the pulmonary capillaries is the most important cause of cardiac
dyspnoea (broken pulmonary compensation). Hence it will not be sur-
prising that dyspnoea from this cause is an early and important symptom
of mitral insufficiency, and that its disappearance depends upon other
factors which tend to deplete the pulmonary capillaries. (Diminution in
the amount of blood entering right ventricle, or weakened suction-pump
action of left.) The capillary area is sufficiently elastic to accommodate a
considerable amount of regurgitant blood before this furnishes an obstruc-
tion to the pulmonary artery, just as is the case with the capillaries of the
splanchnic area, but after a time or in severe lesions the intrapulmonary stasis
finally makes its effect felt in the pulmonary artery. The pressure there rises
(Gerhardt) . When the pulmonary stasis becomes extreme the right ventricle,
too, becomes overloaded and dilated. Broken systemic compen-
sation sets in (Fig. 183, IV). Stasis occurs in the systemic wins,
oedema and ascites take place, and a secondary functional insufficiency of
the tricuspid valve may usually be demonstrated. With the occurrence nt
this secondary leak at the tricuspid orifice, less blood is pumped into the
pulmonary circulation, the congestion hero diminishes, the dyspnoea dimin-
326
DISEASES OF THE HEART AND AORTA.
ishes also, and in spite of the increased gravity of the condition the patient
may experience some temporary relief from his symptoms. This phenom-
enon was noted by T. W. King in 1837, and was designated by him "the
safety-valve action of the tricuspid valve." The relief is, however, only
transitory, as the accumulation of CO2 in the blood soon gives rise to
dyspnoea from stimulation of the respiratory centre in the medulla, and the
real state of cardiac failure manifests itself. If the condition is allowed to
continue, the outcome is death.
NORMAL
ir
COMPENSATED
III
BROKEN
PULMONARY
COMPENSATION
IV
BROKEN
SYSTEMIC
COMPENSATION
FIG. 183. — Diagram showing the effects of mitral insufficiency upon the circulation. I. Normal.
II. Compensation through filling of the auricle in systole but complete emptying in diastole. III. Broken
pulmonary compensation. IV. Broken systemic compensation.
Effect of Increase in the Strength of the Left Ventricle.— If, on the
other hand, the force of the left ventricle increases, it can throw more
blood out into the aorta and arteries; and this blood must first be drawn
from the left auricle and pulmonary circulation. So that if the output
from the ventricle increase, it will soon be pumping more blood into
the aorta than the right ventricle (whose force has remained practically
unchanged) pumps into the pulmonary artery. Accordingly more blood
leaves the lungs than enters them, and the engorgement passes off. The
whole condition may be summed up by the statement that a weakly
acting left ventricle overfills the lungs with blood,
while a strongly acting left ventricle bails them out.
The whole of pulmonary engorgement is, as rightly
claimed by v. Basch, a problem not of the right ventri-
cle, but of the left.
CLINICAL MANIFESTATIONS.
MITRAL INSUFFICIENCY WITHOUT SYMPTOMS.
The earliest circulatory disturbance in mitral insufficiency is stasis in
the pulmonary capillaries, which, as v. Basch and his pupils have shown,
leads to cardiac dyspnoea. Accordingly, it is not surprising that dyspnoea
should be one of the earliest symptoms of mitral insufficiency. But the
MITRAL INSUFFICIENCY. 327
pulmonary stasis does not occur or does not persist when the action of the
left ventricle is sufficiently vigorous, and hence in the milder cases shortness
of breath may be absent for a long time after the actual formation of the
lesion and may make itself evident only upon exertion.
Thus, a young friend of the writer, a boy of eleven, in 1907 contracted tonsillitis accom-
panied by the typical signs of mitral insufficiency. He was kept moderately quiet on account
of the throat lesion and had apparently recovered completely, so that the family did not
notice any abnormality until a year afterward, when he became somewhat short of breath
upon walking uphill. Since a little caution has been exercised against fast walking he no
longer becomes short of breath and remains perfectly free from symptoms. The prognosis
is very favorable. In some more vigorous individuals the lesion does not manifest itself
at all. The writer has in mind a young man of twenty-one who has shown signs of mitral
insufficiency for eight years, but during that period has excelled at football, wrestling, and
all the severe forms of sport; also a professor of forty who has had a mitral lesion of rheumatic
origin for some time without the slightest physical inconvenience. These cases, though
scarcely to be regarded as the rule, are encountered with great frequency in patients who
are examined for some other cause. Occasionally such persons have been informed of their
trouble, sometimes given a grave prognosis, and come to the physician in great mental
distress because they have been 'told that they have "organic heart trouble," and yet
they may reach middle or even old age without serious inconvenience. It is not extremely
uncommon to find cases in whom a mitral lesion has been present thirty or forty years with-
out greatly affecting the patient's activity or enjoyment of life.
Pulmonary Complications of Mitral Disease. — The prolonged stasis and high pres-
sure in the pulmonary capillaries may, however, give rise to permanent changes in their
walls and in the tissues about them and facilitate the occurrence of a chronic bronchitis.
This bronchitis resulting from stasis may be considered analogous in origin to the ulcerations
and weeping eczema found upon the legs in association with varicose veins or cardiac oedema.
The presence of this chronic bronchitis is liable to arouse a suspicfon of tubercu-
losis when the trouble is really cardiac. The suspicion is sometimes still further aroused
in the cases in which the walls of the capillaries in some area of the lungs have become
eroded and occasional pulmonary hemorrhages take place. Thus, Osier and A. G. Gibson
mention the case of a physician who suffered from occasional haemoptysis due to
mitral insufficiency over a period of twenty-five years, each attack giving rise to great relief
of his cardiac symptoms by relieving the engorgement of the left auricle. The diagnosis in
such cases is often difficult, but may be made when there is continued absence of tubercle
bacilli from the sputum, and especially from the ejected blood, associated with the signs of
a definite mitral insufficiency. Further confirmation may be gained by a negative cuta-
neous or ophthalmic reaction with tuberculin, or if necessary by a negative subcutaneous
injection of the latter.
MITRAL INSUFFICIENCY WITH SYMPTOMS.
Second Stage of Mitral Insufficiency (Broken Pulmonary Compensa-
tion).— A more severe stage with less favorable prognosis is that in which the
lesion manifests itself by subjective symptoms. As in most other cardiac
disturbances, palpitation occurs early in the disease. Palpitation is, how-
ever, common in healthy persons, and, as shown by Hirschf elder (see page
157), cannot as yet be regarded as signifying functional weakness, so that
its presence scarcely suffices to direct suspicion to the cardiac valves.
The earliest symptom of real importance is shortness of breath.
This occurs at an earlier stage in affections of the mitral than of the aortic
valves, but is more marked in early mitral stenosis than in early mitral
insufficiency. Nevertheless, it may be quite severe in compara-
tively mild grades of the latter, especially on exertion. As has
been stated above, the dyspnoea is due to the pulmonary engorgement, as
328 DISEASES OF THE HEART AND AORTA.
shown by v. Basch. It is therefore liable to pass off when the left ventricle
hypertrophies and the systolic output is increased and the suction-pump
action is increased. For practical purposes, therefore, such persons whose
cardiac function has been restored by the hypertrophy of the left ventricle
may be said to have passed from the second stage insufficiency back into
the first. They often remain in this excellent condition for a number of
years, and sometimes oscillate between the first and the second stages for
a number of years more.
Tonicity of the Heart as a Factor Governing the Leak. — A most
important factor in preserving this balance is the tonicity of the car-
diac muscle; for when the tonus is maintained the cusps of the valve
are approximated as tightly as possible about the thickening, and the
amount of leak is reduced to minimal, whereas when the tonicity is low
the organic leak is further supplemented by a papillary or a relative insuf-
ficiency. A small leak is thus, if only for a time, transformed
into a large one. When tonicity is low it is harder for the heart to
recover from such an additional strain than if the latter occur at a time
when the tonus is increased. The added functional insufficiency may thus
become permanent. We have here another example of the vicious circle:
Leak at mitral valve
Leak increased ,
t
Papillary or Heart strain
relative insufficiency Diminished tonicity
It is evident, therefore, that in spite of the comparative ease with
which patients may recover from the symptoms of mitral insufficiency
when the case is placed under favorable conditions as soon as possible, yet
the case may rapidly become a grave one if these precautions are neglected,
so that, in the words of Osier, mitral insufficiency may be either the mildest
or the gravest of valvular lesions.
Third Stage of Mitral Insufficiency (Broken Systemic Compensa-
tion). — The second stage of mitral insufficiency represents the physiological
conditions shown in Fig. 183, IV, when the stasis is in the lungs and the
work of the right ventricle is gradually increasing. The third stage repre-
sents that in which the right ventricle also has begun to fail,
and Jplood begins to stagnate in the systemic veins as well. The pressure
in tnese veins increases two- to threefold (from 5-8 cm. H2O to 20-30 cm.)
as can be shown by the method of Eyster and Hooker. As a result they
dilate and the flow through them is slowed, changes occur in the capillary
walls, and oedema soon takes place — first in the feet, later in the shins,
thighs, genitalia, and back. With the onset of these manifestations the
shortness of breath becomes extreme, a dyspnoea of medullary origin adding
its effect to the pulmonary engorgement. The patient is compelled to sit up
all the time, gasping for breath, occasionally with paroxysms of real cardiac
asthma and palpitation, sometimes with pains in the heart, severe cough,
and expectoration of considerable amounts of sputum which often contains
cells loaded with blood pigment (Herzfehlerzellen) . The urine becomes
scant and loaded with albumin and casts. Ascites may set in and may
MITRAL INSUFFICIENCY.
329
even become so great as to require repeated tapping. The same is true of
hydrothorax. On this account it is more common upon the right side.
Unless the course of the disease is checked, death may follow after this
stage has set in ; but if the work of the heart can be diminished and its action
strengthened it may soon pump out the stagnating blood and lower the
venous pressure. From this cause, and owing to the concomitant increase
in cardiac tonicity, the dilatation diminishes. The element of regurgitation
which is of functional origin disappears and the amount of blood regurgi-
tating is once more reduced to that which flows past the vegetations. The
work of the heart is again brought to its minimum, and thus it is that
almost unhoped-for recoveries may occur in mitral insufficiency
when properly treated.
PHYSICAL EXAMINATION.
Inspection. — The typical picture of mitral disease is seen in the flushed
pink cheeks with slight tinge of purple, slightly dilated venules, and bright
watery eyes, giving on superficial inspection the appearance of superabundant
health — the so-called mitral facies. This is in sharp contrast to the pale,
pasty, or sallow color of aortic insufficiency, or the livid purple of emphysema.
The lips show a moderate cyanosis. There is, as a rule, no special throbbing
seen in the carotids. The venous pulse is usually well seen and is of the
normal "double" type. Since
the disturbance of function in
the first two stages is in the pul-
monary circulation and not in
the systemic, no change in the
jugular pulsation is to be found
nor would be expected until the
third stage, when the onset of
tricuspid insufficiency causes it
to assume the " single " or ven-
tricular form.
The chest may show pre-
cordial bulging, especially in
children and in cases of long
standing. The apex impulse if
visible is displaced out-
wards toward the axilla
rather than downwards.
It is frequently of a slow heav-
ing character, while in cases of
long-standing pulmonary stasis there may be also a wavy systolic retrac-
tion of the interspaces which mark the hypertrophy of the right ventricle.
Occasionally a systolic impulse in the second left interspace shows the
vigorous pulsation of the pulmonary artery. In very large hearts it is not
uncommon to find a systolic retraction present along the outer border of
dulness, even when adherent pericardium is absent.
In long-standing cases changes in the extremities also take place,
especially slight clubbing of the fingers.
FIG. 184. — Distribution of the murmur in mitral in-
sufficiency. Distribution upon the chest wall. Light
line, outline of cardiac dulness; heavy line, outline of
cardiac flatness. Shaded area shows distribution of the
murmur. The diagram at the right indicates the relation
of the murmur to the cardiac cycle.
330
DISEASES OF THE HEART AND AORTA.
FIG. 185. — Cross section of the body show-
ing how the thrill and murmur reach the chest
wall. The heavily stippled areas indicate the areas
over which the murmur is heard.
Palpation usually reveals a strong, slow, heaving impulse with a more
or less intense thrill lasting throughout the period of systole. This thrill
is probably due to the impact of eddy currents passing by the vegetation
and striking the heart wall, whose impact sets the valve into vibrations
that are communicated along the chordae tendinese to the walls of the
heart and then to the chest. It is most
intense at the apex, but is often pal-
pable over the entire precordium, oc-
casionally in the axilla, and sometimes
at the back in the left interscapular
region. The thrill at the back is rarely
felt except in children and thin-
chested persons, but as it represents
the direct impact of regurgitation
it is very characteristic. In a few
cases the thrill from a mitral lesion
can be felt in the vessels of the
neck, and sometimes also over the
entire chest.
The shock accompanying the second heart sound is practically un-
changed, though it is often more distinct, especially over the pulmonary area.
Percussion. — The characteristic cardiac outline in mitral insufficiency
shows an increase in area horizontally (M L) towards the left, which is some-
times enormous and may reach well into the axilla and as much as 22 cm.
from the midline by percussion. When the apex approaches the axillary
convexity, as shown by Moritz,
the area of dulness usually
extends somewhat beyond the
actual outline of the heart ; but
with the lightest possible percus
sion (the threshold percussion)
this error may often be reduced to
a centimetre or less. In contrast
to the cardiac outline in aortic
insufficiency, the left border
of dulness or of the
shadow seen with the
X-ray is increased diag-
onally upwards and out-
wards, as well as outwards in
the horizontal diameter (Fig.
186). The upward extension
may reach the second rib and pass outward into the second left inter-
space. According to the autopsy findings of Harris, this is not due to the
dilatation of the left auricle, but to the increase in size of the conus arte-
riosus of the right ventricle and to some dilatation of the pulmonary artery.
Harris has shown that even an extremely dilated left auricle is not visible from
the front of the chest under these circumstances. As is therefore to be expected, such dila-
tions correspond to the later rather than to the earlier stages of the disease, and are also
FIG. 186. — Radiograph of a patient with mitral in-
sufficiency, showing horizontal enlargement of the heart
to the left. (After Bougsch and Schittenhelm.)
MITRAL INSUFFICIENCY.
331
more common in mitral stenosis than insufficiency. The cardiac dulness is not increased
to the right until the third stage of the disease.
The Systolic Murmur. — The data obtained from auscultation usually
furnish the basis for the diagnosis of mitral insufficiency. The character-
istic sign is the presence of a murmur heard at the apex and in the
left axilla throughout systole, — i.e., last-
ing up to the second sound. The sounds
of different systolic murmurs are described
by the French writers as resembling the
rasping of a file, the sawing of wood, the
hissing of a jet of steam, the cooing of a
dove ! These variations depend upon many
sound-producing factors so complex that it
is impossible to predict the characteristics
of the lesion upon the valve by the murmur
to which it gives rise. In general, rough,
roaring, sawing, and purring murmurs are
very often produced by thickened or calcified
vegetations, which act more or less as sound-
ing-boards, while whispering or blowing mur-
murs are produced by regurgitant streams
passing over smooth-walled valves, and
occur especially in functional insufficiencies.
However, exceptions to this are frequent.
Digital Imitation of the Mitral Systolic Murmur. — The mitral systolic murmur can be
reproduced by Larned's or Smith's methods by a stroke across the elbow or across the
back of the hand. To imitate a murmur accompanying the first sound the latter should
be produced by a slow flexion of the finger, which combines the blow and the strok-
ing. For demonstrations to a group of students these manoeuvres may be carried out
upon a derby hat. The stroke should be of long duration and should be followed
immediately by the tap which represents the second sound.
Excellent phonographic tracings of
this murmur have been made by Eint-
hoven as well as by Weiss and Joachim.
These observers have shown that in con-
trast to the murmur of aortic stenosis the
murmur of mitral insufficiency always
begins synchronously with the first sound.
It is loudest at the time of th«e
first sound, which it may entirely re-
place and may then be uniform through-
out the period of systole or take
on a decrescendo character, in
murmur which folio ws the f i r st
FIG. 187. — Diagram of Fig. 180,
showing the directions in which car-
diac enlargement has taken place. The
broken line represents the outline of the
normal heart. The arrows indicate the
conjugates (ML and L) which are most
enlarged.
FIG. 188.— Graphic records of the heart
sounds, showing the systolic murmur.
(Kindness of Prof. Einthoven.) 1, 2, heart
sounds. The vibrations between 1 and 2
and some of those composing 1 are due to
the murmur.
contrast to the aortic
sound and is crescendo in character.
They have shown further that in some cases the first sound and murmur precede
the carotid wave by a greater interval than normally (lengthening of the presphygmic
period from .08-.09 sec. to .12-. 15 sec.). At the very beginning of systole blood rushes
back into the auricle. This escape causes the pressure in the ventricle to rise more slowly
than usual and hence aortic valves open a little later. Hence the presphygmic period is
332 DISEASES OF THE HEART AND AORTA.
later. It is possible that the duration of the presphygmic period may serve as a guide
to indicate the degree of leakage, — shortening indicating an improvement, lengthening
an increase in leakage. However, other observers find lengthened presphygmic periods
from different causes.
In the accidental murmurs of anaemia Weiss and Joachim have found a normal
presphygmic period.
It is stated by some writers that functional murmurs occur late in systole, mesosystolic
or telesystolic, because comparatively little regurgitation occurs until the intraventricular
pressure has reached its maximum and the papillary muscles begin to weaken. There are
no graphic records supporting this claim, and the subject demands experimental investiga-
tion rather than clinical speculation.
As regards distribution, the murmur of mitral insufficiency is heard
over those areas of chest wall which are nearest to the left ventricle and
left auricle, namely, the apex and the neighboring areas to the left (Fig. 184).
The reason why the murmur of mitral insufficiency is heard so loudly at the apex is
not perfectly clear, since this propagation is opposite to the direction of the regurgitant
stream. It is possible, however, that the vibrations of the mitral valve may be transmitted
to the anterior papillary muscle and apex by the papillary muscles which act like violin
strings. This would also explain why the murmur is so loud in the anterior part of the left
axilla at a considerable distance from the left auricle but near the anterior papillary muscle
(Fig. 185).
In children and in many persons with small, thin-walled chests the
murmur is also heard over the left interscapular region to which it is trans-
mitted directly from the left auricle. This distribution is the one which is
most typical, since it represents transmission in the direction of leakage,
and the comparative infrequency with which it is heard is due entirely to
the thickness of the chest wall and the layer of lung. Certain excellent
German observers,, however, are unwilling to diagnose mitral insufficiency
unless this murmur is present.
In order to obviate these disturbing factors, August Hoffmann and later Gerhartz
have attempted to use the oesophageal auscultation described on page 104,
but it is unpleasant to the patient, and, besides, the murmur may be no more distinct
than at the apex.
Another rarer site for the systolic murmur of mitral insufficiency, as shown by Naunyn,
is the pulmonary area — the second and third left interspaces at the sternal margin and
as far out as the parasternal line. Naunyn thinks that in this region the vibrations are
communicated by the hypertrophied and dilated left auricle to the pulmonary artery. This
murmur must always be carefully differentiated from the accidental pulmonary murmur
heard in this region and from that due to pulmonary stenosis and sclerosis.
Over the right ventricle, that is from the left parasternal line to the
left sternal margin, the murmur of mitral insufficiency is usually heard,
diminishing in intensity as the distance from the apex increases.
Differentiation from Accidental and Tricuspid Murmurs. — This is in
sharp contrast to the accidental or "haemic" murmurs which are
loudest over the right ventricle and especially over its upper portion (in the
second and third left interspaces) . These murmurs diminish over the apex
while the mitral murmur increases. They are rarely heard to the left of the
apex. They are later, softer, shorter, more superficial; they vary with
inspiration, expiration, and change of position; and the heart is, as a rule,
not hypertrophied. On the other hand, there is no reason to believe that
the distribution of the murmur due to functional mitral insufficiency differs
from that due to vegetations upon the valves, and it is frequently impos-
MITRAL INSUFFICIENCY. 333
sible to differentiate between the two conditions.1 The common statement
that murmurs of organic origin are transmitted to the axilla while those of
functional origin are not is due to a confusion of " functional " with " acci-
dental" murmurs. All loud and rough murmurs are transmitted further
than soft ones, and murmurs due to vegetations are usually louder than
functional murmurs, but a soft murmur of organic origin is probably no
louder than many murmurs of functional origin.
The murmur due to tricuspid insufficiency is heard loudest over the
lower portion of the sternum, the epigastrium, and often also to the right
of the sternum. That of aortic sclerosis or aortic stenosis is loudest over
the second and first right interspace, and is usually transmitted to the
carotid and axillary arteries. The same applies to the murmur due to
aneurism. Moreover, as stated by Boy-Teissier, it is always meso- or
telesystolic, and therefore follows but never replaces the first sound.
The Second Sound. — The second sound at the apex and over the aortic
area shows no special change, but over the pulmonic area it may be greatly
accentuated. This is not always the case, because, as seen in Fig. 183, the
pressure in the pulmonary artery is not always increased; but during the
course of a mitral insufficiency the intensity of the second pulmonic may
change. In interpreting the significance of this change it must be remem-
bered that rise of pulmonary pressure may occur either when the force of
both ventricles is increasing or when extreme engorgement of the pulmo-
nary vessels has occurred. In the former case it will be accompanied by the
general signs of improvement in the left ventricle, larger pulse, increased
maximal blood-pressure, increased pulse-pressure; in the latter case by fail-
ure of the left ventricle. Regarding the role which vasomotor changes in
the pulmonary vessels play under clinical conditions little is known; but
they also can affect the intensity of the second pulmonic.
Pulse. — The pulse in mitral insufficiency shows no characteristic
changes. Dependent upon blood-pressure, systolic output, and pulse-pres-
sure which vary considerably, it may be large or small, hard or soft. De-
pendent upon the condition of the heart muscle and especially of the left
auricle, it may be regular or irregular. The condition of the individual
patient at any single stage of the disease must be viewed in the light of
these determining factors.
Blood-pressure. — As has been seen above, the sudden production of
mitral insufficiency both in animals and on the model is followed directly by
a fall of blood-pressure and diminution of pulse-pressure, unless the strength
of the ventricle and its systolic output be increased. Such an increase does
take place, however, during hypertrophy, and hypertrophy of the left
ventricle is the rule in mitral insufficiency. Moreover, when the output
into the arteries is diminished by the backflow into the left auricle, these
vessels undergo a compensatory constriction and narrow the blood channel.
However, as the left ventricle hypertrophies, its systolic output increases
at the expense of the residual blood. These two compensatory factors
combine to maintain the blood-pressure and pulse-pressure at their original
1 The confusion of the terms " hsemic " (accidental) and " functional " murmurs so
common in clinical notes seems therefore to be both unnecessary and misleading, and should
be carefully avoided.
334 DISEASES OF THE HEART AND AORTA.
level, and at times even exceed it. For example, a prominent medical
educator who has a mild leak at the mitral valve but suffers no symptoms,
has a maximal pressure of 140, a minimal of 95, and a large full pulse. The
compensation in this case has more than balanced the disturbance in the
circulation. This increase of pulse- and blood-pressure is not always indica-
tive of improvement, but may occur also as terminal events under the
stimulation of medullary asphyxia (see page 27). On the other hand, the
presence of a rather small pulse and rather low blood-pressure and pulse-
pressure may merely represent the natural effect of the lesion unaltered by
compensatory changes on the one hand, or on the other may represent the
failure of the left ventricle to maintain the circulation. The presence of
arteriosclerosis may in itself tend to modify the blood-pressure, and to
increase a blood-pressure and pulse-pressure that would otherwise be small.
In any case the blood-pressure shows no characteristic features in mitral
insufficiency, and the figures obtained are to be viewed as the algebraic
sum of various circulatory factors, rather than as absolute measures of
cardiac vigor. It must be remembered further that the cardiac symptoms
are due mainly to changes in the pulmonary circulation, while the blood-
pressure changes are concerned only with the systemic.
Arrhythmia. — The action of the heart is often irregular in mitral dis-
ease, so that the arrhythmia in these conditions is frequently described as
"the mitralized pulse..7' Physiologically, the "mitralized pulse"
represents an irregularity probably due to numerous extrasystoles arising
in the left auricle but so frequent as to disturb the rhythm completely.
In contrast to the absolute irregularity arising in the right auricle, the a
wave upon the jugular tracing may persist in spite of the arrhythmia, for
the right auricle may not be paralyzed. Joachim has shown by oesophageal
tracings that the left auricle is often paralyzed under such circumstances.
With the irregularity there are often very feeble early extrasystoles too
weak to open the aortic valves and to cause a pulse wave. The second
heart sound is lacking with these beats because the valves are not opened.
The origin of the irregularity is probably in the distended left auricle
(cf. also page 75). It is sometimes, but by no means always, accompanied
by paralysis of the auricle, as shown by the venous tracings, but the exact
mechanism by which this form of irregularity is produced requires further
investigation in order that its diagnostic and prognostic significance may
be thoroughly understood.
The condition of the radial, temporal, and other arteries may vary
considerably, but, especially in patients above 40, may show considerable
grades of arteriosclerosis. This is more common and somewhat more exten-
sive in patients suffering from any cardiac disease than in persons with
normal hearts (Wild).
Lungs. — Examination of the thorax and lungs in mitral insufficiency
reveals the usual signs corresponding to the pulmonary changes described
above — small, moist, and piping rales corresponding to the bronchitis often
associated with hyper-resonance on percussion. Over areas of hydrothorax
there are absolute flatness on percussion, absence of vocal fremitus and
breath sounds, Koranyi's flatness over the lower thoracic spines, and
Grocco's triangle, para vertebral dulness to the left of the midline.
MITRAL INSUFFICIENCY. 335
Abdomen. — The abdomen rarely shows any .special change during the
milder stages of the disease. Occasionally one finds, as in a young girl
recently under the writer's observation in the Johns Hopkins Dispensary,
the remains of an old splenic infarction, characterized by enlargement,
hardness, and tenderness of the organ. This may persist for some months.
Enlargement and pulsation of the liver and ascites (portal stasis) belong to
the stage of broken systemic compensation (see page 338) . The same also
applies to oedema of the feet, ankles, and legs, which occurs in the mildest
form of broken compensation. These phenomena, though of serious import,
are by no means harbingers of death, for with proper treatment many cases
outlive one or even several breaks in compensation for many years.
The following represent the course of typical cases of mitral insuf-
ficiency.
CASE OF MITRAL INSUFFICIENCY.
C. H., ship carpenter, aged 63, first admitted to the Johns Hopkins Hospital in No-
vember, 1899, complaining of shortness of breath. Family history negative. The
patient has always been a robust man. He gives a doubtful history of rheumatism,
but a definite history of pneumonia five years before admission. No venereal his-
tory. He has always been a hard eater, hard drinker, and a hard worker.
The present illness began with attacks of paroxysmal dyspnoea upon
exertion eight or nine months before admission. Two months before admission an
attack came on spontaneously while in a warm room. During the past month he has
not been able to lie down in bed owing to dyspnoea and the onset of
a smothering feeling. He has had no cough, no haemoptysis. Examination on this admis-
sion showed a stout, well-nourished man with mucous membranes a trifle purple and dilated
venules over the face. His chest was barrel shaped and there was a little fluid (flatness and
impaired breath sounds) at the bases behind.
Heart. — A p e x was situated in the 6th interspace 16.5 cm. from the midline. The
area of cardiac dulness reached upward to the second costal cartilage and 5 cm. to the
right of the sternum. There is a well-marked systolic murmur heard over the
body of the heart and over the anterior part of the axilla. The second sound is every-
where clear; the second aortic booming.
The liver is slightly enlarged, being just palpable; the spleen is not. The abdomen is
full, the flanks bulge, and there is slight movable dulness in the flanks. Genitalia normal.
There is slight oedema of the ankles. Blood count normal. Urine is dark sherry
colored, specific giavity 1024, acid, contains a small amount of albumin and some hyaline
and granular casts.
The patient was put to bed on soft diet, given daily purgation with
magnesium sulphate (30 Gm., 5i), also 8 doses of -tincture of digitalis (1 c.c., TI\XV)
at intervals of four hours, followed up by strychnine 1.5 mg. He was also given
potassium iodide 1 Gm. (gr. xv) after meals.
(Edema disappeared and orthopnoea also, so that within ten days the patient could
sleep with his head low and could walk without dyspnoea. He then left the hospital.
He was next seen three years later, having been perfectly well until
he took cold one month before, since when he had shortness of breath on exertion and
on lying down. He had some cough and slight swelling of the feet. The physical
condition was about as on the first admission, except that the systolic murmur
entirely replaced the first sound and was well heard in the axilla.
Maximal blood-pressure' 182 mm. Hg. He again improved rapidly and left the hospital
in two weeks.
He entered the hospital again one year later with the same signs, the liver being now
2 cm. below the costal margin. Once more he improved rapidly under treatment; the liver
receded, and he was discharged, only to be readmitted in the same condition five weeks later,
when symptoms dated from exposure to the wet. He then had some tenacious sputum
streaked with blood and numerous moist rales were heard everywhere over his chest. Re-
covery was once more uneventful.
336 DISEASES OF THE HEART AND AORTA.
COMPLICATIONS AND SEQUELAE.
There are few complications and sequelae which are more character-
istic of mitral insufficiency than of other valvular diseases. Those symp-
toms due to pulmonary engorgement; bronchitis, haemoptysis, and
pulmonary oedema have already been discussed. Embolism from loosening
of vegetations upon the mitral valve or of clots which have formed in the
left auricle during periods of stasis is an occasional occurrence, especially
in severe cases, but less common than in mitral stenosis. As the result
of this there may be the production of infarcts in the various organs-
spleen, kidneys, and brain — and of ecchymoses in the skin.
In contrast to mitral stenosis, pulmonary tuberculosis occurs in mitral
insufficiency with the same frequency as in otherwise normal individuals
(Meisenburg) .
As may be seen in Fig. 166, mitral insufficiency is very frequently asso-
ciated with other valvular diseases, 29 per cent, of all the cases of valvular
disease at the Johns Hopkins Hospital being accompanied by aortic insuffi-
ciency, 21 per cent, by mitral stenosis. In these cases the mitral insuffi-
ciency is sometimes the original lesion, the other lesion resulting from a
metastatic infection or subsequent organization. On the other hand, the
mitral insufficiency associated with aortic insufficiency may also be a func-
tional one due to overfilling of the ventricles. The mitral insufficiency
which appears late in the course of mitral stenosis is due to the inability of
the thickened valves to close. Coronary sclerosis, as shown by Wild, is
more than usually common in chronic valvular disease, and hence should
be borne in mind in establishing the prognosis.
Pericarditis is one of the common complications, especially in children,
in whom adhesive pericarditis is to be feared.
Since the majority of cases of mitral disease are of rheumatic origin,
diseases of the rheumatic cycle, tonsillitis, articular rheumatism, chorea
in children, and affections of the urticarial group, are particularly common.
Of these arthritis is the most frequent as well as the most stubborn
and dangerous.
TREATMENT.
The management of cases of mitral disease does not depart in any
essential particular from the general type of treatment of cardiac disease.
It should be directed to three ends:
1. Removing the overstrain;
2. Increasing the strength of the heart;
3. Avoidance of infection, and removal of the foci.
In the mildest cases, the insufficiency shown by signs but not by symp-
toms, due especially to the formation of a new vegetation, it is most impor-
tant that the cardiac t o n i c i t y should be maintained, that the amount of
leakage should thus be kept down to its minimum, and that cardiac hyper-
trophy should be induced before symptoms have set in. It is therefore
most important to spare the heart every effort. If the patient is seen at
the onset of the disease he should be kept at absolute rest in bed for at
least a couple of weeks after temperature has returned to normal and all
MITRAL INSUFFICIENCY. 337
signs of acute disease have passed. Too much care cannot be exercised
at this time, since this is the crucial epoch in determining the severity of
the case. It is important not only to maintain the tonicity of the heart
muscle but to preserve the valves from all further injury until the vegeta-
tions have become thoroughly organized and lined with endothelium, and
the germs have disappeared from the original focus of infection. When
the tonsil is the source of infection, it should be completely dissected
out as soon as acute infection has passed off, in order to prevent reinfec-
tion of the valves from this source. The results obtained in the Medical
Clinic of the Johns Hopkins Hospital, where this practice has been carried
out at Prof. Barker's suggestion, have been very gratifying. In many
cases the recovery from the first attack has been more rapid than had been
usual before this treatment had been resorted to (see page 317), and it
seems probable that reinfection of the valve is of less frequent occurrence
thereafter. Similar results are seen in gonorrhoeal endocarditis after treat-
ment of the urethritis.
In these mild cases drug treatment may not be absolutely necessary.
In how far Cloetta's suggestion as to the early use of digitalis should be
carried out is still unsettled, but at least the administration of strychnine
in doses of from 1 to 3 mg. (-gV to -^ gr.) is advisable in order to increase
the tonicity of the heart muscle. However, the blood-pressure and hence
the strain upon the valves should not be materially increased (not more
than 10 mm. Hg), and the dose of strychnine should be reduced if it rise
above this level. Digitalis is not necessary in cases of this type.
The bronchitis which frequently accompanies cases of this type does
not differ greatly from the ordinary forms of chronic bronchitis, and is
associated with the usual pulmonary bacteria found in these conditions—
the streptococcus, pneumococcus, influenza bacillus, Friedlander's bacillus,
etc. Treatment is therefore the same as for ordinary bronchitis, a soothing
steam inhalation being very useful. The following are to be recommended :
Oleum pini sylvestris, or
Creosoti, oiss; 5
Tr. benzoin, co.,
Tr. opii camphorat., aa Siiss 75
A teaspoonful inhaled with steam from an atomizer, or from a funnel
above a glass jar into which a teaspoonful of the remedy and a pint of
boiling water have been placed. Codein .015 to .030 Gm. (gr. J to i) or
heroin 2.5 mg. (gr. ¥V to TV) may be given by mouth to relieve the cough
by reducing bronchial secretion and irritability.
Physical Re-education. — When the stage of acute symptoms has passed
the stage of re-education begins. The heart though injured must be trained
to perform the day's work without strain. To do this the heart muscle
must be stronger than normal; it must have hypertrophied. The process
of hypertrophy after valvular lesion, like the heart hypertrophy of an athlete
in training, requires time. However, the amount of hypertrophy setting
in after a valvular lesion is greater than that after a prolonged period of
muscular exercise, and hence may be expected to take a longer time. At
this stage Nauheim baths and resisted movements may be dispensed with
22
338 DISEASES OF THE HEART AND AORTA.
as long as a reasonable supervision is kept over the patient. He should
never be allowed to become either very tired or short of breath, and six
months or a year should elapse before he is allowed to run, participate in
games, severe exercise, or manual labor. The current statement that the
prognosis is doubtful during the first year after the occurrence of a valvular
lesion is due largely to the intercurrence of acute overstrain of the heart
muscle before hypertrophy is complete.
The condition is quite different, however, when the mitral insufficiency
is of long standing before it is encountered by the physician, as is frequently
the case in routine examinations for life insurance, civil service, etc. The
disease may then be said to have cured itself already, and beyond gently
admonishing the patient against over-exertion no further precautions are
necessary. It is often unwise to inform a man or woman of nervous tem-
perament that a heart lesion is present, since worry may in itself contribute
to the cardiac overstrain.
Cases of functional mitral insufficiency are rarely devoid of cardiac
symptoms, and hence will be considered under the second group.
; i Treatment of the Second Stage. — The second stage of mitral insuffi-
ciency, in which dyspnoea and other symptoms of cardiac origin are present,
represents a condition of chronic cardiac overstrain. Indeed it is the
abnormal severity of these symptoms following some slight exertion which
usually calls attention to the existence of the lesion. The treatment does
not depart in any essential particular from that which has already been
discussed in the case of chronic overstrain of the myocardium. Just as in
the milder cases the most important element in the treatment is absolute
rest in bed, continued until long after symptoms have subsided. The
diet should at first be very light (see page 167), and should be very gradually
increased after symptoms have subsided. As in the milder cases, vigorous
doses of strychnine (2 to 3 mg. [gr. -^ to 2\r] every four hours) should
be begun at once. The bowels should be kept moving freely by means
of Seidlitz powders, Epsom salts, Hunyadi water, Mistura ferri aperiens,
or some other mild laxative. It is important that the patient should sleep
well at night, and trional (1 Gm. = gr. xv) or some other soporific may be
given, if necessary with the addition of codein (15 mg. = gr. ss). If symp-
toms have not diminished after a couple of days of this treatment, digi-
talis should be resorted to (see page 178), for it is important not only to
reduce the strain but also to strengthen the heart muscle as rapidly as pos-
sible in order to prevent the overstrain from becoming permanent. Indeed
it may be said that this is the all-important stage in the course of mitral
insufficiency and of all other valvular lesions, the stage which determines
whether the patient may hope to return to a life of activity or must
look forward to one of permanent invalidism, and this question is often
decided by the promptness or tardiness with which the symptoms dis-
appear when the patient is at rest. In this stage the primary source
of infection or reinfection should be treated just as in the milder ones, but
the period of rest should be longer and the period of physical re-edu-
cation and gymnastics should be very carefully undertaken. The
more systematic methods, such as those of Schott, Herz and Oertel, are
especially valuable, as are also the Nauheim baths. The important factor,
MITRAL INSUFFICIENCY. 339
however, is that, whatever the method of treatment, the patient should
never be allowed to become fatigued or short of breath, he should be
gradually trained up to his optimum strength, and he should never be
allowed to attempt to exceed his limit.
Treatment of the Third Stage. — In the third stage of mitral insuffi-
ciency, that of broken compensation, the burden of the cardiac fail-
ure has been shifted from the left ventricle to the right. The treatment
therefore follows the rules laid down for broken compensation due to any
cause whatever: absolute rest, immediate use of digitalis (especially along
with nitroglycerin, sodium nitrite, or erythrol tetranitrate) , free purgation,
and very light diet being the essential features. Hypodermic injections
of morphine (8 to 15 mg., gr. J to J) may be necessary, but they should
be used with caution, since they decrease the irritability of the respiratory
centre and thus lead to accumulation of CO2 and cardiac asthma. Since
many of the symptoms are due to a high pressure in the vena cava and
consequent dilatation of the right auricle and ventricle, venesection is often
followed by great improvement, and should be regarded as an important
therapeutic measure during the acute stage of the overstrain. But in
the presence of anaemia it should not be resorted to. Intravenous
strophanthin (0.5 to 1 mg.) is of the greatest value when the symp-
toms have become alarming, and should be followed by the usual course
of digitalis, or by daily intramuscular injections of strophanthin.
As symptoms subside, the condition and its treatment pass into
those of the second stage, and a gradual return to normal may occur.
On the other hand the symptoms may increase, hydrothorax and ascites
may become extensive and may require tapping, and the oedema may
become extreme. To diminish these it may be advisable to use diuretics,
such as theobromin acetate (agurin), theocin, or acettheocin sodium, or
else potassium acetate and citrate.
PROGNOSIS.
Exactly how much benefit can be effected by treatment varies with
each individual case, and depends upon factors which are difficult to fore-
tell. It is especially true of mitral insufficiency that while there is life
there is hope, for the patient may almost completely recover from one or
more attacks of broken compensation and yet remain comparatively free
from symptoms for a number of years.
As regards the prognosis for the individual attack no absolute rule
can be laid down, but much importance may be attached to the rapidity
of change for the better or for the worse. A rapid improvement during
the first two days may be construed as favorable for the ultimate outcome;
a slow recovery usually indicates a severe residuum of trouble; an increase
of symptoms in spite of treatment is of grave significance.
Between attacks the patient's ability to hold his own or even to im-
prove his condition depends entirely upon his ability to keep himself free
from overstrain and reinfection. In all cases the physician should be some-
what guarded in his statements regarding the future.
340 DISEASES OF THE HEART AND AORTA.
BIBLIOGRAPHY.
MITRAL INSUFFICIENCY.
Krehl, Geipel. Quoted on page 246.
Roy and Adami: The Failure of the Heart from Overstrain, Brit. M. J., Lond., 1888, i,
1321 and 1395.
Kiilbs. Quoted on p. 212.
Weber and Deguy: Du role des hsemorrhagies intracardiaques dans les retre'cissement
mitral, Presse me"d., Par., 1898. La region mitro-aortique; etude anatomique et
pathologique, Arch, de med. exper. et d'anat. path., Par., 1897, ix, 235.
Meigs, V. A.: A New Method of making a Hydrostatic Test of the Mitral and Tricuspid
Valves, Med. News, Phila., 1884, xlv, 533.
Bleichroeder: Die Funktionspriifung der Mitralklappe, Arch. f. path. Anat., etc., Berl.,
1902, clxix, 159.
Gibson, G. A.: Diseases of the Heart and Aorta, Edinb. and Lond., 1898.
Weiss, O., and Joachim, G.: Registrierung und Reproduktion der menschlichen Herz-
tone und Herzgerausche, Arch. f. d. ges. Physiol., Bonn, 1908, cxxiii, 341.
Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris,
1881.
Gerhardt, D.: Ueber die Compensation von Mitralfehlern, Arch. f. exper. Pathol. u. Pharm.,
Leipz., 1901, xlv, 186.
King, T. W.: An Essay on the Safety-valve Function in the Right Ventricle of the Human
Heart, etc., Guy's Hosp. Rep., Lond., 1837, ii, 104.
Osier, W., and Gibson, A. G.: Modern Medicine, Phila. and N. Y., 1908, iv, 205.
Moritz, F.: Einige Bemerkungen zur Frage der percutorischen Darstellung der gesammten
Vorderflache des Herzens, Deutsch. Arch. f. klin. Med., Leipz., 1906, Ixxxviii, 276.
Cf. also article by Dietlen and Simon in the same volume.
Harris, Th.: Some Clinical and Post-mortem Observations on the Cardiac Dulness in
Cases of Mitral Disease, etc., Med. Chron., Manchester, 1892, xvii, 287.
Groedel, F. M.: The Examination of the Heart by the Roentgen Rays, Arch. Roentg.
Ray and Allied Phenom., Lond., 1908.
Hofmann, Aug_ Quoted on p. 119.
Gerhartz, H.: Zur Frage des Stethoskops, Deutsch. Arch. f. klin. Med., Leipz., 1907, xc,
501.
Naunyn, B.: Ueber den Grund weshalb hin und wieder das systolische Gerausch bei der
Mitralinsufficienz am lautesten in der Gegend der Pulmonalklapp zu vernehmen ist,
Berl. klin. Wchnschr., 1868, v, 189.
Boy-Teissier: L'auscultation retrosternale, Rev. de Me"d. Paris, 1892, xii, 169.
Wild, R.: A Contribution to the Pathology of the Coronary Arteries, Med. Chron., Man-
chester, 1892, xvi, 223.
Meisenburg: Ueber das gleichzeitige Vorkommen von Herzklappenfehlern und Tuber-
kulose, Ztschr. f. Tuberk., etc., 1902, iii, 378.
III.
MITRAL STENOSIS.
HISTORICAL.
After mitral insufficiency the most common affection of the mitral
valve is that which leads to mitral stenosis. This condition was first de-
scribed by John Mayow in 1669 in the case of a young man who died after
several years of dyspnoea, palpitation, and attacks of syncope. " At autopsy
he found dilatation and hypertrophy of the right ventricle and almost
complete closure of the left auriculo ventricular orifice by a 'cartilaginous
product/ so that the blood could scarcely traverse the left ventricle and
was compelled to flow backward to the pulmonary vessels, hence the disten-
tion of the right ventricle." Vieussens (1715) described similar findings,
noting also that the papillary muscles were changed to small short tendons,
and that the right ventricle was so dilated as to allow reflux of blood past
the tricuspid valve. He further noted weakness and irregularity of the
pulse, and ascribed it to "too small quantity of blood which the left ven-
tricle furnished to the aorta . . . and the irregularity of its contrac-
tions." Senac (1749) and others described cases, so that the lesion became
quite familiar to pathologists in the early part of the nineteenth century.
PATHOLOGICAL ANATOMY AND PATHOGENESIS.
Pathologically, it is brought about by a chronic inflammatory process
taking place in the tissue of the valve which leads to thickening and fusion
of the cusps. By this fusion the valve comes to form a sort of funnel, some-
times elongated, sometimes short
and shallow. The walls are much
thicker than those of the normal
valve, owing to a chronic infiltra-
tion and proliferation of the con-
nective tissue within them. They
are usually more or less rigid, some-
times smooth, sometimes rough from
remains of old vegetations and calci-
fications, and the auricular surface
is often puckered or thrown into
folds. The lower margin of the
valve is attached to the chordae
tendinese, which become shortened
and thickened very early in the process. The orifice thus formed is
sometimes circular, sometimes oval or button-holed, sometimes irregular
(Fig. 189). According to Sansom, the funnel shape is more common in
341
Fio. 189. — Human heart, showing mitral (3f)
and tricuspid (T) stenosis. Viewed from above.
The auricles have been cut through.
342 DISEASES OF THE HEART AND AORTA.
children, while the buttonhole is more common in adults and represents
a lesion of longer duration. The orifice may often become very small
before death ensues, sometimes barely large enough to admit a goose-quill
(Sansom) . In some long-standing lesions the margin of the valve may
become so thick and stiff (sometimes calcified, cartilaginous, or ossified)
that it does not close during ventricular systole; in others the edges
become retracted so that they no longer cover the orifice. In either case
secondary mitral insufficiency may result.
Occurrence. — According to the studies of Lockhart Gillespie, mitral
stenosis is most common in women, increasing in frequency up to the
age of 29. In men it is scarcely more than half as common, but reaches
its maximum frequency a decade later. The males affected die earlier than
the females, however; the average period of death being from 30 to 39 with
the former, while with the latter it is 40 to 49. The presence of the double
mitral lesion does not shorten the average period of life.
Etiology. — As regards etiology, Cheadle, Samways, Duroziez, and
Dyce Duckworth agree that rheumatism is the etiological factor in at
least 60 per cent, to 78 per cent, of the cases, other acute infections, chlo-
rosis (Goodhart), chronic nephritis, gout, arteriosclerosis, and puerperal
infections representing the other etiological factors. Potain also believes
that pulmonary tuberculosis is an important factor, but this is disputed
by many writers; most of whom agree with Traube that tuberculosis is
far less frequent (5 per cent.) in the presence of mitral stenosis than in
normal individuals (12 per cent.) or in those with other heart lesions
(Meisenburg, Tileston).
Pathogenesis. — As regards pathogenesis, Huchard (I.e.) divides the
cases of mitral stenosis into three groups:
1. The congenital form, resulting from fetal endocarditis, which,
as Sansom has shown, is very rare.
2. The endocarditic form of infectious origin (due especially to
rheumatism, scarlet fever, measles, typhoid fever, smallpox, etc.), resulting
from the organization and fusion of old vegetations. This is the most com-
mon form, since rheumatism alone can be demonstrated as an etiological
factor in about 70 per cent, of the cases.
3. The sclerotic form, which is associated with general arterio-
sclerosis, gout, and plumbism. In this group no traces of endocarditic vege-
tations occur upon the valve, and the process is more closely allied to that
within the vessel walls in arteriosclerosis. Under this group should also fall
the large group of cases associated with chlorosis and other anaemias in
which no other causal factor is present to explain the presence of the lesion.
Goodhart, who lays especial stress upon this group, believes that the
chronic overstrain of the anaemic heart muscle is followed by cedema
and petechia3 in the substance of the mitral valve, as has been demonstrated
experimentally by Roy and Adami. He thinks that this cedema is followed
by cellular infiltration and finally by proliferation of fibrous tissue resulting
in the mitral stenosis. While this view is suggestive, no careful histological
or experimental studies have been made to bear it out. On the other hand,
it must be remembered that most anaemic and gouty persons are subject to
repeated slight infections which might suffice to produce chronic changes in
MITRAL STENOSIS.
343
the heart during the lapse of years. Weber and Deguy have shown that
hemorrhage occurs often in the valves after labor, etc. This is followed
by infiltration and organization and finally by sclerosis of the valve.
PATHOLOGICAL PHYSIOLOGY.
The nature of the disturbance to the circulation in mitral stenosis was
already discerned by Vieussens in 1715, who noted that owing to the inabil-
ity of the blood to pass through the mitral orifice with sufficient rapidity,
it had become dammed back in the pulmonary veins and pulmonary arte-
ries, increasing the work of the right ventricle and leading to insufficiency of
the tricuspid valve. At the same time the force of the pulse (blood-pressure)
and amplitude of the pulse were diminished, owing to the diminution of the
blood which entered or was forced out of the left ventricle. Vieussens
noted further that the force and rhythm of contraction were irregular.
NORMAL
ii
BROKEN
PULMONARY
COMPENSATION
III
BEGINNING
FAILURE OF LEFT
VENTRICLE
FIG. 190. — Diagram showing the changes in the circulation due to mitral stenosis. The stage of
perfect compensation is not shown, since there are practically no pressure changes. II represents the
stage at which pulmonary compensation is broken but systemic circulation has not yet become affected.
Ill represents the stage in which there is broken pulmonary compensation, and the left ventricle has failed
to maintain the arterial pressure. The last pressure changes in the last stage, with broken systemic com-
pensation as well, correspond exactly to those in the last stage of mitral insufficiency.
The changes of pressure corresponding to these phenomena have been studied experi-
mentally by Bettelheim and Kauders, D. Gerhardt, and MacCallum and McClure, who have
found that the production of a mild grade of experimental stenosis causes distinct rise
in the mean pressure within the left auricle, the pulmonary veins
and the pulmonary artery.
Filling of the Ventricles. — The effect of the stenosis upon the filling
of the ventricles as shown in the volume curve has recently been investi-
gated by the writer, aided by Mr. J. M. Wolfsohn. As shown in Fig. 191,
the first effect of the mitral stenosis is to slow the inflow into the left ven-
tricle. As a result of this the left auricle is more than usually full at the
time of its systole, and forces an unusually large quantity of blood into the
ventricle (Fig. 192, AS). This increase in auricular output at first suffices
to complete the filling of the ventricle, but as the lesion progresses a little
further even this fails to do so and the amount of blood entering the ven-
tricle falls below normal. As a consequence of this, the ventricle forces
344
DISEASES OF THE HEART AND AORTA.
less blood into the aorta, the arterial blood-pressure falls and the pulse-
pressure diminishes. This is the condition as observed in the experiment.
In man, however, where the pathological change is a gradual one, the
arteries gradually accommodate themselves by constriction of their chan-
nels until the blood-pressure has returned to about its normal level.
The pressure in the systemic veins is diminished, as has been shown by
Kornfeld.
LIGATURE TIGHTENED
VOL.
CAR.
FIG. 191. — Volume of the ventricles in experimental mitral stenosis. (Kindness of the Johns
Hopkins Hospital Bulletin.) Tracings obtained* from a dog's heart in experimental mitral stenosis.
VOL., volume curve ; CAR., carotid pressure. The arrow indicates the moment at which the stenosis
was produced. The filling of the ventricles (downstroke) was slowed, diastasis (horizontal part of curve)"
sets in prematurely, and the part of the curve due to auricular systole (second downstroke) becomes
more pronounced. The heart rate is practically unchanged.
S D
NORMAL
S D
II
S D
III
S D
IV
FIG. 192. — Diagram illustrating the variations in the volume curve of the ventricles in increasing
degrees (I, II, III, IV) of mitral stenosis. S, systole; D, diastole, AS, inflow into the ventricles due to
systole of the auricles.
As the narrowing of the mitral orifice progresses, a further change
occurs in the filling of the heart. It now requires a greater difference in
pressure to drive the blood from auricle to ventricle and as a consequence
it is seen that during a great part of diastole little or no blood is flowing in.
Diastole is thus divided, according to Henderson's terminology (cf. page
9), into three periods:
I. A period of early diastole, during which the ventricle fills with moderate rapidity,
though more slowly than normally.
II. A period of diastasis (Henderson), during which little or no filling occurs. Experi-
ments upon the excised heart (cf. page 9) indicate that the mitral valves close
suddenly just at the beginning of this period and remain completely or almost
completely closed until the next.
III. This is followed by the third event of diastole, when more blood is driven into the
ventricle by the forcible contraction of the left auricle. The latter must now con-
tract more forcibly than ever and as a consequence hypertrophies. Indeed Ger-
hardt has shown, from the autopsies of two cases with very mild grades of stenosis,
that hypertrophy of the left auricle is the first change resulting from the lesion,
and that hypertrophy of the right ventricle is a later phenomenon. Pulmonary
congestion always occurs, however, and in all but the very mildest cases hypertrophy
of the right ventricle results.
MITRAL STENOSIS. 345
With further narrowing the filling of the left ventricle diminishes, its
total volume and systolic output diminish, and the blood-pressure falls
unless the constricting power of the vasomotor is taxed to the utmost to
preserve it. The left auricle, on the other hand, becomes overloaded and
distended, its capacity even rising from 60 c.c. to 2500 c.c. (G. Miiller) or
3000 c.c. (Minkowski). Under these circumstances paralysis of the
auricle sets in, the auricular wave disappears from the curve of
filling (Hirschf elder) , from the jugular pulse (Mackenzie), and the cesoph-
ageal tracing (Joachim), and the presystolic rumble is no longer
heard. At this stage the rhythm of the heart usually becomes irregu-
lar, due no doubt to the effort of the auricle to empty itself by means of
abnormal contractions. This stage of irregularity with auricular paralysis
is more or less characteristic of cardiac overstrain in mitral stenosis, and
may disappear when the work of the heart is relieved, or its strength is
increased by digitalis (see Fig. 199), when the presystolic rumble
reappears. As the lesion progresses further, the stasis in the pulmo-
nary circulation increases, and broken compensation follows, just as it
does in mitral insufficiency.
As can be seen from the above description, the problem of maintain-
ing compensation in mitral stenosis is quite different from that in mitral
insufficiency. In the latter condition the important factor was seen to be
the emptying of the left ventricle, whereas in mitral stenosis the
difficulty lies in the filling of this chamber, and the hypertrophy
necessary to bring this about affects not the left but the right ven-
tricle and the left auricle. Since this can be accomplished only by increas-
ing the pulmonary engorgement, it is evident that after the lesion has
reached a certain stage perfect compensation becomes impossible, and the
re-establishment of compensation is always more difficult than in a corre-
sponding grade of mitral insufficiency.
SYMPTOMS AND SIGNS.
The symptoms, color, and general appearance of patients with mitral
stenosis are very much the same as in those with mitral insufficiency,
except that they are somewhat more pronounced and more persistent.
Haemoptysis and precordial pain are more frequent than in mitral insuffi-
ciency, as are also attacks of pulmonary oedema.
Hofbauer, Alexander, Miecslaw, Frischauer, and Osier have called
attention to the hoarseness and s t e n o t i c (brassy) cough as
a symptom in mitral stenosis. Osier has shown at autopsy that under
these conditions the left recurrent laryngeal nerve is compressed against
the arch of the aorta and the ligamentum Botalli by the dilated left auricle,
and then undergoes degenerative changes.
Andre" Petit recognizes three clinical groups of persons with mitral stenosis:
I. The chlorotic type affecting mainly young girls. The skin and mucous mem-
branes are pale, the complexion sallow. The patients readily become short of
breath, are subject to nose-bleeds, menstrual disturbances, dyspepsia, constipation,
and nervousness. Only auscultation reveals the nature of the disease.
II. The pseud otuberculous type in young women, characterized by repeated
attacks of bronchitis, dry, hacking cough, and haemoptysis, especially at menstrual
346 DISEASES OF THE HEART AND AORTA.
periods. The patients are pale and emaciated and closely resemble consumptives
in appearance.
III. The dyspnoeic type into which any of the other types may merge. There is
dyspnoea on exertion, frequently also attacks of cardiac asthma at night. These
patients usually have flushed faces, with slight dull tinge of cyanosis (the typical
mitral facies), due to imperfect aeration of the blood in the lungs.
PHYSICAL EXAMINATION.
Except for the findings in the immediate vicinity of the heart, the
results of physical examination in cases of mitral stenosis are practically
the same as in mitral msufficienc}^. The pulse, however, is rarely of as
long volume as in the latter, and the pulse-pressure is usually smaller.
Irregularity is about as common and is of the same type (absolute irregular-
ity, with or without auricular paralysis) in both conditions.
The Cardiac Impulse. — The findings about the heart are, however,
characteristic. The apex impulse, sometimes in the normal position and
sometimes out in the axilla, is usually well marked, sudden, short, and
tapping or flapping. This peculiar appearance is due to the seesaw move-
ments of the chest wall over the right and left ventricles; There is a wavy
movement in the third, fourth, and fifth interspaces, which when accurately
timed or recorded is found to consist of a systolic
retraction of these interspaces over the hyper-
trophied right ventricle (see page 209). The
systolic impulse of the pulmonary artery may
sometimes be seen in the second left interspace
at the sternal margin.
Palpation. — The findings of palpation are
perfectly characteristic. At the apex, and
usually over this area only, the shock of the
first sound can be felt, short, sharp, and tap-
ping. In the typical cases, up to the last stage
(auricular paralysis) this is preceded by a short
presystolic thrill, having a "purring" character
(fremissement cataire, Corvisart, Laennec),
FIG. 193.— Diagram showing the leading up to the shock which accompanied the
direction of the stream entering firgt sound. It Can be increased bv slight
the left ventricle through the ste- , ." ,. ° ,
notic mitral orifice. exercise. It is, as a rule, sharply localized
about the apex in an area of about 3 cm. in
diameter (or about the size of a stethoscope bell), probably because it is
produced by the impact of the narrow stream driven by the forcible
auricular contraction directly against the apical portion of the walls of
the left ventricle.
Indeed Oestreich, Lenhartz, and Burk have shown that this stream may finally cause
a bulging of the ventricular wall at the point where it has been striking. The vibra-
tions transmitted from the chordae tendinese and papillary muscles are also factors in its
production.
Occasionally a tap or thrill is also to be felt in early or m i d - d i a -
stole accompanying the third heart sound or the diastolic rumbles
about to be described. The sensation thus imparted by the presystolic
thrill and the tapping first shock are so characteristic that the diagnosis
MITRAL STENOSIS.
347
of mitral stenosis may often be established from palpation alone. The
shock accompanying the second sound is usually very distinct, and becomes
markedly accentuated as the pulmonary area is approached.
Percussion. — The typical area of dulness on percussion and the cardiac
outline as seen by the X-ray (Groedel) often show the outline of the left
ventricle (lower border and lower half of left border) to be normal, though
in almost equal frequency it is extended to the left. Thus, in 32 cases
Sansom found the left ventricle
Normal in 12
Hypertrophied in 9
Dilated in 5
Dilated and hypertrophied in . . 3
Small in 3
Thin walled in . . .1
Above, the area of dulness
extends higher and further to
the left than normal, often
reaching as high as the second
rib (though usually not above
the third) and embracing an area
of 2 to 5 cm. in the second left
interspace.
As shown by the autopsies of Th.
Harris, this area of dulness corre-
sponds to the dilated conus
a rteriosus and dilated pulmonary
artery and not to the dilated left
{iuricle. Except when general failure
has set in, the right border of the
heart is normal, but the cardiac flat-
ness may be increased and reach to
the right sternal margin (hypertrophy
dulness in mitral stenosis is therefore
left margin (Fig. 194).
Auscultation. — Presystolic Rumble. — The auscultatory findings in mitral
stenosis are quite unique, and usually furnish the basis for diagnosis. The
characteristic sign is a rumbling or echoing sound in late diastole (auriculo-
systolic in time), increasing in crescendo up to the beginning of the first
heart sound. Like the presystolic thrill and the diastolic sounds, this
presystolic rumble is usually heard over an area of 2-3 cm. only, at or a
little to the right of the apex.
The rumble and the first sound thus come to have the phonetic equivalent of Trup,
tr-rr-rup, Turnip (Steel), Rou fut (Duroziez). It was first described by Gendrin in
1842 and by Fauvel in 1843 in cases of mitral insufficiency, but its diagnostic significance
was definitely established by W. T. Gairdner, of Edinburgh, in 1861. Gairdner and the
older writers considered it to be produced by systole of the left auricle (auricular-systolic)
driving the blood forcibly through the narrow mitral orifice. This view has been practi-
cally proved by the observations of James Mackenzie that the presystolic murmur is present
only when the venous tracing shows contractions of the auricles, and disappears when the
auricle becomes paralyzed. Joachim has also demonstrated this for the left auricle by
O3sophageal tracings. The writer (1. c.), moreover, has been able to demonstrate this
parallelism in experimental mitral stenosis. Einthoven's curves of the
FIG. 194. — Cardiac outline and distribution of the
presystolic rumble in mitral stenosis. The area of cardiac
dulness is indicated by a light line, the cardiac flatness by
a heavy line. The area over which the presystolic rum-
ble and snapping first sound are heard is indicated by a
circle. The relation of these sounds to the cardiac cycle
is shown in the small diagram at the left. The systolic
retraction over the right ventricle is indicated by the
inverted cardiogram.
of the right ventricle). The typical area of cardiac
a short, wide oval with a bulging upon its upper
348
DISEASES OF THE HEART AND AORTA.
heart sounds in man, as well as those of Weiss and Joachim, also prove the time of its
occurrence. It is quite certain, therefore, that the rumble does not occur in the early part
of ventricular systole, as claimed by Ormerod, Barclay, Turner, Dickinson, and Brockbank.
The protodiastolic and mid-diastolic rumble remains, however, in spite of auricular paralysis.
FIG. 195. — Radiograph from a case of mitral
stenosis, taken with the plate behind the patient,
showing increase of the shadow due to the dilated
left auricle. (Kindness of Prof. C. M. Cooper.) The
left ventricle is not dilated.
FIG. 196. — Diagram representing the shadows
shown in Fig. 195. The broken line indicates the
outline of a normal heart. The arrow indicates the
enlargement upward in the transvere oblique diam-
eter. LA, left auricle; PA, pulmonary artery;
AO, aorta; LV, left ventricle.
Snapping First Sound. — The nature of the first heart sound is also char-
acteristic. It is short and sharp, and may resemble the second sound so
closely as to be mistaken for the latter. This is especially common in
cases in which the second sound is not well heard at the apex.
Fenwick and Overend believed that it was of higher pitch than the normal first sound,
but this is not borne out by the curves of Weiss and Joachim, who found waves of about
normal pitch but of much greater amplitude (Fig. 197). It is possible
that Fenwick and Overend may
have heard higher overtones than
accompany the normal heart sound.
Owing to its loudness and sharp-
ness, it may so closely resemble the
normal second sound as to be mis-
taken for it. According to Haycraft,
it is the valvular element which
imparts the high-pitched notes to
the first sound, and this is naturally
accentuated in mitral stenosis, for
the stiff mitral valve plays a
greater role in sound production
than in the normal.
Broadbent and Acland be-
lieved that the ventricular walls
"close down rapidly because their cavity is not distended with blood" and thus give rise
to a more sudden sound. However, the snapping sound is quite as pronounced in the
numerous cases in which the ventricle is dilated; and moreover, on the other hand, the
cardiometer shows that diminution in ventricular volume occurs at exactly the same rate
as in the normal heart.1
CAROTID
SOUND
FIG. 197. — Graphic record of carotid pulse and heart
sounds in mitral stenosis. (After Weiss and Joachim.) Upper
line, carotid pulse ; middle line, phonogram ; lower line,
time in Tun seconds ; P, presystolic rumble; 1, 2, heart sounds.
1 On account of the smaller amount of blood discharged at the usual rate, the dura-
tion of systole is shorter; but Einthoven's tracings show that the duration of the first sound
is normal.
MITRAL STENOSIS.
349
This applies only to the first sound produced in the left ventricle,
and hence heard only over a small area about the apex from which it is
transmitted for a short distance upward and to the night. Over the right
ventricle the first sound is normal until the latter stages of the disease,
when it is often replaced by the murmur of tricuspid insufficiency. The
second sound at the apex is usually faint, and may even become quite
inaudible in the latter stages of the disease, probably owing to the low
arterial blood-pressure, but over the pulmonic area it is markedly accen-
tuated.
JNTRAVENTB ICULAR
PRESSURE
VENTRICULAR 3
VOLUME 2
CURVES
1
SOUNDS
CORRESPONDING TO
VOLUME 2
CURVES
«» ,__^
FIG. 198. — Diagram showing the relations of the various sounds heard in uncomplicated mitral
stenosis to events in the filling and emptying of the ventricle. N, normal. Light, heavy, broken, and dot-
ted lines correspond with sounds whose base lines are made with these lines.
Digital Imitation of the Presystolic Rumble and Snapping First Sound.— While the
ordinary vowel and consonant sounds fail to give any close imitation of the sounds heard
in mitral stenosis, these may be quite closely reproduced by the method of H. L. Smith
(page 115), tapping on the knuckles with four fingers in rapid succession.
Systolic Murmur in Mitral Stenosis with Mitral Insufficiency. — Since the mitral cusps
.are much deformed and thickened in mitral stenosis, and the chordae tendinese shortened,
it is not surprising that leakage at this valve should be present in the greater number of
«ases (Fig. 179). The group of signs due to the insufficiency of the valve associated \\iih
stenosis do not present striking differences from the signs of the former lesion when existing
alone. Hypertrophy of the left ventricle occurs in almost all these cases, and the heart is
enlarged horizontally to the left. A blowing systolic murmur accompanies and follows the
snapping first sound; and occasionally, when the second sound at the apex is absent or
very soft, this murmur may seem to bo diastolir. Careful timing by comparison with the
shocks and the time of the pulmonic second sound, however, will prevent this error.
350
DISEASES OF THE HEART AND AORTA.
Sounds in Early and Mid=diastole. — The sounds heard in early and mid-
diastole, however, are quite as well marked as is the presystolic murmur.
These sounds are of three types:
1. An early diastolic sound, the third sound of a proto-
1 2 3
diastolic gallop rhythm (rup - tat - ta) , which Bouillaud observed in 1841
in association with mitral stenosis. This sound is heard in about 65 per
cent, of all cases of mitral stenosis (Steell). Though somewhat louder it
does not seem to differ from the third sound of the normal heart in mode
of production, and is probably due to the sharp closure of the mitral cusps
when the period of rapid ventricular rilling has come to an end. It is there-
fore to be regarded as a "closing snap" of the mitral (Hirschfelder, I.e.),
and not as an "opening snap" as thought by Duroziez, Sansom, and Potain.
As the filling of the ventricle is somewhat less complete than normal, this
sound occurs a trifle early (Thayer). That it should be louder and more
readily produced is due to the rigidity of the altered mitral valve.
FIG. 199. — Venous pulse of a patient with mitral stenosis during an attack of acute heart failure.
A. Tracing taken on Dec. 4, 1907. The presystolic rumble has disappeared. The a (auricular) wave is
absent from the venous pulse. There is absolute arrhythmia. B. Tracing taken five days later, after
return of compensation. The presystolic rumble has returned; the a wave is present on the venous pulse.
The rhythm is regular. The arrows mark the time when auricular contraction should occur.
2. One of the commonest sounds in mitral stenosis is a rumble
in early or in mid-diastole of the same character as the pre-
systolic rumble. According to Huchard, it may resemble the sound of a
flag fluttering in the breeze, causing the cardiac cycle to resemble the words
1 2
"rup - tat - rarou." This rumble may follow almost immediately after
the second sound. It may last throughout diastole and be continuous
with the presystolic rumble, or it may be separated from the second sound
and also from the presystolic by short intervals. On the other hand, when
the presystolic rumble has disappeared during auricular paralysis it may be
the only sound heard during diastole.
These rumbles occur, therefore, at the time when the blood is flowing rapidly into the
left ventricle. At this phase of diastole, owing to the stasis in the pulmonary veins, the
auricular pressure is relatively high. It is, therefore, not surprising that the stream pass-
ing through the narrowed auricular channel under about the same pressure should give
rise to a rumble similar to that produced later in diastole when the same stream is pro-
pelled through the same orifice at about the same rate by the force of the auricular con-
traction. Nor is it, therefore, surprising that, as shown by Mackenzie, the early diastolic
MITRAL STENOSIS. 351
rumbles produced by a pressure which is continually diminishing should be always
decrescendo in character, while the presystolic rumbles produced by the rapidly
increasing auricular contraction should, on the contrary, be crescendo.
3. A blowing diastolic murmur not unlike the ordinary mur-
mur of aortic insufficiency is occasionally heard in mitral stenosis (Graham
Steell, Huchard, Cabot and Locke, Bard). This murmur, however, never
replaces the second sound as does the aortic murmur, but follows it after
a short pause. It becomes louder and lasts longer as the pulse-rate dimin-
ishes. The murmur is intense at the apex, but is also heard above and
to the left of the latter. It is not heard over the aortic area nor over the
sternum, though sometimes heard at the upper left sternal margin. Whether
this murmur is caused by a secondary functional insufficiency of the pul-
monary valves, due to dilatation of the right ventricle (cf. page 390), or is
a cardiopulmonary murmur (cf. page 111) induced by the increased activity
of the right ventricle, is still unsettled. It is probable that each is met with
in some cases.
STAGES OF MITRAL STENOSIS.
It is difficult to divide the course of mitral stenosis into well-defined
stages. From a physiological and diagnostic stand-point it might be con-
venient to distinguish four stages, — which differ slightly from those de-
scribed by Broadbent (I.e.). These are characterized by the following
phenomena:
First Stage. — Presystolic rumble, snapping first sound and second
sound are well heard at the apex, — compensation is good, — the left auricle
contracting forcibly as shown by the presystolic rumble, also the left ven-
tricle as shown by well-marked second sound. The second pulmonic sound
is increased. The sounds of early and mid-diastole may or may not be
present. Broadbent says of this stage, " I have never known serious symp-
toms to arise from the condition of the heart, and I have seen serious ill-
nesses of different kinds passed through without the intervention of embar-
rassment of the circulation."
Second Stage. — The presystolic rumble and first sound persist and the
early and mid-diastolic rumbles may be present, but the second sound at
the apex has completely or almost completely disappeared. This indicates
that the force of the left ventricle is beginning to diminish (Fig. 190, III),
but the left auricle is still contracting forcibly. At this stage the presystolic
rumble is sometimes mistaken for the first heart sound and the snapping
first sound for the second, so that if there is a systolic murmur present a
diagnosis of mitral insufficiency may be made, and a less severe prognosis
is sometimes given. This error may be avoided by carefully timing the
heart sounds by palpation or by no'ting the change in sounds on gradually
passing the stethoscope from base to apex.
Third Stage. — The presystolic rumble and thrill have disappeared. The
snapping first sound and sounds of early diastole persist ; the second sound
at the apex may or may not be heard. Paralysis of the left auricle has set in.
Overlapping of Second and Third Stages. — In some cases this occurs
earlier than the disappearance of the first sound at the apex, and these
two stages overlap or may even replace one another chronologically.
352 DISEASES OF THE HEART AND AORTA.
This depends upon the relative strength of left ventricle and left auricle, as well as
upon the degree to which the mitral orifice is narrowed; for a comparatively weak left
auricle sometimes fails without materially affecting the cardiac filling, while, on the other
hand, a vigorously beating auricle may produce a loud sound while forcing a small amount
of blood through the narrowed orifice, and yet the amount of blood thus entering the left
ventricle may be too small to maintain the arterial blood-pressure and to cause a distinct
second sound.
Dyspnoea, haemoptysis, and the usual features of stasis in the pulmo-
nary circulation occur in the second and third stages of the disease.
Fourth Stage. — Broken systemic compensation, venous stasis, oedema
of the extremities, enlargement of the liver, gastric and digestive disturb-
ances, ascites, hydrothorax, and all the other features of broken compen-
sation of the right ventricle set in. In the later stages there are well-marked
signs of tricuspid insufficiency, positive venous pulse, and positive pulsa-
tion of the liver.
PULSE.
Exactly as in mitral insufficiency, permanent irregularity of the pulse
due to the numerous extrasystoles may occur quite early in cases where
both the presence of the presystolic rumble and the venous pulse tracing
CAR.
JUG.
FIG. 200. — Permanent arrhythmia in a case of mitral stenosis, showing persistence of the auricular
contractions (a wave) upon the venous pulse. The right auricle (at least) is still contracting. The tracing
shows the presence of persistent auricular extrasystoles.
show that the auricles are still contracting forcibly (Fig. 200). Owing to
the greater circulatory disturbance entailed in the filling of the left ventricle,
arrhythmia causes a somewhat greater circulatory disturbance in mitral
stenosis than in insufficiency, although in neither is it a harbinger of immedi-
ate danger and it may last for years. The pulse is usually small in mitral
stenosis, owing to the contracted condition of the radial and other medium-
sized arteries.
The blood-pressure is, as a rule, very little changed, owing to the com-
pensatory changes in the arterial bed. The most common change is a
diminution in pulse-pressure due to a rise in the minimal pressure brought
about by the vasoconstriction. A large pulse-pressure, such as is frequently
seen in well-compensated mitral insufficiency, is not common in mitral
stenosis.
DIAGNOSIS.
In the absence of aortic insufficiency and adherent pericardium the
diagnosis of mitral stenosis is comparatively simple, and is based upon the
presence of the presystolic or diastolic rumble or thrill at the apex, together
with a short snapping first sound in this region, and a markedly accentuated
second pulmonic sound.
MITRAL STENOSIS. 353
However, it sometimes happens that these signs appear only occasion-
ally while the patient is under observation.
Some years ago the writer had under his care for several months a patient with per-
nicious anaemia in whom a presystolic murmur was heard on only one occasion, though the
heart's action was fairly vigorous and regular. A gallop rhythm had been present during
her entire illness. The diagnosis of a mild grade of mitral stenosis was verified at autopsy.
Occasionally, on the other hand, the patient is seen after auricular
paralysis has set in and when there is no diastolic rumble present whatever
and only the sounds of the second and third stages. Such cases show the
need of frequent auscultation of the patient.
Differentiation between Aortic Insufficiency and Mitral Stenosis.— In
the presence of aortic insufficiency it must be remembered that the presys-
tolic and diastolic murmurs described by Austin Flint may closely simulate
those arising in mitral stenosis (see page 371). In aortic insufficiency the
thrill is rarely as well marked as in mitral stenosis, and the first sound is
rarely sufficiently short and snapping to be mistaken for mitral stenosis.
The two conditions were found together in 4.2 per cent, of the 1781 cases
of valvular disease at the Johns Hopkins Hospital, — i.e., in about one-
seventh of all the cases of mitral stenosis and one-tenth of all the cases of
aortic insufficiency, so that it is not a condition of extreme rarity. When,
as not infrequently happens, the mitral stenosis is the first condition present,
there is no difficulty, as the late diastolic blow of mitral stenosis is rare and
scarcely ever mistaken for aortic insufficiency. But when the aortic insuffi-
ciency is the first lesion to occur, the diagnosis of the second lesion becomes
much more difficult. Occasionally in doubtful cases a slight exercise
or a few forced expirations with glottis closed (Valsalva's experiment) will
increase the work of the left auricle and cause the presystolic thrill and
rumble to become so intense that the presence of mitral stenosis is unmis-
takable. A diagnosis should never be made unless the heart has been
examined in various stages of its activity. In spite of such precautions
errors are not infrequent, and are made by the most skilful observers. It
must be frankly confessed that there are many cases in which the diagnosis
cannot be made with any degree of certainty.
According to Phear, adhesive pericarditis can also be mistaken for
mitral stenosis, since occasionally a presystolic rumble may occur, due no
doubt to the stretching of the fibrous strands under the influence of the
auricular contraction of the ventricular filling, and here also the diagnosis
of two coexistent lesions should be made with caution.
Presystolic Gallop Rhythm. — Another condition which on rare occa-
sions may be confounded with mitral stenosis is one of slight cardiac weak-
ness in which there is a presystolic gallop rhythm. Under these circum-
stances, as Sewall states, the ventricles are overfilled with blood and the
auricle encounters some difficulty in forcing blood into them. There may
even in some cases be a slight functional stenosis like that discussed on
page 106. Sewall believes that under these conditions the contraction of
the auricle becomes audible and may even be mistaken for mitral stenosis.
Quite recently the writer has had under his care in the Johns Hopkins Dispensary
a girl of 13 years who presented this picture. She had had a slight attack of rheumatism
and tonsillitis and shortly afterwards began to have palpitation, weakness, nervousness,
23
354 DISEASES OF THE HEART AND AORTA.
and a little pain in the precordium and around the lower part of the left axilla. On exami-
nation the heart was not enlarged, but the shock accompanying the first sound was quite
sharp and there was a well-defined impulse which began with vibrations that suggested a
presystolic thrill. These were somewhat increased on exercise. The second pulmonic
was not abnormally accentuated. The pulse-rate was 120 and regular. There was no
anaemia. The signs were not quite definite enough to warrant a diagnosis of mitral stenosis.
The patient was given digitalis for a few days and this was followed by a prolonged treat-
ment with iron, quinine, and strychnine. She improved steadily, and for several weeks
past no presystolic sounds or impulse can be elicited even by quite severe exercise. As it
seems quite unlikely that an auricular paralysis would set in coincident with these condi-
tions of improvement, and in the absence of any arrhythmia, it seems most likely that this
case represented one of very loud presystolic gallop rhythm, and that no organic lesion
is present.
CASE OF MITRAL STENOSIS WITH INSUFFICIENCY, ANGINA PECTORIS, AND
PULMONARY SCLEROSIS.
O. A. K., farmer, aged 34, was admitted to the Johns Hopkins Hospital, June 2,
1903, complaining of heart trouble and shorthessof breath. Family history
negative. Patient has always been healthy except for chorea at 14 and acute
articular rheumatism at 18. He is rather subject to headaches. Has smoked and
drunk in excess, but for the past few years does so in great moderation. He is much ex-
posed to the weather.
For the past six or seven years he has been short of breath and has had
pain over the heart. Six months before admission he developed ascending
oedema, which disappeared under treatment, but his breath remained short and the
cedema reappeared within a couple of months. During the past month he has had spells
of dizziness and fainting during exertion and had one chill followed by fever.
On examination the patient is seen to be a well-nourished man with anxious appear-
ance and flushed face, deeply cyanotic. He is quite dyspnoeic. The teeth are
bad; the pharynx is injected. The veins of the neck are prominent, but do not pulsate.
The chest is full, and coarse rales are everywhere heard.
Heart. — The apex impulse is seen in the 6th left interspace 12 cm. from
the midline. Dulness extends upward to the second left interspace and 4 cm. to the right
of the sternum. There is a loud systolic murmur heard over the entire heart
and left axilla. The heart's action is irregular in force and rhythm. Pulse-rate 76. The
radial is somewhat sclerotic. Maximal blood-pressure 130 mm. Hg.
His liver and spleen were not enlarged. There was no cedema of the feet.
He was kept in bed, purged freely, given tincture of digitalis
(8 doses of 1 c.c. [TT\,XV] each). During the following two months his condition i m -
proved markedly, in spite of the occurrence of a fibrinous pleurisy. His dyspnoea
diminished and he felt much improved. Coincident with this improve-
ment a presystolic rumble and thrill gradually appeared and a snap-
ping first sound preceded the systolic murmur. Three months after admis-
sion his cyanosis had almost entirely disappeared. The heart was still enlarged (the apex
11 cm. from the midline); a well-marked presystolic thrill was felt and a presystolic mur-
mur was heard at the apex. The first sound was snapping and was accompanied and
followed by a loud blowing systolic murmur.
The blood-pressure during his stay in the hospital ranged between 120 and
135 mm. Hg.
After leaving the hospital at this time the patient felt well for about six weeks,
during which period he could even run for a car without distress. Then he caught a
cold which persisted for four months, being aggravated by exertion. He had two more
fainting spells on exertion. Oedema returned, the lower extremities and
of late even the face and eyes being swollen. Urine less frequent than normal.
On readmission he was very cyanotic and very dyspnoeic.
Moist rales were heard over the entire chest. The apex is now in the 6th left
interspace 15.5 cm. from the midline. The presystolic rumble and sys-
tolic murmur are well heard, as at the last discharge. Red blood-corpuscles 5,000,000;.
haemoglobin 105 per cent.; leucocytes 5500.
MITRAL STENOSIS. 355
On the night of admission the patient felt badly and had attacks during
which he felt faint and "saw stars." Venesection caused much releif
in the symptoms and the blood-pressure rose from 120 mm. Hg to 140mm.
The patient's condition then gradually improved, but on January 24 he had a definite
attack of precordial pain and constriction lasting 1-3 minutes.
Feb. 23. Has had pain in head and the left side of the face due to a beginning otitis
media.
During the next few weeks he had several attacks of angina pee-
to r i s , the pain being usually most marked behind the lower part of the sternum. In
one attack it radiated to the left shoulder and down the left arm to the hand (left ventric-
ular pain).
On April 20 he complained of pain in the left axilla and back, com-
ing in paroxysms lasting for 15-20 minutes (left auricular pain).
May 6. Sputum bloody. From this time on he gradually improved,
cyanosis and dyspnoea almost disappeared, and he was discharged in August
in fair condition. From that time until his readmission in November he suffered from
numerous attacks of angina pectoris, beginning in the left hand and
passing up the arm to the shoulder and heart. He also had an attack of rheu-
matism and severe tonsillitis. His physical condition was like that on pre-
vious admission, but the anginal attacks were more frequent. He was given hypodermic
injections, sometimes of morphine, sometimes of distilled water, to relieve them.
His condition gradually improved, most markedly after venesec-
tion. Toward the end of his stay, while up and about, he became subject to sudden
paroxysms of acute dyspnoea (respirations 130 per minute), with small moist rales filling
the lungs (acute pulmonary oedema). These persisted in spite of repeated rest and digitalis
treatments. He was discharged on July 11, 1905, seven months after admission. (Edema
and dyspnoea returned within ten days, and he was soon back in the hospital again. Dur-
ing this admission he never thoroughly rallied. His blood-pressure remained
low, 105 mm. maximal pressure (as compared with 120-130 mm. on previous ad-
missions). The pulse was irregular. Rales were constantly present in his chest. The
liver was palpable. A slight pleurisy developed on October 13 and he died on Octo-
ber 20.
At autopsy the mitral orifice was found to have the form of a small
button -hole barely admitting the tip of the little finger (about 5 mm. in diameter).
The left auricle was dilated and hypertrophied. The left vehtricle
was not dilated, but was much hypertrophied, its walls being 15 mm. thick. The right
auricle and ventricle were much dilated, the tricuspid orifice admitting four fingers
(13-14 cm. in circumference). The coronary arteries were patent but showed
scattered areas of sclerosis. There were old fibrous patches upon the pericardium.
The pulmonary arteries were markedly sclerotic; the sclerosis extended
into their smaller branches. The aorta and peripheral arteries showed less sclerosis. There
were also chronic passive congestion of the other viscera, anemic infarctions of the spleen,
hemorrhagic infarction of the lungs, acute bronchitis, bronchopneumonia,
acute ulcerative follicular colitis, old tuberculous foci in the lymph-glands and lungs,
chronic adhesive pleuritis, and adhesive peritonitis.
COMPLICATIONS.
As seen by the table in Fig. 179 mitral stenosis is frequently associated
with other valvular lesions. Mitral insufficiency, present in one-half of the
Johns Hopkins cases and in 75 per cent, of Steell's cases, may be regarded
as an essential part of the disease rather than a special complication, and
its presence does not shorten the average length of life.
The association of aortic disease, and indeed of any additional burden
upon the circulation, increases the gravity of the condition.
Tricuspid stenosis is an occasional concomitant, though rarely as often
found as by Samways, who encountered it in severe grade in 21 out of
356 DISEASES .OF THE HEART AND AORTA.
autopsies upon cases of mitral stenosis, and in mild grade in 8 additional
cases. In the Johns Hopkins Hospital it was found clinically 7 times
among 298 cases of mitral stenosis.
• A certain degree of myocarditis is the rule, especially in cases in the
third and fourth decades.
Acute pericarditis is quite common in the youthful rheumatic cases,
frequently leaving a residual adherent pericardium, a lesion which aggra-
vates the condition considerably and greatly shortens the life of the patient.
One of the most important and dangerous complications arising with
mitral stenosis is pregnancy (see Chapter IX) .
Thrombosis in the Left Auricle. — Another not uncommon complica-
tion of mitral stenosis, more than any other valvular lesion, is thrombosis
within the left auricle. This may occur even while the auricle is still
contracting vigorously, as shown by the presystolic thrill and rumble.
The thrombus may remain quiescent in the tip of the auricle or it may
obstruct the pulmonary veins. Sometimes it is so large as to stop up the
narrow mitral orifice and kill the patient. More frequently it is small
enough to pass through, and if carried on by the blood current gives rise
to a small area of embolism.
Embolism. — Embolism of the middle cerebral artery may give rise
to paralysis or aphasia. Embolism in other organs gives rise to correspond-
ing signs and symptoms.
Pulmonary embolism and infarction are caused by thrombi from the
right auricle and ventricle; and hence are due to secondary stasis in the
latter and not primarily to the mitral stenosis. However, as failure of
the right ventricle is particularly common in mitral stenosis, pulmonary
embolism is especially frequent in this disease.
A few months ago a patient was admitted to the medical service of the Johns Hopkins
Hospital with gangrene and anaesthesia of both lower extremities, due to plugging of the
abdominal aorta by such an embolus. He had a well-marked mitral stenosis, with purring
presystolic thrill and loud presystolic rumble, showing that his left auricle was contracting
vigorously. Needless to say, nothing could be done to relieve him, and he died within a
few days.
TREATMENT.
The treatment of mitral stenosis is practically the same as that of
mitral insufficiency, except that, since the lesion is a more uniformly pro-
gressive one, greater care must be exercised in the general hygiene, espe-
cially the avoidance of infection and overstrain. Digitalis is given about
as in mitral insufficiency, especially when the left ventricle is dilated.
Amyl nitrite and the other drugs of the nitrite group may
prove of value when there is a broken pulmonary compensation. Hydro-
therapy and gymnastics may be used after the pulmonary compensation
has been re-established, but must be administered with even greater care
than in mitral insufficiency, for acute pulmonary engorgement and pulmo-
nary oedema are more liable to set in. Since it is particularly important to
guard against dilatation and hypertrophy of the right ventricle, vene-
section should be performed promptly in failure of the latter, especially
if there are signs of pulmonary oedema, unless marked ansemia is present.
MITRAL STENOSIS. 357
Hypodermic injections of atropine 0.5-1.0 mg. (gr. TTC—BTT) may be given
to relieve the pulmonary cedema or to ward it off. '
Owing to the role of anaemia in the etiology of mitral stenosis, it is
especially important that the haemoglobin be kept at a normal level. If
anemic, the patient should be given as complete rest as possible, with
maximal amount of fresh air and sunshine, a diet especially rich in eggs,
on account of the lecithin, and iron preparations, especially Blaud's pills
(0.3 Gm., gr. v), or Vallet's mass (same dose), or Ferrum oxidatum saccha-
ratum solubile (one teaspoonful in water), should be administered three
times a day. When the hemoglobin is near 60 per cent, or the progress
slow, arsenic should be given by the mouth, especially as Fowler's or Dono-
van's solution, in increasing doses until 1 c.c. (15 minims) is reached. Prof.
J. O. Hirschfelder obtains excellent results by the hypodermic injection
of 1 per cent, sodium arsenate (1 c.c., 15 minims) daily. However, this
must sometimes be discontinued on account of pain, in which case atoxyl
may be substituted.
W. Arbuthnot Lane and later (1902) Sir Lauder Brunton suggested
that in the light of modern surgical technic it might be possible
to slit the narrowed valve with a fine knife and thus
remove the stenosis. The experiment of slitting the mitral valve has been
performed by Gushing and Branch in hearts of normal dogs. It does not
present extreme difficulties, but the recoveries were few, in spite of the
fact that the heart muscle of these dogs was in good condition. Bernheim
in the same laboratory arrived at similar results. Lauder Brunton had
advocated the operation only for cases which were otherwise doomed;
and it is evident that here the danger from a weakened myocardium would
be far greater. Moreover, even if successful, the mechanical effect of sud-
denly converting a severe mitral stenosis into a severe mitral insufficiency
would impose an intense strain upon the hgart, and might, even in that
way, do more harm than good.
PROGNOSIS.
In spite of the numerous complications and the progressive character
of the lesion, the average duration of life in mitral stenosis is not extremely
short, being 33 years for males, 38 for females. This is due to the large
number of cases in which the process is dormant or progresses very slowly,
and indicates in the individual case the importance of avoiding everything
which may start it afresh, particularly infections and overstrain. In many
cases the condition then remains dormant for many years, the patient con-
tinuing to live a normal if somewhat careful life without further trouble.
Lenhartz has seen cases pass through seven pregnancies without manifest-
ing signs of cardiac distress, and endurance of equal magnitude may be
met with in men. On the other hand, the lesion may progress rapidly and
death may occur within a few years. In the more severe cases it may
come on without warning, often due to the loosening of an embolus from
the left auricle.
358 DISEASES OF THE HEART AND AORTA.
BIBLIOGRAPHY.
MITRAL STENOSIS.
Mayow. John, and Vieussens. Quoted from Huchard, Maladies du coeur, vol. iii, 3d ed.,
Paris, 1905.
Sansom, A. E. : The Pathological Anatomy and the Mode of Development of Mitral Stenosis
in Children, Am. J. M. Sci., Phila., 1908, xcix, 229.
Gillespie, A. Lockhart: An Analysis of 2368 Cases admitted with Cardiac Lesions into the
Royal Infirmary, Edinburgh, Edinb. Hosp. Rep., 1898, v, 31.
Cheadle. Quoted from Sansom.
Samways, D. W.: Mitral Stenosis, a Statistical Inquiry, Brit. M. J., 1898, i, 364.
Duroziez. Quoted from Petit.
Duckworth, Dyce: On the Etiology of Mitral Stenosis, St. Barth. Hosp. Rep., Lond.,
1877, xiii, 263.
Goodhart, J. H.: On Anaemia as a Cause of Heart Disease, Lancet, Lond., 1880, i, 479.
Meisenburg: Ueber das gleichzeitige Vorkommen von Herzklappenfehlern und Lungen-
schwindsucht, Ztschr. f. Tuberkl. u. Heilstattenwesen, 1902, iii, 378.
Tileston, W.: Passive Hypersemia of the Lungs and Tuberculosis, J. Am. M. Asso., Chicago,
1908, 1, 1179.
Bettelheim, K., and Kauders, F.: Experimentelle Untersuchungen ueber die kiinstlich
erzeugte Mitralinsufficienz und ihren Einfluss auf Kreislauf und Lunge, Klin, exper.
Unters. a. d. Lab. S. v. Basch, Berl., 1891, i, 144.
Kornfeld, S.: Experimentelle Beitrag zur Lehre vom Venendruck bei Fehlern des linken
Herzen, ibid., 1892, ii, 126.
Gerhardt, D.: Ueber die Compensation von Mitralfehlern, Arch. f. exper. Pathol. u. Phar-
makol., Leipz, 1901. xlv, 186.
MacCallum, W. G., and McClure, R.: On the Mechanical Effects of Mitral Stenosis and
Insufficiency, Tr. Ass. Am. Phys., Phila., 1906, xxi, 5; also Bull. Johns Hopkins
Hosp., Baltimore, 1906, xvii, 260.
Hirschfelder, A. D. : The Volume Curve of the Ventricles in Experimental Mitral Stenosis
and its Relation to Physical Signs, Bull. Johns Hopkins Hospital, Baltimore, 1908, xix.
Muller, G.: Ungewohnliche Dilatation des Herzens und Ausfall der Vorhofsfunction,
Ztchsr. f. klin. Med., Berl., 1905, Ivi, 520.
Harris, Th. Quoted on p. 340.
Petit, A.: Retrecissement mitrale, Traite de Med. (Charcot, Bouchard, Brissand), Paris,
1893, v, 247.
Corvisart, J. N. : An Essay on the Organic Diseases of the Heart, etc., translated by Jacob
Gates, Phila., 1812.
Gendrin and Fauvel: Arch, de Med., Paris, 1843, Ser. iv, i, 1. Quoted from Gairdner.
Gairdner, W. T.: A Short Account of Cardiac Murmurs, Edinb. M. J., 1861, vii, 428; also
Clinical Medicine, 1862.
Mackenzie, James: The Study of the Pulse and Movements of the Heart, Lond., 1903.
The Extrasystole, etc., I, Quart. J. M., Lond., 1907, i, 131, 481.
Minkowski, O. : Demonstration eines Herzens mit ungewohnlich starker Dilatation der
Vorhofe, Miinchen. med. Wchnschr., 1904, li, 182.
Hofbauer: Rekurrenslahmung bei Mitralstenose, Wien. klin. Wchnschr., 1902. Also
Alexander: Berl. klin. Wchnschr., 1904; and Frischauer: Wien. klin. Wchnschr.,
1905. Quoted from Thorel, C. : Pathologic der Kreislauf organe, Lubarsch-Ostertag's
Ergebnisse der Path., Wiesb., 1907, ii, iite Abth., 386.
Osier, W.: De la paralysie du nerf recurrent gauche dans les affections mitrales, Arch, des
malad. d. coeur, Par., 1909, ii, 73. Reviewed in an editorial, J. Am. M. Ass., Chicago,
1909, liii, 35.
Einthoven, W., with the assistance of Flohil and Battaerd: Die Registrirung der mensch-
lichen Herztone mittelst des Saitengalvanometers, Arch. f. d. ges. Physiol., Bonn,
1907, cxvii, 461.
Brockbank, E. M.: The Murmurs of Mitral Disease, Edinb. and Lond., 1899.
Fenwick, W. S., and Overend, W.: The Production of the First Cardiac Sound in Mitral
Stenosis, Am. J. M. Sci., Phila., 1893, ex, 123.
MITRAL STENOSIS. 359
Haycraft, J. B.: The Cause of the First Sound of the Heart, J. Physiol., Camb., 1890, xi,
486.
Broadbent, W. H., and J. F. H.: Heart Disease and Aneurism, N. Y., 1906.
Acland. Quoted from Fenwick and Overend.
Steell, G.: The Auscultatory Signs of Mitral Obstruction and Regurgitation, Med. Chron.,
Manchester, 1888, viii, 89. The Diagnosis of Mitral Regurgitation through a Con-
stricted Orifice, ibid., 1891-2, xv, 361. The Conduction of the Murmur of Mitral
Regurgitation, ibid., 1892, xvi, 116. The Distinction between Mitral Stenosis and
Muscle-failure in Certain Heart Cases, ibid., 1892-3, xvii, 24. The Auscultatory Signs
of Mitral Stenosis; a Statistical Inquiry, ibid., 1895, N. S. iii, 409. Case of Mitral
Stenosis presenting a Widely Distributed To-and-fro Murmur Resembling that of
Aortic Incompetence, ibid., 1896-7, N. S. vi, 174. Mitral Stenosis, Internat. Clin.,
Phila., 1898, s. viii, iii, 1411.
Huchard: I.e., p. 569.
Cabot, R. C., and Locke, E. A.: On the Occurrence of Diastolic Murmurs without Lesions
of the Aortic or Pulmonary Valves, Bull. Johns Hopkins Hosp., Baltimore, 1903, xiv.
115.
Bard, L.: Die Physikalische Zeichen der Mitralstenose, Samml. klin. Vort., I^eipz., No. 45,
Inn. Med. No. 137, 1907.
Flint, A.: The Mitral Cardiac Murmurs, Am. J. M. Sc., 1886, xci, 27.
Phear, A. G.: On Presystolic Apex Murmur without Mitral Stenosis, Lancet, Lond., 1895,
ii, 718.
Weber and Deguy: Du role des hsemorrhagies intracardiaques dans le retrecissement
mitral, Arch/de M6d. Exper., Par., 1897, and Presse m&L, Par., 1898.
Sewall, H.: A Common Modification of the First Heart Sound, etc., Trans. Ass. Am. Phys.,
Phila., 1909, and Am. J. M. Sc., 1909.
Brunton, T. Lauder: Preliminary Note on the Possibility of Treating Mitral Stenosis by
Surgical Methods, Lancet, Lond., 1902, i, 352. Discussed by Shaw, L. E., ibid., 1902,
i, 619.
Cushing, H. W., and Branch, J. R. B.: Experimental and Clinical Notes on Chronic Val-
vular Lesions in the Dog and their Possible Relation to a Future Surgery of the Cardiac
Valves, J. Med. Research, 1908, xii.
Bernheim, B. M.: Experimental Surgery of the Mitral Valve, Johns Hopkins Hospital
. Bull., Baltimore, 1909, xx, 107.
IV.
AORTIC INSUFFICIENCY.
HISTORICAL.
Our knowledge concerning lesions of the aortic valves producing leak-
age at that orifice (aortic insufficiency, aortic regurgitation, aortic incom-
petency) dates from 1705, when the
English anatomist Cowper first de-
scribed the occurrence of stiffening
and thickening of the valves so that
they "did not apply adequately to
each other, whence it happened some-
times that the blood in the great
artery would recoil and interrupt the
heart in its systole." Shortly after
this, and quite independently of Cow-
per, Vieussens (1715) described two
similar cases, noting also the presence
of a very full quick pulse, like the
rebound of a tightly-stretched cord,
associated with palpitation of the
heart so severe that it prevented lying
down. Morgagni also described sev-
eral cases, in one of which he recog-
nized both aortic insufficiency and
aortic stenosis. Hodgkin in 1829 de-
scribed a number of cases, and also
noted for the first time the diastolic
murmur, but did not recognize any
diagnostic features; so that the clear
clinical picture of aortic insufficiency may be said to date from the
publication of Dominic Corrigan in 1832.
FIG. 201. — Specimen showing vegetations
upon the aortic valves. The arrow points to the
vegetation.
PATHOLOGICAL ANATOMY.
Modern classifications of aortic insufficiency differ little from that of
Corrigan, and we distinguish, as he did—
1. Organic forms of aortic insufficiency due to pathological changes in the valves.
2. Functional or relative aortic insufficiency due to dilatation of the mouth of the
aorta (Fig. 202, D).
The organic forms of aortic insufficiency may be of three types:
1. Endocarditic, due to the occurrence of inflammatory changes upon the valves,
usually vegetations, occasionally to calcified atheromatous plaques (Fig. 202, A).
360
AORTIC INSUFFICIENCY. 361
2. Rupture of the valves, sometimes from mechanical strain, sometimes from ulcera-
tion (Fig. 202, B).
3. Sclerotic shrivelling of the cusps, usually associated with arteriosclerosis (Fie;.
202, C).
1. The pathology of the endocarditic lesions has been sufficiently dis-
cussed in a preceding chapter (page 299) , since they represent quite typi-
cal vegetations. This form of lesion results from the usual causes of
endocarditis, especially rheumatism, scarlet fever, pneumonia, as well as
gonorrhoeal, puerperal, septicaemic, and other acute infections (see page
301). It is the most common form in persons below thirty-five, whereas
the sclerotic is more common in later life.
2. Rupture of the valves is one of the less frequent but by no means
rare occurrences, and usually takes place suddenly during a period of great
muscular strain, such as wrestling, lifting a heavy weight, drawing a heavy
burden, or even during a bicycle race (Huchard), or else after severe blows
upon the chest (Osier). Under these circumstances, as has been seen,
the blood-pressure may suddenly rise to a tremendous height (see page 132),
FIG. 202. — Schematic, showing the various forms of lesion producing aortic insufficiency. A. Vegetation.
B. Perforation. C. Arteriosclerotic shrinking. D. Dilatation of the aorta.
and the blood stream tears its way through the valve at the weakest point-
usually near the base of the sinus of Valsalva. The ruptured valve may
have an apparently normal structure, but probably contains minute areas
of degeneration, since it is impossible to rupture a normal valve experi-
mentally by subjecting it to the highest pressures that are ever reached in
the animal body. In many cases the ruptured valves show arteriosclerotic
changes which have tended to weaken the tissue. Where endocarditic
changes are already present, rupture or perforation of the valve takes place
spontaneously and at ordinary or even lowered blood-pressures.
3. The sclerotic form of the lesion is not only the most common,
but produces the lesions which are most uniformly severe and progressive,
since it usually occurs in later life and is associated with general arterio-
sclerosis (Fig. 202, C) . The lesion is in every way similar to the sclerotic proc-
ess elsewhere in the aorta, and may assume any of the types which occur
in general arteriosclerosis — thickening with contraction, calcification, ancu-
rismal dilatation, perforation. In any individual case the symptoms
depend upon the size of the leak as well as upon the state of the peripheral
vessels and the heart.
The etiological factors bringing about this lesion are the same as those
given for general arteriosclerosis (see page 254), infections, alcohol, tobacco,
lead poisoning, nephritis, hard work. Osier (I.e.) especially calls atten-
tion to the fact that syphilis is one of the most frequent causes of sclerosis
362 DISEASES OF THE HEART AND AORTA.
about the root of the aorta in men under thirty-five, and that the lesions
commonly involve both the aortic valves and the mouths of the coronary
arteries. He considers this factor next to endocarditis in order of impor-
tance as a cause of aortic insufficiency in young men. Collins and Sachs
and Longcope have recently obtained a positive Wassermann reaction in
about half the cases of aortic insufficiency in which there had been no out-
spoken rheumatism.
Sex. — In women aortic insufficiency is far less frequent than in men,
constituting 8.4 per cent, of all heart lesions in the former as compared with
28.5 per cent, in the latter (Ciillespie).
Moreover, as shown by Romberg and Hasenfeld, the presence of aortic
insufficiency from causes other than sclerosis in itself leads to the produc-
tion of general arteriosclerosis, and hence the presence of any other form
of the lesion predisposes to the superposition of sclerosis.
Functional Aortic Insufficiency. — The existence of leaks at a dilated aortic orifice
was already suspected by Corrigan, especially when there was an aneurism near the base of
the ascending arch. This has been verified by subsequent observers and a diffusely dilated
aorta with insufficiency of the valves is not a rare finding. As regards the presence of tran-
sitory leaks from dilatation Gibson has al^b shown experimentally that such a dilata-
tion may occur as a result of too high pressure in the excised heart, and Stewart claims to
have produced it by cutting the aortic ring muscle. But since transitory aortic insufficiency
does not often accompany the high blood-pressures of uraemia, meningitis, and brain tumor,
it is probable that this factor plays little role clinically. The cases of supposed functional
aortic insufficiency are rare, but Anders has reported a considerable number. In some at
least it is possible that the phenomena (diastolic murmur, collapsing pulse, etc.) are due
to other causes, especially functional pulmonary insufficiency. Cardiopulmonary
murmurs, like those described by Potain, must also be excluded. However, the possi-
bility of functional aortic insufficiency must be borne in mind by the clinician; but it can
rarely be verified, and the clinical diagnosis is, at best, hazardous.
FIG. 203. — Effect of aortic insufficiency in the mechanical model. (After Marey.) The horizontal
line shows the point of production of aortic insufficiency. P.V., intraventricular pressure; PR, arterial
pressure; O, auricular systole. The diastolic pressure in the ventricle after aortic insufficiency is consid-
erably higher than in the normal condition and approximates the diastolic pressure in the aorta. The
wavelet o', due to contraction of the auricle, is less marked.
PATHOLOGICAL PHYSIOLOGY.
The mechanical effects of aortic insufficiency upon the circulation were
first studied experimentally in horses and dogs, as well as on the mechanical
model, by Marcy and Chauveau.
AORTIC INSUFFICIENCY.
363
They produced the lesion by pushing a probe down one carotid artery and through a
cusp of the aortic valve, while they registered the pulsation in the other carotid by means
of a cannula. They were thus able to reproduce the phenomena observed clinically,
especially the occurrence of the murmurs, the violent beating of the heart and arteries,
and the large collapsing pulse which had been described by Corrigan. They were also
able to reproduce these phenomena in a mechanical model of the circulatory system.
The experiments of Marey and Chauveau on animals have been repeated and con-
firmed by Cohnheim, Rosenbach, de Jaager, Kornfeld, Romberg and Hasenfeld, and those
upon the model by Moritz. The subject was again investigated under the writer's direction
by Dr. H. A. Stewart in the Johns Hopkins Medical Clinic. The method employed by
.Stewart differed from that of previous observers in the fact that he recorded simultaneously
the volume of the ventricles, the maximal and minimal blood-pressures, and the pulse-
curve from the carotid artery. He found in animals, as had been shown by Marey upon
the mechanical model, that the production of aortic insuffici en c v *i s at
NORMAL
II
COMPENSATED
LOW PERIPHERAL
RESISTANCE
III
COMPENSATED
HIGH PERIPHERAL
RESISTANCE
IV
BROKEN
PULMONARY
COMPENSATION
Fin. 204. — Diagram of the circulation in aortic insufficiency. The vertical black bars represent the
volume of the left ventricle, the shaded portions representing the residual blood, the portions indicated by
the white arrows showing the amount of blood regurgitating, the solid black indicating the systolic output.
The black arrows indicate the change in condition or pressure that has taken place. MAX, MIN, max-
imal and minimal blood-pressures. The white curve indicates the absolute sphygmogram corresponding.
AO, l'.\, If A, LA as in previous diagrams.
once followed by a great fall in pressure during diastole,
which is, at least in part, due to the regurgitation into the ventricle. This great fall in
diastolic pressure is the most characteristic feature of aortic insufficiency.
The actual amount of blood regurgitating, both in animals (Stewart)
and in model experiments (Moritz), is usually not more than one- tenth of the
total forced out at each systole.
As in the case of flow through any orifice, the factors influencing this
rcgurgitation are: (1) the size of the hole in or between the valves; (2)
the head of pressure in the aorta; (3) the length of time during which
leakage occurs.
Cardiac Tonicity. — The experiments performed by Stewart and the
writer indicate that the chief factor antagonizing the reflux is the elasticity
•of the heart muscle, or the cardiac tonicit y.
It is evident that, with a given lesion and a constant heart rate, the
fact or affecting the regurgitation is, therefore, the antagonism between the
height of blood-pressure dining diastole, on the one hand, and the cardiac
tonicity, on tlie other. However, the pressure within the ventricle is not
364
DISEASES OF THE HEART AND AORTA.
constant throughout diastole, but is continually increasing; while the pres-
sure in the aorta is continually decreasing, and the reflux will cease alto-
gether at the instant when pressure within the ventricle + cardiac tonicity
= pressure within the aorta. Consequently, the lower the pressure in the
aorta (diastolic pressure) or the higher the cardiac tonicity, the earlier this
will occur and the less will be the amount of blood regurgitating.
AORTIC PRESSURE
INTRAVENTRICULAR PRESSURE
AMOUNT OF BLOOD
REGURGITATING
FIG. 205. — Diagram showing how the high cardiac tonicity (T -f ) hastens the equilibrium between aortic
pressure, intraventricular pressure, and tonicity, and thus diminishes the amount of blood regurgitating.
It was found, however, that whenever this occurred the hearts
dilated and the animals died. Those animals which survived the shock of
the operation were able to increase their systolic output by the amount
regurgitated, and thus in spite of the lesion to keep the maximal pressure
at the same height as before. In these animals positive intraventricular
pressure during diastole acts as a load to the heart muscle, which responds
T +
VOL.
NORMAL
DILATATION
DIMINUTION IN VOLUME
FIG. 206. — Effect of rupturing an aortic valve in a dog, showing a transitory dilatation followed by a
permanent diminution in size. (After Stewart.) CA R., carotid; VOL., volume of the ventricles. Down-
strokes represent systole, upstrokes diastole. The maximal blood -pressure remains unchanged (122 mm.
Hg), the minimal pressure falls from 90 to 45 mm. Systolic output is somewhat increased. a-& repre-
sents the tonicity of the ventricles before producing the lesion; c-d represents tonicity after the lesion. A
represents the point at which, the aortic valve was ruptured.
by increased tonicity, and fills somewhat less completely than it otherwise
would; so that the total volume of the ventricles after aortic insufficiency,
just as after any other strain, may be smaller than before it. In these hearts
total volume is decreased, systolic output increased, and residual blood
greatly decreased.
Romberg and Hasenfeld (1. c.) have denied that this increased tonicity is always
beneficial, claiming that by inhibiting the inflow from the auricle it impedes the circulation.
However, Kornfeld found that the pressure in the left auricle is not affected by experi-
AORTIC INSUFFICIENCY. 365
mental aortic insufficiency as long as the strength of the left ventricle remains unimpaired.
As the influences which maintain tonicity are in almost every instance the same as those
which increase the strength and volume of the systole, it is probable that Romberg and
Hasenfeld are in error.
As regards the role played by tonicity in aortic insufficiency two views
are held:
1. Romberg and Hasenfeld claim that an increased tonicity hindering
the influx of blood from the auricle is distinctly harmful.
2. Stewart and the writer have shown that the most dangerous event
in experimental aortic insufficiency is overdilation, and this is antagonized
by increase in tonicity. Moreover, Cloetta has found that the hearts of
rabbits with experimental aortic insufficiency which had been treated with
digitalis were less dilated and were much stronger than those of normal
rabbits. Almost all the influences which bring about increased systolic
output are the same as produce increase in tonicity. Fear of evil results
from this cause seems, therefore, quite unwarranted.
Blood-pressure. — As regards blood-pressure, it was found that when
the peripheral resistance was increased, as by clamping the thoracic aorta,
the force of the heart-beat increased correspondingly, and both maximal
and minimal (systolic and diastolic) pressures increased about equally
and pulse-pressure remained high. With the increase in diastolic pressure
upon clamping, the regurgitation through the orifice increased (Fig. 214),
and, as systolic output changed no further, the heart dilated considerably,
showing that high peripheral pressure represents the condition which
produces the greatest embarrassment of the circulation. With the increase
in peripheral pressure, however, the form of the pulse curve changed
from collapsing to flat-topped and anacrotic, a fact which will be referred
to later.
Rate. — Corrigan thought that if the heart were slowed and diastole
were prolonged the heart would undergo great dilatation, but in the experi-
ments performed by Stewart and the writer it can be seen that this dilata-
tion soon reaches its limit, and the volume of the ventricles need not exceed
the normal volume for the same rate (Fig. 206). This is due to the fact
that, as the aortic pressure falls during a prolonged diastole, it approaches
the intraventricular pressure, and the above-mentioned equilibrium is
soon reached.
As a result of experiments upon animals, it would appear, therefore,
that the conditions most favorable to the heart are low peripheral resist-
ance and moderately high tonicity; and, as will appear later, therapy should
be directed toward this end.
Pulmonary Circulation. — As stated above, Kornfeld's experiments
show that the aortic lesion has no effect upon the pulmonary circulation as
long as the left ventricle is acting powerfully. ' When the left ventricle
begins to fail, pulmonary stasis and rise in auricular pressure occur (Korn-
feld), which, as Stewart and the writer have found, are frequently associated
with the occurrence of a functional mitral insufficiency. Pulmonary stasis
in aortic insufficiency is, therefore, a secondary phenomenon dependent
upon failure of the left ventricle. The clinical importance of this fact will
be referred to subsequently.
366 DISEASES OF THE HEART AND AORTA.
Hypertrophy. — As a result of the increased strain upon the left ventricle,
the walls of this chamber undergo great hypertrophy. The cavity of the left
ventricle, owing to the regurgitation during diastole, is often much dilatedr
especially in the infrapapillary or aortic portion of the chamber.
The left auricle, on the other hand, is rarely hypertrophied. The right
ventricle, however, usually shows some hypertrophy, resulting either from
slight increase in pulmonary pressure or from continuity of the fibres with
those of the left ventricle.
SYMPTOMS.
The symptomatology of aortic insufficiency differs considerably from
that of the mitral lesions. When the lesion is well compensated and no
pulmonary stasis occurs, dyspnoea may not appear for years, and in the
meantime the patient may enjoy excellent health. On the other hand,
he may also be considerably annoyed by the throbbing of his arteries,
headache, roaring in the ears, by loss of memory, by periods of depression
often alternating with periods of great exhilaration, by the appearance of
motes or muscse volitantes before the eyes.
Hallucinations of sight, especially that of the veiled gray figure, of hearing
(rhythmic knocking or bell-tolling), and of smell are relatively common in aortic disease,
and are usually associated with pain in the precordium or down the arms and tenderness
over the upper left chest (Head) . Head states that these always disappear
when mitral insufficiency sets in.
There are often pains over the heart, especially over the base, and
down the left arm, and typical attacks of definite angina pectoris. These
symptoms are especially common in the sclerotic forms, in the later stages
of the disease, but may occur even when the coronary arteries are unaffected.
After the break in compensation, dyspnoea is usually intense, and the patient
is compelled to sit up in bed, not only on account of shortness of breath
but also on account of extreme palpitation.
Cheyne-Stokes respiration (of the cardiac type) is some-
what more common in aortic insufficiency than in other forms of cardiac
disease. Undoubtedly this is due to some disturbance in the medullary
circulation, but the exact explanation is still uncertain.
Sudden agonizing attacks of cardiac asthma are very fre-
quent, accompanied by intense orthopnrea, in which the patient gasps for
breath for several minutes or even half an hour. No doubt they are asso-
ciated with sudden overfilling of the left ventricle, secondary functional
mitral insufficiency, and pulmonary stasis. Sudden death may occur dur-
ing such attacks, and is indeed more common in aortic insufficiency than
in other forms of valvular disease. Both the maximal and the minimal
pressures may be high up to the instant of death, as in one case observed
by the writer in which the blood-pressures were 150 mm. Hg and 110 mm.
respectively until the instant when the pulse suddenly ceased.
PHYSICAL EXAMINATION.
The appearance of persons suffering from aortic insufficiency is usually
quite characteristic. The eyes are bright, with conjunctiva? moist, the
pupils often dilated and palpebral slits wide, giving a peculiar staring ap-
AORTIC INSUFFICIENCY. 367
pearance which sometimes for an instant suggests exophthalmic goitre.
The sclera? are' usually pale and bluish. The cheeks are somewhat sunken,
the complexion usually pale and sallow (aortic facies).
One of the features which at once atfracts the attention of the observer,
as already the case with Vieussens in 1715, is the intense and sudden visi-
ble pulsation in the arteries, especially the carotids, temporals, and
brachials. Often this pulsation is so great as to shake the entire head,
even when the patient is asleep (Frankel). There is sometimes a visible
pulsation of the entire uvula (F. Miiller) and of the arteries in the retina
(Becker).
Not only the larger but also the smaller arteries pulsate visibly, as
can be seen in the so-called capillary pulse (Quincke), the to-and-
fro movement of the red border of an area of hypera^mic skin synchronous
with each pulse-wave. This can be observed at any place where an area
of erythema borders upon an area of pallor, especially along the margin
of an area of skin which has been caused to redden by slight friction, beneath
the finger-nails, or in the lips or gums when gently compressed with a glass
slide. This appearance coupled with the presence of the bounding and
collapsing pulse is usually very typical. Indeed, it is said that Oppolzer
won his professorship at Vienna by casually making a diagnosis of aortic
insufficiency while walking down the wards of the hospital and merely
resting his hand upon the dorsum of the patient's foot.
However, Oppolzer might readily have come to grief had he encountered one of those
not very rare cases in which all these phenomena result from arteriosclerosis alone. Lenn-
hoff, v. Weissmayer, and Huber have termed these cases pseudo-aortic insuffi-
ciency. In these cases the arteries are large and rigid and there is a high pulse-pressure
but no other manifestations of aortic insufficiency. The whole phenomenon is due to a
high pulse -pressure in rigid arteries (page 261).
The chest and lungs show no abnormalities until the later stages of
the disease are reached and pulmonary congestion has set in with bronchitis,
pulmonary oedema, or hydrothorax.
Cardiac Impulse. — Over the heart there is usually some bulging of the
chest wall, and usually a well-defined apex beat in the fifth or sixth inter-
space to the left of the mammillary line. The impulse is systolic in time
and heaving in character (dome-like, "choc en dome")> owing to the fact
that the entire apex is usually made up of the hypertrophied left ventricle
(Bamberger). In the /second right interspace there is often another
systolic impulse, caused by the throbbing aorta, which may lead to the
suspicion of aneurism.
On palpation nothing abnormal is noted except that the second aortic
shock is often lacking. In about 40-50 per cent, of the cases a p r c -
systolic thrill (Thayer) and in 15 per cent, /a tapping systolic shock
may be felt at the apex. This is very similar to that observed in mitral
stenosis but less intense, while in most cases the impulse is strong and
heaving. In about 16 per cent, of Thayer's cases an actual mitral stenosis
was present as well, and this association must always be borne in mind.
Systolic thrills are often felt, especially over the aortic area, caused by the
roughenings of the aortic valves, and also over the apex in cases where
mitral insufficiency is present.
368
DISEASES OF THE HEART AND AORTA.
Percussion and X=ray Shadow. — As stated above, the cardiac outline
in aortic insufficiency shows a marked elongation of the long axis (L) , due
to the hypertrophy and dilatation of the left ventricle. There is little
increase in the transverse diameter (Q), so that the area of cardiac dulness
LOWING
DIASTOLIC MURMUR
BLOWING
DIASTOLIC MURMUR
(AXILLARY)
PRESYSTOLIC
RUMBLE (FLINT)
FIG. 207. — Area of cardiac dulness and distribution of the cardiac sounds and murmurs in aortic
insufficiency. Heavy curved line, outline of the heart; heavy straight line, longitudinal diameter.
Parallel lines indicate the distribution of the aortic diastolic murmur. Black dot indicates maximum
intensity. Small circle indicates the distribution of the presystolic rumble (Flint). Small diagram at the
left indicates the murmur heard in each area.
and the X-ray show (Figs. 207, 208, and 209) the form of a narrow elongated
oval whose long axis is inclined more obliquely downward than is that of
the normal heart. In this way it presents a marked antithesis to the out-
FIG. 208. — Radiograph of a case of aortic insuf-
ficiency, showing elongation of the long axis of the
heart. (Kindness of Prof. C. M. Cooper.) The plate
is at the back of the patient, the tube in front.
FIG. 209. — Diagram of Fig. 208, showing the
hypertrophy of the left ventricle. The broken line
indicates the normal cardiac outline; the arrow indi-
cates the direction of enlargement; AO indicates
the shadow of the dilated aortic arch.
line of mitral stenosis, in which the oval is a broad and rather short one,
and to the broad, elongated oval of mitral insufficiency. The X-ray shadow
often shows a marked dilatation of the aortic arch, which may correspond
to an area of dulness in the second right interspace and over the adjacent
portions of the sternum, but this can be differentiated from aneurism by
AORTIC INSUFFICIENCY. 369
fluoroscopic examination with oblique illumination. Indeed, examination
with the X-ray shows this condition to be much more frequent than had
previously been suspected, and discloses many cases of dilated aorta which
had previously been regarded as true aneurisms. On the other hand, the
tremendous strain upon the vessel walls in aortic insufficiency tends to
bring about the formation of aneurisms, and the latter is a relatively fre-
quent complication of aortic insufficiency.
The Aortic Diastolic Murmur. — The characteristic and almost pathog-
nomonic sign of aortic insufficiency is the blowing, hissing, or occasionally
musical murmur heard over the heart in early diastole. This murmur was
first described by Hodgkin in 1829 as "a constant bruit de scie,
which presented this peculiarity, that it was double, attending the systole
as well as the diastole."1 However, it remained for Corrigan (1832) to
recognize its diagnostic significance. The murmur is caused by the regurgi-
tant stream passing through the orifice between the closed valves, and its
quality, like the noise made by a jet of steam, depends upon the size and
character of the opening and the pressure in the vessel during diastole
rather than upon the size of the orifice. Indeed, a small leak passing
through a narrow orifice, especially with irregular and calcified walls, at
a high diastolic pressure, may cause a much more intense murmur than
a large leak through a wide orifice (cf. page 110). Balfour even goes so far
as to state that when the diastolic murmur is loud over
the base but not over the carotid artery the regur-
gitation is small, whereas when it is loud over the arteries but not
heard over the base the leak is a large one. In occasional cases of ulcera-
tive endocarditis separation of an entire cusp may occur without the pres-
ence of the characteristic murmur. Moreover, it is frequently observed
that the diastolic murmur is totally absent when the heart is rapid and
weak, but reappears as the rate falls and the force of the beat increases.
The consistency of the valves also plays a considerable role. A rigid and
calcified orifice forms a better sounding-board and gives rise to a louder
and more roaring murmur.
As to the region in which it is best heard, the statements of different
authors vary. The following list shows the region of maximum intensity
given by various authors:
V. Jurgenson Second right interspace and adjacent portions of
sternum.
Gerhardt Left of sternum.
Romberg Second and third left interspaces.
Huchard Third right costal cartilage.
Sibson Lower part of left margin of sternum.
Broadbent Sternum near origin of third left costal cartilage.
Osier Midsternum, third costal cartilage, or along left
border of sternum as low as ensiform.
Cole and Cecil have called attention to the fact that in many cases of
aortic insufficiency the diastolic murmur not only can be heard but under-
goes an accentuation as the stethoscope passes outward from the apex
into the left axilla. The writer can confirm this observation.
1 Evidently there was a systolic as well as a diastolic murmur present.
24
370 DISEASES OF THE HEART AND AORTA.
The discrepancies in the statements of the different observers may be due to the
direction taken by the regurgitant stream. Foster, Balfour, and Grocco suggested that
this might depend upon the aortic segment which happened to be affected. It is easy for
any one to demonstrate to his own satisfaction that this view is at least partially correct.
A calf's heart may be obtained from a butcher's shop and a cannula connected with a pres-
sure bottle inserted into the aorta. A window is cut into the left ventricle, and a hole is
then made in one of the aortic leaflets. A regurgitant stream issues from the hole, taking a
direction nearly perpendicular to the plane of the valve. The stream emerging from a
hole in the left cusp strikes the septum, that from the posterior cusp strikes the left wall
of the ventricle in the vicinity of the apex or anterior papillary muscle, while that from
the right cusp strikes against the anterior cusp of the mitral valve. The higher the pressure
under which these streams pass the more their direction is deflected toward the apex. A mod-
erate change in pressure will make a great difference in the direction taken by the stream.
FIG. 210. — Direction of the primary regurgitant streams in aortic insufficiency. (Schematic.) I. Re-
gurgitant streams passing through orifices in the aortic cusps. II. 1, Direction taken by a stream regurgi-
tating at low pressure; 2, direction of stream regurgitating througn the same orifice at high pressure. III.
A, direction naturally taken by a stream regurgitating through an orifice in the aortic cusp; B, direction
to which the stream through the same orifice is deflected by irregularities upon the surface of the vegetation.
If the orifice from which the stream emerges is an irregular one like that at the margin
of a vegetation, the direction of the stream may be totally deflected from its original course
(Fig. 210) and this is probably the case in most clinical conditions. No hard-and-fast rules
hold for all lesions of any individual segment. However, the important fact is that the
regurgitant stream continues as a well-defined jet, whose sound would naturally be loudest
near the point where it strikes and which would be transmitted more or less nearly in the
direction of its course. The walls of the heart and the chordae tendineae aid in transmitting
these murmurs for some distance beyond their point of impact.
It is evident, therefore, that the mere variations in the direction of
the regurgitant streams due to the form of the leak, the blood-pressure ,
and the position of the heart may give rise to the greatest variations in
the point at which the murmur is maximal, and may account for the dis-
crepancies in the clinical findings of excellent observers.
Murmurs over the Arteries. — Owing to the roughening of the aortic
valves and sometimes to the presence of aortic stenosis, a systolic murmur
is also heard over the aortic area and transmitted along the blood stream
to the arteries.
In the carotid and brachial arteries a diastolic or to-and-fro murmur
may also be heard. This was described by Corrigan in 1832 and by Da
Costa Alvarenga in 1856, but it is most frequently and easily heard over
the femoral arteries, where it was first noticed by Bouillaud and described
by his pupil, Duroziez, in 1861. It is usually known as Duroziez's
double murmur. The diastolic portion is probably due to a slight
regurgitant stream from the periphery toward the larger arteries.
AORTIC INSUFFICIENCY.
371
VOL.
Flint's Presystolic Rumble. — Another and very important murmur is
the presystolic rumble heard only at the apex (Flint murmur), first de-
scribed by Austin Flint in 1862 in cases of aortic insufficiency without any
mitral involvement. This rumble is in
every respect similar to that of mitral
stenosis, and it is extremely difficult to
determine whether the latter is absent. PR.
Indeed, Flint, in his original paper, supposed
that the murmur was due to the existence of a
functional narrowing of the orifice between the
mitral cusps, which, as Baumgarten (1843) and
Hammernjk had shown, was closed at the beginning
of auricular systole. Guiteras and Thayer believe
that the murmur is due to the vibration of the ante-
rior cusp of the mitral valve set in motion by the
regurgitant stream. Thayer and also Gibson deny
the existence of such a functional stenosis. How-
ever, the writer has been able to show on the excised
heart, by the method of Baumgarten and Gad, that
although the mitral valve usually opens along its
entire extent, yet when the pressure within the ven-
tricle is increased, the separation of the cusps occurs
at only a small portion of the lineof closure (Fig. 212) .
An actual functional stenosis is, there-
fore, present exactly as assumed by Flint.
Snapping First Sound. — The first sound
at the apex in 30 per cent, of these cases
has the snapping character present in mitral
stenosis, but more commonly is loud and
booming. The systolic murmur transmitted to the left axilla is present
in many cases in which mitral insufficiency is associated.
Aortic Second Sound. — When there is great destruction or great retrac-
tion of the aortic cusps and they do not ap-
proximate, the second sound may completely
disappear; but if the edges are sclerotic or
calcified, or covered with hard vegetations,
the closure may even cause an intensification
of the second sound, in spite of the presence
of a larger regurgitation.
Third Heart Sound. — Besides these sounds
Prof. Thayer has called attention to the ex-
treme frequency of a loud third heart sound
(protodiastolic gallop rhythm) in aortic insuf-
ficiency, associated with the protodiastolic
wave upon the cardiogram. If, as has been sug-
gested by Hirschfelder, Gibson, and Thayer,
this sound is due to the closing snap in diastole,
it is quite natural that it should be unusually loud in aortic insufficiency
when the mitral valves are forcibly clapped together by the high diastolic
pressure in the ventricle. It can be readily shown on excised hearts that
the snap is then more abrupt than under normal conditions.
FIG. 211. — Relation of murmurs in
aortic insufficiency to the cardiac cycle.
PR., intraventricular pressure; VOL., vol-
ume curve of the ventricles. 1, simple
aortic diastolic murmur; 2, Flint presys-
tolic rumble and aortic diastolic murmur;
3, presystolic rumble, diastolic murmur,
and third sound; 4, mitral and aortic in-
sufficiency murmurs replacing both sounds
(machinery murmur).
mitral
FIG. 212. — Functional mitral ste-
nosis in aortic insufficiency as d«-m<m-
-t rated mi tin- c\cis(Ml heart by Baum-
garten's method. (Semi-schematic.)
372
DISEASES OF THE HEART AND AORTA.
BLOOD-PRESSURE.
The blood-pressure in patients with aortic insufficiency presents the
same characteristics as in experimental animals, — namely, a constantly
high pulse-pressure. This may be due eithe,r to a considerable
fall in the minimal pressure (as, for example, maximal pressure 120, mini-
mal 50), as is most common in the endocarditic group, or to a considerable
rise in the maximal pressure with relatively little change in the minimal
(170 and 90 respectively), such as is usual in the arteriosclerotic form.
Occasionally one encounters cases in which an aortic diastolic murmur
and normal pulse-rate are present with normal maximal and minimal pres-
sures (120 and 90), but all the experimental evidence indicates that in
these cases the leak must be a small one, just as is the case in animal experi-
ments when a thrombotic deposit plugs the hole in a punctured valve
(see page 299). In such cases, therefore, there is a definite lesion of the
aortic valves, producing but little leakage yet a well-marked murmur.
Any disturbances to the circulation in such a case are due to sclerotic and
myocardial factors rather than to the aortic lesion. Although this class
of cases has not been studied extensively, it seems probable that a careful
functional diagnosis based upon the blood-pressure findings might prove
very useful for prognosis.
FIG. 213.— Variations in the form of the pulse-wave encountered clinically in aortic insufficiency. (After
Marey.) 1, normal form; 2, collapsing (Corrigan); 3, 4, 5, 6, anacrotic pulse.
PULSE.
The typical pulse of aortic insufficiency is very characteristic, and
since the time of Corrigan has been known as the Corrigan pulse (water-
hammer pulse, see page 47). The wave is large, with a quick upstroke
(pulsus celer et altus) and sudden fall, leaving the artery quite
AORTIC INSUFFICIENCY.
373
small and soft during diastole (collapsing pulse).1 In the typical sphygmo-
gram these characteristics are very marked. The criterion for designat-
ing a pulse-tracing as collapsing is not the steepness of the up-and-down
strokes, for these depend chiefly upon the speed at which the smoked sur-
face is travelling, but lies in the fact that the dicrotic notch in the
collapsing pulse falls below the middle of the pulse-
wave, while in the normal and anacrotic pulse it lies above the middle
(Mackenzie and Broadbent). Since Marey and Huerthle have shown that
the systolic period occupies the time before the dicrotic notch and the
JSEC.
CAROTID
VOLUME OF
VENTRICLES
VOLUME OF
VENTRICLES
FIG. 214. — Tracings from a dog with experimental aortic insufficiency, showing the conversion of a
collapsing (A) into an anacrotic pulse (B) by clamping the descending aorta. (After Stewart.) A, before;
B, after clamping. The figures on the first pulse curves indicate the time from the base to the summit of
the pulse- wave. The figures on the second wave indicate maximal and minimal pressures in the carotid.
Downstrokes upon the volume curve represent systole. Clamping the aorta causes the ventricle to dilate
somewhat, and to fill more quickly in diastole.
diastolic after it, it is but a paraphrase to state that in the collapsing pulse
over half the fall of pressure occurs during systole, while
in the normal pulse the fall occurs chiefly during diastole. Moreover
the volume curves by Stewart and the writer have shown that the collapse
occurs while the blood is still flowing out of the ventricle into the aorta,
and not at the time when the regurgitation is occurring. On the other
hand, increasing the peripheral resistance, either by clamping
the descending aorta or by the administration of adrenalin, etc., which
1 ( 'orrigan called attention to the fact that elevating the arm caused the pulse to
have a more collapsing quality, but Stewart has shown that this is due to hastening the
venous return and not to increased regurgitation. It can be prevented by slightly con-
stricting the arm.
374 DISEASES OF THE HEART AND AORTA.
caused an actual increase in the amount of blood regur-
gitated, caused the collapsing form of the pulse-wave to
be replaced by one of typically anacrotic form (Fig. 214).
The pulse-pressure, however, remained high. Moreover, the pulse-tracings
of Marey (Fig. 213) showed almost all possible variations of form to occur
in cases of aortic insufficiency, and Stewart found that the collapsing pulse
was absent in 42 per cent, of the tracings at the Johns Hopkins Hospital.
There is also a certain number of cases in which the clinical note describes
the pulse as collapsing, while no such character appears on the tracing. In
these cases there is usually ,a large pulse-pressure, and the discrepancy is due
tothe*fact that the finger appreciates the amount of the changes in pressure
while the sphygmograph records mainly the suddenness of the change.
The cause of the collapsing character of the pulse seems, therefore, to
be situated in the peripheral arteries, though the relatively small backflow
into the ventricles and the high intraventricular pressure during diastole
also play important roles.
Hasenfeld and Romberg have shown that these vessels become greatly
dilated after the lesion has been produced, and Stewart has shown that
this is due to a stimulation of the depressor nerve at the aortic ring which
the increase in intraventricular pressure may render continuous. Eastman
has found by measurements of skin temperature that in typical aortic
insufficiency the peripheral vessels are actually dilated. The blood there-
fore passes rapidly into the small arteries, and the aorta empties itself
rapidly, so that this factor coupled with the backflow into the ventricle
causes the great fall in pressure during diastole.
It is sometimes thought that the absence of a collapsing
pulse in a case of aortic insufficiency indicates the presence of aortic
stenosis. However, as not only the above-mentioned experiments but
many autopsy findings
demonstrate, this is not
the case. It merely indi-
cates that there is high
peripheral resistance,
which is common in arte-
FIG. 215. — Radial pulse tracings from patient (R. C.) showing .
extrasystoles (E) which are probably of ventricular origin. The riOSCierOSlS.
heavily shaded portion represents the systolic period in one cardiac PiilcA-rafA TV»o
cycle. The pulse is collapsing.
pulse-rate depends largely
upon the degree of compensation, being little faster than normal in cases
without symptoms, but usually ranging from 80 to 120 in hospital cases.
The pulse-rate is usually regular; but when the heart's action is very
labored, ventricular extrasystoles may result from the over-distention,
and thus produce an irregular or a bigeminal pulse.
CASE OF AORTIC INSUFFICIENCY.
R. M. C., colored laborer, aged 46, entered the hospital on May 20, 1904, complain-
ing of soreness and swelling of the abdomen and shortness of breath. He has
always befen healthy except for measles, mumps, and whooping-cough as a child, diph-
theria at 21, and chills and fever. He has had gonorrhoea but denies syphilis.
He passes water once a night. He has worked hard, exposed to wet and cold and doing
heavy lifting. Does not use alcohol or tobacco.
AORTIC INSUFFICIENCY. 375
About two years before admission he had cough, palpitation, short-
ness of breath on exertion, and some orthopnoea, of which he was cured
at the dispensary. The present trouble began about two months ago, with violent
beating of the heart and shortness of breath which were worse at night. These symp-
toms came on in paroxysms, which may be produced by stooping down. He has
severe paroxysmal coughing spells. During the past few days his abdomen has
been swollen, but his feet have not been at all so.
The patient is a poorly nourished man, propped up in bed without respiratory dis-
tress. There is marked pulsation visible in all the large arteries,
and a to-and-fro murmur can be elicited over them by heavy pressure with the
stethoscope. The lungs are clear on percussion and auscultation, except for a few coarse
mucous rales at both bases.
Heart. — There is considerable pulsation over the precordium, the apex being
located in the seventh left interspace 18 cm. from the midline. Dulness
extends upward to the second left interspace and 5 cm. to the right of the midline in the
fourth interspace. There is a well-defined presystolic thrill over the apex.
A blowing systolic murmur replaces the first sound and is heard over the whole axilla, also
a short blowing diastolic murmur and a short presystolic rumble
(Flint murmur). Passing inward and upward the sounds are replaced by a loud to-
and-fro murmur, loudest over the insertion of the fourth rib and scarcely
heard to the right of the sternum. In the second right interspace the systolic mur-
mur is very harsh and the first sound is loud; the diastolic murmur is well heard.
The pulse is of good volume, regular, markedly water-hammer in charac-
ter. Maximal blood-pressure 170 mm. Hg.
Abdomen is full ; the hepatic dulness extends 9 cm. below the costal margin ;
the liver is soft and tender. There is well-marked oedema of the legs.
Red blood-corpuscles 5,000,000; haemoglobin 75 per cent.; leucocytes 75 per cent.
He was put at rest, soft diet, and given 1 c.c. of tincture of digi-
talis and strychnine, 1.5 mg. (gr. ^) every four hours, and purged freely.
He immediately improved. The oedema disappeared, and within three weeks he
was up and about, feeling well, with a pulse- rate of 80-90 per minute. He was
discharged on June 16. His shortness of breath and oedema returned, however,
within a week, and he re-entered the hospital on June 26 so dyspnceic that
he was scarcely able to speak. The signs were about as before. He did not improve
as before, however, in spite of treatment, and remained dyspnoeic throughout the
month, subject to spells of intense cardiac asthma, so that he was com-
pelled to seek relief by being propped up continually in a wheel-chair instead of
lying in bed. During this period his maximal pressure remained high (150-
170), his minimal pressure about 110 (Erlanger apparatus). During the after-
noon of August 1 the cardiac asthma was particularly intense. His maximal pressure was
150 mm. Hg, the minimal 110. Venesection was contemplated. Before this could be
done, .however, while the patient was being examined and perfectly conscious, the maximal
blood- pressure suddenly fell to 110, the pulse stopped suddenly, and
the patient dropped back dead.
At autopsy the aortic segments were found to be thickened at
their edges, and the valve was clearly incompetent. The aortic orifice meas-
ured 8.5 cm. in circumference, the pulmonic 8.5 cm. The edge of the mitral valve was
slightly thickened, the tricuspid also; but there was no stenosis of either. The tricuspid
orifice, on the contrary, measured 14 cm. There was much dilatation and hy-
pertrophy of the left ventricle, the heart weighing 760 Gm. The coro-
nary arteries were clear. There were numerous thrombi along the walls of
the right ventricle. Corresponding to this finding there were numerous areas of
embolism of the branches of the pulmonary arteries, evidently from the loose-
riiing of such thrombi. Along the pericardium there were numerous raised irregular pearly
til nous patches. There were chronic passive congestion and oedema of the lungs, right-
sided hydrothorax, chronic passive congestion of the abdominal viscera, and chronic
<r:istritis.
376 DISEASES OF THE HEART AND AORTA.
DIAGNOSIS.
The diagnosis of aortic insufficiency usually presents little difficulty.
The following conditions may, however, give rise to blowing diastolic mur-
murs over and near the sternum which may be mistaken for aortic insuf-
ficiency (Cabot and Locke).
1. Dilatation of the aorta.
2. Intense anaemia.
3. Tuberculous mediastinitis and similar conditions (murmur is cardio-
respiratory, loudest in inspiration).
4. In association with mitral disease and dilatation of the pulmonary
artery (functional pulmonic insufficiency).
These conditions are, as a rule, easily excluded, and do not frequently
obscure the diagnosis.
On the other hand, as has been seen, it is often difficult to exclude
complications such as mitral stenosis in the presence of a well-marked
Flint murmur, or of aortic stenosis when the pulse is not collapsing.
The dilatation of the aorta, which often follows as a sequela of aortic
insufficiency, is frequently mistaken for aneurism. It may be accompanied
by very marked pulsation in the second right interspace and even of the upper
portion of the sternum, with dulness in these regions. Even the X-ray when
taken in the anteroposterior diameter may be ambiguous, and oblique illumi-
nation may be necessary to remove the suspicion of aneurism (Holzknecht) .
The existence of a functional aortic insufficiency from transitory
dilatation of the aortic ring can only be definitely diagnosed when an aortic
diastolic murmur and an abnormally high pulse-pressure have been present
and have passed off. This is indeed a rare occurrence. Other complications
are few, and are generally those of arteriosclerosis. Bronchial features may
be present, as in any other form of cardiac disease when the pulmonary
compensation is broken. Anginal attacks and coronary sclerosis may
usually be regarded as a feature of the sclerotic form of aortic insufficiency
rather than a complication. On the other hand, one of the cases under the
writer's care was very subject to severe attacks of definitely anginal charac-
ter, and yet at autopsy the coronary arteries were found to be clear. It is
possible that in such cases the pain may be due to either vasomotor ischsemia.
or ischaemia due to the low mean pressure in the coronary arteries.
TREATMENT AND PROGNOSIS.
For purposes of prognosis and treatment the course of the disease
may be divided into three stages.
1. Freedom from symptoms, the left ventricle performing
its work perfectly without either dilatation or pulmonary stasis. In this
stage the high pulse-pressure, low diastolic pressure, and collapsing pulse
and throbbing arteries are, nevertheless, prominent. The only indication
is to aid nature by avoidance of overstrain, overeating, alcohol, coffee,
tobacco, unhygenic surroundings, and exposure to infectious diseases.
When hypertrophy is good, the lesion may persist for years without pro-
ducing the slightest symptoms.
AORTIC INSUFFICIENCY. 377
Three years ago the writer examined a medical student twenty-five years old who
has been in perfect health since an attack of rheumatic endocarditis at the age of ten.
In spite of his lesion he has become an athlete, was a member of his class crew at Yale, and
excelled in long-distance running; he smokes and takes alcohol in moderation. Cases
like this may persist for thirty-five years or more (Osier), but manifest themselves sooner
or later after infectious diseases or with the onset of the arteriosclerotic period of life.
In cases with arteriosclerosis, potassium iodide, 0.3 Gm. (gr. v), or
sodium nitrite, 0.2 Gm. (gr. iii), three times a day, is advisable, to help
check the progress of the arteriosclerosis and to keep down the blood-pres-
sure. Occasional Nauheim baths, warm salt baths, or even ordinary warm
baths are useful in promoting the vasodilation. Cardiac tonicity must be
maintained at all costs and dilatation must be prevented.
2. The second stage is that of dilatation of the left
ventricle. This is the stage when symptoms appear, some arising
in the sensory nerves of the ventricle and manifesting themselves in the
forms described above — palpitation, referred pain, psychic disturbances,
anginal attacks; some arising in the pulmonary circulation as a result of
stasis, presenting the various forms of respiratory disturbance. According
to Head, the stage of cardiac sensation never merges into the stage of re-
spiratory distress, but disappears when the functional mitral insufficiency
and the latter symptoms set in. There is a "safety-valve" action
of the mitral valve.
As has been seen, the important factors producing distention of the
ventricle are diminution of tone and high peripheral resistance. Treatment
should therefore be directed toward counteracting these conditions. The
usual cardiac procedures, rest, light diet, free purgation, should be resorted
to, and, when improvement warrants, the Nauheim baths and gentle
exercises free from much resistance.
Digitalis and the Nitrites. — The use of digitalis has been much disputed.
Corrigan stated that "in every case of this disease in which digitalis has
been administered it has invariably aggravated the patient's sufferings."
Broadbent believes that it should be used with caution and that it may
even precipitate sudden death, but that it is certainly indicated after mitral
insufficiency has set in. Romberg thinks it should always be used with
caution. It is probable that any deleterious property which the drug may
possess lies in its vasoconstrictor action, and hence from a priori reasons
it should be combined with nitroglycerin or other nitrites, or preferably
strophanthus substituted. Indeed, strophanthus seems to be the drug par
excellence in these conditions, but with this drug it is well to give nitro-
glycerin. The pharmacological researches of Cameron demonstrate that
the nitrites possess the two properties most needed in aortic insufficiency,
—that of increasing tone and of dilating the peripheral vessels; and the
writer's clinical experience bears out the view that, either alone or with
strophanthus or digitalis, they furnish great relief and are to be strongly
recommended.
A beautiful series of animal experiments recently carried out by
Cloetta merits consideration.
Cloetta found that the administration of digitalis over prolonged periods caused no
changes in size and strength of normal rabbits' hearts. If aortic insufficiency were pro-
duced and the animals left untreated for a year, their hearts hypertrophied and gained
378 DISEASES OF THE HEART AND AORTA.
SO per cent, of their original heart weight, but the animals lost in strength and endur-
ance. If they were treated with digitalis immediately after producing the lesion, and the
treatment continued throughout the year, the hearts were smaller (hypertrophy 30 per
cent.), but the hearts were almost as strong as those of normal rabbits. The aortas of
untreated animals had widened much more than those of the treated.
Cloetta claims to have had equally good results in patients by early
and continuous treatment with digitalis, but the matter must be studied
upon a larger series of cases before attaining general acceptance. It is
chiefly applicable to early rheumatic cases, though it seems probable that
long-continued administration of very small doses of digitalis (0.3 c.c., or
5 minims, of the tincture) may exert this beneficial effect without pro-
ducing the harmful effects sometimes met with.
For the extreme palpitation and anginal attacks, little can be done
beyond the administration of amyl nitrite in the latter. Ice-bags to the
precordium are often of value, as is the Finsen light treatment, galvanism
of the vagus (J. O. Hirschf elder) , etc. Stewart has found excellent results
after a lumbar puncture, even when the cerebrospinal pressure was low.
It is not unlikely that acupuncture over the neural segment afflicted might
have the same effect.
3. The third stage is the stage of failure of the right ventricle,
presenting the usual signs and symptoms except that anginal attacks,
spasms of cardiac asthma, and Cheyne-Stokes breathing are a little more
common than in other diseases. In the treatment of this condition the aortic
insufficiency is 'more or less disregarded, digitalis, purgatives, and diuretics
being given quite freely. The administration of nitrites is, however, still
to be advised.
What can be accomplished occasionally in such cases is shown by the case cited on
page 154. a farmer, aged 33 years, who came under the writer's care in November, 1903,
entering the hospital after a year's suffering with orthopncea so great that he had been
compelled to sleep in a chair for six months, and oedema and ulceration of the legs, as
shown in Fig. 123. Under digitalis and free purgation improvement set in rapidly, and in
ten weeks he left the hospital free from oedema and almost free from dyspnoea. He has
remained quite well, and has continued his work as a farmer during the past five years.
On the other hand, failure of compensation is usually a more serious
event than in mitral insufficiency, since the factors producing weakening
of the ventricles from over-distention are more intense and more persistent.
The writer has found in several instances that broken compensation in
aortic insufficiency is associated with a high diastolic pressure which falls
as the case improves in many cases shortly before death. It is probable
that this is due to asphyxial vasoconstriction and furnishes another example
of the vicious circle :
( Broken compensation 1
^, < Slowed circulation > N*
( Medullary asphyxia J
f Increased regurgitation ) f Vasoconstriction )
{ Weakening of ventricle J ( Increased peripheral resistance }
Venesection is not indicated except when there are a considerable
grade of venous stasis, high venous pressure, and dilatation of the right
auricle; but in the writer's experience its results are then excellent.
AORTIC INSUFFICIENCY. 379
In the anginal attacks and the spells of dyspnoea or for insomnia,
codein, .03 Gm. (gr. ^), or morphine, .0075 Gm. to .03 Gm. (gr. J to gr. i),
hypodermically, may be necessary, but should always be used as sparingly
as possible, since the habit is readily formed and the patient injures himself
by feigning dyspnoea in order to get the drug.
BIBLIOGRAPHY.
AORTIC INSUFFICIENCY.
Cowper: Phil. Trans., 1705, No. 299. Quoted from Osier and Gibson, Diseases of the
Valves of the Heart, Modern Med., Phila. and N. Y., 1908, iv, 205.
Vieussens: Nouvelles decouvertes sur le coeur, 1706. Traite" nouveau de la structure et des
causes du mouvement natural du coeur, Toulouse, 1705. Quoted from Huchard, Mai.
du C03ur, 3d ed., Paris, 1905, iii.
Morgagni: also quoted from Huchard.
Hodgkin, T.: On Retroversion of the Valves of the Aorta, Lond. M. Gaz., 1829, iii, 433.
Corrigan, D. J.: On Permanent Patency of the Mouth of the Aorta or Inadequacy of the
Aortic Valves, Edinb. M. and S. J., 1832, xxxvii, 225.
Gillespie, A. L.: An Analysis of 2368 Cases admitted with Cardiac Lesions into the Royal
Infirmary, Edinburgh, Edinb. Hosp. Rep., 1898, v, 31.
Hasenfeld, A., and Romberg, E.: Ueber die Reservekraft des hypertrophischen Herz-
muskels, u.s.w., Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1897, xxxix, 333.
Gibson, G. A.: Jugular and Triscupid Reflux, Edinb. M. J., 1880.
Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris,
1881.
Cohnheim, J.: Vorlesungen ueber allgemeine Pathologic, Berl., 1882, i.
Jaager: Arch. f. d. ges. Physiol., Bonn, xxxi.
Rosenbach, O.: Arch. f. exper. Pathol. u. Pharmakol., Leipz., 1878, ix, 1.
Kornfeld, S.: Ueber den Mechanismus der Aorten-insufficienz, Ztschr. f. klin. Med., Berl.,
1896, xxix, 91, 344.
Moritz, F.: Ueber ein Kreislaufsmodell als Hilfsmittel fiir Studium und Unterricht,
Deutsch. Arch. f. klin. Med., Leipz., 1899, Ixvi, 349.
Stewart, H. A.: Experimental and Clinical Investigation of the Pulse and Blood-pressure
Changes in Aortic Insufficiency, Arch. Int. M., Chicago, 1908, i, 102.
Head, H.: On Disturbances of Sensation, with Especial Reference to the Pain of Visceral
Disease, Brain, Lond., 1896, xix, 153. Certain Mental Changes that accompany Vis-
ceral Disease, ibid, 1901, xxiv, 345.
Frankel: Des secousses rhythmique de la tete chez les aortiques, Rev. de M&l., Paris,
1902, 664.
Miiller, Fr.: Pulsation des Gaumens bei Aorten-insufficienz, Charite Annalen, Berl., 1889,
251.
Becker: Ueber Retinalarterienpuls bei Insuffizienz der Aortenklappen, Monatsschr. f.
Augenheilk., 1870.
Quincke, H.: Beobachtungen ueber Kapillar-und Venenpuls, Berl. klin. Wchnschr., 1868.
Lennhoff: Ueber Pseudoaorteninsuffizienz, Diss., Berl., 1893.
V. \Veissmayer, W.: Insuffizienz der Aortenklappen ohne Gerausch und Pseudoaortenin-
suffizienz, Ztschr. f. klin. Med., Berl., 1897, xxxii, 29.
Huber: Ueber Pseudoaorteninsuffizienz, Berl. klin. Wchnschr., 1898.
Flint, A.: On Cardiac Murmurs, Am. J. M. Sc., Phila., 1862, xliv, 29.
Thayer, W. S.: Observations on the Frequency and Diagnosis of the Flint Murmur in
'Aortic Insufficiency, Am. J. tfed. Sci., Phila., 1901, cxxii, 538.
V. Jurgensen, Th.: Valvular Disease of the Heart, Nothnagel's Encyclopaedia of Practical
Medicine, Amer. edition, trans, by G. Dock, Phila., 190S.
< lerh.-irdt . Quoted from v. Jurgensen.
Romberg, E.: Lehrbuch der Knmkheiten des Herxens und der Blutgefasse, Stuttgart, 1906
Huchard, 1. c., Sibson, quoted from Huchard.
Broadbent, \V. II.: Heart Disease and Aneurism of the Aorta, 4th ed., N. Y., 1906.
Osier, W.: The Principles and Practice of Medicine, 4th ed., N. Y., 1901.
380 DISEASES OF THE HEART AND AORTA.
Cole, R. I., and Cecil, A.: The Axillary Diastolic Murmur in Aortic Insufficiency, Johns
Hopkins Hosp. Bull., Baltimore, 1908, xix, 353.
Foster, B.: Essays on Clinical Medicine, Lond., 1874.
Balfour, G.: Diseases of the Heart, Lond., 1898.
Grocco: Arch. ital. riv. clin., 1888. Also Borgherini, A.: Ueber das Verhalten des riick-
laufigen Blutstroms bei Insuffizienz der Semilunarklappen der Aorta, Deutsch. Arch,
f. klin. Med., Leipz., 1898, Ix, 139.
Eastman, T. J. E.: The Diagnosis of Circulatory Conditions by Temperature Measure-
ments, Bost. M. and S. J., 1908, clviii, 639.
Holzknecht, G.: Die roentgenologische Diagnostik der Erkrankungen der Brusteinge
weide, Hamb., 1901.
Cloetta, M. : Ueber den Einfluss der chonischen Digitalisbehandlung auf das normale und
pathologische Herz, Arch. f. exper. Path. u. Pharmakol., Leipz., 1908, lix, 209.
V.*
AORTIC STENOSIS.
PATHOLOGICAL ANATOMY.
In a certain percentage of cases (10 per cent.) in which the aortic valves
are diseased, the cusps become fused into a ring by which the orifice into
the aorta is narrowed (aortic stenosis). Owing to the force within the ven-
tricle, this ring is usually pushed
upward into the lumen of the aorta
until the orifice has a sort of dome-
shaped appearance (Figs. 216 and
217, A).
The inflammatory or atheroma-
tous changes most commonly begin
in the cusps separately, and the
process extends until their edges be-
come fused with an organization or
atheroma at the line of union. Oc-
casionally there is a progressive
uniform diffuse sclerosis like that
which often occurs in mitral lesions.
The condition almost always arises
from the same conditions as aortic Flo 2ir)._Specimen showing aortic stenosis,
insufficiency, but in rare cases may viewed from above,
also be of congenital origin.
Naturally many of the manifestations depend upon the degree of
stenosis, which is sometimes so extreme that a quill can barely be passed
B r
FIG. 217. — Forms of stenotic aortic orifices. A. Lateral view of the specimen shown in Fig. 216. B,
6. Aortic stenosis, with edges of cusps flexibly fixed at ring shown by broken line, but capable of move-
ment indicated by arrows. C, c. Aortic stenosis with rigid cusps.
through the orifice. On the other hand, the orifice may be, relatively speak-
ing, wide, and the valves retain sufficient flexibility to close it during dias-
tole, so that a pure aortic stenosis occurs without any insufficiency
381
382 DISEASES OF THE HEART AND AORTA.
whatever (a condition present in about 60 per cent, of the cases). In the
other 40 per cent, the orifice is not only narrowed but the cusps are so
fused and rigid that they do not close the aortic orifice during diastole,
and an aortic insufficiency is present along with the ste-
nosis (double aortic lesion).
OCCURRENCE AND ETIOLOGY.
Aortic stenosis is by far the rarest of left-sided valvular lesions, occur-
ring in only 5 per cent, of the 1781 Johns Hopkins cases and in 2.73 per
cent, of Romberg's cases. This is in accordance with the experience of
most writers. Gillespie's statistics, in which it was supposed to occur in
18 per cent, of all the heart cases in the Edinburgh Royal Infirmary, are
unique and arouse the suspicion that the fault lay in the diagnosis.
The etiological factors are practically the same as in aortic insuffi-
ciency. Syphilis and arteriosclerosis play a relatively important role. Con-
genital stenosis also occurs occasionally. In rare cases there is a double
stenosis, — one at the aortic orifice, and one occurring within the ventricle
by the formation of a fibrous ring from the septum to the anterior cusp of
the mitral valve. The disease is rare among women.
PATHOLOGICAL PHYSIOLOGY.
The changes in the circulation due to stenosis of the aortic orifice were
very completely shown by Luderitz under the guidance of Prof. Gad. Liid-
eritz found that if the aortic orifice were narrowed by the tightening of a
clamp, the aortic blood-pressure might or might not fall, but the form of the
CAR.
INT.
FIG. 218. — Carotid pulse and intraventricular pressure in experimental aortic stenosis. (After
Luderitz, Ztschr. /. klin. Med., xx.) | St marks the point at which aortic stenosis was produced. The carotid
pulse (CAR.) shows the gradual development of the pulsus tardus, with a fall in blood-pressure, while the
intraventricular pressure (INT.) increases tremendously.
pulse-curve changed. The upstroke changed from sudden to.
gradual and slanting, ending with a broad rounded top whose sum-
mit was reached near the end of systole (pulsus tardus). This form of
pulse, as will be seen, is perfectly typical of aortic stenosis, and furnisher
the basis for the diagnosis.
AORTIC STENOSIS.
383
Rise of Intraventricular Pressure. — The pressure within the ventricle, on the other
hand, rises greatly, often as much at 100 per cent., without affecting the aortic pres-
sure; for the greater part of the contraction is unable to force much blood into the
aorta. The excess of intraventricular over aortic pressure is therefore much greater than
in any other condition. The conditions under which the contraction takes place conform
more or less to those for the execution of an isometric contraction, and the curve of intra-
ventricular pressure comes to resemble that of an isometric contraction, the summit
changing from flat to the dome-shaped, as is typical for the latter (as shown by Frank
and by Huerthle). That is, the pres-
sure does not at once reach its maxi- NORMAL [ AOHTIC STENOSIS
mum, but rises gradually, coinciding
quite well with the rise of the curve
in the aorta. It is the direct com-
munication of this progressive rise of
pressure to the aorta which gives rise
to the pulsus tardus, as well as the
fact that the volume of blood flows
into the aorta more slowly than usual.
The duration of systole is prolonged
considerably, seven to ten per cent,
in mild grades of stenosis, ten to fifty
per cent, when stenosis is extreme.
When the ventricle is not
able to expel its quota even by
the end of systole, extrasystoles
are likely to occur, and this fre-
quently assumes the form of
a continuous bigeminal pulse.
Such overfilling of the left ventricle naturally leads to stasis in the auricle
and pulmonary veins, with rise of pressure in these parts, pulmonary con-
gestion, cardiac dyspno3a (v. Basch), oedema of the lungs (Welch), and
secondarily also of the right ventricle. These in turn lead to dilatation
and hypertrophy of the left ventricle and left auricle and hypertrophy of
the right ventricle, which are usually found to be present at autopsy.
FIG. 219. — Diagram of the circulation showing the
effect of aortic stenosis. The broken line indicates the
intraventricular pressure. The vertical black line indicates
the volume of the heart, the shaded portion representing
the amount of residual blood.
SYMPTOMS AND CLINICAL COURSE.
Aortic stenosis is probably the most chronic of all valvular lesions, and
persists for years without affecting the duration of life. However, as soon
as the stenosis becomes marked, so that the left ventricle has difficult} in
emptying itself completely, slight exertion, excitement, or emotion brings
on disagreeable symptoms, palpitation, constriction, substernal pain or
anginal attacks, and shortness of breath. These sensory stimuli probably
arise in the depressor nerve as the result of distent ion of the ventricle, for
experiments of Sewall and Steiner have demonstrated that distention ha>
this effect in animals. The symptoms at first j>a>s oft when the patient
rests or leads a quiet and hygienic life, but as the disease persists they
become more frequent and persistent. Sudden death is relatively common,
and is probably due to acute dilatation.
Compensation. — As in mitral stenosis, compensation is dif-
ficult. The left ventricle may by increasing its power continue to drive
enough blood into the aorta to maintain the blood-pressure, and even to
cause the pulse to resume the normal form (l-'iu. '2'2X), but this is done :it
384
DISEASES OF THE HEART AND AORTA.
an enormous waste of energy, which sooner or later brings on heart failure.
Moreover, the lesion itself is slowly progressive, and this constantly increases
the difficulty of maintaining the circulation. In the final stage broken
compensation sets in exactly as in other advanced valvular lesions.
When aortic insufficiency coexists the circulatory difficulty is naturally
increased, since the ventricle must drive an even excessive amount of blood
into the aorta in order to maintain the circulation, in spite of the difficulty
under which it already labors. Moreover, these are often the cases with the
most advanced pathological lesions, so that the coexistence of aortic insuffi-
ciency renders the prognosis less favorable than that of pure aortic stenosis.
PHYSICAL EXAMINATION.
The most striking feature upon general physical examination in aortic
stenosis is the presence of a well-marked systolic thrill and bruit over the
larger arteries. Over the chest there is usually a certain amount of pre-
cordial bulging. The apex impulse is sometimes well marked and heaving,
situated quite outside the mammillary line in the fifth or sixth interspace ;
frequently, however, it is not visible nor palpable. Between the apex and
the sternum there is often some
systolic retraction of the inter-
spaces from the contraction of
the hypertrophied right ventri-
cle. The left ventricle hypertro-
phies, increasing in size along its
long axis (obliquely downward) .
Palpation. — Palpation re-
veals a systolic thrill which is
usually very marked and felt
over the whole heart, especially
over the aortic area. It is pres-
ent in the carotid and brachial
arteries, and is transmitted in
the direction of the blood stream
(see page 92). The intensity
of this thrill is often the most
striking feature of all the phys-
ical signs, and may far exceed
that which is found in any other
condition. The shock of the first sound is usually felt, while that of the
second is often, though not always, absent.
Percussion and X=ray examination reveal no peculiarities other than
an area of cardiac dulness enlarged along its longitudinal axis, as in aortic
insufficiency; but, owing to the presence of functional mitral insufficiency
and dilatation of the conus arteriosus, the area of dulness may be higher
and broader than in aortic insufficiency and resemble that found in organic
mitral insufficiency.
Auscultation. — On auscultation one is immediately struck by the pres-
ence of a loud systolic murmur most intense over the aortic
area, and transmitted thence to the first right inter-
FIG. 220. — Diagram showing the cardiac outline and
distribution of the murmur in aortic stenosis. The par-
allel shading indicates the distribution of the systolic
murmur and thrill; the dot indicates the point at which
they are most intense.
AORTIC STENOSIS. 385
space and along the course of the arteries, where it is,
as a rule, still loud and distinct. It is also heard over the pulmonic area,
body of the heart, and over the apex, but far less loudly than in the aortic
area and the arteries.
This murmur is usually the loudest that is heard in any form of valvular
disease, and is often heard several feet away from the patient. The mechan-
ism of its production exemplifies perfectly the simple experiment for the
production of thrills and murmurs described on page 92. Since it cannot
be produced until the blood
begins to flow into the aorta,
this murmur does not begin
until an appreciable in-
terval after the begin-
ning of systole (Boy- SOUNDS
Teissier, Romberg, Weiss and
Joachim) and follows the
first sound in that region Tio SEC
as well as at the apex (Fig. IMUR
221) Weiss and Joachim have FlG 221._Murmur of aortic stenosi~ (After Weiss
recorded thlS murmur With their and Joachim.) Upper curve, carotid pulse; middle curve,
nhonosronp and find that it heart sounds; lower curve- time: one vibration equal
.Ope, anf to ^ second. The second sound is practically absent.
Sets in With a Crescendo Char- The murmur is composed of a crescendo followed by a
, ,1 i f . i ~ decrescendo character loudest with the upstroke on
acter at the very end of the first the pulse-wave.
sound. The crescendo continues
until the crest of the carotid pulse, after which it changes to decrescendo
throughout the rest of systole. The form of the carotid wave portrays the
amplitude of the vibrations and the variations in loudness of the murmur.
When mitral insufficiency (organic or functional) is present, the mitral
murmur may enter into or replace the first sound.
The second sound may vary considerably in aortic insufficiency.
If the valves are fused throughout their whole extent, it will be entirely
absent, but if portions of the cusps remain freely movable their closure
may give rise to a sound. Owing to the small excursion, this sound may
not be as loud as it would be if no stenosis were present, but this factor
may be more than balanced by the presence of sclerotic plaques and calcifi-
cations whose concussions may actually render the second sound louder
than normal.
PULSE.
Aortic stenosis may be said to be the only disease in which the absolute
diagnosis is determined by the pulse-tracing. The pulse is small, hard
(high diastolic pressure), and in typical cases rises and falls very slowly
(pulsus tardus). Like the curves in experimental aortic stenosis (Fig. 219),
the typical radial pulse-curve (Fig. 222) shows a very oblique ascent
which lasts throughout systole, the summit of the curve appearing just be-
fore the dicrotic notch. This is produced by the slow, gradual, and progres-
sive filling of the arteries from the gradually increasing intraventricular
pressure. It may be recalled that during the period of the up-stroke upon
the pulse-wave blood is flowing into the aorta 'more rapidly than onward
25
386
DISEASES OF THE HEART AND AORTA.
to the periphery; that during the period of the plateau the inflow and out-
flow are equal; and during the period of fall blood is flowing onward to the
periphery more rapidly than it flows into the aorta.
The pulse of aortic stenosis, there-
fore, reflects the true condition, that
blood is flowing into the aorta less
rapidly than usual and out of it also
less rapidly. However, it must be
admitted that this typical form of
pulse is rather rare. Most commonly,
either the aortic stenosis does not reach
this stage without being complicated
by an insufficiency which changes the
pulse form or death intervenes before
these signs of inability of the heart
to empty itself have set in. Indeed, many practitioners may pass through
long lives of busy practice without encountering a single example of aortic
insufficiency with pulsus tardus. The anacrotic pulse is so much more
FIG. 222. — Diagram showing the pulsus tar-
dus and the anacrotic type. Solid line, pulsus
tardus, showing the slow gradual rise; broken
line showing the anacrotic form with sudden
almost vertical rise surmounted by a plateau
which takes up the greater part of systole.
VI
VII
FIG. 223. — Pulse tracings from cases of aortic stenosis. The heavily shaded curve represents the sys-
tolic portion of the tracing. I. Anacrotic pulse from a case of tricuspid insufficiency but no aortic stenosis,
showing quick upstroke with only the summit sloping. II, III. Pulsus tardus from a case of aortic ste-
nosis (L. S.). IV. Tracing from a case of aortic stenosis and insufficiency. V, VI, VII. Tracings from
another case of aortic stenosis and insufficiency. V. Taken on February 28 soon after admission; symptoms
of cardiac weakness well marked; maximal blood-pressure 130 mm. Hg. The upstroke is gradual and slop-
ing. VI. From same patient on March 24 after recovery from cardiac symptoms. Maximal pressure 160.
The strong heart forces blood rapidly through the stenosed orifice and causes a sudden upstroke. VII.
Pulse tracing taken immediately after VI, with other arm raised. The increased resistance changes the
tracing to a pulsus bisferiens.
common in aortic stenosis that examples of it are given in many text-books
erroneously labelled pulsus tardus. A pulse-curve with a sud-
den perpendicular up-stroke, however, is not a pulsus
tardus, but an anacrotic pulse, whatever may be the form of its summit.
AORTIC STENOSIS. 387
It indicates that blood is flowing into the aorta from the heart more rapidly
than it is flowing out of the aorta toward the periphery, a condition which
occurs in aortic stenosis only (1) when the orifice is so slightly narrowed
that the hypertrophied left ventricle is able to drive blood through it with
great rapidity, and (2) when the peripheral vasoconstriction is so great that,
in spite of a slow inflow into the aorta, the blood still enters the latter much
more rapidly than it can leave it. The former is the more common condi-
tion; and it would appear that the hypertrophy of the ventricle can usually
keep pace with the advancing stenosis until a very late stage is reached.
The pressure within the ventricle produced under these conditions is prob-
ably tremendous.
These facts are well illustrated in Curves V, VI, VII (Fig. 223). The first (V) was
taken when the patient's heart was weak, and the blood-pressure shows a gradual up-stroke
and is fairly typical of aortic stenosis. The other curves (VI and VII), taken after his
heart had improved, have taken on the characters of aortic insufficiency and have lost those
of aortic stenosis.
Arrhythmia. — The rhythm of the heart in man, as in animal experi-
ments, is frequently irregular; small beats and dropped beats being
frequent, due to the occurrence of a pulsus alternans or to extrasys-
toles arising in the left ventricle when that chamber is unable to empty
itself sufficiently. Exercise, emotion, or any other form of cardiac over-
strain, on the one hand, or of cardiac weakening, on the other, precipitates
this irregularity.
Blood-pressure. — The blood-pressure in aortic stenosis is usually
slightly elevated (maximal pressure 130 to 160 mm.), due in part to the
accompanying arteriosclerosis, in part to the increase in the intraventricular
pressure, especially when the heart hypertrophies.
DIAGNOSIS.
In typical cases the diagnosis of aortic stenosis is extremely simple.
The presence of slow, gradual pulse, the pulse-tracings, the enlarged heart,
the very intense systolic thrill, the thrill and murmur over the aortic area
and arteries, and the absence or marked diminution of the aortic second
sound, present a perfectly characteristic picture. In certain cases, however,
and especially when there is arteriosclerosis or aortic insufficiency, it may
become extremely difficult to decide whether a mild grade of stenosis is
present.
CASE OP AORTIC STENOSIS.
Mrs. L. S., housewife, aged 58, entered the Johns Hopkins Hospital, April 29, 1904,
complaining of heart trouble. She has always been healthy; has had no infectious diseases
and never had rheumatism, but occasionally has had sore throat. She has occasionally
had fainting spells and palpitation after mental excitement, and during
the past year has had to void three or four times a night. Except for these symptoms she
was quite well until a year before admission, when one night after a heavy meal she awoke
with extreme dyspnoea, palpitation, and a feeling of extreme weakness. She had no pain,
but felt considerably alarmed. Immediately after this her feet became swollen
and in spite of a sojourn in bed she became subject to attacks of extreme dyspnoea. The
oedema of the feet subsided, however, but reappeared after exertion.
At the time of examination the patient was propped up in bed, with slight
dyspnoea. She was fairly nourished, pale, sallow, lips very cyanotic. Lungs
388 DISEASES OF THE HEART AND AORTA.
clear on percussion and auscultation, except at both bases, where the note is impaired and
the breath sounds are accompanied by crackling rales.
Heart. — The apex impulse is barely visible in the sixth left interspace
13 cm. from the midline, from which point dulness extends upward to the third rib,
as well as 3 cm. to the right of the midline. There is slight impairment of the percussion
note over the sternum. A soft systolic murmur is heard at the apex and in the
axilla, becoming louder, however, as the sternum is approached, and maximal over
the second right interspace, where it becomes rough in character. It is
transmitted to the carotids but not to the subclavians. The second pul-
monic sound is louder than the second aortic. There is a wrell-marked thrill
over the base and manubrium, most marked in the second right interspace.
Slight pulsation over the manubrium. No tracheal tug. The pulse is small,
regular, 100 per minute. The left radial pulse is a trifle larger than the right. Tracing
shows a well-marked pulsus tardus (Fig. I and II). Blood-pressure 150
m m . Hg.
The abdomen is distended but does not contain fluid. The legs are very oedematous.
Urine is reddish; specific gravity 1030; acid, and contains a large number of
hyaline casts.
Red blood-corpuscles 5,300,000; haemoglobin 85 per cent.; leucocytes 10,000.
During the first week she improved under rest, purgation, and digi-
talis; but on May 8 had a severe spell of dyspnoea not controlled by morphine
or nitroglycerin, but somewhat relieved by strychnine, 3 mg. (^ gr. hypo.). During the
attack the aortic murmur was much less marked than it had been before.
The cardiac outlines were unchanged. There was very slight development of fresh
rales, indicative of pulmonary oedema. After the attack and the nitroglyc-
erin there was unequal dilatation of the peripheral venules. Cheyne-Stokes respiration
developed during the night. A few purpuric areas were seen over the extremi-
ties and the sacrum.
On the next day she had another attack of dyspnoea, after which cyanosis deepened,
respiration became labored, the pulse weakened, and the blood-pressure fell gradually
until the patient died in the early evening.
•At autopsy the three aortic cusps were found to be fused together
by a calcareous cement, leaving an orifice not more than 3 mm. in
diameter. The left ventricle was markedly hypertrophic, the right
less so. Both were dilated. The heart weighed 600 Gm. There were slight atheroma of
the aorta below the transverse arch, infarction and cedema of the lungs, left hydrothorax,
left pleural adhesions, chronic passive congestion of the liver (nutmeg), spleen, and kid-
neys; general anasarca.
TREATMENT.
As regards treatment there is little to be said. Fortunately, the disease
is very chronic in its course, especially when it begins after the period of
adolescence has passed. A quiet life under the best possible hygienic con-
ditions, with avoidance of infections, excitement, and all forms of stimulants
and overstrain, usually serves to stave off the onset of symptoms for many
years. When these once appear in spite of quiet, the case is practically
hopeless. Absolute rest, light diet, moderate purgation, and lessening of
the peripheral resistance by means of the nitrites and the Nauheim baths
constitute the most important means of treatment. Digitalis is of
value until the heart reaches its limit of hypertrophy, after which it merely
precipitates overwork and irregularity of the heart.
In the acute attacks of acute heart failure, venesection should be
resorted to promptly, in order to lessen the residual blood in the left ven-
tricle by diminishing the inflow into it.
AORTIC STENOSIS. 389
BIBLIOGRAPHY.
AORTIC STENOSIS.
Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart,
1906.
Gillespie, A. L.: An Analysis of 2368 Cases Admitted with Cardiac Lesions into the Royal
Infirmary, Edinburgh, during the Five Years 1891-1896, Edinb. Hosp. Rep., 1898,
v, 31.
Liideritz, C.: Versuche ueber den Ablauf des Blutdrucks bei Aortenstenose, Ztschr. f.
klin. Med., Berl., 1892, xx, 373.
Welch, W. H.: Zur Pathologie des Lungenoedems, Arch. f. path. Anat., etc., Berl., 1878,
Ixxii, 375.
Sewall, H., and Steiner, D. W.: A Study of the Action of the Depressor Nerve, etc., J.
Physiol.r Camb., 1885, vi, 162.
Boy-Teissier: L'auscultation retrosternale, Rev. de Me"d., Par., 1892, xii, 169.
VI.
PULMONARY INSUFFICIENCY.
Insufficiency of the pulmonary orifice usually occurs either as a con-
genital lesion or as a result of a severe endocarditis in which other valves
are involved. Even as such it is a very rare disease, only 3 cases having
been seen among 24,000 admitted to the medical service of the Johns Hop-
kins Hospital.
Lesions of the pulmonary valves had been described by Morgagni, but
the first clinical cases of pulmonary insufficiency were described by Norman
Chevers in 1846, and after him by Frerichs, Benedikt, Walshe, and Stokes.
Barie in 1891 was able to collect detailed records of 58 cases with 24
autopsies.
PATHOLOGICAL ANATOMY.
The conditions leading to regurgitation at the pulmonary orifice may
be divided into six groups:
I. Congenital malformations of the valve resulting in
atrophy and deformity. The presence of only two, or, on the other hand,
of four cusps does not usually bring about any leakage. In this category
may also be mentioned stenosis of the orifice.
II. Endocarditic vegetations upon the valves, especially
arising in very acute attacks of endocarditis with lesions of other valves.
III. Arteriosclerotic changes in the cusps, often associated
with dilatation and arteriosclerosis of the pulmonary artery.
IV. Aneurisms of the cusps.
V. Ruptures of the cusps during coughing or strain, especially of
cusps already diseased.
VI. Dilatation of the pulmonary artery and conus arteriosus lead-
ing to a functional insufficiency of the valves.
According to many writers, especially Gibson, a functional insuffi-
ciency of the pulmonary valve of more or less transitory duration takes
place as a result of dilatation of the artery and of the right ventricle.
This would naturally occur most frequently in cases of mitral stenosis
with broken pulmonary compensation, and would account for the blow-
ing diastolic murmur which is sometimes heard to the left of the sternum
in these cases.
The experimental data upon this subject are more or less uncertain. G. A. Gibson has
shown upon the dead heart that the pulmonary valves become insufficient under much lower
pressures than are necessaay to cause leaks at the aortic. He has also shown that these
leaks can be prevented from occurring in the dead heart if the pulmonary orifice be pre-
vented from dilating (as by surrounding it with a string). His studies would therefore
lead one to believe that such regurgitations would occur readily in hearts whose tonicity
was diminished and in which the fibres about the pulmonary orifice stretched accordingly.
390
PULMONARY INSUFFICIENCY.
391
On the other hand Sollman has shown in the living excised cat's heart perfused with Ringer's
solution and other salt mixtures that the pulmonary orifice can withstand tremendous
pressure without leaking.
However, Stokes, Kolisko, Bristowe, Coupland, Litten, Chauffard,
Gouget and Preble, have reported cases of relative pulmonary insufficiency,
supported by autopsy. In all these cases there was dilatation of the right
ventricle, and in three of them a mitral lesion with pulmonary stasis. It
seems quite likely, moreover, that such a pulmonary insufficiency was
present in cases W. H. (page 402) and B. I. (page 417), though the water
test was not applied to the valves at autopsy.
NORMAL
INSUFFICIENCY
ETIOLOGICAL FACTORS.
Barie*'s statistics collected from 50 cases of organic pulmonary insuf-
ficiency show that the two sexes are affected with equal frequency. It was
found in patients of all ages from birth to 75 years, but 37 out of 46 cases
(80 per cent.) occurred between the ages of 18 and 34 years. In 40 per cent,
the disease was congenital, but in these it never occurred as the sole lesion,
being usually associated with stenosis. Rheumatism was the etiological
factor in 16 per cent, of the cases. Puerperal infection, gonorrhoea, and
the other infectious diseases rank next in frequency. There is also an
arteriosclerotic group due to
syphilis, alcohol, and other ™™,T PULMONARY
affections especially associated
with mitral stenosis and scle-
rosis of the pulmonary artery.
PATHOLOGICAL PHYSIOLOGY.
Pulmonary insufficiency
bears the same relation to the
lesser circulation that aortic
insufficiency bears to the sys-
temic circulation. The effect
of the leak is to bring about a
lowered diastolic pressure and
an increased pulse-pres-
sure in the pulmonary
artery, accompanied by a
somewhat greater systolic out-
put from the right ventricle to compensate for the leak. The increased
intraventricular pressure in the right ventricle during diastole gives rise to
hypertrophy when the strain is compensated, and dilatation when the
strain becomes too great. As a result of this dilatation, functional
insufficiency of the tricuspid valve very readily sets in.
The results of these secondary changes are, therefore:
1. To slow the circulation through the lungs.
2. To cause a marked rise of pressure and stasis in the systemic veins.
3. When this occurs less blood enters the left ventricle than before. This would
naturally lead to a fall in blood-pressure; but, just as in mitral stenosis, it is compensated
Fio. 224. — Diagram of the circulation in pulmonary
insufficiency. I. Normal. II. Moderate grade of pul-
monic insufficiency.
392
DISEASES OF THE HEART AND AORTA.
by constriction of the peripheral vessels and the blood-pressure maintained. The vaso-
constriction, however, manifests itself in the smallness of the arteries and of the pulse, which
thus presents a striking contrast to the pulse of aortic insufficiency. The pulse-pressure
also is never increased, as is the rule in the latter condition.
SYMPTOMS.
The symptoms and complications are chiefly respiratory in origin:
dyspnoea, especially in intense paroxysms which are brought
about by slight exertion; cough and bronchitis, resulting from the poor
circulation through the lungs. The intense pulsation of the pulmonary
vessels weakens their walls and predisposes to haemoptysis and the
expectoration of blood-tinged sputum. Phthisis is a common complication.
Palpitation is sometimes noted.
Anginoid attacks and pressure
at the base of the sternum are
frequently met with; also pain,
which, in contrast to that aris-
ing in aortic insufficiency, is
more commonly referred to the
right shoulder and down the
right arm.
Sudden death is rela-
tively common, sometimes re-
sulting from over-distention of
the right ventricle, sometimes
from embolism
nary artery.
in the pulmo-
FIG. 225. — Distribution of the murmur in pulmo-
nary insufficiency. The parallel shading indicates the
area over which the murmur is heard. The dot indicates
the point at which it is loudest; the diagram at the right
indicates its position in the cardiac cycle. The diagrams
over the shaded area represent the pulsations, i. e. the
systolic impulse over the pulmonary area and the systolic
retraction over the right ventricle.
PHYSICAL SIGNS.
Cyanosis, as a result of
the slowed circulation in the
lungs, is one of the earliest signs.
It is usually very marked and
is liable to occur in paroxysms. Signs of bronchitis or often of
bronchopneumonia are found in the chest.
Examination of the heart shows, as a rule, some precordial bulging,
with well-marked pulsation of the conus arteriosus in the second
left interspace, and a systolic retraction in the third, fourth, and fifth left
interspaces and epigastrium, due to the vigorous beating of the right ven-
tricle. The area of cardiac dulness is increased to the right in the trans-
verse diameter, owing to dilatation of the right auricle. Very often it
extends upwards in the second left interspace as well (dilated conus arterio-
sus), where it extends 5-6 cm. to the left of the midline. The area of
cardiac flatness is increased to both left and right, and forms a scalene
triangle extending to the right border of the sternum. On palpation the
vigorous beating of the conus arteriosus may be felt in the second left
interspace^ also a diastolic or systolic and diastolic thrill in this region and
over the right ventricle. On auscultation the sounds at the apex may be
clear. The characteristic feature is the presence of a very superficial dias-
PULMONARY INSUFFICIENCY. 393
tolic murmur maximal over the pulmonary area, varying from short and
soft to loud, rough and hissing in character and not infrequently musical.
It is also heard along the left sternal margin, but less distinctly over the
aorta. The difference is accentuated on coughing. Owing to the presence
of other lesions in the pulmonary artery, there may also be a loud systolic
murmur at the base, while over the base of the sternum a systolic mur-
mur, due to the secondary tricuspid insufficiency, may also be present.
The pulse, in contrast to aortic insufficiency, with which this con-
dition may be confounded, is small and weak; the blood-pressure is prob-
ably but little affected. Marked systolic pulsation of the veins and liver
(positive venous pulse) is frequently present, due to the secondary tricus-
pid insufficiency. In the extremities oedema sets in readily, and there is
often clubbing of the fingers and toes even in cases which are not
congenital.
The following notes are taken from the records of the medical service of the Johns
Hopkins Hospital:
CASE OF PULMONARY INSUFFICIENCY.
R. R., a colored laborer, aged 48, was admitted on Feb. 8, 1900, complaining of
pain in the stomach and chest.
He had measles and whooping-cough as a child, several attacks of tertian malaria,
syphilis in 1897, rheumatism in 1899, and several attacks of gonorrhoea.
He uses alcohol and tobacco in moderation.
Present illness began two years ago, coincident with the onset of u r e t h r a 1
discharge and an attack of rheumatism (gonorrhoeal ?). This caused him to
stop work. Since then the rheumatism has become better, but he has been troubled with
shortness of breath and palpitation, though these are not very severe.
Note by Dr. Henry Harris states that the patient is a well-nourished man, not dys-
pnoeic nor cyanotic. Lungs clear except for a few moist rales over the upper fronts.
The note on the heart by Dr. Osier on Feb. 10, 1900, is as follows: "Chief
impulse is in the fourth left interspace just at the nipple, also a little
impulse above. The impulse in the second left interspace extends 5-6
cm. outside of the left sternal border. No impulse in the aortic area; no
dilated veins; no visible pulsation of the arteries. On palpation there is no
thrill. There is not a very large area of cardiac dulness. The pulse is easily com-
pressed and not collapsing. In the fifth interspace, at the apex, and over
the aortic area the sounds are practically normal. In the fourth left
interspace and at the nipple itself both sounds are loud. There is a short, distant, slightly
rumbling murmur before the first sound, becoming distinct on moving towards
the sternum.
" At the third interspace 5 cm. from the left sternal border a short,
loud diastolic murmur is heard, much louder as the left sternal border is
approached, maximal at the, left sternal border. There is also a roughness of
the first sound. The diastolic murmur disappears in the sternum, being very
circumscribed. At the second left interspace 5 cm. from the left
sternal border the diastolic is louder. At the left sternal border it has
a maximal intensity. There is a short systolic, and a loud somewhat booming dia-
stolic, with a rough somewhat vibratory quality. In the first interspace the murmur
diminishes, being just feebly heard. In the second interspace the murmur practically
abolishes the second sound, which is clearly heard at the aortic area.
" No thrill after walking about. No evidence of congenital heart
disease .
"The condition is most likely pulmonary insufficiency.
There is a possibility of aneurism, but firm pressure with the stethoscope
far out in the second left interspace gives no sense of lifting and no diastolic
shock. There is no tracheal tugging and no diastolic shock."
394 DISEASES OF THE HEART AND AORTA.
DIAGNOSIS.
The diagnosis of pulmonary insufficiency is rarely made during life.
The history of very severe endocarditis or evidence of affection of several
valves or of a lesion dating from birth leads to the suspicion of right-sided
valvular disease. It is always difficult to exclude aortic insufficiency or
the presence of the two lesions at once. The small size of the pulse,
the absence of visible pulsation of the large arteries, the small pulse-pres-
sure, the marked pulsation of the conus arteriosus (both against the chest
wall and as shown by the fluoroscope) , the retraction of the interspaces
over the right ventricle, the increase in the horizontal diameter of dulness
to the right and not to the left, and especially the dulness in the second
left interspace furnish the basis for the diagnosis. This is also confirmed
when there is pain down the right arm instead of the left. On the other
hand, the congenital heart lesions — open ductus Botalli, open septum
auriculorum or ventriculorum, etc. — are very difficult to exclude, and will
be dealt with in connection with congenital heart diseases.
The diagnosis of functional pulmonary insufficiency is based upon the
presence of a transitory diastolic murmur along the left sternal border
during periods of pulmonary stasis, in the absence of other signs of aortic
insufficiency. No doubt this diagnosis may sometimes be made correctly
especially in cases of mitral stenosis, but it is one of which even Gibson
cannot feel certain in any individual case.
TREATMENT.
Treatment is the usual procedure for cardiac overstrain of any sort, —
rest, light diet, purgation, and digitalis. Venesection, by relieving the
distention of the right auricle and ventricle, is particularly useful, and, as
stated by Alexander Morison, yields remarkably good results in this
condition.
The main hope, however, lies in bringing about the hypertrophy
of the right ventricle and in preserving the balance between the strength
of the right ventricle and the strain put upon it. Symptomatic treatment
of the bronchitis and pulmonary complications may do much to relieve
the patient.
THE PROGNOSIS is bad when pulmonary stenosis is present, but in the
presence of a pure insufficiency depends greatly upon the condition of the
right ventricles and the amount of cardiac embarrassment caused by the
lesion. As seen from Barie's cases, patients may reach the age of
seventy-five in spite of the lesion. These cases are, however, rare.
BIBLIOGRAPHY.
PULMONARY INSUFFICIENCY.
Chevers, N.: A Collection of Facts illustrating the Morbid Conditions of the Pulmonary
Artery, Lond. M. Gaz., 1846.
Frerichs: Insufficient valvularum arteriae pulmonae, Wien. med. Wchnschr., 1853, iii,
817 and 833.
PULMONARY INSUFFICIENCY. 395
Benedikt, J.: Ein Fall von insufficientia valvularum semilunararum arteriae pulmonae,
ibid., 1854, iv, 547.
Walshe: A Practical Treatise on Diseases of the Lungs, Heart, and Aorta, Lond., 1854.
Barie", E.: Recherches sur 1'insuffisance des valvules de 1'artere pulmonaire, Arch, de m6d.
ge"n., Paris, 1891, i (vol. xxvii), 650, and 1891, ii (vol. xxviii), 30 and 183.
Gibson, G. A.: Jugular Reflux and Tricuspid Regurgitation, Edinb. M. J., 1880, xxv, 978.
Preble, R. B.: Relative Insufficiency of the Pulmonary Valves, J. Am. M. Asso., Chicago,
1897, xxviii, 1012.
Aforison, A.: On Dextral Valvular Disease of the Heart, Edinb. M. J., 1880, xxv, 102, 439,
515, 619. 748.
VII.
TRICUSPID INSUFFICIENCY.
ORGANIC AND FUNCTIONAL TRICUSPID INSUFFICIENCY.
Insufficiency of the tricuspid valve occupies a unique position among
the valvular lesions. In the functional form, due to dilatation of the right
ventricle, it is extremely common, and indeed probably occurs at some
stage in every dying or failing heart. In the organic form, on the other
hand, it is rare, occurring only 16 times in 1781 cases of valvular disease at
the Johns Hopkins Hospital (0.85 per cent.) and in less than 0.7 per cent,
of Gillespie's cases at Edinburgh.
The organic forms occur more frequently in severe or malignant endo-
carditis, as is indicated by the fact that in none of the Johns Hopkins
cases was it the only valve affected, mitral stenosis being present in 10,
aortic insufficiency in 7 of the cases. Three valves, the aortic, mitral, and
tricuspid, were involved in 7 of these cases, the pulmonary orifice once.
Although severe rheumatic fever is perhaps the most frequent cause,
streptococcus and gonococcus infections are relatively common etiological
factors (see Chapter I), more so than in the milder valvular affections.
Occasionally it occurs as a congenital 'lesion, the result of endocarditis
during fetal life.
Anatomically the lesions of the tricuspid valve exactly resemble those
of the mitral, with which they are so frequently associated, being due to
vegetations, thickenings, ulcerations, hemorrhages, and occasionally tumors
or malformations upon the valves.
Functional Tricuspid Insufficiency. — Our knowledge of functional tri-
cuspid insufficiency dates from the remarkable anatomical and physiolog-
ical studies of T. W. King in 1837.
King stated that " the right ventricle is liable to dilatation and that the dilatation
deranges its valves.
" The last proposition is thus explained. The cavity is formed by the solid septum
of the heart for its inner wall, and by a thinner, more extensive and yielding layer of muscle
for its outer or right wall; whilst each of these walls affords points of attachment to the
cords of the valves. ... In the progress of post-mortem examinations, I have found in
hearts thus dilated, or only greatly distended by the final congestion, that upon injecting
the ventricle by the pulmonary artery the tricuspid curtains when stretched out were under
all circumstances a great deal too small to close the opening, .... and it appears from
careful examination that the united areas of these valvular portions are scarcely more than
equal to the mean extent of the oval opening I have shown that upon injecting
fluids into the ventricles by their respective arteries (the semilunar valves destroyed) the
left or bicuspid valve (human heart) was always seen to close completely and firmly, the
curtains being so extensive as to fold together in the form of a cone or wedge within the
ventricle, whijst the tricuspid valve was constantly found in its ordinary state incapable
of preventing a considerable reflux. With every attempt to induce an accurate closure
of this valve, its scanty and divided curtains united imperfectly or
scarcely met, and were only sufficient at the best to form a plane
396
TRICUSPID INSUFFICIENCY. 397
equal to the area of the opening No position in or out
of water, no degree of gentleness or force, no state in anywise
natural to the organ that I was able to induce, would prevent
a considerable riband-like stream of regurgitation between the
ill-apposed edges of the valve...
The only possible means of obtaining a nice,
though weak, adjustment of the tricuspid
curtains was to compress the ventricle, and
by the same means to lessen the extent of
the valvular aperture. ... I have twice
had an opportunity of experimenting on the
human heart at the earliest period that
propriety could admit of. In one of the
cases (of which I have not hitherto spoken),
after performing the experiment and eliciting
results similar to those related, the heart
was set aside, with the expectation that its
tonicity would gradually contract the
ventricles and fleshy pillars, which accord-
ingly occurred. The first trial of this heart FIG. 220.— The outline of a normal heart super-
was made with warm water, and the fluid S^X1*flSS&t£rt£
was thrown in at first gently, and after- shown in light shading, dilated heart shown in
wards pretty forcibly; but the regurgitation black, the diameter of the orifices in white and
at this time was always considerable. Now black bars' resPectively.
upon repeating this experiment oh the same
heart when contracted after the lapse of a few hours, the tricuspid valve was still found
to be much less incomplete; still in this case there was some refluent stream. In the
second case, however, under precisely similar circumstances, I obtained at least an
almost perfect valvular action."
King also confirmed these observations by extended experiments
upon the hearts of a great variety of mammals and birds during life as well
as after death. His experiments were repeated and substantiated by G. A.
Gibson in 1880, who showed that merely narrowing the orifices by
constricting them with a cord was sufficient to prevent the reflux. Fran-
cois-Franck in 1882 was able to demonstrate the production of tricuspid
insufficiency in the living animal under conditions which led to cardiac
dilatation, and to demonstrate its disappearance under digitalis. The
frequency with which such functional insufficiencies occur in heart failure
during life was shown by Friedreich, Mahot, Riegel, Mackenzie, Hirsch-
felder, and a host of other writers. In hearts which have been dilated
for a long period there is a considerable stretching of the valvular orifice,
as was already noted by King. This has lately been very clearly shown
by Keith's figures of the hearts of Mackenzie's patients, in which the
stretching was so great that the usual narrowing at the auriculoventricular
opening had completely disappeared (Fig. 226).
PATHOLOGICAL PHYSIOLOGY.
As Rosenbach has shown, the production of tricuspid insufficiency
has in itself little effect upon the systemic circulation. Blood-pressure
in the arteries remains unchanged, and there is no characteristic change
in the pulse. In the pulmonary circulation there may be a slight fall of
pressure as a result of the regurgitation. On the other hand, this may be
compensated by a slight increase in the systolic output of the right ventricle
and no change may occur.
398
DISEASES OF THE HEART AND AORTA.
The principal effect of tricuspid re gurgitation is
exerted upon the circulation in the systemic veins.
The blood thrown back into them at each systole causes the pressure to
rise, so that in such cases the pressure may reach as high as 26 cm. H2O
(20 mm. Hg) (Hooker and Eyster). The stasis thus occurring also affects
the peripheral circulation of the limbs and body, giving rise to oedema and
ascites; stasis in the kidneys causing diminished excretion of a concen-
trated urine rich in albumen and casts, also stasis in the medulla oblongata
where the accumulation of CO2 causes a general reflex vasoconstriction.
The secondary effect of this vasoconstriction is rise of general blood-pres-
sure, further increase of the work of the heart, and increased heart failure —
the vicious circle of asphyxia (see page 27).
NORMAL
TRICUSPID
INSUFFICIENCY
FIG. 227. — Diagram showing the changes in the circulation in tricuspid insufficiency. The arrows
show the rise in pressure in the right auricle (RA ) and vena cava, and the fall of pressure in the pulmonary
artery (PA). The white curves represent the pulse-waves, that above RA showing the ventricular type
of the venous pulse.
Venous Pulse in Tricuspid Insufficiency. — In contrast to the normal
(negative, presystolic, diastolic, "double") venous pulse, the typical pulsa-
tion in tricuspid insufficiency is synchronous with and of the same frequency
as ventricular systole (single venous pulse) (Friedreich, Riegel, Mackenzie,
Hirschf elder) . Since there is a free communication between auricle and
ventricle, the jugular pulse-wave (Fig. 228) closely resem-
bles the curve of intraventricular pressure, with its
up-stroke and plateau during systole and its fall during diastole. In the
advanced stages the wave (a) due to auricular systole is absent, since the
auricles are paralyzed (Mackenzie).
Mackenzie states, however, that, contrary to preconceived notions,
all cases with tricuspid insufficiency do not necessarily show a positive
venous pulse, and in a number of his cases which at autopsy showed both
organic and functional insufficiencies the positive venous pulse was absent.
Mackenzie finds in these cases that the up-stroke of the wave (v), which is
due to stagnation in the ventricle, begins earlier than usual. As the lesion
increases, this wave (reflux) begins sooner and sooner after the beginning
of systole, until finally it takes up the entire systolic period, and the posi-
TRICUSPID INSUFFICIENCY.
399
JUG.
BRACK.
live or ventricular type is assumed. These observations have been con-
firmed in man by Gibson and Sewall, and in animals with tricuspid lesions
by J. Rihl, who found that as long as the regurgitation was slight the
auricular type of venous pulse persisted, but when it became severe this
gave way to the ventricular type. As Sewall states, " among patients pre-
senting themselves for examination on account of a wide range of func-
tional disorders, I have been
struck with the uniformity
with which evidences of cardiac
insufficiency could be distin-
guished, based upon the nature
of the symptoms and the char-
acter of the venous pulse . . .
The v wave has a double crest;
or rather, the wave v, which
begins just at the moment of
closure of the aortic valves, as
determined by the dicrotic
notch in the lower tracing, is
immediately preceded by a wave ^^SS^S^SSS^SS^S^S^Si i SEC.
which is completed during the
last moments of ventricular
outflow." He believes that
this last-mentioned wave (the
t wave of Bard) is produced by
a slight regurgitation due to
weakness of the papillary mus-
cles, and is indicative of such
regurgitation, but he does not take into account the fact that it may
be present without any other signs of tricuspid insufficiency. On the other
hand, as shown by Theopold, Hewlett, and others (page 75), the positive
venous pulse may be present without any regurgitation at the tricuspid.
FIG. 228. — Venous pulse of patients with tricuspid
insufficiency (positive venous pulse). JUG., pulsation
over the jugular vein; BRACH., pulse in the brachial
artery; c, moment of onset of the pulse-wave in the
carotid artery. The tracing shows an elevation through-
out systole, with a very slight depression (perhaps due to
fling) immediately following the upstroke. The curve
corresponds almost exactly to the curve of pressure in
the right ventricle.
J u VJD
x_y
Fio. 229.— Venous pulse of another patient. VJD, right jugular pulse; ACS, left carotid artery.
The slow slanting upstroke indicates a slightly less smaller leak than in the preceding case. There is no
fling, and hence no midsystolic depression.
SYMPTOMS.
The condition of patients with tricuspid insufficiency well illustrates
the fact that this is one lesion which is not often compensated, though com-
pensation can take place through increased suction-pump action of the
right ventricle. They are usually markedly dyspnceic or orthopnceic, weak
and readily exhausted by the slightest effort, often drowsy and somnolent.
400 DISEASES OF THE HEART AND AORTA.
Palpitation may be extreme. One of the early symptoms is pain in the
region of the liver, from the stretching of the capsule. This is often accom-
panied by slight jaundice; and the appearance of an icteroid hue is one of
the unfavorable signs in tricuspid insufficiency, since it marks an intense
hepatic stasis. Gastric disturbances, loss of appetite, and indigestion are
the rule and vomiting is frequent.
PHYSICAL EXAMINATION.
The patients are usually quite pale and deeply cyanotic. When
secondary renal changes have set in, the face may be puffy. Emaciation
and slight jaundice, the result of catarrhal cholangitis from stasis in the
portal system, are among the most suggestive signs that tell the onset of
tricuspid insufficiency. The veins are full and show well-marked pulsation,
systolic in time and synchronous with the carotid pulse. There is often
oedema of the extremities, genitalia, and back, and large ecchymoses are
not uncommon. Ascites and right-sided hydrothorax are seen in the last
stages of almost every case. Examination of the eye-grounds usually shows
distention of the retinal veins (Black). The urine is usually scant and
concentrated, and contains a large amount of albumen and casts in large
numbers.
Heart. — The precordium often bulges, and the very vigorous beating
of the hypertrophied right ventricle is seen in the retraction of the inter-
spaces between the parasternal line and sternal margin. In the epigastrium
and over the liver a systol.c pulsation is seen and felt. Percussion
shows a marked extension of the cardiac dulness to the right of the sternum,
due to dilatation of the right ventricle. It often reaches 5-6 cm. from the
midline, but the cardiohepatic angle remains acute. There may be or may
not be extension of dulness to the left mammillary line, dependent upon
the presence of weakness of the left ventricle. The characteristic modifi-
cation of the heart sounds is the presence of a systolic murmur
which is over and near the lower third of the sternum, but may also be
heard over the greater part of the heart, over the ensiform cartilage, and in
the epigastrium. It is loudest in the fourth and fifth right interspaces,
between the parasternal and the midline. Occasionally, as in Case J. D., this
murmur cannot be heard when the patient is lying on his back or even
standing, but can be elicited by causing him to bend forward to an angle
of 45°. This does not increase the accidental murmur which is often heard
over the entire right ventricle, nor does it augment cardiopulmonary mur-
murs over this area.
The murmur is often accompanied by a systolic thrill over the lower
sternum and neighboring portions of the chest wall. The distribution to
the right of and behind the sternum corresponds to the wall of the right
auricle, the chamber into which the regurgitant stream is conducted (see
Figs. 230 and 231). The area to the left of the sternum over which the
murmur is loudly heard corresponds to the wall of the right ventricle. As
in mitral insufficiency, it is difficult to explain the loud transmission of this
murmur in*a direction opposite to that of the leakage, but it seems possible
that the vibrations of the valve may be communicated to the ventricular
wall along the tense chordaB tendinea? The murmur is rarely transmitted
TRICUSPID INSUFFICIENCY.
401
FIG. 230. — Distribution of the murmur and cardiac
outline in tricuspid insufficiency. The shaded area indi-
cates the region over which the systolic murmur is heard,
the diagram at the left indicates its relation to the cardiac
cycle. The heart is seen to be enlarged to the right. The
systolic pulsation of the liver is indicated by the small
diagram and the arrows.
as far as the pulmonary area, though a systolic murmur of different origin
(accidental murmur) is often heard in the latter area in cases with tricuspid
insufficiency as well as in others. The tricuspid murmur is, as a rule, not
transmitted to the apex. Most frequently in dilated hearts there is also a
functional mitral insufficiency
coexisting, and it is this which
gives rise to a systolic murmur
at the apex and in the axilla, but
this is usually less superficial
than the tricuspid murmur and
it can usually be differentiated
from the latter. Moreover, there
is, between the two areas at
which each murmur has its
maximum, a zone, correspond-
ing to the interventricular sep-
tum, at which both murmurs
diminish in intensity.
As Hering and others have
shown, a systolic murmur is
not heard in all cases of tricus-
pid insufficiency, especially in
those in which the heart is too
weak to give rise to a loud
sound or in which the aperture
of leakage is too loud to produce one (large leaks) . Sometimes the murmur
has a musical character. Occasionally, as in Case W. H., in which the pres-
ence of tricuspid insufficiency was demonstrated conclusively by venous
and liver tracings during life and by autopsy, peculiar diastolic murmurs
are heard over the right ventricle,
especially along the left sternal mar-
gin. They are sometimes blowing and
sometimes rumbling (mid-diastolic in
character), and may perhaps be caused
by functional insufficiency of the pul-
monic valves due to the dilatation of
the right ventricle.
Organic murmurs are frequently
rough, while those due to functional
insufficiency are usually soft and blow-
ing, and sometimes barely audible.
Hering states, as the result of pro-
longed experimental investigation,
that functional insufficiency which gives rise to distinct murmurs is
usually of slight grade, but when the orifice is much dilated and the leak
is a large one no murmur is heard. This aphony of the valves corre-
sponds to the condition described on page 110.
Except for the accompanying murmur which often replaces the first
sound, the cardiac sounds are not greatly modified. The sounds at the
26
FIG. 231. — Cross section of the body, show-
ing the paths of propagation of the murmur of
tricuspid insufficiency.
402 DISEASES OF THE HEART AND AORTA.
base are very considerably dependent upon the pulmonary and aortic pres-
sures and on the degree of arteriosclerosis, and hence their relative loudness
varies considerably.
Pulse. — The radial pulse in tricuspid insufficiency is usually small and
weak and often irregular. The arrhythmia usually assumes the character
of permanent absolute irregularity (pulsus irregularis perpetuus) (see page
75) and is accompanied by paralysis of the auricles.
BIood=pressure. — The blood-pressure is usually normal or a little below
normal; but there are no characteristic features, and secondary rises of
blood-pressure from medullary asphyxia are common.
The liver is usually enlarged and may extend far below the costal
margin or even below the umbilicus. It is usually hard and its edge smooth,
and often shows a distinct systolic pulsation (Fig. 232).
i ii
SYSTOLIC PULSATION SYSTOLIC RETRACTION
FIG. 232. — Tracings of liver pulsation. I. Systolic pulsation of the liver in tricuspid insufficiency.
LIV, tracing from the liver; BRACH, tracing from the brachial artery; b, pulse- wave in the brachial ar-
tery; c and d have their usual significance. The upstroke of the arrow indicates a protrusion, the downstroke
a retraction. II. Systolic retraction over the liver from a case of marked hypertrophy of the right heart.
CAR, tracing from the carotid artery.
A s c i t e s and oedema of varying grades may be but are not
always present, dependent upon the patient's condition. "Broken com-
pensation" does not always indicate "tricuspid insufficiency," nor vice
versa.
CASES OF TRICUSPID INSUFFICIENCY.
MYOCARDITIS WITH TRICUSPID INSUFFICIENCY AND PROBABLY ALSO PULMONARY
INSUFFICIENCY.
W. H., colored driver, aged 48, first admitted to the Johns Hopkins Hospital on May
12, 1896, complaining of swelling of the feet and shortness of breath. He
had always been healthy except for measles and chicken-pox in childhood and malaria in
1861. Gonorrhosa at 33 but no lues. Drinks and smokes in moderation.
Present illness began during the past winter, with gradually developing shortness
of breath, especially on exertion. After such attacks the extremities would swell very
much. A few days before admission his testicle also began to swell.
On examination by Dr. Thayer at this time he was found to be a well-formed colored
man, mucous membranes of good color. Lungs clear except for moist rales over the right
front. The apex was then in the sixth interspace at the mammillary
line. The first sound was feeble, but no murmurs were heard. The abdomen was full;
liver and spleen not palpable. Slight oedema of the extremities. The oedema dis-
appeared under rest and digitalis. The patient gained in strength and was discharged in
three weeks. He returned again three years later, with similar symptoms, and again
made a rapid recovery. On this admission the liver was felt by Dr. McCrae.
He was treated in the hospital repeatedly during the next few years, always presenting
TRICUSPID INSUFFICIENCY. 403
about the same clinical picture. On Dec. 9, 1903, the apex was 14.5 cm. to the
left of the midline, and Dr. Thayer noted that the sounds were clear in the tricuspid area.
There was, however, a soft diastolic and a rumbling presystolic murmur
heard over the heart between the left parasternal line and the sternal margin (pulmonary
insufficiency). When he first came under the writer's care in July, 1904, during a similar
attack of cardiac failure, this diastolic murmur, and indeed all the other murmurs,
had disappeared, the heart sounds were very feeble and the heart action
irregular. As his condition improved under treatment, the former murmur
reappeared and increased to about the
previous intensity, though heard only with the
larger beats. During the next admission a few
months later the rumble was definitely mid-dias-
tolic and very rough.
Blood-pressure during these admissions
ranged from 130 to 160 mm. Hg.
He was readmitted for the last time in
October, 1905, the sounds being about as before,
the oedema somewhat greater. There was severe
. « i v j ir *1G- 233- — Systolic pulsation of the liver
right-Sided hydrothorax. Venous of patient W. H. Car., carotid arterial
tracings showed a positive venous pulse of pulse; «, onset of ventricular systole.
the ventricular type, and there was
systolic pulsation of the liver (tricuspid insufficiency) (Fig. 233).
The blood-pressure during this admission was 110 mm., but rose to 130
mm. on the day before death.
Autopsy showed dilatation of the right auricle and ventricle,
dilatation of the pulmonary artery, marked sclerosis of the c o r -
"onary arteries, very marked chronic fibrous myocarditis (cardiosclerosis),
and relative tricuspid insufficiency. There was marked cardiac hyper-
trophy, the heart weighing 620 Gm. There were also chronic passive congestion of the
viscera, cirrhosis of the liver, chronic interstitial nephritis, chronic fibrous pleurisy, and
acute gastritis. There v.'ere no valvular lesions and there was no tricuspid steno-
sis to account for the middiastolic rumble. It is quite probable that there was during life
a functional pulmonary insufficiency.
CASE OF MITRAL AND TRICUSPID INSUFFICIENCY.
J. D., painter, aged 69, came to Johns Hopkins Dispensary complaining of swell-
i n g of the limbs. He has always been healthy except for inflammatory rheu-
matism off and on during the last twenty years. Denies venereal disease. Has not
worked during the past twenty years.
He has had swelling of the feet and legs after exertion during the past four years,
some shortness of breath, but can always sleep without a pillow. His legs
and penis have been swollen for the past month.
The patient is a well-nourished man, looking much younger than he acutally is.
His color is a trifle sallow but not icteroid. Pupils equal. No glandular enlargement.
No lead line on the gums, in spite of his occupation. The chest is clear on percussion
and auscultation except for a few wheezing rales at the bases.
The heart is markedly enlarged, d u 1 n e s s extending to the anterior ax-
il 1 ar y line in the fifth left interspace, above to the middle of the second left interspace
and 5 cm. to the right of the midline. At the apex the first sound if
replaced by a blowing systolic murmur heard distinctly throughout the entire
left axilla, this diminishes in intensity to the right of the mammillary line. When the
patient is standing and bending forward at an angle of 45°, a loud
blowing systolic murmur of different character is heard over the entire tri-
cuspid area, but this is not evident in any other position. In the pulmonic area
there is a loud blowing mesosystolic murmur, also heard in the second right interspace,
but not transmitted to the carotid arteries. The heart's action is somewhat irregular;
the jugular veins are distended but do not pulsate; the venous pressure, as shown
by Gaertner's method, is high. (The veins of the back of the hand and wrist
do not empty until the hand is about 20 cm. above the level of the heart.)
404 DISEASES OF THE HEART AND AORTA.
The liver is not palpable. There is little if any fluid in the abdominal cavity. The
scrotum and penis are markedly oedematous, as are also the legs and thighs.
The patient entered the hospital, where he died of heart failure a few days later.
DIAGNOSIS.
The absolute diagnosis of tricuspid insufficiency depends upon the
presence of a dilatation of the right auricle (increased dulness to the right) ,
a systolic murmur loudest at and about the base of the sternum, a positive
venous pulse of the ventricular type, and an enlarged liver with systolic
pulsation.
As has been seen above, these features are not always present. Hering has summed
up the whole question in the following conclusions:
1. A large tricuspid insufficiency may give no murmur, but small regurgitations
usually give distinct murmurs.
2. A small tricuspid regurgitation may cause no change in the venous pulse, but a
large leakage gives rise to a positive venous pulse of the ventricular type. Hence,
I. Loud murmur + auricular (presystolic, diastolic, double, physiological) venous
pulse = slight tricuspid regurgitation.
II. No murmur + positive ventricular venous pulse + systolic pulsation of liver =
severe tricuspid regurgitation,
TREATMENT.
Frangois-Franck showed, in his experiments upon functional tricuspid
insufficiency, that the administration of digitalis caused the signs of insuffi-
ciency to disappear. This is in perfect harmony with the clinical experience
that "broken compensation" (and tricuspid insufficiency) is in general
the signal for digitalis, and the administration of this drug furnishes the
main therapeutic measure. Absolute rest is necessary for prolonged periods;
but after the tricuspid insufficiency has persisted for months in spite of it,
it is useless to reduce the patient to a permanently bedridden condition
in the hope of final recovery. It is better to render his life as pleasant as
possible under the conditions, to let him sit up. and move quietly about the
house, go driving, or indulge in other pleasant diversions which do not
entail exercise, effort, or excitement. It must not be forgotten that worry
and nervousness bring on palpitation and cardiac overstrain almost as
readily as does exercise; and, conversely, mental diversion and cheerfulness
assist in re-establishing conditions favorable for cardiac recovery. The
important feature in this phase in the management of the case is the avoid-
ance of dyspnoea. The simple methods of counting between steps on a
staircase or of taking for one's gait one step for each inspiration may give
the patient considerable latitude for accomplishment without strain or
injury.
Diet should always be light, partly to avoid the strain on the heart,
partly on account of the disordered digestion, gastritis, and catarrhal
jaundice, which are entailed by portal stasis.
The bowels should be kept open with saline purgatives and several
movements a day should be secured.
In stages of acute heart failure when the venous pressure is high and
the right auricle much distended, venesection should be resorted
to promptly and continued until the right border of the heart has receded.
TRICUSPID INSUFFICIENCY. 405
The best results are obtained when venesection is accompanied by intra-
venous injection of strophanthin (£ mg.) (see page 177) and this followed
by free purgation and digitalis.
BIBLIOGRAPHY.
TRICUSPID INSUFFICIENCY.
Gillespie, A. L.: An Analysis of 2368 Cases admitted with Cardiac Lesions into the Royal
Infirmary, Edinburgh, Edinb. Hosp. Rep., 1897, v, 31.
King, T. W. : An Essay on the Safety-valve Function in the Right Ventricle of the Human
Heart, Guy's Hosp. Rep., Lond., 1837, ii, 104. Part II. On the Safety-valve Action
in the Mammalia, ibid., 142. Part III. Of the Safety-valve in Birds, ibid.
Gibson, G. A.: Jugular Reflux and Tricuspid Regurgitation, Edinb. M. J., 1880, xxv, 979.
Franc,ois-Franck : Sur la part importante qui revient a 1'etat du muscle cardiaque dans la
production des insuffisances tricuspidiennes transitoires, Compt.-rend. Soc. Biol.,
Paris, 1882, xxxiv, 88.
Friedreich, N.: Ueber den Venenpuls, Deutsch. Arch. f. klin. Med., Leipz., 1866, i, 241.
Mahot: Des battements du foie dans Tinsuffisance tricuspide, These, Paris, 1869.
Riegel, F.: Ueber den normalen und pathologischen Venenpuls, Deutsch. Arch. f. klin.
Med., 1882, xxxi, 26.
Mackenzie, J.: The Venous and Liver Pulses, and Arrhythmic Contractions of the Cardiac
Cavities, J. Path, and Bacteriol., Edinb. and Lond., 1894, ii, 84, 273. The Study of
the Pulse and Movements of the Heart, Lond., 1903. The Interpretation of Pulsa-
tions in the Jugular Veins, Am. J. M. Sci., Phila., 1907, cxxxiv, 12.
Hirschfelder, A. D.: Graphic Methods in the Study of Cardiac Diseases, ibid., 1906, cxxxii,
378. Inspection of the Jugular Vein; its Value and its Limitations in Functional
Diagnosis, J. Am. M. Asso., Chicago, 1907, xlviii, 1105.
Keith, A.: An Account of the Structures concerned in the Production of the Jugular Pulse,
J. Anat. and Physiol., Lond., 1907, xliii, 1.
Rosenbach, O.: Ueber artifizielle Herzklappenfehlern, Arch. f. exper. Path. u. Pharmakol.,
Leipz., 1878, ix, 1.
Hooker, D. R., and Eyster, J. A. E.: An Instrument for the Determination of Venous
Blood-pressure in Man, Bull. J. Hopkins Hosp., Balto., 1908, xix, 274.
Gibson, G. A.: Our Debt to Ireland in the Study of the Circulation, Reprint from the
Dublin J. M. Sci., 1907.
Rihl, J.: Ueber den Venenpuls nach experimenteller Lasion der Trikuspidalklappe, Ver-
handl. d. Kong. f. innere Med., Wiesbaden, 1907, xxiv.
Sewall, H.: Safeguards of the Heart-beat, Am. J. M. Sci., Phila., 1908, cxxxvi, 32.
Hering, H. E.: Ueber pulsus irregularis perpetuus, Deutsch. Arch. f. klin. Med., Leipz.,
1908, xciv, 185.
VIII.
TRICUSPID STENOSIS.
OCCURRENCE AND ETIOLOGY.
Stenosis of the tricuspid orifice belongs to the rarer valvular lesions,
and also to the group which rarely occurs alone. In the 24,000 cases which
have been admitted to the Medical Service of the Johns Hopkins Hospital
tricuspid stenosis has been found in only seven cases, in all of which other
lesions were present. W. W. Herrick has recently given the following
statistics from 187 cases collected from the literature:
SUMMARY OF REPORTED CASES.
Sex.
Male 38
Female 133
Sex not known 16
Age.
10 to 20 years 16
20 to 30 years 59
30 to 40 years 38
40 to 50 years 28
50 to 60 years 10
60 to 70 years 6
Not known . . 30
_187
Previous History.
Rheumatism 61
Doubtful rheumatism or chorea 11
No rheumatism 33
Not known . . 82
Association of Valvular Lesions.
Tricuspid alone 14
Tricuspid and mitral 102
Tricuspid and aortic 64
Tricuspid and aortic and pulmonary 1
Tricuspid and endocardium of left auricle 1
Tricuspid, mitral, and pulmonary 2
Total cases .184
Cases showing adherent pericardium 12
In Leudet's series rheumatism was an etiological factor in over 50 per
cent., puerperal fever in 5 per cent. Syphilis has also been assigned as a
causal factor.
406
TRICUSPID STENOSIS. 407
In the cases in which the tricuspid stenosis follows the mitral stenosis
the same etiological factors are concerned as for the single lesion. In view
of the work of Goodhart, Roy and Adami, and Weber and Deguy quoted
above (page 359) , it is not unlikely that the overstrain of the right ventricle,
brought about by the latter conditions, leads to oedema and hemorrhage
into the tricuspid valve, and that these processes usher in the fibrosis. In
other words, the mitral stenosis itself becomes an etiological factor in the
tricuspid lesion, and the pathological process completed in the mitral is
now transferred back one step in the circulation and repeats itself in the
tricuspid.
Occasionally, as in a case reported by Gairdner, a fibrinous ball, a
tumor, or a hemorrhage into the valve may assist in producing the stenosis.
A certain percentage of the cases are congenital in origin.
PATHOLOGICAL ANATOMY.
The anatomical changes in the valve are exactly similar to those
which occur upon the mitral in stenosis of that orifice : a progressive fibro-
sis accompanied by fusion of the cusps along their line of closure, and
gradual web-like extension of the valvular membrane, which grows down-
ward between the shrunken chordae tendinese forming an elongated funnel
with narrow outlet.
The liver is usually enlarged, though in some cases it may be smaller
than usual, owing to the cirrhotic changes and perihepatitis which result
from the prolonged stasis.
PATHOLOGICAL PHYSIOLOGY.
The changes which tricuspid stenosis produces are exactly similar
to those already seen in mitral stenosis, except that they affect the systemic
veins instead of the pulmonic. The filling of the right
ventricle is retarded. The amount of blood which enters it
passively in early diastole is diminished, and the amount driven in by the
auricle is increased. The auricle thus begins to hypertrophy.1 Its strength
increases, and the presystolic wave which it produces in the venous pulse
increases in size. In well-marked cases the force of auricular contraction
may be great enough to produce a definite presystolic pulsation in the
liver with a wave exactly similar to that found in the vein (Mackenzie).
When the tricuspid orifice is narrowed to such an extent that the
increased force of the auricle no longer empties the latter, the auricular
contraction begins to drive the blood back into the veins and to increase
the already high venous pressure, thus still further impeding the circula-
tion through the heart and lungs, so that the aeration of the blood is greatly
interfered with and marked cyanosis produced. This in turn gradually
predisposes to polycythaemia (red blood count 8,000,000 to 9,000,000).
The latter condition causes increased viscosity of the blood, and still
further increases the burden upon the heart. On the other hand, the
1 The right ventricle is almost always hypertrophied in tricuspid stenosis, owing to
the presence of mitral stenosis and tricuspid insufficiency.
408
DISEASES OF THE HEART AND AORTA.
NORMAL
TRICUSPID STENOSIS
hypertrophy of the right auricle gradually reaches its limit, and when
the venous pressure becomes too high from exercise or
other cause, this chamber becomes dilated and paralyzed, and the pre-
systolic wave disappears from the jugular and liver pulse (Mackenzie).
Unlike lesions of other valves, no further compensation is now
possible, and only rest of the heart can prevent the over-distention of
the veins. Consequently slight
overstrain results at once in
venous stasis, oedema, etc.,
which may pass off readily
when the patient is at rest.
The liver is often, though
not always, enlarged; and a
pulsation presystolic in time
may be felt in it as long as
the right auricle is beating
strongly (Mackenzie). (Edema,
ascites, and hydrothorax may
be present as in other cardiac
diseases.
The pulse is usually
small because the peripheral
arteries are constricted in or-
der to maintain the blood-
pressure, which may be per-
fectly normal. The rhythm
may continue regular or may become irregular as the disease advances.
Still more common are attacks of heart failure and dropsy.
In many cases, notably those of Shattuck and Mackenzie, such attacks
may recur at intervals during a decade or more. At first the condition
yields readily to rest and treatment, but later the attacks become more
and more frequent and persistent.
FIG. 234. — Diagram showing the changes in the circu-
lation in tricuspid stenosis. The arrows indicate the rise
in venous pressure in the right auricle (RA) and the vena
cava, and the fall in pressure in the pulmonary artery
(PA). The pressure in the left auricle and ventricle may
remain unchanged or may fall.
SYMPTOMS.
Fortunately for the patients, the course of tricuspid stenosis is usually
a chronic one, the development of the lesion generally lagging behind the
concomitant stenosis of the mitral or the other lesions that may be present.
As a consequence, the lesion may be present for a number of years without
manifesting any signs other than cyanosis, and no symptoms whatever.
Osier quotes a case reported by Hirtz and Lemaire who was known as
"I'homme bleu" for two years before he developed any symptoms. On
the other hand, in the case mentioned by Shattuck there was said to be " no
cyanosis."
There is nothing pathognomonic about the symptoms. Dyspnoea on
the slightest exertion sets in and becomes progressively worse. Pain
down either arm is relatively common, occasionally pain about the right
side and abdomen due to distention of the auricle or of the liver. Sudden
death is quite common.
TRICUSPID STENOSIS.
409
PHYSICAL SIGNS.
On inspection the extreme cyanosis is striking, and there may be dila-
tation and accentuated pulsation of the veins. When carefully timed this
pulsation is seen to be presystolic, and is often a "double" pulse of the
physiological type. Those characteristics are brought out more clearly
by a venous tracing. In long-standing cases the fingers may be clubbed.
The lungs usually show signs of bronchitis, oedema, or often of tuber-
culosis. Pulmonary infarction, with the presence of areas of consolidation
and the expectoration of dark red or "prune-juice" sputum, is relatively
common. In the physical exam-
ination of the heart the real
lesion is often overlooked. Ex-
cept for the systolic retraction
over the right ventricle, there
may be nothing abnormal on
inspection. The area of cardiac
dulness is increased to the right,
corresponding to the dilated
right auricle; occasionally also
to the left, as a result of con-
comitant lesions other than the
tricuspid stenosis.
Palpation sometimes re-
veals a presystolic thrill over
the lower part of the sternum
and just to the left of the latter,
but it is rarely as distinct in
the former situation as in the
latter (due to concomitant mitral stenosis). The shock accompanying the
first sound over the right ventricle may be tapping. The second pul-
monic shock is usually less marked than might be expected to result from
the lesions present.
The characteristic sign on auscultation is the pres-
ence of a short presystolic rumble, which is maximum over the
base of the sternum and different in character from the presystolic rumble
heard at the apex. There is also a snapping character to the first sound in
this area, and it may be accompanied by a tricuspid systolic murmur.
This murmur is, however, often absent, indistinct, or merges so gradually
into the mitral murmur that its existence is not noted. Except when other
lesions are present the second aortic and pulmonic sounds are not as loud
as might be expected.
DIAGNOSIS.
So indistinct are the murmurs due to the tricuspid lesion and so com-
pletely are they overshadowed by those of the mitral or other orifices that
the diagnosis before death was made in only six of Leudet's 114 cases. The
correct diagnosis has been almost equally Tare since then. It may be made
with certainty in the presence of marked cyanosis, dilatation of the right
FIG. 235. — Cardiac outline and distribution of the
presystolic rumble and snapping first sound in tricuspid
stenosis.
410 DISEASES OF THE HEART AND AORTA.
auricle (increase of dulness to the right), presystolic thrill and rumble, and
presystolic liver pulsation. But these signs disappear as the auricle begins
to weaken, and in very many cases the existence of the lesion is one that
can be suspected rather than proved.
CASE OF TRICUSPID STENOSIS.
The following notes are from one of the rare cases in which the diagnosis
was made during life. This diagnosis was made by Professor T. B. Futcher,
who has kindly permitted the writer to make use of the notes.
Mrs. A. J., aged 37, entered the private wards of the Johns Hopkins Hospital on
April 30, 1909. The family history was negative. She was not a blue baby;
has been healthy since childhood, but subject to occasional sore throat. She has never
had acute articular rheumatism. At the age of nineteen she had an obscure fever lasting
several weeks.
She has been somewhat short of breath for the past nineteen years, and since an
attack of grippe about twelve years ago has complained of palpitation on
exertion or after eating. "These symptoms became much more marked four years ago,
when oedema of the feet and ankles and cyanosis appeared for the first time.
This condition passed off under treatment, but returned again two years later, again pass-
ing off, only to return with increased severity eight weeks before admission. During this
attack she has been blue and has had severe orthopnoea.
Note by Dr. Futcher, May 1, 1909: "Patient is of short stature, a little overstout;
very marked cyanosis of ears, lips, cheeks, and finger-nails, although this is
nothing as compared with the day she reached Baltimore. There is a distinct jaun-
diced tint to the face and sclerotics. Propped up in bed; considerable dyspnoea. Tongue
moist, only a trifle coated; pupils normal size and equal, react to light and accommodation.
" Still impossible to count pulse at wrist, although very faint beats are occa-
sionally appreciable. Thorax well formed, expansion good and equal on both sides.
Lower left axillary region expands slightly less than right. Lungs: Right side clear
throughout front and axilla on percussion. There is an occasional crackling rale heard at
the base. Fairly numerous fine moist rales audible throughout whole back. Left lung
(in semi-recumbent posture) flatness reaches to level of fourth interspace in anterior axil-
lary line. In midaxillary line it reaches nearly to apex of axilla, and in posterior scapular
line to a point about 3 cm. above left scapula. Slight movable dulness in
front with change of position. On auscultation, breath sounds are harsh above and below
clavicle, as in compensatory breathing. Below level of flatness there is absence of vocal
fremitus and distant tubular breathing and distant nasal quality of the voice sound.
" Heart. — Point of maximal impulse seen and felt in fifth interspace 11 cm. to
the left of the midsternal line and just in the mammillary line. There is very slight pre-
cordial bulging, but practically no pulsation or heaving. Systolic shock distinctly tap-
ping at apex; no definite thrill. Relative cardiac dulness commences at the upper
border of the third rib, in fourth right interspace, extends 8.5 cm. from
midsternal line, and merges into the fluid flatness to left, but apparently dulness extends
considerably outside of midline. There is no apparent Rotch's sign to the right. The
absolute cardiac dulness begins at the upper border of the fourth rib at the left sternal
margin, extends to right sternal margin at level of fourth rib and to point of maximal
impulse in fifth left interspace. On auscultation, the first sound is very snap-
ping at apex. There is as yet no definite presystolic murmur, but there is a slight echo-
ing rumble in diastole. There is no systolic bruit at the apex. The second sound is
not audible here. In the fourth and fifth interspace at the left ster-
n a 1 border the snapping quality of the first sound is even more marked
than at the apex and the tapping systolic shock is very striking here.
The second sound is audible and there is definitely reduplicated. There is no
rumbling presystolic murmur here. In diastole, however, there is, on
very careful auscultation, a faint, soft, prolonged, blowing diastolic
murmur. At the aortic area yesterday there was a faint systolic thrill.
It is just perceptible this morning. The first sound is audible and is accompanied
by a very rough systolic bruit transmitted upwards to stenoclavicu-
TRICUSPID STENOSIS. 411
lar articulation. The second aortic is quite loud and, if anything,
accentuated. There is no aortic diastolic bruit heard here. Pulmonic sounds clear,
second pulmonic accentuated. The external jugulars are only slightly distended.
''Liver. — Absolute flatness extends from sixth rib to a point apparently on a
level with the costal margin m right mammillary line. In median line it reaches only to
tip of ensiform. Owing to cedematc'is abdominal walls, it is not possible to palpate for
liver edge. No visible or palpable liver pulsation.
"Abdomen moderately distended, walls oedematous, tympanitic in elevated and flat
in dependent portions. Undoubtedly some ascites. There is very marked oedema of
dependent portions of trunk, moderate of arms and hands, very marked of thighs and legs.
"Over dorsal surfaces of both wrists there are quite numerous pin-head
sized petechiae."
The urine was very scant (300 c.c.), of orange color, specific gravity 1015, acid, con-
tains a trace of albumin and many hyaline and finely granular casts.
Her chest was aspirated by Dr. Henry on May 1, and 500 c.c. of dark straw-
colored clear fluid removed. She became worse, however, and her kidneys refused to act.
On May 3 her pulse became irregular, cyanosis increased, and the
petechial eruption on the dorsum of wrists became more extensive. She died at
3.15 P.M.
Intra vitam diagnosis by Dr. Futcher: Aortic stenosis and insuffi-
ciency, mitral stenosis, probable tricuspid stenosis.
Autopsy showed tricuspid, mitral, and aortic stenosis, dila-
tation and hypertrophy of the auricles, contraction and atrophy of the
ventricles, chronic passive congestion of all the tissues except the
lungs , generalized oedema, pleural and pericardial effusion, compression and atelectasis
and oedema of the lungs, hemorrhagic infarctions of lungs, acute diphtheritic hemorrhagic
colitis, generalized narrowing of arteries and thickening of veins.
TREATMENT.
Except for rest, purgation, and palliative treatment, little can be said
in this condition. Digitalis is sometimes of value to restore tone to the
auricle and increase the force of the ventricular contraction, but it very
frequently fails- In the spells of acute heart failure a free venesection
may ward off impending death by lowering the venous pressure, relieving
the heart failure; and by diminishing the viscosity of the blood may afford
more lasting relief. Free purgation is often also of great benefit, because it
may lower the pressure in the veins.
PROGNOSIS.
The prognosis depends entirely upon the degree of stenosis and the
rapidity of its progress. As has been said, this is frequently very chronic.
Mackenzie's famous case, which is typical, was a woman whose lesion
probably dated from an attack of rheumatism in 1880, at the age of twenty-
nine. In 1892 she complained of weakness and shortness of breath, and
at that time the liver showed a presystolic pulsation. She was subject to
numerous temporary attacks of extreme heart failure and died in 1899.
However, this woman was under excellent care during the last seven years
of her life, and lived a tolerably discreet and hygienic existence. Had she
been compelled to do heavy work her life would probably have been much
shorter.
412 DISEASES OF THE HEART AND AORTA.
BIBLIOGRAPHY.
TRICUSPID STENOSIS.
Herrick, W. W.: Tricuspid Stenosis, with Report of a Cure,1 Arch. Int. Med., Chicago,
1908, ii, 295.
Huchard, H.: Maladies au coeur, tome iii, Paris, 1905; based upon statistics of Leudet,
R. : Essai sur le retrecissement tricuspidien, Paris, 1888.
Herrick. J. B.: Tricuspid Stenosis, with Report of Three Cases with Autopsies, etc., Bost.
M. and S. J., 1897, cxxxvi, 245.
Goodhart, Roy and Adami, Weber and Deguy. See page 359.
Gairdner. Quoted from Herrick.
Mackenzie, J.: Notes on a Case Presenting some Novel Features in Cardiac Symptoma-
tology, Edinb. Hosp. Rep., 1897, v, 22. Studies on the Pulse and Movements of the
Heart, N. Y., Edinb., and Lond., 1902.
1 Probably intended to be, "with Report of a Case."
IX.
PREGNANCY AND LABOR IN CASES OF HEART DISEASE.
PULSE-RATE AND BLOOD-PRESSURE.
The effect of pregnancy upon the heart is influenced by several factors.
The gradual pushing of the diaphragm as the uterus grows causes the heart
to assume a more transverse position (raising the apex to the fourth inter-
space in 28 out of 35 cases observed by Stengel and Stanton) , and thus plac-
ing it in a position which embarrasses its action. Moreover, a reflex vagus
inhibition is often present, which causes the pulse-rate to become slowed.
Blot has reported a pulse-rate as low as 36; 40 per cent, of Vegas's cases
were slow, but only 26 per cent, of Skabo's cases were below 75 per minute.
There is also an increase in the width of the blood channel through the
uterine vessels, which is manifested by the presence of a dicrotic pulse.
In order to overcome these factors and to keep up the equilibrium of the
circulation, the heart is compelled to put forth increased efforts. Siemens
and Goldsborough in a most careful series of observations have found the
following figures, which accord well with the previous findings of O. Fellner,
Stengel and Stanton, and Vogeler.
They found the following figures : l
BLOOD-PRESSURES.
Pulse-
Cardiac
Work of heart.
Max.
Min.
Pulse-
pressure.
Mean pressure
(min.-t-i P. P.)
rate.
output
P.P. x P.R.
Mean pi . x pulse-
rate.
Normal .
110
65
45
80
72
3240
259,000
(Erlanger)
Pregnancy . . .
127
74
53
91.6
80.5
3325
49
(primig.)
Primig.
in primig.
5332
195,000 to 429,000
60
(multip.)
Multip.
in multip.
421,000to 1,065,000
Puerperium . .
115
72.5
42.5
86.5
70.5
3000
Primig.
290,000 to 327,000
Multip.
156,000 to 337,000
HYPERTROPHY.
This prolonged increase in work was supposed by Larcher to bring
about hypertrophy of the heart, a fact which has found some support in
the weighings of certain observers; but the more careful work of W. Miiller
and of later observers (average weight of heart during pregnancy 227 Gm.)
1 While this method of calculation is not intended to be regarded as quantitatively
accurate (see p. 24), it shows the qualitative changes fairly well.
413
414 DISEASES OF THE HEART AND AORTA.
fails to substantiate this view. The increase in size supposed to represent
hypertrophy is probably due in part to dilatation of the heart, and in part
to the apparent increase in cardiac area which occurs when the heart lies
in a more transverse position. However, a very slight hypertrophy, like
that of the athlete's heart, arising from the slightly increased work of
the heart during nine months, would not be surprising. During labor an
additional strain is thrown on the heart, but this is of comparatively short
duration.
FUNCTIONAL TRICUSPID INSUFFICIENCY AND OVERSTRAIN DURING LABOR.
James Mackenzie has shown, moreover, that the dilatation during
pregnancy affects the right heart particularly, and that in very many cases
even of otherwise normal women a definite insufficiency
of the tricuspid valve may appear, disappear, and reappear accord-
ing to the condition of the patient. The presence of this insufficiency
is shown by both the positive venous pulse and the systolic murmur in the
tricuspid area. The effects during the labor pains are exactly comparable
to those of heavy lifting, defecation, etc. (exercises of strain of maximal
intensity), and are accompanied by forced expiration with glottis closed
(Valsalva's experiment) as well as by very general muscular contractions.
Dr. Slemons informs the writer that during the labor pains there is often a
rise of fifty millimetres of mercury in the maximal pressure, though these
elevations are of short duration. It is therefore not surprising that some
hearts should fail and that pulmonary oedema should be an occasional com-
plication, especially in mitral stenosis where the pulmonary circulation is
already engorged. It is perhaps surprising, however, that so few cases actu-
ally succumb during the strains of labor. Schlayer's results typify the gen-
eral experience in this regard. He lost eight out of twenty -five cases (32 per
cent.) of severe heart disease, but only two of these (8 per cent.) died during
labor. From this, as well as from the work of Slemons and Goldsborough
and the metabolism experiments of Williams and Slemons, it would appear
that the act of labor itself does not impose a much more severe strain
upon the organism than that arising during the course of pregnancy.
CAUSE AND FREQUENCY OF DEATH FROM LABOR.
The immediate cause of death during labor is usually pulmonary
oedema from failure of the left ventricle. However, as above stated, only
about one-fourth of the fatal cases die during labor, the greater number
surviving some days, weeks, or months. In the cases of mitral stenosis,
apoplexy or cerebral embolism is not uncommon, owing to loosening of
thrombi which form in the left auricle during the periods of stasis.
As regards the results obtained by different writers in cases with heart
lesions the greatest divergence is found. The following represent the
mortality reported by various writers: Macdonald 61 per cent., v. Guerard
34 per cent., Lublinsky 60 per cent., v. Ley den 55 per cent., Schlayer 48
per cent., Wessner 49.3 per cent., Lwoff 12 per cent., Gusserow 6 per cent.,
Jess 31.5 per cent., Wiesenthal 12.5 per cent., Schneider 7.1 per cent.,
Miiller 3 per cent.
PREGNANCY AND LABOR IN HEART DISEASE. 415
A very careful study of these conditions has been made by O. Fellner
in Schauta's clinic in Vienna. Fellner noted that the percentage of heart
cases reported in obstetrical clinics was far too low for the general prev-
alence of cardiac disease, and upon careful routine examination found that
about six cases out of seven of compensated heart dis-
eases were actually escaping detection in the clinics.
So little effect had heart disease made upon the course of pregnancy
and labor! Of the cases that had been recognized in the obstetrical
clinic in ten years he found the following:
Cases.
Mother
died.
Child
died.
Mitral insufficiency,
Compensated . . . .
26
0
3
Uncompensated
14
1
2
Mitral stenosis,
Compensated . . . ....
Uncompensated . ...
4
0
3
Mitral stenosis plus insufficiency,
Compensated
10
0
2
Uncompensated . .
17
1
10
Aortic insufficiency,
Uncompensated
2
1
1
Aortic insufficiency plus mitral insufficiency,
Compensated . . .
3
0
1
Uncom pensated
5
0
4
Total
81
3
26
In the 900 cases occurring since his own routine examinations of the
heart were instituted, he found:
Cases.
Mother
died.
Child
died.
Mitral insufficiency,
Compensated . ....
14
0
4
Uncompensated .
1
0
0
Mitral stenosis plus insufficiency,
Compensated
3
o
1
Uncompensated .
1
1
0
Aortic insufficiency plus mitral insufficiency,
Compensated
1
0
0
FACTORS INFLUENCING PROGNOSIS.
These statistics from unselected cases are much more favorable than
the previous reports would indicate, and are in accordance with the con-
clusions of Hicks and French that few women with heart disease are sterile,
that they are not particularly liable to abort, and that most of them bear
416 DISEASES OF THE HEART AND AORTA.
children well. Blacker, in a most excellent resume of the subject, coin-
cides with these opinions, but finds 53 deaths (12 per cent.) in 453 cases of
heart disease taken from the literature.
Most writers believe that the variety in the results is due to the severity
of the cases which happen to be encountered, or at least recognized; but
the excellent statistics from Schauta's clinic would indicate that skill in
the management of the case plays a considerable role. It must not be
forgotten that the recognition of an organic valvular lesion in a pregnant
woman may be by no means easy, for the functional or accidental systolic
murmurs at the apex, occurring during pregnancy, may closely simulate
those from an organic mitral insufficiency; and, unless their disappearance
is noted by the end of the puerperium, this discrepancy may not be noted.
The constancy of the murmur, its roughness, its transmission to the axilla
and the increase rather than decrease in intensity at times when the condi-
tion of the heart improves favor the diagnosis of an organic mitral insuffi-
ciency; while in the presence of a soft murmur occurring with a dilated heart,
a rapid pulse, and a break in compensation the presumption is temporarily
in favor of the more common functional insufficiency. The diagnoses of
mitral stenosis and of aortic insufficiency are probably more uniformly
correct and present less difficulty.
Broken Compensation in Pregnancy. — On the other hand, it may be
difficult to judge when compensation should be considered broken. The
pushing up of the diaphragm by the pregnant uterus causes some short-
ness of breath; anemia is also a factor. The pressure upon the pelvic
veins may give rise to oedema of the feet and legs and even of the genitalia.
And, moreover, a relative tricuspid insufficiency of muscular origin may be
present as a result of the pregnancy without organic lesion, but may never-
theless give rise to the same signs and practical effects as the latter.
The diagnosis of broken compensation in pregnancy therefore depends
upon signs which are relative rather than absolute, since, as Mackenzie
shows, a certain degree of broken compensation is an almost normal phe-
nomenon in the later months of pregnancy. This again is relative, for
some women are almost as active throughout pregnancy as at other times,
while other quite normal women may be almost invalids throughout the
entire period. It is upon degree rather than upon actual symptoms that
the diagnosis of a pathologically broken compensation should be made.
Dyspnoea and cyanosis on very slight exertion, such as quietly walking a
distance of a few hundred yards or less, walking up a few stairs, etc., and
the presence of a small rapid pulse, persistent cough, enlargement of the
liver, and oedema of the feet and legs may be regarded as the most impor-
tant symptoms. The earlier in pregnancy they occur the more alarming
they are. Persistent dyspnoea or orthopncea and cyanosis alone, especially
in the presence of a valvular lesion, are in themselves most significant
and should warrant immediate attention.
MANAGEMENT OF CASES OF HEART LESIONS IN PREGNANCY.
The correct management of a case of heart lesion complicated by
pregnancy is, as stated by Blacker, to treat the heart disease
without regard to the pregnancy until the break in
PREGNANCY AND LABOR IN HEART DISEASE. 417
compensation is seen to persist, and then to termi-
nate the pregnancy. In other words, as long as compensation is
good the patient should merely be carefully watched but no medication
need be resorted to. At the first signs of cardiac weakening and dilatation
(dyspnoea and cyanosis, etc., on slight exertion) absolute rest should be
insisted on and digitalis or strophanthus should be given. This procedure
should be insisted on even if the diagnosis of organic valvular lesion is not
definite, for these procedures will afford quite as much relief in cases of
functional tricuspid insufficiency. Moreover, they should be repeated at
the slightest indication (see page 180), especially toward the end of pregnancy.
It is advisable in such cases to give a few prophylactic doses of digitalis
when labor seems imminent, or a few doses of strophanthus at the begin-
ning of labor pains, so as to have the tonus of the heart muscle at its opti-
mum by the time the strain of the second stage is imposed upon it. At
periods of acute dilatation, and especially when pulmonary oedema sets
in, venesection affords the greatest relief.
If cardiac symptoms disappear the patient may be gradually allowed
up and around, but she must be more careful than before, and if
signs of a second break in compensation occur, terminating the pregnancy
should be seriously considered. This is especially true in cases of mitral
stenosis, in which the cardiac accidents of pregnancy are particularly fre-
quent. Women with compensated mitral stenosis may pass through five,
six, or seven pregnancies without appearing to be injured by them (Len-
hartz), but when cardiac symptoms appear in a case of this disease during
the course of a pregnancy it is nearing the danger line, and if these persist
in spite of rest and treatment or when compensation is once broken, the
danger becomes great.
Fellner's low mortality (21 cases with 1 death) is probably due to the
careful practice of Schauta's clinic, which he summarizes in the advice to
"terminate pregnancy in cases of mitral stenosis as soon as the slightest
signs of broken compensation appear," or in cases in which signs of danger
had been present in previous pregnancies.
CASE OF MITRAL STENOSIS WITH PREGNANCY AND LABOR.
The danger of disregarding this advice was well illustrated by a patient under the
writer's care during the past year. She was a young married woman of twenty-six, and
was seen in November, 1907, in the sixth month of pregnancy, complaining of
shortness of breath and was quite c y a n o t i c . Her trouble dated from
the birth of her first child nine months before, at which time she had
evidently received a mild puerperal infection. The veins were rather full;
her heart was not enlarged, and at the apex the first sound was snapping
and preceded by a slight presystolic rumble. This varied in intensity from time
to time. Occasionally a blowing diastolic murmur was heard along the left
border of cardiac dulness, but not over the aortic area. The pulse was small
and weak, not collapsing, usually regular. There was slight oedema of the
shins and ankles. The patient was placed in the hospital, and her condition improved at
once, so that within two weeks she was allowed to enter the waiting ward of the obstet-
rical department. It was then proposed that lal>or should be induced, but the obstetrical
house staff did not regard the case as imperative. She left the hospital contrary to advice,
and on January 1, 1908, in the seventh month of pregnancy, she was delivered of a
healthy premature child. The labor was easy. She insisted upon giv-
ing the infant the breast for a couple of weeks, but remained in bed and quiet, suffering
27
418 DISEASES OF THE HEART AND AORTA.
from orthopnoea. This continued in spite of digitalis. Her liver was enlarged, and
oedema of the legs gradually set in. She finally returned to the hospital, but never recu-
perated, and died in June, 1908. The child, which had always been under the
care of a district nurse and later in the Thomas Wilson Hospital, also died dur-
ing the same month.
Termination of Pregnancy. — In an almost exactly similar case Hellendal
performed an abortion as soon as the signs of broken compensation were
definite, and eight days later resected both tubes to prevent subsequent
pregnancy. The patient made a perfect recovery and her life is no longer
endangered.
In deciding the question of terminating pregnancy, it must be borne
in mind that in from 25 to 40 per cent, of patients with
severe heart lesions the pregnancy does not reach
term, but premature labor occurs spontaneously owing to partial asphyxia
of the foetus. The placental circulation is slowed, the aeration is poor, and,
as Fellner has shown, there is often a large necrotic border about the pla-
centa. This probably results from thrombosis. Moreover, the statistics
of the obstetrical clinics, even of Schauta's, are far more favorable than the
end results would show. Our own case above mentioned would be classed
in such statistics as "improved" at the end of the puerperium and the
child as "living"; while, as a matter of fact, both died within six months
after the labor. Since most statistics are compiled from the histories of
hospitals, where the cases are subsequently lost sight of, it is probable that
this represents a very large class of cases. The children are especially deli-
cate, and, even if they survive, succumb more easily to pulmonary and gastro-
intestinal infections during the first or second year than do other children.
The inevitably high child mortality and the danger to the mother,
especially in mitral stenosis, somewhat lessen the moral responsibility of
terminating pregnancy. Moreover, as Weber and Deguy have shown,
pregnancy and labor are in themselves causal factors in valvular disease,
and especially mitral stenosis, through the occurrence of hemorrhages into
the substance of the valves (see Chapter III), or, as in the case of our
patient, bring about the recurrence of a slumbering endocarditis, and thus
leave the patient worse than before, often with a progressive lesion. When
it has been decided to terminate pregnancy, this should be done as soon as
possible. The procedure of choice depends upon the severity of the symp-
toms and the necessity for immediate emptying of the uterus. They have
been summed up by Fellner in the following scale: (1) Induction of
labor with de Ribes bag or packing the cervix; (2) craniotomy; (3) forceps;
(4) version and extraction; (5) Caesarean section. In general it must be
said that the less the operative interference with the physiological course
of each stage, the less shock to the patient and the better the end result.
On the other hand, each stage of labor is likely to be prolonged in such
cases and this must be avoided. When the condition is alarming, the
relief should be rapid. Pulmonary oedema is often at once relieved by
tapping the fetal membranes, removing the fimniotic fluid, and allowing
the diaphragm to descend; although the labor then becomes much harder.
The patients usually stand the operative interference well. As in other
conditions, ether is preferable to chloroform where the heart is diseased.
PREGNANCY AND LABOR IN HEART DISEASE. 419
AORTIC DISEASE IN PREGNANCY.
As aortic disease is comparatively rare in women, it usually receives
little mention. It is significant, however, that in Fellner's series there was
a very high mortality (60 per cent.) in the fcetus. Newell reports a case
in which there was little cardiac discomfort throughout pregnancy, but a
hard labor set in. Forceps were used. Collapse and pulmonary cedema
ensued, and the mother died four hours after labor. The child died also.
This is simply an example of the acute heart failure (probably acute dila-
tation of the left ventricle with sudden onset of functional mitral insuffi-
ciency) so characteristic of aortic insufficiency. Mitral lesions are usually
more dangerous than aortic, but they usually give signs of gradual progres-
sion. The danger in aortic insufficiency may, as in Newell's case, come on
very rapidly and result in the death of the patient.
SUBSEQUENT PRECAUTIONS.
In cases in which dangerous breaks in compensation occur during the
course of pregnancy and termination of the latter becomes necessary, as
well as in those which reach a natural termination under conditions in which
the life of the mother is endangered, measures must be taken to prevent
subsequent conception. As Feis points out, the physician's advice to a
married woman to absolutely avoid coitus is so rarely followed that for
practical purposes it is scarcely worth giving. To rely entirely upon it
therefore savors of hypocrisy. Feis believes that in these cases prophylactic
measures against conception should be advised. Fellner and Hellendal
go one step further. They both advise and practise sterilization of the
mother by resection of the tubes, an operation which is not fraught with
much danger, and which then relieves her from the sword of Damocles
that otherwise hangs over her head.
MATRIMONY AND HEART DISEASE.
The question also arises under what condition may women with heart
disease be permitted to marry. As Fellner's statistics show, the danger
is not very great. Blacker sums up the facts in the statement that all
women with heart lesions will suffer from them sooner or later, and that
this period need not be much accelerated by pregnancies. Some writers
even go so far as to state that pregnancies do not alter the duration of life
at all, but this view is much too optimistic. The best proof, however,
that the compensated heart lesion should not be a bar to matrimony is
shown by Fellner's statistical proof that six out of every seven heart lesions
are not even suspected in the average obstetrical clinic. On the other hand,
if compensation is poor, marriage, like any other strain, should of course
be forbidden. This again, as Fellner points out, depends as much on socio-
logical as on physical factors, for a woman in poor circumstances may be
able to live more quietly and avoid cardiac strain more readily in married
life than when supporting herself by her own work. Under such circum-
stances the patient should be made fully aware of the dangers of conception
and coitus. All things being considered, compensated mitral stenosis cannot
420 DISEASES OF THE HEART AND AORTA.
be made an exception to these rules, although its presence warrants a cer-
tain foreboding in the physician consulted, and should direct his advice
toward the side of caution. If compensation has once been broken in a
case of mitral stenosis, conception should be forbidden and marriage
strongly advised against. The same applies to well-marked chronic
myocarditis or nephritic cardiopathy when these can be
diagnosed with probability, since they run a more unfavorable course for
both mother and foatus than do the cases of valvular lesions.
BIBLIOGRAPHY.
Stengel, A., and Stanton: Heart and Circulation in Pregnancy and the Puerperium, Trans.
Asso. Am. Phys., Phila., 1904, xix, 520.
Vejas: Mittheilungen ueber den Puls und die vitale Lungencapacitat, etc., Samml. klin.
Vortr., Leipz., 1886, No. 269.
Szabo: Ueber die Bradykardie im Wochenbette, Frommel's Jahresb., 1901, 700.
Siemens, J. M., and Goldsborough, F. C.: The Obstetrical Significance of the Blood-
pressures and their Relation to the Work of the Heart, Johns Hopkins Hosp. Bull.,
Bait., 1908, xix, 194.
Fellner, O.: Herz und Schwangerschaft, Monatschr. f. Geburtsh. u. Gynakol., Berl., 1901,
xiv, 370.
Vogeler, W.: The Blood-pressure during Pregnancy and the Puerperium, Am. J. Obstetr.,
1907, Iv, 490.
Macdonald, A.: The Bearings of Chronic Diseases of the Heart upon Pregnancy, Parturi-
tion, and Childbed, Lond., 1878.
Leyden: Ueber die Complication der Schwangerschaft mit chronischer Herzkrankheit,
Ztschr. f. klin. Med., Berl., 1893, xxiii, 1.
Schlayer, Schneider, and Vinay. Quoted from Feis.
Miiller, W.: Die Massenverhaltnisse des menschlichen Herzens, Berl., 1878.
Mackenzie, J.: Pulsations in the Veins, with the Description of a Method for Graphically
Recording Them, J. Path. u. Bacteriol., Edinb. and Lond., 1893, i, 53.
Schlayer. Quoted from Fellner.
Hicks and French. Quoted from Blacker.
Blacker, G. F.: Heart Diseases in Relation to Pregnancy and Labor, Brit. M. J., Lond.,
1907, i, 1225.
Hellendal, H.: Herzfehler in der Schwangerschaft und operative Sterilisation, Med. Klinik,
Berl., 1907, 763.
Newell, F. S.: Valvular Diseases of the Heart Complicating Pregnancy, Surg., Gynecol.,
and Obstet., Chicago, 1907, iv, 610.
Weber and Deguy. See Part III, Chapter III.
Feis, O.: Ueber die Komplication von Schwangerschaft, Geburt, und Wochenbett mit
chronischem Herzfehler, Samml. klin. Vortr., Leipz., Gynakol. No. 78.
The articles by v. Rosthorn and by Lenhartz, H., Die Beziehungen der weiblichen Gesch-
lechtsorgane zu innere Erkrankungen, Verhandl. d. Kongr. f. inn. Med., Wiesb., 1908,
xxv, 29; Tuszkai, Uterus, Graviditat und Herz, ibid., 1908, xxv, 118, and the sub-
sequent discussion contain much valuable information.
X.
CONGENITAL HEART DISEASE.
DEVELOPMENT OF THE HEART.
In the human heart, as in all other complex anatomical structures,
there are many portions whose form and function are obscure and difficult
of comprehension when considered only in the light of conditions pres-
ent in the adult, but which become
quite clear when seen in the various
stages of their development. A
brief consideration of the embryol-
ogy of the heart will therefore greatly
simplify the study of the anatomy.
Moreover, it must be borne in mind
that occasionally some portion of
the adult heart fails to develop
beyond the embryonic stage, giving
rise to the signs and symptoms of
congenital heart disease; and there-
fore a knowledge of the embryologi-
cal development is necessary for pur-
FIG. 236. — Very early stage in the development of the human circulatory system. (Drawn from
a model of a human embryo 2.5 mm. long, about two weeks after fertilization. From Prof. F. P. Mall's
collection. The model was prepared by Mr.'W. E. Dandy.) The specimen shows the two aortee (AO) leading
the blood to the chorionic villi, and the two umbilical veins (UMB V) leading it back to the primitive
heart (//). The five branchial or aortic arches (.4.4) which connect the heart with the aorta are shown
also. A. Dorsal aspect. B. Lateral aspect of the head end of the same embryo.
poses of practical diagnosis and prognosis as well as for anatomical study.
The earliest stage of the circulatory system in the mammalian embryo
consists in the formation of a number of small blood-vessels and capillary
421
422
DISEASES OF THE HEART AND AORTA.
AA
plexuses, which arise from the mesoblast over the surface of the yolk-sac.
These soon unite to form a definite symmetrical vascular system.
Eternod has carefully described the earliest development of the circu-
latory system in a human embryo 1.2 mm. long, estimated at about eleven
days after fertilization. Another embryo of almost the same age (Fig. 236)
has recently been discovered by Dr. Mall and modelled by Mr. W. E. Dandy.
In this embryo the venous system is represented almost entirely by the
umbilical veins (Umb V), which carry the blood that has been aerated in the
placenta back to the heart. They follow the border between the embry-
onic area and the yolk-sac and pass forward to the
head end of the embryo. Here (H) the two veins
unite, and at the union there are given off a second
set of vessels consisting of a group of four upon
each side, the aortic arches (A A), which pass
backward more or less parallel to the midline
and soon reunite to form a single vessel on each
side, the primitive aortse (AO). These two
aortse carry the blood from the embryo proper
back on each side of the midline to the numer-
ous ramifications in the placenta, whence, as
we have seen, it is returned through the umbil-
ical veins. At this stage the heart is simply a
small dilatation of the venous tube, and the
FIG. 23?.— Human embryo 4 blood is propelled by the pulsations of the ves-
mm. long (about the fourth week •, ,1 i .-, . .. -, .•, rp,
after fertilization), showing the sels throughout their entire lengths. There is
further development of the heart scarcely a widening of the lumen to mark the
and of the branchial or aortic . i • i i Y «n j i
arches (A A). (Modified from site at which the heart will develop, — namely,
His ) The heart has assumed at the point Qf union of tne tWO Umbilical
an S shape, and is divided into ••i_i»ii
a truncus arteriosus (TR A), a veins just behind the place where the aortic arches
single ventricle (V), and a single
auricle (AUR). The inner en-
dothelial cardiac tube (shaded
MUS
are given off.
At a little later stage (Fig. 237) we find
the heart the form of an S-shaped tube just
On each side the jugular veins ventral to the pharynx of the embryo to which
(JUG) from the head unite with ., . ~ , 111 TI , , • *
the cardinal veins (CA RD) from it is fixed, and already two dilatations have
the trunk to form the duct of taken place in the lumen, forming the primitive
Cuvier (D CUV) which empties / . ' • i / , • \
into the sinus reuniens cs #). sacs of the ventricle (V) and the auricle (atrium)
(A). The point of union of the veins (sinus
reuniens, S R) has been pushed further backward. The umbilical veins
have received veins entering from the yolk-sac (vitelline veins) as well
as a branch (duct of Cuvier, D Cuv) from the body wall on each side.
The duct of Cuvier is in turn formed by the union of a branch to the
head (jugular vein, Jug) and a branch (cardinal vein, Card) extending
downward along each side of the body wall and giving off branches to
the muscle segments. The veins to the intestine arise from the vitelline
vein, while the umbilical or omphalomesaraic veins continue as before
to carry the blood back to the placenta and yolk-sac.
Anteridrly the arterial portion of the circulatory system may now be
observed to be composed of the truncus arteriosus (Tr A), a continuation
of the ventricle, and four aortic arches each now corresponding to a definite
CONGENITAL HEART DISEASE.
423
visceral (or gill) arch of the embryo (V A). These branches of the aorta
are of great importance, for from them the carotid, axillary, innominate,
and pulmonary vessels will develop.
As the embryo grows older (Fig.
240) the heart is still more S-shaped,
FIG. 238. — Heart of an embryo slightly older
than that shown in Fig. 237, showing the earliest
stages in the formation of two auricular and two
ventricular pouches. (Drawn from a His model.)
5.R.
FIG. 239. — A diagram showing the interior of
this heart; AO., aorta or truncus arteriosus; SEPT.
V., septum of the ventricles; OA V., auriculoventric-
ular orifice; CA., canalis auricularis, or auricular-
ventricular channel; AUR., auricles; S.R., sinus
reuniens, or common chamber into which the two
venae cavae empty, which corresponds to the sinus
venosus of the lower vertebrates.
FIG. 240. — Schema to show the development of the arterial system from out of the primitive aortic
arches. A. Schema of the circulatory system at about the same stage as Fig. 237. I-VI, aortic or bran-
chial arches (the fifth branchial arch described by Tandler arises from and anastomoses with the fourth,
which is the largest of the branchial arches). AO, AO, primitive aortse; PA, PA, rudimentary pulmonary
arteries; V, primitive common ventricle; RA, LA, auricular pouches. B. Schema of the adult arterial
system derived from the aortic arches. EXT CAR, external carotid artery (3d arch); INT CAR, in-
ternal carotid artery (connecting bars of first three arches); COM CAR, common carotid artery connect-
ing bar between third and fourth arches. A. The aorta is seen to be derived from the fourth branchial arch,
the pulmonary arteries arise along the course of the sixth. The ductus arteriosus (Botalli) represents the
distal end of the sixth branchial arch. The dotted lines indicate the outline of embryonic arteries which
have atrophied.
and at the junction of the two halves of the S a small crescentic infolding
of the muscular and endothelial wall has begun to protrude into the cavity
of the ventricle (interventricular septum, Sept. V.), while the ascending
limb of the lower half of the S represents a stenosis in the lumen, the canalis
auricularis (CA.), whose narrowest part forms a small slit, the ostium
auriculoventriculare (atrioventriculare) (OAV.).
424
DISEASES OF THE HEART AND AORTA.
The development of the interventricular septum continues rapidly
(Fig. 241), and also a similar ridge appears running longitudinally along
the truncus arteriosus, changing the lumen from circular to U-shaped,
each arm of the U being a channel leading to the corresponding half
of the ventricle.
The auricular (or atrial) cavity is now also widened into two symmet-
rical pouches, the right and left auricles, the cavity of which is continuous
with the junction of the veins.
SEPT V.
FIG. 241. — A. Heart of slightly older embryo viewed from the dorsal aspect, showing the separation
of the aortic and the pulmonary channels in the truncus arteriosus. (Drawn from a His model.) B.
Diagram of the auricular portion of the same heart. Lettering as in Fig. 239. VE, Eustachian valve,
separating the sinus from the auricular portion of the heart. The arrows indicate the course of the
blood -cur rents. C. Diagram of the ventricular portion of the same heart, showing the course of the cur-
rents through the separate channels of the truncus arteriosus.
The trunks of the veins have already undergone considerable changes,
such that the left duct of Cuvier is now atrophied, and most of the blood
from the head and upper limb returns to the heart through the right duct
of Cuvier, foreshadowing the superior vena cava, while the blood from the
placenta returns through the two omphalomesaraic (or omphalomesen-
teric) veins, which along with anastomoses from the body wall, intestinal
tract, and liver will form the inferior vena cava. The junction of the
two venae cavse forms the sinus reuniens which opens into the auricular
cavity. In the wall of the sinus reuniens at this stage there is a longi-
tudinal valve-like fold of endothelium (VE, Fig. 241, B), so arranged that
blood from the superior vena cava flows over it into the right auricle
(atrium), while the blood arriving from the placenta is directed under it
into the left auricle.
CONGENITAL HEART DISEASE.
425
\
FIG. 242. — Still later stage, showing com-
plete division of the truncus arteriosus into
pulmonary artery and aorta. (Drawn from a
Born model of a rabbit's embryo 10 mm.
long.) The arrows show the course of the
blood-stream. DA, ductus arteriosus.
Very shortly after this stage the most important changes take place
in the heart (Fig. 242). The two channels of the truncus" arteriosus are
now completely separated off from one
another, and exist as distinct vessels,
the aorta (^4.0) and the pulmonary ar-
tery (PA), connected with each other
at only one point through the ductus
arteriosus (DA). The interventricular
septum (septum ventriculorum, Sept V.,
Fig. 241, C) is now found to be almost
completely closed, and the originally
single auriculoventricular opening is
now divided into two portions (mitral
and tricuspid, Mil. and Trie.} separated
by the ingrowth of the septal ridge. In
the auricles also great changes have
occurred. The greater portion of the
sinus reuniens has been drawn into the
cavity of the auricle, and exists there as
a separate chamber, whose right margin
opening into the right auricle is formed by
the longitudinal valve (VE) (described
in connection with the previous stage of
development, now known as the valvula venosa dextra, or Eustachian
valve) . The left wall of the right auricle is formed by the septum auricu-
lorum, which has grown considerably,
partly through the gradual ingrowth
of the septal ridge and partly by the
pushing in of a mass of connective
tissue arising from the latter and from
the left wall of the sinus reuniens
and known as the- septum inter-
posit um. The left wall formed in
part by the wall of the vein is imper-
fect, and on the left the cavity extends
over to the auricular septum (sep-
tum atriorum). This septum has
also not completely closed, and the
reconstruction (Fig. 243) from a
model by Born at this stage shows a
double opening between the two auri-
cles. At a later stage (Fig. 245, B)
these openings have broken down
into one, the foramen ovale, and
it is the opinion of Born, in opposi-
tion to His, Sr., that the latter struc-
ture is of secondary formation and does not arise directly from the
primitive interauricular openings, although it performs the same function,
—namely, of allowing the blood to pass from the right into the left auricle.
FOR.OV
TRIC
FIG. 243. — Auricular end of the same heart.
The blood enters through the superior and inferior
vena cava (SUP.V.C., INF.V.C.) into the sinus
reuniens (SR), which is separated from the right
auricle (R.AUR.) by the Eustachian valve (VE),
which at this stage forms a large partition between
the two cavities. The foramen ovale (FOR.OV.)
connects the sinus reuniens with the right ventri-
cle; it is divided into two parts by a thin lamina
formed from the interauricular septum. TRIC,
tricuspid orifice: P.V., pulmonary veins.
426
DISEASES OF THE HEART AND AORTA.
In the later stages a valve-like flap of connective tissue projects over the
foramen, allowing the blood to flow only from right to left.
DEVELOPMENT OF THE PERICARDIUM.
The pericardial cavity develops as a part of the original body cavity
or coelom, from which it is separated at a later stage. In the earliest em-
bryos (Fig. 236) the pericardial cavity arises as a small space lined with
endothelium, surrounding the blood-vessels on each side of the embryo
(Fig. 244, A). These two spaces or cavities unite at the head end of
the embryo to form a single pericardial cavity which surrounds the
primitive heart. At a slightly later stage the heart and the pericardial
ANTER.
MEOIAST.
FIG. 244. — Development of the pericardial cavity. A. Earliest stage in the development of the
pericardial cavity. (After Robinson.) Embryo corresponding roughly to the stage shown in Fig. 236. E,
ectoderm; C, co3lom; En, entoderm; PB, primitive blood-vessel. The pericardial cavity is represented by
the part of the crelom present at this level. B. Later stage showing the division of coelom into pleural
and pericardial cavity. (Schematic.) The arrow points to the channel connecting the two cavities. C.
Relations of the pericardium in the adult. (Schematic). ANTER. MEDIAST., anterior mediastinum.
cavity lie upon the ventral aspect of the pharynx and the pericardial
and pleural cavities together form the anterior or cephalic portion of
the coelom.
At a later stage (Fig. 244, B) the heart has grown to fill almost all the
ventral portion of the coelom in its vicinity, and about its contour the
connective tissue of the body wall is closing in, as shown by the arrow,
beginning to divide the original coelomic cavity into a pleural and a
pericardial portion.
CONGENITAL HEART DISEASE. 427
In Fig. 244, C this closure has become complete, and we have,
represented in rough diagram, the conditions present in the adult chest.
The pericardial cavity is completely separated from the pleural cavity,
and is lined throughout by a single layer of flat endothelial cells,—
the portion growing directly upon the heart called the epicardium,
and the portion forming the opposite wall of the pericardial cavity, the
pericardium proper.
The pleural cavity has now grown more extensive than before, owing
to the growth of the lungs, which have pushed forward along the sides to
well in front of the heart and almost to the midline, leaving a narrow pleural
cavity between them and the chest wall. Like the pericardial cavity the
pleural cavity is lined with endothelium which extends partly over the
lung (visceral pleura) and partly along the thoracic wall (parietal pleura).
The anterior portion of the visceral pleura passes over the pericardium,
from which it is separated only by a very thin mass of connective tissue,
occasionally containing fat-cells. The three layers — pleural endothelium,
connective tissue, and pericardial endothelium — are so closely fused that
together they are generally designated as the pericardium, of which one
speaks of the pleural and pericardial surface. The pericardium does not
extend quite to the chest wall, while the pleura does so, and ventral to
the heart we find a small space filled by connective tissue and known as
the anterior mediastinum.
PHYSIOLOGY OF THE FETAL CIRCULATION.
The blood of the foetus is aerated in the placenta and passes back
through the umbilical veins and through the ductus venosus (D.V.) to
the inferior vena (V.C.I.), without passing through the liver. The sinus
reuniens has now become part of the main cavity of the auricle, and the
inferior vena cava (V.C.L) empties into the latter near the septum ventric-
ulorum. Over its mouth pass the remains of the Eustachian valve (val-
vula venosa dextra) which directs the blood not into the right auricle but
away from it across the right auricle to the limbus fossa? ovalis. According
to the views of Galen and Harvey, the blood from the superior vena cava
and that from the inferior are mixed in the right auricle before any of
the stream passes to the left auricle. Haller and Sabatier, however, believed
that no such mixing took place, but that all the blood from the inferior vena
cava (aerated blood) passed across to the left auricle, while the blood from
the superior vena cava passed down into the right ventricle. Pohlman
has recently given an excellent review of the subject. He has investigated
it experimentally on the fetal pig's heart by injecting starch granules into
the superior vena cava in some living fetal pigs and into the inferior vena
cava in others. The hearts were then removed, and the bloods in the two
ventricles and auricles were shown to contain the starch granules in equal
amounts, confirming the theory of Galen and Harvey. Pohlman introduced
capillary glass tubes into the two ventricles and demonstrated that the
pressures within them were equal. The blood from the left ventricle passes
at first to the innominate and carotid and subclavian arteries, below which
the aorta is joined by the ductus arteriosus Botalli. The blood from the
428
DISEASES OF THE HEART AND AORTA.
right ventricle passes into the main trunk of the pulmonary artery, from
which about one-fifth enters the rami passing to the lungs and about four-
fifths passes onward through the ductus arteriosus and enters the descend-
ing aorta. As the ductus arteriosus carries a little more blood than the
descending aorta, the volume of blood in the aorta is more than doubled
and the lumen considerably widened below its entry. The blood below this
point goes to the kidneys, the alimentary tract, the bladder, and the lower
limbs, and the rest goes on through the umbilical arteries (Umb. A.), to be
aerated in the placenta and returned as described above.
FORAMEN OVALE
EUSTACHIAN VALVE
FIG. 245. — A. The circulation in the foetus just before birth. Course of the blood to and from
the placenta. (Semi-schematic.) UMB A, UMB V, umbilical artery and umbilical vein; DV, ductus
venosus. B. The heart just before birth. The course of the blood-stream is indicated by the arrows.
VCS, VCI, superior and inferior vena cava.
These are the conditions present up to the time of birth. After the
first respiration the expansion of the lungs greatly reduces the resistance
in the pulmonary circuit, so that it becomes less than that in the aorta,
and most of the blood is diverted from the ductus arteriosus into
this new channel of low resistance. Hence it persists only a year
or so after birth and soon becomes changed into a simple strand of
connective tissue.
On the other hand, the pressure in the left auricle becomes greater
than that in the right, and the valve of the foramen ovale is therefore
kept closed against the septum, and soon becomes organized as a part
of the latter.
With fche cessation of placental circulation, the ductus venosus loses
its physiological importance and soon undergoes atrophy and closure.
CONGENITAL HEART DISEASE. 429
CLASSIFICATION OF CONGENITAL HEART LESIONS.
Classifications of congenital heart lesions are difficult, and from a
clinical stand-point not always satisfactory. From the anatomical stand-
point they may be classified as follows:
I. Malformations about the heart.
1. Malformations of the chest wall (ectopia cordis).
2. Malformations of the pericardium.
II. Abnormalities in the position of the heart.
1. Heart on the right side (dextrocardia or dexiocardia).
2. Position of all the organs inverted (situs trans versus).
3. Heart situated in the neck (cervical heart).
4. Heart situated, within the peritoneal cavity (abdominal heart).
III. Abnormalities of the valvular orifices.
1. Pulmonary stenosis or atresia.
2. Supernumerary or defective cusps of pulmonary valves.
3. Tricuspid stenosis or insufficiency; malformation of the valve.
4. Aortic stenosis; atresia of the aorta; malformations of the aortic valve.
5. Mitral stenosis; malformation of the mitral valve.
IV. Defects in the septa.
1. Interventricular septum.
a. In the septum membranaceum.
b. In the muscular part of septum (below).
2. Interauricular septum.
a. Defect or absence of valve of the foramen ovale.
6. Valve normal but not closed.
c. Defect between the muscle strands in the lower portion of interauricular
septum.
V. Abnormalities in the cavities.
1. Supernumerary septa.
2. Cor biatriatum triloculare.
3. Cor biloculare.
4. Cor biventriculatum triloculare.
5. Bifid apex.
6. Double heart.
VI. Deviations of the septum cordis with transposition of vessels.
VII. Persistence of ductus Botalli.
VIII. Abnormalities of the aorta.
1. Coarctation of the aorta.
a. Above the ductus arteriosus.
6. Below the ductus arteriosus.
2. Hypoplasia of the aorta.
3. Malformations of the aortic arch.
IX. Abnormalities in thg arrangement and formation of the veins.
GENERAL CHARACTERISTICS.
Such a purely anatomical classification, though sufficiently complete,
does not furnish a good basis for the study of the cardiac malforma-
tions, because it does not take into account the relation of the indi-
vidual lesions to one another. For, since these lesions are
usually produced in groups rather than singly, it
is quite as important from a clinical stand-point to recognize these
groups and understand their effect upon the circulation as to recognize
the individual lesions.
Moreover, as will be seen, the mere clinical manifestations show giv:it
similarity in the various lesions, and may be summed up in what may be
430 DISEASES OF THE HEART AND AORTA.
termed the "syndrome of congenital heart lesions;" orr
in the words of Peacock (1866), "the characteristic symptoms
of malformations of the heart — cyanosis (especially
from birth), palpitation, dyspnoea, faintings, occa-
sional convulsive attacks and lividity.' Moreover, the
most common physical sign of many congenital lesions is a loud superficial
murmur, most intense in the second and third left interspaces at the sternal
margin in both systole and diastole and often heard over the entire pre-
cordium and the arteries as well.
ETIOLOGY.
As Lancereaux has well said, "cardiac teratology repre-
sents the pathology of intra-uterine life." The chief
pathological conditions which affect the development of the foetus may
be classed as —
1. Inflammation (fetal endocarditis or myocarditis, the formation of
adhesions about the heart or vessels, etc.).
2. Abnormal torsions of the cardiac tube.
3. Underdevelopment of heart or branchial arches.
These processes lead directly to the production of malformations
which may be designated as primary congenital lesions, such as stenosis
and atresia of the pulmonary artery, transposition of the great vessels,
stenosis at the isthmus of the aorta, etc. The presence of these lesions in
the foetus in turn exercises its effect upon the circulation, which alters the
course of development and brings about secondary congenital lesions.
The developmental mechanics which results in the formation of such
groups of lesions is well illustrated in pulmonary stenosis and atresia, the
commonest of congenital heart lesions which may be considered as the
prototype.
PULMONARY STENOSIS AND ATRESIA.1
The commonest of all the primary congenital lesions is pulmonary
stenosis, occurring in 254 (68 per cent.) of the 366 cases of congenital heart
disease reported by Peacock and by Keith. Two causes have been ad-
vanced to explain its occurrence: (1) endocarditis in fetal life; (2) defec-
tive development of the pulmonary artery.
1. Bouillaud (1835) ascribed it to endocarditis in fetal life.
This theory seems certainly to be applicable to those cases in which the semi-
lunar valves have already formed, but just as in the adult have fused along
the lines of closure. This is well shown in Fig. 2^6 and in a case figured by
Peacock. Moreover, a number of cases have been reported in which rheu-
matism or infectious disease in the pregnant mother has led to the occur-
rence of endocarditis in the foetus. On the other hand, it must be borne in
mind that in 329 (82.5 per cent.) of 399 cases of pulmonary stenosis col-
lected from the reports of Rauchfuss, Vierordt, and Abbott the interven-
1 Atresia — (Greek arprjToq (atretos), riot perforated), from a = not, and rprja^ = a bor-
ing = absence or extreme constriction of any natural passage or opening of the body.
CONGENITAL HEART DISEASE.
431
tricular septum remained incomplete, indicating that the primary lesion
had taken place before the time at which the septum had closed (eighth
week of embryonic life). As Osier has pointed out, "It is not easy to
imagine a fet'al endocarditis localized to so small an area as the pulmonary
valves must be before the eighth week of fetal life." To this very objec-
Fio. 246. — Pulmonary stenosis due to fusion of
the cusps. (Drawn from a specimen in the Army
Medical Museum, Washington, D. C.) There is
also a patent interventricular septum.
INF.
FIG. 247. — Pulmonary stenosis due to a lesion
of the infundibulum. (Drawn from a specimen in
the Army Medical Museum, Washington, D. C.)
INF, infundibular portion of the right ventricle.
tion, however, the advocates of this theory might reply that in very many
cases the lesion is by no means confined to the cusps of the valves, but in-
volves the entire infundibulum, over which the endocardium may be thick-
ened and shrivelled (Fig. 247). Nor does it necessarily follow that even
though the interventricular septum has once closed it must remain so,
PATENT
INTERVENTRICULAR
SEPTUM
PULMONARY ARTERY
PULMONARY ORIFICE
Fio. 248. — Complete pulmonary atresia. (Drawn from a specimen in the Army Medical Museum,
Washington, D. C.) The pulmonary artery ends as a blind sac (shown by broken lines) just above the
dot which marks the closed pulmonary orifice.
since it may rupture under increased pressure or ulceration may result
from the fetal endocarditis. Such phenomena have occasionally been
observed (Abbott) .
2. The malformation may also arise by " irregular evolution
of the branchial arches." Panum has shown that malformations
can be produced experimentally in birds by raising the temperature of
incubation (fever in the mother) ; and His believes that at least a consider-
432
DISEASES OF THE HEART AND AORTA.
able portion of malformations result from "disturbances of developmental
conditions caused by insufficient nourishment, insufficient aeration of the
blood, and mechanical causes resulting from malpositions of the uterus, dis-
turbed placental circulation, etc."
It must be recalled that, as shown by Rathke in 1843, the pulmonary
artery separates from the rest of the truncus arteriosus about the eighth week
of embryonic life, along with the remains of the sixth1 left branchial arch
which forms the ductus arteriosus and the right pulmonary artery which
springs directly from this arch (Figs. 240 and 249) . The right pulmonary
artery, according to Bremer, has sprung in a similar manner from the right
fifth branchial arch, but the latter has atrophied and is now represented
only by the small segment con-
necting the right pulmonary
artery with the truncus pul-
monalis. In the twisting of the
cardiac tube and separation of
the ventricles the part of the
truncus arteriosus corresponding
to the pulmonary artery pro-
trudes ventrally while the aortic
portion protrudes dorsally. The
truncus pulmonalis thus repre-
sents the ventral half of the
truncus or bulbus arteriosus and
springs directly from the in-
f undibulum of the right ventricle
(Fig. 249). Stenosis or atresia
may therefore take place from
arrest of development in three
places: 1. In the trunk of the
pulmonary artery between the
semilunar valve and the point
of branching, — i.e., where the
pulmonary artery is in close
contact with (and perhaps
pressed upon by) the main trunk of the aorta. (This condition is represented
in a case of Peacock's series.) 2. At the orifice itself (as in Fig. 246),
from fusion or stenosis of the valves. 3. Below the valves and within the
infundibulum of the right ventricle, as in Fig. 247. In some cases a
supernumerary septum may separate the infundibulum from the main
cavity of the right ventricle, thus producing the so-called third ventricle.
Peacock regarded this structure as representing the condition present
in the turtle, but states that "such separation" (into two cavities)
FIG. 249. — Schema illustrating the genesis of pul-
monary stenosis. A. Fusion of the cusps. B. Fetal
endocarditis affecting the infundibulum. C. Normal
mode of development of the aortic branchial arches.
D. Maldevelopment of the sixth branchial arch, leading
to pulmonary atresia.
1 Rathke, His, and the older writers speak of the last branchial arch from v/hich the
pulmonary artery arises as the fifth branchial arch; but Tandler (Zur Entwicklungsges-
chichte der Kppfarterien bei den Mammalia, Morphol. Jahrb., Leipz., 1902, xxx, 275) has
recently shown that a small rudimentary arch is present upon the same stem with the
fourth. He terms this small arch (which plays no important role in development) the
fifth, and the pulmonary arch accordingly becomes the sixth.
CONGENITAL HEART DISEASE. 433
" may be produced in different ways. It may depend simply on undue
development of the ordinary muscular bands, or on this in conjunction
with thickening of the endocardium or subjacent fibrous tissue." Re-
cently Arthur Keith, of London, has revived Peacock's idea that this is
the portion of the heart which is homologous with the bulbus cordis of
the lower animals, and which, as Greil has shown, becomes incorporated
into the substance of the ventricle (infundibulum) just as the sinus is
swallowed up by the auricle. Keith believes that the period during
which this is taking place represents the crucial epoch in the production
of malformations.1
Certain it is that most fetal lesions arise about the time when the
pulmonary artery and the aorta and the remnants of the branchial arches
are taking their final form, the interventricular septum is becoming com-
plete, and the original portions of the branchial arches are disappearing,—
i.e., between the fourth and the eighth week of fetal life.
SECONDARY MALFORMATIONS.
As has been stated above, stenosis of the pulmonary orifice results
in stasis within the right ventricle, and the blood is forced to take a
new channel.
Patent Interventricular Septum with Pulmonary Stenosis.— In 80 per
cent, of the cases of pulmonary stenosis the interven-
tricular septum is still open, and the blood is forced through
the open septum and passes up through the aorta. As the condition is a
permanent one, the current through the septum continues and its closure is
prevented (stasis theory of William Hunter and Kussmaul). In rare cases,
and especially those in which the stasis appears at a very early stage, the
blood current eddies through and keeps open a passage between the muscle
strands at the base, in contrast to the usual defect at the septum mem-
branaceum. This opening at the base of the septum is often accompanied
by defects in the mitral or tricuspid valves.
Dextroversion (Rechtslage) of the Aorta. — Moreover, the pressure
upon the septum tends to deflect it toward the left and still further enlarge
the septal opening (Figs. 248 and 250).
In most cases the deflection of the septum to the left is so great that
the aorta comes to lie in the axis of the right ventricle. The cavities thus
come to form an inverted Y whose arms are formed by the ventricles and
whose shaft is the aorta. Since the shaft is inclined to the right, this gives
the appearance as though the aorta arose directly from the right ventricle
(Rechtslage — dextroversion of the aorta). This condition is present in
the majority of the cases reported by Abbott, especially in those in which
there is complete atresia of the pulmonary artery (Fig. 248).
1 It is possible that in some cases, like those figured by Keith, the rudimentary septa
represent endocardial pockets upon the wall of the ventricle. Schminke (Endokardiale
Taschenbildung bei Aorteninsuffizienz, Arch. f. path. Anat., etc., Berl., 1908, cxcii, 50)
has shown that similar pockets may be formed in the left ventricle by the impact of a re-
gurgitant blood stream.
28
434
DISEASES OF THE HEART AND AORTA.
Open Ductus Botalli. — When the stenosis reaches a considerable grade,
much of the blood that reaches the lungs must pass to them from the aorta
back through the duct us arteriosus (Botalli) (Fig. 256), which is therefore
forced to remain open after birth.
Open Foramen Ovale. — If the
intraventricular septum has closed
before the pulmonary stenosis has
occurred, the resulting stasis causes
a rise of pressure in the right auricle,
and the path of least resistance to
blood flow is through the foramen
ovale to the left auricle. The stream
in this direction is therefore larger
than usual and prevents the initial
sclerosis about the foramen, or even
preserves a channel in the lower part
of the septum, so that sometimes (as in
Fig. 250) the valve of the foramen may
close and a breach through this por-
tion of the septum still remain patent.
Three=chambered Heart (Cor bia=
triatum triloculare) . — When the
atresia is complete and the intraven-
tricular septum is closed, the right
ventricle becomes converted into a
blind sac into which no more blood
can enter. The tricuspid orifice thus
falls into disuse, and the valve under-
goes stenosis and atresia until it is
completely closed. The cavity of the
right ventricle remains only as a small
blind sac in the wall of the left, from
which the aorta arises, cor biatriatum
triloculare (Fig. 251).
Lesions of the Peripheral Vessels.
— The abnormalities in structure sec-
ondary to congenital heart diseases are
by no means confined to the heart, but
especially involve the finer ramifica-
tions of the vessels. Recent experimen-
tal investigations throw much light
upon the distribution and formation
of these abnormalities in a manner
which is of great practical importance.
J. Loeb in 1893 was the first to demonstrate experimentally the effect of injury to
the heart upon development. He poisoned the hearts of fish (Fundulus) embryos by tem-
porary immersion in 1.5 per cent. KC1 solution, and found that, though the hearts of such
embryos did not beat at all, nevertheless these embryos reached adult stage, and differed
from normal fish chiefly in the irregular structure of their blood-vessels. Knower, working
with frog tadpoles, has recently confirmed Loeb's observations, but studied the changes
FIG. 250. — Currents and lines of force in the
embryonic heart which result from pulmonary
stenosis and tend to produce patency of the septa
and of the ductus arteriosus. A. Ventricular
end of the fetal heart (before the eighth week of
embryonic life). B. Auricular end of the fetal
heart at the same stage. P A, pulmonary artery;
D A, ductus arteriosus (Botalli); R A, right auri-
cle; R V, right ventricle; L A, left auricle; L V,
left ventricle; F O, foramen ovale. The large
arrows indicate blood currents, the black within
the ventricles, the white those within the auricles.
The small arrows indicate the forces tending to
dilate the heart and to deflect the septa. In
cases of extreme grades of pulmonary atresia
the current in the ductus arteriosus flows from
aorta to pulmonary artery, instead of in the
reverse direction.'
CONGENITAL HEART DISEASE. 435
in more detail, and has found that after mechanical or chemical (acetone-chloroform)
injury to the heart the embryos usually become very oedematous and are less advanced
than the controls. These embryos, according to Mall, are very similar to the oedematous
moles frequently met with in gynaecological practice. Knower also found that the devel-
opment of the brain, intestines, liver, and pancreas is retarded, "both arteries and veins
are very much distended, and follow very irregular courses. ... Inmost cases
the first precapillary loops are represented by large sinuses,
. . . . but there is a notable absence of capillaries in the fin. The
smaller vessels do not push out nor form characteristic plexuses. Their development is
inhibited. The weaker the heart-beat in fact the less does the blood flow outward from
the larger vessels and precapillary loops." Similar changes had already been described
by Panum and Dareste in chick embryos, by Stockard upon fish embryos poisoned with
lithium, and by Bardeen upon toads which had been fertilized with sperm previously
exposed to the action of X-rays. Knower also notes that similar malformations are com-
mon in frogs at the end of the breeding season (when the sperm may well be weakened).
The secondary changes in man, outside
of the heart, are quite homologous with those
in animals. These are especially underdevel-
opment in stature and in intelligence and the
occurrence of malformations of the arterioles
and venules. Just as in Knower's frogs, there
is a dilatation and irregularity of venules often
in the skin, viscera, and retina (Fig. 253), from
which hemorrhages frequently take place.
Thickening and clubbing of the ends of the
fingers (clubbed fingers, Fig. 254) also take
place, from proliferation of the connective
tissue as a result of the venous stasis.
FIG. 251.— Three-chambered heart
P A TWOT r^Tri A T T>H VGTOT r\f- v (cor kiatriatum triloeulare) produced
PATHOLOGICAL PHYSIOLOGY. by complete atresia of the pulmonary
and tricuspid orifices. (From a speci-
The effect Of pulmonary StenOSIS Upon the men in the Army Medical Museum,
mechanics of the circulation in the adult is
Very marked. In the first place it brings ventricle; F O, foramen ovale. The
, * e 11 • i i i /i A i • i arrows indicate the course of the
about a fall in blood-pressure (both arterial blood stream.
and venous) in the pulmonary artery and
in the lungs (Fig. 252), and consequently a corresponding secondary
lowering of pressure in the aorta.
The extent to which other areas of the circulatory system are affected
depends as much upon the correlated defects as upon the stenosis itself.
If the stenosis is the only lesion, it produces a fall of pressure in the
pulmonary artery, a rise of pressure (from stasis) in the pulmonary veins,
and a marked increase in pressure within the right ventricle, like that
which Liideritz found in the left in aortic stenosis (Fig. 252, light broken
line). This always leads to hypertrophy of the right ventricle and right
auricle, and usually to the signs of congenital venous congestion to be
described later.
Between these two grades of severity there exist all stages of cardiac
insufficiency, the most important being the overloading or weakening of
the right ventftcle, which leads to transitory venous stasis, tricuspid insuf-
ficiency, and cyanosis. The pressure in the pulmonary vein and left auricle
436
DISEASES OF THE HEART AND AORTA.
is by virtue of the pulmonary stenosis lower than usual, while that in the
right auricle is for the same1 reason higher. Accordingly the tendency is
for venous blood to pass into the left auricle and ventricle in diastole to a
much greater degree than when the pulmonary orifice is normal, and hence
to cause a greater tendency to cyanosis and dyspnoea than in the uncompli-
cated patent foramen ovale.
When the foramen ovale is patent but the septum ventriculorum closed
(12 per cent, of Abbott's cases), the effect upon the circulation varies.
Owing to the pulmonary stenosis, the path of least resistance is through
the open foramen ovale into the left auricle without passing through the
lungs, and much blood may circulate in this way. Whether or not this
gives rise to cyanosis depends upon the actual amount entering the lungs
through the pulmonary artery. Under ordinary circumstances this may
NORMAL
PULMONARY
STENOSIS
AND ATRESIA
FIG. 252. — Diagram of the circulation in pulmonary stenosis and atresia. Simple pulmonary stenosis.
The arrows show the fall of pressure in the aorta and pulmonary artery and the rise of pressure in the vena
cava and right auricle. The broken line indicates the high intraventricular pressure in the right ventricle.
Pulmonary atresia, with patent interventricular septum (SV\ patent ductus arteriosus (DA), and patent
foramen ovale (FO). The blood current passing through the patent interventricular septum is indicated
by the heavy broken line; the light broken lines indicate intraventricular pressure. The shaded curves
indicate mixed blood. BR, bronchial arteries. The relation of the new channels to the other arteries
is shown in the diagram below.
keep enough blood aerated to avoid cyanosis, but in exercise or exertion
when more CO2 is produced, this excess may show in the patient's color.
Moreover, the venous pressure may rise until the pressure in the right
auricle still further exceeds that in the left, and thus a larger proportion
of this non-aerated blood enters the left side of the heart, giving rise to the
vicious circle of the open foramen ovale (Fig. 250, B).
Cyanosis,
Asphyxia
/ Increased work of heart
\ Passage of unae rated blood
into left auricle
High pressure in
vena cava
SYMPTOMS.
The classical picture of pulmonary stenosis and especially of pulmonary
atresia is the "morbus cceruleus" or "blue sickness," as which it has been
known since the time of Senac (1749). The patient is usually a small child
COXCKMTAL HEART DISEASE. 437
or youth below the normal size and intelligence. He is said to have been
blue at b i r t h (as in 74 of Peacock's 101 cases), or to have become so
during the first year or two of life (as in almost all of Peacock's other cases).
He has suffered from cough most of his life, as well as shortness of breath.
The latter becomes extreme or may come on in severe paroxysms after
exertion. During these attacks of dyspnoea, the patient may
become extremely blue or even black in the face, and they may end in a
fainting spell or an epileptiform convulsion (due to venous stasis
and cerebral ischsemia). He may also have frequent headaches. His
hands and feet are usually cold (venous stasis). He is subject to frequent
bleedings from the nose, mouth, intestines, or other mucous membranes
(due to congestion in dilated venules) , which may even suggest the diagnosis
of haemophilia.
On the other hand, persons with a considerable grade of congenital
pulmonary stenosis may remain free from symptoms and even perform
heavy work, as in the case quoted by Peacock of a man of forty-four who
worked as a navigator until six weeks before his death. Such cases, however,
constitute only a small percentage of every series.
Pulmonary Stenosis with Patent Interventricular Septum.— However,
when the interventricular septum is defective the condition is entirely
different. The lowered pressure in the pulmonary artery usually continues
unless fully compensated by the anastomotic circulation. The right ven-
tricle hypertrophies until it equals or even exceeds the left in thickness,
and, owing to the dextro version of the aorta, sends its large quota of blood
into the aorta. The pressure in the systemic veins, therefore, depends not
upon the pressure within the right ventricle but upon the ability of the
right ventricle to force the blood onward and prevent it from accumulating
in the veins. The presence, extent, or absence of symptoms, on the other
hand, depends upon the aeration of blood in the lungs. Peacock well says
that " in cases of this description the open state of the foramen ovale and
the imperfection in the ventricular septum, so far from adding to the danger,
really afford the means of relief to the overcharged right auricle and ven-
tricle without which life could not be prolonged for any considerable period."
That the outlook in cases where defective septa accompany the pulmonary
stenosis is graver than in cases where the stenosis occurs alone is due merely
to the fact that in the latter case the lesion is usually formed late in fetal
life, and hence is comparatively mild; or, if formed early, it is too slight to
give rise to the stasis which keeps the septa open.
PHYSICAL SIGNS.
The patients, usually children, are of stunted growth, with eyes
watery, veins of forehead, face, and arms large, very numerous, and
anastomosing frequently.
Cyanosis. — So striking and so frequent is the occurrence of intense cya-
nosis in congenital heart disease that this term has become almost synony-
mous with the "morbus cceruleus" (blue sickness) described by Senac.
The patients may be persistently livid or the cyanosis may be present
only at times of exertion or ill health. It may then come in attacks asso-
438 DISEASES OF THE HEART AND AORTA.
elated with dyspnoea and sometimes convulsions. The patients may be-
come quite black in the face and may remain so for some time.
The mode of origin of the cyanosis in congenital heart disease is a
matter not only of scientific interest but of the greatest practical importance in diagnosis
and prognosis. Theories: 1. Mixture of venous with arterial blood. Senac (1749), William
Hunter, Forget, Meckel, Corvisart, Gintrac, Favre, Paget, and others supposed that the
cyanosis was due to the passage of venous blood directly into the left auricle or ventricle
through the open foramen ovale or interventricular septum. While this may play a role
in some or indeed in most cases, Moreton Stille (1844) has shown "that complete
admixture of the blood may take place without cyanosis
This is conclusively demonstrated by the two following cases.
"First. — Foramen ovale open; pulmonary artery arose from both ventricles, gave
off pulmonary branches, and formed the aorta descendens. The aorta gave off the branches
to the head and upper extremities and joined the pulmonary artery by the ductus arterio-
sus. No cyanosis. Age eight months.
"Second. — Heart with two cavities; aorta and pulmonary arising from the ventricle.
No cyanosis. Age eleven days."
Numerous other observations in the literature have confirmed Still's contention.
On the other hand, when there is mixing of venous and arterial blood, a relatively slight
stasis or cardiac weakness from overstrain or disease may bring about intense cyanosis,
which would not occur in persons with healthy hearts.
2. The second theory, proposed by Morgagni (1761) and subsequently advocated by
Louis. Bouillaud, Valleix, Hasse, Stille, and Rokitansky, was that owing to the pulmonary
stenosis there was stasis in the systemic veins, and that the cyanosis resulted from that
factor only. To this theory Grancher adds the fact that the capillaries and precapillaries
are already markedly dilated (for reasons given above on page 434) and that in these dilated
capillaries slight stasis brings about marked cyanosis.
Another factor, to which attention has been called by Vaquez, Osier, and others, is
that in such cases cyanosis is usually accompanied by intense polycythaemia, and the in-
crease in the amount of the CO2 hemoglobin intensifies the cyanosis which might other-
wise be present in moderate degree.
None of these theories, however, explains the absence of cyanosis in cases where all
the venous blood passes into the aorta. In these cases the ventricles are strongly exerting
both their suction-pump and force-pump action, so that blood does not accumulate in
the veins. On the other hand, the pressure in the aorta (ranging from 90 to 120 mm. Hg)
is about three times as high as the pressure normally present in the pulmonary artery,
and hence is capable of forcing a very large amount of blood through the wide bronchial
arteries or open ductus arteriosus (Botalli) to the lungs.
Whether admixture of venous blood will or will not produce cyanosis depends largely
upon the amount of CO2 which the abnormal pulmonary circulation can take care of, and
which in most cases is more limited than in the normal individual. When excessive exer-
cise, strain, or cardiac weakening causes an abnormal increase of CO2, cyanosis makes its
appearance, and owing to the congenital dilatation of the capillaries the cyanotic effect
is magnified.
The cases in which cyanosis occurs in spells are probably examples of transitory
venous stasis (in congenitally enlarged capillaries and capillary plexus). In cases with
open foramen ovale stasis in the systemic veins and right heart will divert an abnormally
large amount of venous blood through the foramen ovale (Fig. 250).
The head occasionally shows signs of other abnormalities in form. There may be
deficient formation of bones of skull, abnormalities in the form of the ears, hare-lip, cleft
palate, etc.
Vascular Changes in the Retina. — Marked changes in the vessels of
the retina, seen upon examination with the ophthalmoscope, were first
reported by Knapp in 1861. In cases with marked cyanosis elsewhere
there are often irregularities in the lumina of arteries and veins, which are
tortuous ("resembling large angle-worms," Posey) and in some places
very wide (twice as wide as normal) , in others very narrow. " Both veins
CONGENITAL HEART DISEASE.
439
FIG. 253. — Dilatation and irregularity of the reti-
nal vessels. V, vein; A, artery. (After Posey.)
and arteries become much darker than normal, the former assuming a deep
violet color, while the arteries resemble normal veins. The peripheral
twigs of the retinal vessels are distended, and vessels which are usually
invisible may be seen over the entire fundus Small hemor-
rhages are of frequent occurrence" (Posey) (Fig. 253). In doubtful cases
this feature may be of great diag-
nostic value, but it can be expected
to occur only in those cases in which
there is a considerable degree of cy-
anosis and in which the prenatal
slowing of circulation has probably
been marked.
Clubbed Fingers (Hippocratic Fin-
gers).— The ends of the fingers under-
go peculiar changes (clubbed fingers,
Hippocratic fingers) (Fig. 254), which
also occur in chronic pulmonary dis-
eases, tuberculosis, chronic cardiac
disease, especially in children and in
conditions producing long-continued
local or general venous stasis (Eb-
stein). The change is confined to the
pulp of the finger, which is thicker than normal and broadest near the tip,
and tapers in a proximal instead of a distal direction. The nails are very
convex in both longitudinal and transverse diameters. They are usually
cyanotic. The form of the bones is practically unchanged. E. Ebstein
has collected a large number of observations
which prove that clubbing of the fingers and toes
results from chronic passive congestion either gen-
eral or local (from pressure on veins). The earlier
in intra-uterine or in extra-uterine life that the
congestion occurs and the longer is its duration
the more marked is the clubbing.
The occurrence of clubbed fingers is dependent
on almost the same factors as cyanosis, and the two
features usually occur together or are both absent.
Cardiac Signs. — The precordium almost always
bulges, and the wavy systolic impulse over the
precordium due to systole of the right ventricle is
usually seen. A systolic impulse at the apex may
or may not be present.- The area of cardiac dulness
is usually enlarged to both right and left. On
palpation a rough systolic thrill is felt over the pulmonary area,
from which it is transmitted diagonally upward toward the left clavicle
and downward over the precordium (Fig. 255). In cases in which there
is a defect in the septum ventriculorum, this thrill is also intensified over
the third and fourth left interspaces near the sternal margin.
The characteristic sign of pulmonary stenosis on auscultation is a sys-
tolic murmur accompanying the above-mentioned thrill and following
FIG. 254.— Clubbed fingers.
440
DISEASES OF THE HEART AND AORTA.
FIG. 255. — Distribution of the pulmonary systolic mur-
mur of pulmonary stenosis.
the first sound, loudest over the pulmonary area or just beyond it in the sec-
ond left interspace. In sharp contrast to the murmur of aortic stenosis, it is
transmitted upward and to
the left. It is also heard
over the precordium, but, un-
less the interventricular septum
or ductus arteriosus (Botalli) is
open, it is not usually trans-
mitted to the systemic arteries.
The second pulmonic sound is
either absent or suppressed in
spite of the respiratory distress.
However, it is noteworthy that
in those cases in which there is
uniform pulmonary atresia ex-
tending over one or two cm.
and where the lesion is actually
most severe, the murmur may
be entirely lacking. The same
applies, of course, to complete
obliteration of the pulmonary artery. Needless to say, the imperfectly
formed valves may be insufficient and a dias^olic murmur due to regurgi-
tation may also be present. However, a murmur
of this type is most frequently due to the defect
in the interventricular septum (see page 444).
Open foramen ovale, when present, rarely
gives characteristic signs, but occasionally may be
diagnosed from a presystolic murmur heard at the
base. The signs due to an open ductus arteri-
osus Botalli are so similar to those of pulmo-
nary stenosis that even in typical cases it is
almost impossible to diagnose in the presence
of the latter. The murmur from the former
is more frequently heard at the back to the
left of the third and fourth dorsal vertebra?
with every marked inspiratory accentuation
and expiratory diminution (Francois-Franck) .
The chest is usually poorly expanded, often
pigeon-breasted.1 Harrison's grooves are often
prominent. Signs of phthisis (areas of dul-
ness, tubular breathing, increased vocal fremitus
and rales) are very common, especially at the
apices (80 per cent, of Abbott's cases), in cases
which have passed the age of infancy, and tuber-
cle bacilli are frequently found in the sputum.
FIG. 256.— Direction of blood-
streams and propagation of mur-
murs accompanying defect in the
interventricular septum, pulmon-
ary stenosis, and open ductus arte-
riosus (Botalli). DEF. SEPT.,
defect in the interventricular sep-
tum; P. ST., pulmonary stenosis;
PAT DA, patent ductus arterio-
sus (Botalli); 1, 2, 3, 4, 5 represent
the corresponding ribs.
1 This flatness of the chest may perhaps be of reflex origin, since F. Kauders (Ueber
einige Experimente zur Lehre von der cardialen Dyspnoe, Wien klin. Wchnschr., 1891),
under v. Basch's direction, has shown that the diaphragm rises when the blood flow through
the lungs is diminished.
CONGENITAL HEART DISEASE.
441
Condition of Other Organs. — The abdomen is often very full, the
liver and spleen enlarged, especially in cases with cyanosis and
venous stasis. The genitalia are usually underdeveloped.
The blood count usually ranges between 6,000,000 and 9,000,000, the
haemoglobin between 110 and 130 per cent.
There are often albumin and casts in the urine, which is frequently
scanty. Occasionally there is blood from the dilated capillaries.
DIAGNOSIS.
As stated by Rauchfuss in 1878, the diagnosis of congenital pulmonary
stenosis can usually be made from the following symptom complex : " Cyan-
osis, from birth or following signs of cardiac affection which were then pres-
ent; signs of dilatation and hypertrophy of the right auricle and ventricle;
systolic murmur and thrill over the conus arteriosus and pulmonary artery,
not transmitted to the carotid arteries." He admits, however, as do all
subsequent authors, that the exact diagnosis of the secondary lesions intra
vitam is almost impossible, owing to the multiplicity of the lesions which
may occur and the fact that so many of the signs overlap one another.
TREATMENT AND PROGNOSIS.
As regards prognosis statistics vary considerably. Of Stoelker's 53
cases 32 died at birth, 12 during the first year, and 1 1 during the first decade.
Only 4 reached the fourth decade.
The age of death in Abbott's series was as follows:
Age at death.
PULMONARY STENOSIS.
PULMONARY ATRESIA.
V. S. closed.
F. O. closed,
detect V.S.
F. O. patent,
defect V. S.
V. S. closed.
F. O. closed,
defect V. S.
F.O. patent,
defect V. S.
Before 1 year
0
2
4
3
6
1
4
16
5
8
3
0
3*
8
4
5
0
0
6
0
0
0
0
0
2
n
0
0
0
0
lot
0
0
0
0
0
1-7..
7-14..
14-20
20-28
28-45
61
36
20
6
5
10
* 9.7 per cent.
t 78 per cent.
One can hardly fail to be struck by the contrast between the cases of
pulmonary atresia and pulmonary stenosis, since 78 per cent, of the former
die in the first year, while this is the case in only 9.7 per cent, of the latter.
Even of these only 36 per cent, survived the age of puberty and only one
reached middle age.
In the individual case the physician may be guided by the intensity
of the symptoms even more than by the physical signs, severe symptoms,
as a rule, portending an early death. When the symptoms in early youth
442 DISEASES OF THE HEART AND AORTA.
are comparatively mild, the prognosis is a little better, but an early death
from phthisis or acute endocarditis is always to be feared, even when the
heart failure is less intense. It is, therefore, most important, as Peacock
suggested: (1) to keep the patient warm by both warm clothing and
sojourn in a balmy climate; (2) to keep him leading a quiet life on a diet
of nourishing but easily digested food. For paroxysms of dyspnoea and
distress free purgation should be resorted to. Venesection, which was recom-
mended by Peacock, though indicated by both the venous stasis and the
high viscosity of the blood, is a dangerous procedure and should be used
only as a last resort, for the coagulation of the blood in these cases is
often retarded. Before performing it the coagulability should always be
determined.
The general cardiac stimulants, such as digitalis and strychnine, are
rarely of much value, since in most cases the heart has already reached the
maximum of its power and cannot be stimulated much further. Vasodila-
tion from amyl nitrite and nitroglycerin may sometimes help, and Peacock
recommends the use of warm baths or mustard baths, especially for the
convulsions of children.
DEFECTS IN THE INTERVENTRICULAR SEPTUM.
OCCURRENCE AND PATHOGENESIS.
As has been stated above, defects in the interventricular septum are
usually with and secondary to other malformations, this being the case in
117 (78 per cent.) of 149 cases studied by Abbott. Pulmonary stenosis or
atresia was present in 75 cases (58 per cent.). In only 24 cases (16.1 per
cent.) were there no other abnormalities.
The circulatory mechanism which keeps the septum from closing in
the presence of pulmonary stenosis has been discussed above under the
latter condition. In the other cases, in which Abbott classes it as a " second-
ary lesion," the mechanism is similar.
In the uncomplicated cases, however, the causation is more obscure.
In a few cases it is accounted for by fetal endocarditis affecting the septum
interpositum before the septum membranaceum has formed. In other
cases the septum membranaceum does not form completely. After birth,
when the pressure in the left ventricle rises high above that in the right,
the rush of blood from the left ventricle into the right may push the septum
along with it and may cause it to protrude as a funnel into the right ven-
tricle (Tate, Hebb) . In still other cases the septum forms and protrudes as
an aneurism of the septum. This aneurism may rupture later anjd give
rise to the defect.
Some cases of apparent defect in the septum are due to ulcerative
septal endocarditis, but these are probably few. Trauma may produce a
similar effect in adult life. McOscar and Voelcker report the case of a man
who was run over by a wagon. Rupture of the interventricular septum
resulted and the patient died eight days afterwards. Reiss states that
pulmonary tuberculosis has been found in every adult in his series, but this
is by no means always the case.
CONGENITAL HEART DISEASE. 443
PATHOLOGICAL PHYSIOLOGY.
When the defect in the septum is secondary to a severe pulmonary
stenosis or atresia, as has been seen, its effect is to allow blood to pass from
the right ventricle into the left, and under any circumstances this is the
case during fetal life.
When there is no such stenosis, however, and the strength of the left
ventricle increases after birth, the current passes in the reverse direction
and aerated blood passes from the left ventricle into the right. The effect
upon the work of the former is consequently about the same as that of a
leak at the mitral valve; intra ventricular pressure is lowered, and the
systolic output must be increased in order to maintain the circulation.
The left ventricle consequently hypertrophies as a result of the strain; the
right ventricle hypertrophies also as a result of the increase in the blood
forced into it. The extent of hypertrophy of the latter chamber depends
largely upon the size of the opening. As the right ventricle hypertrophies
and pressure in the right ventricle increases, the leakage diminishes, so
that the effect of the lesion tends to correct itself; on the other hand, the
pressure in the pulmonary artery increases. But since the ordinary resist-
ance in the pulmonary circulation is much less than that in the systemic,
when the forces of both ventricles approximate one another, the effect on
the pulmonary circulation is the same as though the left ventricle became
weaker and the right remained unchanged. Pulmonary engorgements
may, therefore, result, with consequent dyspnoea. In most cases, however,
the hypertrophy does not reach this point, and it is only when the heart is
stimulated by effort or exercise that pulmonary engorgement sets in.
SYMPTOMS.
In considering the symptoms and signs of defects of the interventricular
septum, one must differentiate sharply between those cases in which the
condition exists alone and those in which it is secondary to other lesions.
In the latter case the manifestations of the primary condition may predomi-
nate; and these are discussed in the corresponding sections.
The symptoms from simple defect in the interventricular septum are
few, and, as a rule, are confined to more or less weakness, dyspnoea, and
palpitation, rather than the extensive symptom complex met with in
pulmonary stenosis.
PHYSICAL SIGNS.
In marked contrast to pulmonary stenosis, marked cyanosis is not
one of the signs of uncomplicated defect in the interventricular
septum, since there is, as a rule, no stasis in the veins and the abnormal
blood stream flows from left ventricle into the right. Cyanosis may occur,
however, as the result of a cardiac overstrain, just as in any other condi-
tion of cardiac weakness, but is not abnormally intense. The fingers are,
as a rule, not clubbed. Over the precordium and epigastrium there is
usually violent systolic retraction, produced by the hypertrophied right
ventricle. There may be violent systolic pulsation of the conus arteriosus
in the second left interspace. The area of dulness may be enlarged to both
444
DISEASES OF THE HEART AND AORTA.
right and left, or there may be no change from the normal. There is
almost always a well-marked systolic thrill over the third left interspace
near the sternal margin.
Auscultation reveals the presence of a murmur which was first described
by Roger in 1879 in the following words:
" It is in general remarkably intense; its maximum is not at the apex
(as in alterations of the auriculoventricular orifices), nor at the right base (as in' aortic
stenosis), nor at the left base (as in
pulmonary stenosis). This maximum
is at the upper third of the precor-
dial region and is median like the ven-
tricular septum itself. It is single
and very prolonged, commencing with
systole and replacing the two normal
sounds. It is fixed without propa-
gation in the large vessels, as is the
case with aortic or pulmonary stenosis,
and decreases in intensity equally in
all directions as one passes away from
this central point The mur-
mur corresponds with a very extensive
thrill which exactly coincides with it.
.... The murmur does not change
in the course of years."
FIG. 257. — Distribution and character of the murmur due
to a patent interventricular septum (Roger's murmur).
However, all writers do not
agree with Roger. Cadet de
Gassicourt, Potain, and Reiss
claim that it occurs during systole only; while in some cases, especially where
the septal defect is a large one, it is totally absent (Bennetz). The murmur
is sometimes transmitted to the carotid arteries, though it is always loud-
est over the precordium. The second pulmonary sound is accentuated.
The pulse may be small and weak, or, as in the case of McOscar and
Voelcker, collapsing. The blood-pressure is usually low.
CASE OF PATENT SEPTUM VENTRICULORUM.
The following notes were obtained from a case admitted to Prof. Barker's service
in the private wards of the Johns Hopkins Hospital:
The patient was a married man, a scientist of some note, aged 59. As a child he had
been subject to bad dreams and disturbed sleep and became short of breath on
slight exertion. This shortness of breath on exertion followed through life, but
in spite of the ordinary diseases of childhood, three mild attacks of typhoid fever, and
continued use of tobacco, alcohol, and strong coffee, he was able to lead an active life until
past middle age.
For six weeks before admission to the hospital he has been very weak and has been
troubled with nocturnal dyspnoea, though these symptoms are probably refer-
able to his renal rather than to his cardiac changes. Swelling of the feet set in a few days
before admission.
On Feb. 15, 1908, Dr. Barker made £he following note on his cardiac condition:
The radials are thickened, the blood-pressure is high; there is a blowing systolic murmur
at the apex, the aortic second sound is fairly loud, the pulmonic second very loud. The
rough systolic murmur is also heard in the pulmonary area,
but is loudest and roughest a little lateral from the tricuspid
area. No aortic diastolic murmur is heard. There is no marked throbbing of the neck;
veins in the neck are a little overfilled. There is some oedema of the ankles and overfilling
df the veins of the lower extremities.
CONGENITAL HEART DISEASE. 445
He passed over 2500 c.c. of urine daily, of specific gravity 1012-1014, containing a
trace of albumen and some hyaline casts. The blood-pressure varied from 220 to 285
mm. Hg, pulse-rate 80-90.
During his stay in the hospital he had occasional smothering spells which were relieved
by venesection. He spat up considerable amounts of red tenacious sputum.
The patient died during the course of the next few months. Autopsy revealed
a funnel-shaped bulging of the membranous septum into the
right ventricle with a perforation »3 -4 mm. in diameter at the
apex of the funnel. (This condition is exactly similar to the lesion described
by Hebb and by Tate.)
There was also a chronic nephritis.
CASE OF PROBABLE PATENT SEPTUM VEXTRICULORUM.
B. J., an unmarried colored woman aged 26, entered the Johns Hopkins Hospital
complaining of pain in the chest. Except for shortness of breath on exertion during the
last ten years, the history is negative.
Her heart was very slightly enlarged to the right. The sounds were clear at the apex,
but over the body of the heart a peculiar intense high-pitched murmur was heard, loudest
during systole but lasting through the whole cardiac cycle (Roger's murmur?). This
murmur is loudest and most intense over the third left interspace
between the parasternal line and the sternum, but it is heard also in
the second and fourth interspaces, where it is much less intense.
Maximal blood-pressure varied from 110 to 125 mm. Hg; venous tracings were normal;
retinal vessels normal. The urine contained a trace of albumen but no casts nor blood-cells.
The subsequent history was uneventful.
DIAGNOSIS.
The diagnosis of defect in the interventricular septum can be made
only when, in the absence of cyanosis or other signs of congenital heart
disease, the vigorous pulsation of the right ventricle is seen in the second
right interspace, and both the peculiar murmur of Roger and the accent-
uated second pulmonic sound can be heard. In the presence of pulmonary
stenosis or other congenital or acquired lesions, signs may merge into one
another in such a way that an absolute diagnosis may be impossible.
Simple acquired endocarditis often occurs, as in Tebb's case, and its signs
may serve further to confuse the clinical picture.
TREATMENT.
Needless to say, there is no treatment that can be directed against
the defect itself. However, the symptoms in many cases arise only during
over-exertion, and the most important factor in the management of the
case is, therefore, directed along the usual lines for the avoidance of over-
strain,— rest, graduated exercise, moderation in diet, avoidance of dyspnoea,
regulation of the bowels, and if necessary digitalis and strychnine. The
most important point is the avoidance of pulmonary congestion.
The PROGNOSIS in simple septal defect depends less upon the extent
of the lesion than upon the apparent impairment of the function. Simple
defects in the septum are compatible with quite long life, and many cases
are reported in which the patients have reached the fourth and fifth decades.
When other lesions are present, such as pulmonary stenosis, abnormali-
ties of the blood-vessels, etc., it is they, rather than the septal defect, which
determines the prognosis.
446
DISEASES OF THE HEART AND AORTA.
PATENT FORAMEN OVALE.
OCCURRENCE AND PATHOGENESIS.
Mere patency of the foramen ovale to the passage of a probe is by no
means pathological. In statistics of 1166 heterogeneous autopsies collected
by Vierordt, it was present 313 times (28 per cent.), and also in 80 (22.3 per
cent.) of Zahn's 357 miscellaneous autopsies upon persons past the age of
40. This non-closure is probably due to the fact that both the auricular
septum and the valve closing the foramen are lined by endothelium, and
no fibrosis takes place between the two surfaces until the endothelial cells
slough off or are injured. The valve itself remains closed against the septum
during life and no symptoms are
produced. Perhaps, when heart
failure from any cause occurs in
such cases and the pressure in the
right auricle exceeds that in the
left, a certain amount of blood may
actually pass through this embryonic
channel, but in too small amounts
FIG. 258. — Open foramen ovale. (From a spec-
imen in the Army Medical Museum, Washington, D.
C. ) The patient was a soldier who had never shown
any cardiac signs or symptoms and no cyanosis.
FIG. 259. — Diagram showing a cross-section
of the same. VC, vena cava; RA, right auricle;
FO, foramen ovale; LA, left auricle.
to give signs or symptoms. On the other hand, in 462 autopsies by Hinze
and by Ogle the foramen was permeable to the little finger (permanently
patent) in only 9 cases (1.9 per cent.).
The mechanism of secondary septal defects (auricular stasis of Mor-
gagni and William Hunter) by which more than the usual proportion of
blood passes through the foramen ovale has been discussed under pulmo-
nary stenosis, and it may occur with other congenital lesions.
The truly pathological lesions of the interauricular septum are shrink-
age or total absence of the valve and perforation of the septum between
the muscle strands (Fig. 260). Occasionally the valve has closed, but is
somewhat weak and forms an aneurismal bulging. Peacock reports one
and Abbott two of these cases, in all of which the protrusion was from right
to left, indicating that the pressure in the right ventricle exceeded that in
the left. »
CONGENITAL HEART DISEASE. 447
PATHOLOGICAL PHYSIOLOGY.
A defect in the interauricular septum has comparatively little effect
upon the circulation as long as the pressures in the two auricles are equal
or nearly so. When the left ventricle begins to fail or the pressure in the
left auricle rises from any cause whatever (mitral stenosis, mitral insuffi-
ciency, etc.), the patent foramen ovale exercises a sort of safety-valve action
and relieves the pulmonary congestion by allowing the excess of blood to
pass back into the right auricle. Ritter (1856) and Rusch (1862) have
shown that when the foramen ovale is open in cases of mitral insuf-
ficiency, the pulsation in the jugular vein assumes the positive ven-
tricular type, owing to the crossing of the regurgitant stream. How-
ever, this is of little value in diagnosis, since the positive ventricular
pulse is common with heart weakness
and auricular paralysis.
On the other hand, when the right
heart begins to fail and pressure in the
l c± • 1 • xu ui i r 11 VALV.F.O.
left auricle increases, the blood follows
the same course as it does in the foetus
and passes from the right into the left FORAMINA!
auricle. Under ordinary circumstances
this would exert no influence whatever,
and would not even produce cyanosis.
But when the heart is already weak, the
circulation slow, and the blood heavily
charged with CO2, this sudden admixture
of venous blood carries the CO2 content
past the physiological limit, and gives FIG. 260.— Openings between strands ot
. j Jj muscle in the interauricular septum. (From
rise tO CyanOSIS and Symptoms. More- a specimen in the Army Medical Museum,
over, the blood entering the coronary Wa-?hin?t?n/TP-H Th1 val,vula 1floraniini?
'. . J ovahs (VA LV. F.O.) is closed and has fused
arteries is also less aerated, the cardiac with the rest of the septum. FORAMINA,
tonicity and cardiac strength are im-
paired, and the vicious circle of the open
foramen ovale sets in, subsiding again with inordinate rapidity as soon
as the pressure in the systemic veins falls below that in the pulmonary.
SYMPTOMS.
In most cases patency of the foramen ovale alone does not give rise
to any symptoms. For example, the patient whose heart is shown in Fig.
237 was able to perform his duties as a soldier in heavy campaigns and
died from dysentery without any symptoms referable to his heart. Pea-
cock mentions the case, reported by Spry in 1805, of a girl of seven years
who had no cyanosis during life and whose foramen was patent and two
inches in circumference (f inch in diameter). On the other hand, he cites
another case, a woman of twenty-one whose foramen ovale was one inch
in diameter, who from the age of three months "presented characteristic
symptoms of malformation of the heart, — cyanosis, palpitation, dyspnoea,
faintings, occasional convulsive attacks, and lividity."
448 DISEASES OF THE HEART AND AORTA.
PHYSICAL SIGNS.
Apart from the paroxysmal cyanosis the physical signs of open fora-
men ovale are extremely variable. Cyanosis and abnormalities in the retina
may be present. On the other hand, all physical signs may be absent. In
some cases systolic, in others diastolic, murmurs are present in the third
left interspace at the sternal margin. Occasionally there is heard a well-
defined presj^stolic murmur which is maximal at this point, and which
when present is the most characteristic sign of the open foramen ovale.
DIAGNOSIS.
The diagnosis rests upon the presence of paroxysmal cyanosis
and of murmurs in the third left interspace without signs
of aortic insufficiency or of hypertrophy of the right ventricle (well-marked
systolic retraction over the right ventricle with or without systolic impulse
in the second left interspace) or of other congenital heart lesions. This is
especially corroborated if the child was a blue baby at birth or within a
few months afterwards, even if only during intervals of a few hours or days.
The retinal changes are valuable signs when present.
In rare cases incidental phenomena may help in the diagnosis. Cohnheim cites a
case in which the diagnosis was made from the occurrence of embolism of the brain when
the primary thrombus was in the veins of the leg (crossed embolism) ; but such cases are
necessarily extremely rare, and before such inferences are made all commoner factors must
be carefully excluded.
TREATMENT.
Treatment between attacks of cyanosis and dyspnoea is confined to
general hygiene and regulation of the patient's life, as described above for
pulmonary stenosis, though, as a rule, more latitude may be allowed.
During the attacks hot baths and vasodilators (such as
amyl nitrite and nitroglycerin) may be resorted to, and, when there is no
diminished coagulability and the attack is severe, venesection may be
performed.
PATENT DUCTUS ARTERIOSUS (BOTALLI).
PATHOGENESIS.
In many cases in which the arterial circulation is markedly disturbed
in the foetus, the ductus arteriosus (Botalli) may be found to remain patent
after birth. This is a common concomitant of pulmonary stenosis and
especially pulmonary atresia, of the corresponding conditions at the aortic
orifice, and of congenital lesions at either of the auriculoventricular valves.
When viewed in the light of its closure, the mechanism of this secondary
non-closure of the ductus is tolerably clear. The ductus arteriosus Botalli
represents the remains of the sixth branchial arch (Fig. 240). It "is in
a direct line with the pulmonary trunk, is the direct continuation of the
same, and is of almost equal size, while it is of greater diameter than the
descending arch of the aorta. A distinct narrowing of the aortic arch is
to be observed just above the entrance of the ductus into it." (Klotz.)
CONGENITAL HEART DISEASE. 449
Closure of the Ductus Arteriosus. — Several theories have been advanced
to explain the closure of the ductus arteriosus at birth:
Haller thought that it results from coagulation of the blood within its lumen. Kiliani
(1826) was the first to show that with the expansion of the lungs at birth the resistance
in the pulmonary circulation was diminished and a large amount of blood thus diverted
from the channel through the ductus. A number of theories have been proposed to explain
the exact manner in which this diversion of blood through the pulmonary channels brings
about the closure of the ductus arteriosus.
Strassman (1894) attempted to explain the closure on purely mechanical grounds.
He called attention to the fact that the ductus arteriosus penetrates the wall of the aorta
at an acute angle, so that the tissue included in this angle forms a sort of valve. He
believed that when the pressure within the aorta became greater than that in the pulmonary
artery (after birth), this flap of vessel wall closed down over the mouth of the ductus and
prevented blood from entering it. Strassman found, moreover, that if he injected fluid
into the aorta of a new-born child at a pressure under 100 mm. no blood entered the pul-
monary artery. These experiments have been very carefully repeated in a large number
of infants by Klotz, who found that "at all times when the ductus arteriosus was unob-
literated by new-formed or forming fibrous tissue the colored fluid found its way into it
for some distance sufficient to stain it." However, the fact that the communication was
not a free one demonstrates that this valvular action is probably a contributing cause in
cutting off the blood flow or in lessening the pressure in the ductus. *
On the other hand, Schulze in 1871 showed that the walls of the ductus arteriosus,
though poor in or lacking elastic fibres, were particularly rich in muscle fibres. He believed
that when the blood-pressure in the pulmonary artery fell, and the blood was diverted
away from the ductus arteriosus, the muscle fibres in the wall contracted down further
until the lumen was finally obliterated. This occurs without any such intravascular co-
agulation as Haller had supposed; but Langer (1857) has found that it is accompanied
by a very active proliferation of the cells in the intima, with sloughing off of the endothelial
lining (Klotz). The proliferation goes on till the wall of the vessel becomes thicker than
that of either the pulmonary artery or the aorta, and it is finally occluded by fibrosis.
Factors Causing Persistence of Ductus. — Under pathological conditions
it is clear that anything which causes obstruction to the flow of blood
through the arch of the aorta during fetal life (aortic stenosis or atresia,
congenital mitral stenosis, coarctation of the arch of the aorta, etc.) will
cause the right ventricle to carry on the greater part of the circulation and
to force more blood than usual through the ductus arteriosus. This condi-
tion, of course, persists after birth; the ductus, which now represents a
main blood channel, remains open. The flow continues in the usual direc-
tion backward from the pulmonary artery into the aorta.
On the other hand, when there is atresia of the pulmonary artery the
pressure in the ductus is low and blood enters it from the aorta, passing
foward (ventrally) into the rami pulmonales. These facts explain the
persistence of the ductus arteriosus in its usual occurrence as a secondary
congenital lesion.
The occurrence as a primary lesion is rare, only 26 cases having been
collected by Vierordt in 1898, 12 more by Abbott. Klotz believes that
these may be "the result of imperfect expansion of the lungs. In these
cases the blood-pressure has never been lowered in the pulmonary system
to the point which allowed the walls of the ductus to overcome it." It
may also result from congenital weakness of the left ventricle causing a
low blood-pressure in the aorta at the time of birth.
The size and structure of the patent ductus may vary greatly, from a
short and narrow passage to an almost aneurismal dilatation. Acute or
29
450 DISEASES OF THE HEART AND AORTA.
malignant vegetations are not uncommon within the lumen, and the pres-
ence of an open ductus tends to predispose to endocarditis. Arterioscle-
rosis of both the ductus and the pulmonary artery also occurs, perhaps as
a result of the high pulmonary pressure.
SYMPTOMS.
The symptoms of uncomplicated patent ductus arteriosus are usually
obscure and slight, and the condition is often found incidentally. Cyano-
sis is slight and transitory. Slight weakness and shortness of breath on
exertion may occur, but many of the cases are devoid of symptoms.
PHYSICAL SIGNS.
Several diagnostic features of open ductus arteriosus have been pub-
lished at various times. Gerhardt in 1867 described a small quadrilateral
extension of the area of dulness in the second (and first)
left interspace. In this region the pulsation of the pulmonary artery may
be seen, and the well-marked systolic retraction is often seen over the inter-
spaces corresponding to the hypertrophied right ventricle. Zinn, de la
Camp, and others have found, on examination with the fluoroscope, that
Gerhardt's area of dulness corresponds to a round shadow of a
small mass along the left upper margin of the cardiac shadow, where
the pulmonary artery and left auricle are usually seen (Fig. 261) . This
mass shows systolic pulsation and corresponds to the dilated ductus arterio-
sus. This dilatation is frequently aneurismal. The picture with the X-ray
is thus of great diagnostic value, but one must carefully exclude an aneu-
rism of the aorta behind the sinus of Valsalva. In contrast to the shadow
of the left auricle, this shadow is magnified when the tube is placed in front
of the body as compared with the illumination from behind.
The signs on auscultation vary considerably. There is usually
a systolic murmur over the precordium, and especially over the
second left interspace, which sometimes replaces but often follows the first
sound. This murmur when not caused by another concomitant lesion is
due to the rush of blood through a narrowed ductus into the wider lumen
of the aorta. Franc,ois-Franck has shown that this murmur is
heard loudly at the left back over the area at which the aorta
comes in contact with the chest wall (level of the third and fourth spines),
to which it is transmitted in a direct line (Fig. 256). He showed that
the loudness of this murmur bears a definite relation to the phases of respi-
ration. It is loudest during expiration, for at that time the resistance in
the pulmonary circuit is greatest, and hence the blood flows through the
ductus more rapidly; but becomes feebler in inspiration when more
blood passes through the lungs and less through the ductus. Franc. ois-
Franck also found that this variation in the blood flow into the aorta
found equally marked expression in the pulse, causing a rise of pressure
and full pulse in expiration, fall and small pulse during inspiration
(pulsus f>aradoxus).
These signs, however, occur only in cases in which there is an efficient
circulation through the pulmonary orifice. In the cases associated with
CONGENITAL HEART DISEASE.
451
pulmonary atresia where the flow through the ductus is in the opposite
direction, the murmur may be absent at the back and will be loudest during
inspiration, for then the inflow into the lungs is greatest. Never-
theless, the pulse will remain a pulsus paradoxus, for the flow
through the aorta during inspiration will be diminished just the same.
This respiratory variation of murmur and pulse is, however,
often absent in spite of the open ductus, as is the systolic murmur itself
in some cases. Neither bears an absolute relation to the degree of patency
of the ductus.
MI
Fns. 261. — Radiograph of a thirteen-year-old boy with patent ductus arteriosus (Botalli) and aneu-
dilatation of the ductu* and pulmonary artery. (After Hochsinger, in Pfaundler and Schlos>rnann's
4 I)ist-:iM'> of Children.") -4.4, arch of the aorta; DB, ductu* Botalli and pulmonary artery dilated like
an aneurism, giving a cap-shaped top to the shadow of the heart; Ml. internal mammary artery, consider-
ably dilated, denoting an internal collateral circulation.
A diastolic murmur is often heard along with the systolic, sometimes
replacing the second sound but more often accompanying or following an
accentuated pulmonic sound. The inequality in pressure between aorta
and pulmonary artery persists during diastole, and the abnormal blood
flow therefore continues and produces the murmur in diastole. When the
difference of pressure is slight, especially with low peripheral resistance,
the diastolic murmur may be absent.
452 DISEASES OF THE HEART AND AORTA.
DIAGNOSIS.
From the above discussion the points upon which the diagnosis of the
open ductus arteriosus may rest are sufficiently clear, — pulsation over the
right ventricle, Gerhardt's dulness, a systolic or double murmur loudest at
second left interspace and heard at the left upper back, expiratory accent-
uation and pulsus paradoxus, and the pulsating mass in Gerhardt's area
seen on X-ray examination. In addition, the history may show that the
patient was blue at birth (before the pulmonary channels have opened up)
but that cyanosis soon passed off.
J. Plesch in Kraus's clinic (Berl. klin. Wchnschr., 1909, xlvi, 391) has attempted
to make the diagnosis by analyses of the expired air. By a very simple device he deter-
mines the percentage to which the blood flowing through the pulmonary artery is satu-
rated with oxygen. Under normal conditions the saturation is 38-70 per cent, of its oxygen
capacity. In patent ductus arteriosus the blood in the pulmonary artery is mixed blood
and hence its oxygen content is higher (80-90 per cent.). The aerated blood
could enter only through a patent ductus arteriosus.
TREATMENT.
Treatment for the persistence of the ductus consists mainly in those
methods which improve pulmonary circulation, — breathing exercises,
careful hygiene, avoidance of exposure to pulmonary infections, and avoid-
ance of fatigue, general muscular and cardiac overstrain. Since the per-
sistence of the ductus is in itself a compensatory process, it calls for no
special remedy. To ligate it, as might readily be done after opening up
the thorax under positive pressure, would be harmful rather than bene-
ficial. Otherwise general hygienic measures and cardiac stimulants are
of value, as in other diseases. But in many cases open ductus Botalli has
no effect upon the duration of life and requires no treatment.
STENOSIS OF THE AORTA.
Stenosis of the lumen of the aorta may occur in three places:
I. At the aortic valve.
II. Stenosis of the arch of the aorta.
1. Above the entrance of the ductus arteriosus Botalli.
2. Just below the entrance of the ductus arteriosus Botalli.
I. Stenosis at the aortic orifice is one of the rarer con-
genital lesions (2 per cent, of Abbott's series), though probably many of
the milder cases escape detection. It is usually due to endocarditis late in
fetal life.
Those which develop earlier in fetal existence, in which true aortic
atresia occurs, are quite analogous to the cases of pulmonary atresia,
except that the posterior instead of the anterior channel of the common
truncus arteriosus fails to develop. The changes in the fetal circulation
are similar to those in pulmonary atresia, but affect the opposite sides of
the heart. The septa remain open, and occasionally one ventricle (the left)
fails to develop. Practically the entire systemic circulation is carried on
by the pulmonary artery through the ductus arteriosus.
The consequences of the lesion are very severe and few cases survive
birth, in striking contrast to pulmonary stenosis and atresia. No doubt
CONGENITAL HEART DISEASE. 453
this is due to the fact that, since the right ventricle is the stronger in fetal
life, it succeeds in establishing a better compensatory circulation after
atresia of its orifice than does the left. Moreover, when the first breath is
taken after stenosis of the aorta, it is venous instead of arterial blood
which is thrown into the organs.
II. Stenosis in the vicinity of the duct us Botalli
is one of the most common congenital heart lesions, occurring in 198 of
Abbott's 412 cases. Like most abnormalities it arises as an exaggeration
of a condition which is normally present in the foetus. As stated above,
Klotz finds that there is a distinct narrowing of the aortic arch just above
the entrance of the ductus into it. This is no doubt due to the fall of pres-
sure in the aorta which occurs below the left carotid artery and the rise
further on when the blood enters from the ductus.
Hamernik in 1844 divided the cases into: (1) stenosis above the
ductus, (2) those at the entrance of the ductus, and (3) those below the
ductus. Bonnet, who made an exhaustive study of the subject in 1903,
discards Hamernik's second group, and distinguishes two types:
1. The type in the new-^orn, in which the stenosis occurs above the
ductus and the latter remains open.
2. The type found in adults, in which the stenosis occurs below the
ductus. The latter is closed and collateral circulation develops.
Bonnet's studies were based upon 160 cases, of which 55 (34.3 per cent.)
were of the new-born type and 105 (65.7 per cent.) were of the adult type.
Type of the New-born. — The cases of the new-born type represent an
exaggeration of the slight narrowing in the aorta which, as Klotz states,
is present above the left subclavian artery and the ductus Botalli. Em-
bryologically, as Longa points out, this represents the branch
joining the fourth and sixth
branchial arteries (Fig. 240)
and might correspond to a failure of
development of this branch. On the
other hand, the amount of blood in the
aorta is very much depleted by the
flow into the innominate, left carotid,
and subclavian, so that its lumen is
naturally smaller until replenished by
the inflow from the ductus. There is
consequently a region of functional
stenosis between these two points
which may be exaggerated by con-
traction of the muscle-fibres in the Flo. 202.— stenosis of the isthmus of the
wall nf thp flnrtfl Thp WPflkpr thp aort« above the ductus .-trteriosus (Botalli).—
type of 1 1,,- now-born. (From a specimen in the
action of the left ventricle the more Army Utdtai MOMBB, WMUo«tao, D. C.)
marked will be this functional steno-
sis. The ductus Botalli therefore takes on more and more of the circu-
lation in the lower parts of the body, and fetal life may be undisturbed as
long as the right ventricle is pumping aerated blood ; but when this con-
dition ceases and the pulmonary channels widen and pressure in the ductus
falls, the aortic circulation may become insufficient and the syndrome of
454
DISEASES OF THE HEART AND AORTA.
congenital heart disease may result. It is rare for these children to live
more than a few weeks, or at most a few months, and many die at birth.
Physical signs are indefinite, confined to double murmurs over
the chest and back and in most cases cyanosis. There are very often asso-
ciated malformations, such as pulmonary stenosis, open septum ventric-
ulorum, etc.
In this form there is very little attempt at establishment of a c o 1 1 a t-
c r a 1 circulation, since the greater part of the systemic circulation
is maintained by the right ventricle through the open ductus arteriosus,
just as it is before birth. Owing to the completeness of this compensation,
there may be little difference between the pulses in the upper and in the
lower extremities, and the clinical diagnosis is scarcely ever made.
Adult Type. — In the second or adult type, which is more
common, the stenosis occurs just below the entrance of the ductus Botalli,
and this vessel is found to be closed. Indeed, the very stasis at this point
assists in its closure. The mode of
origin of the stenosis at this point is
not clear. Bonnet calls attention to
the fact that the lumen of the aorta
at the stenosis (usually 2-4 mm.) is
about that of the normal aorta at the
time of birth, and thinks that the
whole anomaly may be of post-
natal development. It is possible,
as he suggests, that, when the ductus
Botalli is particularly long, the fibro-
sis of the latter brings about a kink-
ing of the aorta at this point, and
with a dilatation above and stenosis
at the point of kinking.
Skoda, on the other hand, has
suggested that the stenosis may
result from a band of fibrosis passing
around the aorta at this point; but, though this theory is alluring, there
is no definite histological evidence in its support.
The stenosis cuts off the circulation from all parts of the body below
the stenosis, but the high pressure due to the stagnation above it causes a
progressive dilatation of other arterial channels, such as the mammaries,
thoracic and scapular arteries, which are always found to be much dilated.
Indeed, the collateral circulation may be so good that the lumen of the aorta
below the stenosis may be as great as above it (hour-glass constriction),
though usually it is somewhat narrow and it may even be funnel-shaped.
Clinically the presence of this type of stenosis does not necessarily
shorten life, though this depends largely upon the completeness of the
collateral circulation. The symptoms are chiefly those of cerebral conges-
tion,— headache, vertigo, buzzing in the ears. Occasionally there are pains
in the chest. Bonnet calls attention to the fact that in his 105 cases there
was never intermittent claudication, showing that the circulation in the
lower limbs is always sufficient.
FIG. 263. — Stenosis below the ductus arteri-
osus (Botalli), — adult type. (After Bonnet, Rev.
<ie Mdd., Par., 1903, xxiii.)
CONGENITAL HEART DISEASE. 455
PHYSICAL SIGNS AND DIAGNOSIS.
Cyanosis is not common and not a sign of the disease. The most
definite indication is the difference in the size and quality of the pulse in
the upper and lower extremities, the carotid and radial pulses being large
and throbbing, the femoral, popliteal, and dorsalis pedis as well as the
abdominal aorta small or impalpable. Though the diagnosis intra vitam
is rare, Lepine was able to make it from these data in two cases. Dr. W. S.
Morrow calls attention to the possibility of diagnosis from marked differ-
ence in the brachial and tibial blood-pressures, but just as in aneurisms
the difference in size and quality of the pulse on palpation would usually
be more marked than that of the blood-pressures. Moreover, Halsted
has found little difference between brachial and femoral pressures in man
after the abdominal aorta has been occluded with metal bands for the treat-
ment of aneurism. The presence of large tortuous mammary, thoracic,
and scapular arteries aids in the diagnosis. There are usually low murmurs
over the arteries, especially at the angle of the left scapula, as was present
in a case diagnosed by Mercier in 1839.
Valvular disease of the heart frequently results from the increased
work thrown upon the heart and dilatation of aortic and mitral orifices,
and their signs complicate the picture. Before making the diagnosis, it is
always necessary to exclude aneurism and mediastinal tumor by the absence
of dulness on percussion and of abnormal shadows on X-ray examination.
TREATMENT.
Treatment depends purely upon symptoms, occasional venesection
being of value to relieve the headaches. It is most important for the
patient who suffers from these symptoms to avoid over-exertion or excite-
ment, which cause too vigorous action of the heart.
DIFFUSE NARROWING OF THE AORTA.
Virchow has also called attention to another form of abnormality in
the lumen of the aorta, a diffuse narrowing of its entire lumen throughout
its whole extent (hypoplasia of the aorta). This condition is associated
with under-development of the elastic and muscular elements in the arterial
walls. As Virchow and other observers have found, it is often associated
with chlorosis of intense grades and occasionally accompanies other con-
genital malformations of the heart.
About the objective finding there is little dispute. The only point in
question is whether the condition is to be regarded as a true congenital
malformation or as a postnatal development, which, like the changes in
rickets, is determined by conditions of growth and nutrition during child-
hood and may be corrected by cure of these conditions. It is possible that
it may be secondary to the conditions which bring on anaemia, and due to
the fact that the aortic walls have never been subjected to the stimulating
influence of an adequately high blood-pressure. That this may be a factor
in the development of and strengthening of blood-vessel walls has been
shown especially by the results of arteriovenous anastomosis and trans-
456
DISEASES OF THE HEART AND AORTA.
plantation, in which the walls of the transplanted vein become thicker and
richer in elastic and muscular elements (Carrel). It is of course extremely
difficult to determine what would have occurred if such cases had recovered
from their anaemia or primary debility and blood-pressure had reached a
normal level. It is equally difficult to determine that any such cases have
recovered under these conditions, though the fact that the lumen of the
radial artery increases (pulse becomes larger) with the recovery from
chlorosis is of course definite.
For the present, therefore, one must hesitate somewhat in classing
hypoplasia of the aorta among the definite congenital malformations.
FIG. 264. — Transposition of the viscera in embryo and adult. (Schematic.) A, B, C, position of organs
in the embryo; a, b, c, position of organs in the adult. A, a, normal; B, b, transposition of the heart and
arteries simple dextrocardia; C, c, complete situs transversus.
COMPLETE AND PARTIAL SITUS TRANSVERSUS.
It is not extremely rare to meet with a case of complete transposition
of the viscera, so that the heart and stomach are found to lie on the right
side (dextrocardia, dexiocardia) and the liver upon the left.
This condition is probably brought about by a change in position of the
cardiac tube in early embryonic development, so that it lies in the position
of £ instead of the normal S (Fig. 264). Maude Abbott suggests that
in these cases there is a change, the embryo lies in an abnormal position
within the chorion so that its right side instead of its left is closer to the
blood supply. At all events the relation of the organs is the mirror image
CONGENITAL HEART DISEASE.
457
of the normal condition. In complete transposition, however, the organs
develop normally, and the condition, though unusual, has no effect upon
the function. Persons whose hearts lie on the right side are quite as free
from symptoms as those whose hearts are on the left, provided the other
viscera are normal; and the condition is usually discovered accidentally
during routine physical examination. In such cases the apex impulse and
PULMONARY ARTERY
TRICUSPID VALVE
AORTA
MITRAL VALVE
INTER VENTRICULAR SEPTUM
FORAMEN OVALE
Fir,. 265. — Transposition of the valves. (From a specimen in the Army Medical Museum, Wash-
ington, D. C.) The course of the interventricular septum is indicated upon the heart wall. The course
of the blood stream is shown by the arrows.
heart sounds are heard in the fifth right interspace, and the second aortic
is heard on the left side instead of on the right. In persons with thick or
barrel-shaped chests, and especially in women whose breasts are large, the
condition is readily overlooked.
Dextrocardia (dexiocardia) without transposition of other viscera is
much rarer. Most frequently it is due to a pushing or pulling of the heart
to the right by intrathoracic growths or adhesions, but occasionally (in 2
PULMONARY ARTERY
AORTA
FHJ. 260. — Pulmonary artery with four cusps. (From a specimen in the Army Medical Museum,
Washington, D. C.)
of Abbott's 412 cases) it is due to alteration in development. Under these
circumstances the pulmonary artery is given off from the left ventricle,
the aorta from the right. Great variations may be seen in the arrangement
of venae cavse, which sometimes enter the left, sometimes the right auricle.
The results, as in other cases in which the blood is mixed, vary greatly.
The syndrome of congenital heart disease may be present, owing to the
mixing of blood, but the exact transposition of vessels can rarely be
diagnosed intra vitam.
458 DISEASES OF THE HEART AND AORTA.
ABNORMALITY OF THE VALVES.
The number and formation of the cardiac valves may also undergo
alteration in fetal life. In the aortic and pulmonic this is usually due to
inflammatory fusion of two cusps forming a bicuspid valve (Fig. 265),
or to the fact that one of the leaflets is divided into two parts by a slit and
finally under the influence of the blood-pressure grows to form symmetrical
cusps (Fig. 266).
In the mitral and tricuspid valves, especially in association with open
septum ventriculorum, there may be a split in the middle of one leaflet,
practically converting it into two separate cusps. s Except for the forma-
tion of valvular insufficiencies which result, multiplicity or paucity of the
cusps has no pathological effects.
A large number of other malformations, such as partial separation of
the two ventricles to form a "bifid apex," defective formation of the chest
wall with exposure of the heart (ectopia cordis), malposition of the heart
causing it to lie in the abdomen or the neck, transposition and malformation
of the great arteries and veins, are encountered. Space does not permit
of a complete discussion of these conditions, for which the reader is referred
to the magnificent article by Dr. Maude Abbott in Volume IV of Osier's
Modern Medicine.
BIBLIOGRAPHY.
DEVELOPMENT OF THE NORMAL HEART.
The development of the normal heart is well discussed in Piersol's, Morris's, and
Quain's anatomies and in the various text-books of embryology.
The following articles may be consulted also:
Eternod: Premiers stades de la circulacion sanguine dans 1'ouef et 1'embryon humains,
Anat. Anzeig, 1899, xv, 181.
His, W.: Anatomie menschlicher Embryonen, Leipzig, 1880. For an excellent series of
figures see also Kollman, J.: Handatlas der Entwicklungsgeschichte des Menschen,
Jena, 1907.
Born, G.: Beitrage zur Entwicklungsgeschichte des Saugethierherzens, Arch. f. mik. Anat.,
Bonn, 1889, xxxiii, p. 284.
Robinson, A.: Early Stages of Development of the Pericardium, J. Anat. and Physiol.,
Lond., 1903, xxxvii, 1.
Pohlman, A. G.: The Course of the Blood through the Heart of the Fetal Mammal, etc.,
Anat. Rec., Phila., 1909, iii, 75.
CONGENITAL HEART DISEASES.
Lancereaux: Das anomalies cardiaques, Gaz. d. hop., Paris, 1880, liii, 850, 875, 883, 890,
906, 930, 981.
Morgagni: De sedibus et causes morborum, Venet., 1761.
Peacock, T. B.: Malformations of the Human Heart, Lond., 1866.
Keith, A.: Malformations of the Bulbus Cordis, Studies in Pathol., Quatercent. Pub.
Aberdeen Univ., 1906, 55.
Bouillaud: Traite" clinique des maladies du coeur, Paris, 1835.
Rauchfuss: Missbildungen des Herzen's, Gerhardt's Handb. d. Kinderkrankh., 1878,
iv, 1 part.
Yierordt, H.; Die angeborene Herzkrankheiten, Nothnagel's Handb. d. spez. Pathol. u.
Therap., Wien, 1901, xv, II part 1.
Abbott, M. E.: Congenital Cardiac Disease, Mod. Med., ed. by Wm. Osier and Thos. Me-
Crae, Phila., 1908, iv, 323.
CONGENITAL HEART DISEASE. 459
Osier, Wm. Quoted from Abbott.
Panum, P. L.: Ueber die Entstehung von Missbildungen, Berl., 1860.
His, Win., Sr. : Anatomic menschlicher Embryonen, Leipz., 1880.
Ii.it like, H.: Die Entwickelung der Arterien, welche beim Saugethier von den Bogen der
Aorta ausgehen, Arch. f. Anat., Physiol. u. wissench. Med., Berl., 1843, 276.
Bremer, J. L.: On the Origin of the Pulmonary Arteries in Mammals, Am. J. Anat., Balto.,
1901-1902, i, 137.
{ireil, A.: Beitrag zur vergleichende Anatomic und Entwickelungsgeschichte des Herzens
und des Truncus arteriosus der Wirbeltiere, Morph. Jahrb., Leipz., 1903, xxxi, 123.
Hunter, Wm.: Medical Observations and Enquiries, 1784, vi, 300. (Qupted from Peacock.)
Kussmaul, A. Quoted from Vierordt.
Loeb, J.: Ueber die Entwicklung von Fisch-embryonen ohne Kreislauf, Arch. f. d. ges.
Physiol., Bonn, 1893, liv, 528.
Knower, H. McE.: Effects of Early Removal of the Heart and Arrest of the Circulation
on the Development of Frog Embryos, Anat. Rec. (Am. J. Anat.), Balto., 1907.
Mall, F. P.: A Study of the Causes underlying the Origin of Human Monsters, J. Morphol.,
Phila., 1908, xix, 3.
Dareste: Recherches sur les monstrosites, Paris, 1891. Quoted from Mall.
Stockard, C. R.: The Development of the Fundulus Heteroclitus in Solution of Litliium
Chloride, with Appendix on its Development in Fresh Water, J. Exper. Zool., Balto.,
1906, iii, 99.
Bardeen, C. R.: Abnormal Development of Toad Ova fertilized by Spermatozoa exposed
to the Rontgen Rays, ibid., 1907, iv, 1.
Senac, quoted from Bard, L., and Curtillet, J.: Contribution a I'dtude de la physiologic
pathologique de la maladie blue. Forme tardier de cette affection. Rev. de me"d.,
Paris, 1889, ix, 993, from whom Grancher et al. are quoted.
Stiile, Moreton: On Cyanosis or Morbus Cceruleus, Am. J. M. Sci., Phila., 1844, N. S. viii, 25.
Osier, Wm.: Chronic Cyanosis, with Polycythaemia and Enlarged Spleen: a new Clinical
Entity, Am. J. Med. Sci., 1903.
Knapp, quoted from Posey, W. C.: Cyanosis Retinae, Am. J. Med. Sci., Phila., 1905,
cxxx, 415.
Tate, W. W. H.: Case of Malformation of the Heart, Trans. Path. Soc., Lond., 1892, xliii, 36.
Hebb, R. G.: Hearts with Congenital Defects and Inflammatory Disease, ibid., 1897,
xlviii, 41.
McOscar, J., and Voelcker, A.: On a Case of Traumatic Rupture of the Ventricular
Septum, ibid., 1897, xlviii, 47.
Reiss, P.: Contribution a l'6tude des malformations congenitales du coeur, Maladie de
Roger, These, Par., 1893.
Roger, H.: Recherches cliniques sur la communication des coeurs par inocclusion du
septum interventriculaire, Bull, de 1'Acad. de M6d., Paris, 1879, se*r. viii, t. ii,
1074 and 1189.
•Cadet de Gassicourt, Potain. Quoted from Reiss, 1. c.
Klotz, O.: The Closure of the Ductus Arteriosus and its Bearing on Arteriosclerosis, Trans.
Asso. Am. Phys., 1907, xxii, 213.
iierhardt, C.: Persistenz des Ductus arteriosus Botalli, Jenaische Ztschr. f. Med. u. Natur-
wissench., 1867, iii, 105. (Quoted from Vierordt.)
:Zinn, W.: Zur Diagnose der Persistenz des Ductus arteriosus Botalli, Berl. klin. Wchn-
schr., 1898, xxxv, 433.
De la Camp, O.: Familiares Vorkommen angeborener Herzfehler; zugleich ein Beitrag
zur Diagnose der Persistenz des Ductus arteriosus Botalli, Berl. klin. Wchnschr.,
1903, xl, 48.
Franc.ois-Franck, A.: Sur le diagnostic de la perseverance du canal arteriel, Cong, de
1'avancement des sciences, Paris, 1878.
Bonnet: Sur la lesion de la ste*nose de 1'isthmus conge*nitale de 1'aorte dans la region, Rev.
de MeU, Paris, 1903, xxiii, 108, 255, 335, 419, 481.
XI.
HEART-BLOCK AND THE ADAMS-STOKES SYNDROME.
HISTORICAL.
In 1827 Robert Adams, of Dublin, reported the case of a revenue
officer, aged 68, whose pulse-rate was 30 per minute and who suffered
from dyspnoea, cough, and attacks of fainting (" apoplectic attacks"),
" during which his pulse would become even slower than usual. . . .
He recovered from them without paralysis." In the same year an exactly
similar case was reported in great detail by Wm. Burnett. Burnett's
observations were reported even more carefully and in greater detail than
those of Adams and ill deserve to have fallen into oblivion. Burnett
further called attention to the fact that Morgagni had described two cases
of " epilepsy with slow pulse" in 1761. Holberton described another case
in 1841, but general attention was not attracted to the condition until
Wm. Stokes published four cases in 1846.
Since then the condition of persistent extreme brady-
cardia with syncopal or convulsive seizureshas been
known asthe Adams-Stokes syndrome, though it may more
accurately be designated by the names of Morgagni-Adams-Stokes, as
Pletnew has done, or by that of Morgagni-Adams-Burnett or Adams-Bur-
nett syndrome.
As but little can be added to the clinical descriptions of these cases,
one of Stokes's histories may be reported in some detail:
"Edmund Butler, aged 68, stated that his health had been robust until three years
before admission, at which time he was suddenly seized with a fainting fit. This occurred
several times during the day and always left him without any unpleasant effects. Since
that time he has never been free from attacks for any considerable length of time, and has
had at least fifty such seizures. The fits are very uncertain as to their period of invasion
and very irregular as to their intensity, some being much milder and of shorter duration
than others. They are induced by any circumstance tending to impede or oppress the
heart's action, such as sudden exertion, distended stomach, or constipated bowels. There
is little warning given of the approaching attack. He feels, he says, a lump first in the
stomach, which passes up through the right side of the neck, where it seems to explode
and pass away with a noise like thunder by which he is stupefied. This is often accompanied
by a fluttering sensation about the heart At first he found that spirits were the
best restorative or prophylactic, but latterly he has not used them, being 'afraid to die
with spirits in his belly.'
"On admission he was haggard and emaciated On percussion the chest
is universally resonant. The respiratory murmur is louder and combined, especially pos-
teriorly, with large mucous rales. The impulse of the heart is slow and of a dull heaving
character The first sound is accompanied by a soft bruit de soufflet. The second
sound is alsp imperfect We remarked to-day that on listening attentively to the
heart's action we perceived that there were occasional semi-beats between the regular con-
tractions,— very weak, unattended with impulse, and corresponding to a similar state of the
pulse, which thus amounts to about 28 in the minute, the evident beats being only 28. ...
460
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 461
" (June.) The cardiac phenomena remain as before, but a new symptom has appeared,
namely, a very remarkable pulsation in the right jugular vein. This is most evident when
the patient is lying down. The number of reflex pulsations is difficult to be established,
but they are more than double the number of manifest contractions. About every third
pulsation is very strong and sudden and may be seen at a distance; the remaining waves
are much less distinct.
"He has scarcely had any of the cardiac attacks since he was discharged."
THE CONCEPTION OF HEART-BLOCK.
Stokes did not appear to have any definite understanding of the nature
of these "semi-beats" nor of the functional disturbance associated with
them. A similar, more accurate observation was made by A. Chauveau.
Chauveau in 1882 made observations upon a case whose usual pulse-rate
was 24 per minute, and who suffered from occasional attacks of vertigo
and loss of consciousness. Tracings made from the apex showed a series
of large beats at regular intervals corresponding to the loud heart sounds
and to the radial pulse, and also a second series of very small notches
occurring at equally regular
ricular beat was absent, and
™_ , i , , Fio. 267. — Tracing of the apex beat in a case of Adams-
Chauveau Correctly Concluded Stokes disease. (After Chauveau.)
that these small notches were
due to the contractions of the auricles, which were beating at a
rate of 66 per minute while the rate of the ventricles was 24. Chau-
veau investigated the matter experimentally, and was able to demon-
strate that in horses upon stimulation of the vagus the auricles could be
observed to beat more frequently than the ventricles. He therefore natu-
rally considered the dissociation of auricular and ventricular rhythm as
due to over-stimulation of the vagus. This conclusion was further war-
ranted by the fact that his patient had pains at the back of the neck, and
the chief of service had diagnosticated a lesion of the medulla at the level
of the vagus nucleus.
While Chauveau was experimenting in France, experimenters in Germany and in
England were unconsciously throwing light upon the condition from different stand-points.
In 1883 Wooldridge, under Ludwig's direction, was investigating the course of the nerves
in the cardiac septum, and for this purpose constricted the interauricular septum by tight-
ening a fine silk ligature introduced so as to embrace only the septum. He observed:
"the auricles and ventricles continue to contract, but no longer with equal frequency.
Stimulation of the vagus causes the auricles to stop beating, the ventricles continue.
"The ligature is removed; at first the auricles and ventricles beat at different rhythms,
then the uniform (normal) beats of both chambers return, and stimulation of the vagus
now inhibits both auricle and ventricle."
Wooldridge's results were confirmed in 1884 by Tigeretedt, who cut through the
septum with a specially devised "atriotoine."
462 DISEASES OF THE HEART AND AORTA.
These observations under Ludwig's direction were made with the
view only of cutting the intracardiac nerves. As a matter of fact, the
muscular connections were severed as well, but the importance of these
was disregarded.
The myogenic conduction from auricle to ventricle was, however, at this-
very period being demonstrated by Gaskell in Cambridge upon the heart
of the tortoise and frog, in which the auriculoventricular function is repre-
sented by a wide band of muscle whose properties differ somewhat from
those of either the auricle or the ventricle. Gaskell demonstrated that "if
this auriculoventricular ring were clamped, the auricle continued to beat
at unaltered rhythm, but as the clamp was tightened the period between
auricular and ventricular contractions (As— Vs interval, on conduction
A -SEC.
JUGULAR
APEX
BRACK.
FIG. 268. — Partial heart-block (3 : 1 rhythm) produced by pressure upon the vagus in a patient with
disturbed conductivity who was also subject to attacks of the Adams-Stokes syndrome. (Tracing made by
Dr. F. W. Peabody and the writer.) A, A, A, A, auricular contractions to which the ventricles do not respond.
time) was gradually lengthened; then the ventricle failed to respond to
some of the impulses from the s auricle, and, according to the tightness of
the clamp, the ventricle could be made to .... respond to every second
contraction of the auricles (partial heart-block), to respond to every third,
fourth, or other contraction, or to remain quiescent. When the clamp
was closed very tightly the ventricle remained still for a variable time,
then, in accordance to its inherent rhythmical power, developed a rhythm
of its own (rhythm of development), the rate of that rhythm when fully
developed and the length of time that the standstill lasted being correlated
with the rhythmicity of the tissues." The condition in which the ventricular
r ventricle no longer follows any of the impulses from the auricles is termed
complete heart-block, in contrast to the partial heart-blocks in which the
impulse ventricle is responding to some, but not all, of the impulses arising
in the auricles.
Gaskell showed that heart-block also set in when the bridge of tissue
connecting the auricles and ventricles was cut down to a sufficiently nar-
row strip. He was able to produce similar blocks between portions of the
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 163
auricle or ventricle by clamping or cutting, just as Romanes had done for
the muscle in the bell of the medusa. Gaskell demonstrated also that the
block between auricles and ventricles remained complete, when the only
connection between the auricles and the ventricles was formed by the
coronary nerve.
THE AURICULO(ATRIO) VENTRICULAR MUSCLE BUNDLE.
Anatomy. — The existence of muscular connections between the auricles
and ventricles in man and mammals was, however, denied until 1893,
when Stanley Kent, of Oxford, found that in the rat and other
mammals there was a large strand of small fusiform muscle cells with
fusiform nuclei which ran in the septum membranaceum and connected
the musculature of the ventricle with that of the auricle.
In the same year Wm. His, Jr., described the presence in the mouse,
dog, and man of a bundle of muscle-
fibres which "arises from the posterior
wall of the right auricle near the inter-
auricular septum, in the atrioventric-
ular groove, lies upon the upper edge
of the muscular interventricular sep-
tum, passes forwards and to the vicin-
ity of the aorta, where it divides into
a right and a left branch. The latter
passes down to the base of the anterior
mitral cusp."
These* anatomical findings of His
have been confirmed by Braeunig,
Humblet, Retzer, and Tawara. The
latter found that the fusiform cells
described by Kent were really Purkinje
fibres, and that the muscle bundle of
His is in reality continuous with the
entire network system of Purkinje
fibres which permeates both ventricles.
Tawara also demonstrated the pres-
ence of nerve-fibres within the His bun-
dle, and Gordon Wilson has recently
demonstrated ganglion cells as well.
In a later research Retzer has stated that this conducting system is
continuous above with the septal portion of the right auricle (Fig. 269), and
that its cells are of the same histological structure us those about the sinus
region. He believes that it is a true sinoventricular bundle, but the recent
work of Lydia de Witt seems to confirm the claims of Tawara. The idea
that the cardiac impulse must pass from sinus to auricle before reaching
the auriculoventricular bundle is borne out also by the observation of Dr.
G. S. Bond that in the frog the auriculoventricular muscle can be seen to
contract considerably later than the auricle but before the ventricle.
Experimental Physiology of the Auriculoventricular Bundle. — The
first experiments upon the physiology of heart-block in mammals \\viv
Fro. 269. — The right branch of the auriculo-
ventricular bundle in the dog'* heart. (After
Barker and Hirschfelder. Arch. Int. Mecl., 1909.)
464 DISEASES OF THE HEART AND AORTA.
performed by Stanley Kent, the discoverer of the auriculoventricular
bundle, in 1893, and were recorded by him in his original publication in
the following words: "By the use of a suitably constructed clamp ... I
have been able to verify for the mammal (i.e., in the excised heart of the
rat), almost all the effects described by Gaskell as obtained in the frog."
Kent thus seems to have forestalled all the later experiments upon the sub-
ject, but the brevity of his physiological note left much to be investigated.
In 1895 His repeated the experiments of Wooldridge and Tigerstedt, and
demonstrated that in order to bring about dissociation of the auricles and
ventricles it was not necessary to injure the entire septum but merely this
auriculoventricular muscle bundle.
In 1899 he applied his anatomical and physiological studies to a case
of Adams-Stokes disease, in which he confirmed Chauveau by finding inde-
pendent action of the auricles and ventricles, and designated this by Gas-
kell's term "heart-block.'7 His also gave an excellent tracing, taken during
a syncopal attack, demonstrating that the auricles continued at their
usual rate while the ventricles ceased to beat for several seconds and then
resumed their beat at a gradually increasing rate (corresponding to Gaskell's
"rhythm of development")-
56
JUG.
'
FIG. 270. — Tracings from the carotid artery and jugular vein of a patient with Adams-Stokes
disease, showing stoppage of the ventricles and continuance of the auricular contractions during the
attack. (After His, Deutsches Arch. f. klin. Med., 1899, Ixiv.) 1, 2, 3, 4, 5, 0 represent the onset of
independent ventricular contractions.
The experiments of Kent and His and their predecessors were con-
firmed by Humblet, Hering, and Tawara, and led to the conclusion:
1. That the slow pulse of Adams-Stokes disease was due to dissocia-
tion between the auricles and ventricles (heart-block) and to the slow
independent rhythm of the ventricles.
2. That the syncopal attacks (Adams-Stokes syndrome) were due
to cessation of ventricular beat but not of the auricular beat.
Experimentally they had produced the former but not the latter in
mammals, while Gaskell had produced it in the frog and tortoise. Nor
had pathological changes in the auricular ventricular bundle been shown
in cases dying from the Adams-Stokes syndrome. The missing link was
supplied by American scientists.
Factors Affecting Degree of Heart=block. — In 1904 E r 1 a n g e r
began a series of experimental and clinical investigations upon this condi-
tion. He first confirmed all of His's findings in man, and refuted Chauveau's
claim, that the heart-block was due to the vagi, by showing that when in
his cases the latter were paralyzed with atropine the heart-block did not
pass off.1 Then he devised a modification of Gaskell's clamp, an L-shaped
hook of steel wire whose arm could be pressed against a brass block by
means of a bolt and screw.
>
1 Edes had previously shown that belladonna had no effect in his cases of Adams-
Stokes disease.
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 465
The hook was introduced into the right wall of the aorta just above its origin (the
pericardial fat having been dissected off), the point passed backwards and downwards
into the left ventricle, and then pushed through the ventricular septum till it entered the
right ventricle (Fig. 271). The brass block was then pushed down over the long arm of
the L and the nut gradually screwed taut. The first effect observed was lengthening of the
conduction time ( Ag-V8 or A-V interval); then alternate ventricular beats disappeared (2 : 1
rhythm), at first occasionally, then regularly. With further tightening of the clamp a
3 : 1 rhythm occurred, and finally complete heart-block.
"After the ventricles have emptied themselves it may be
seen that each contraction of the auricles sends into the
former a distinct wave, upon the subsidence of which the
volume of the ventricles is seen to have been considerably
increased." In many but not in all of his experiments the
complete block began with a complete stoppage of the
ventricles, exactly like that in the Adams-Stokes syndrome,
in which "the ventricles stop beating without warning.
The auricles continue to beat with an apparently unaltered
rate ..... The ventricles enlarge with each contraction
until their distention becomes really huge ..... Respi-
ratory convulsions may begin. Witnesses are almost con-
vinced that the experiment has come to a close when it
may be that after more than twenty seconds the ventricles
suddenly empty themselves with one great effort." This is
sooner or later followed by another and another until the
slow ventricular rate is gradually assumed.
FIG. 271. — The Erlanger
heart-block clamp compressing
the auriculoventricular bundle
(A V B). S M, septum mem-
branaceum; MV, mitral valve.
Factors Affecting Stoppage of the Ventricles.
— This "stoppage" of the ventricles
represents the condition which is the cause of
death and discomfort in man. Patients, as a rule, remain free from symp-
toms while the pulse-rate remains regular. A study of the factors bringing
it about was therefore of the utmost importance. Erlanger was able to
show that it was neither brought on nor prevented by stimulation of the
cardiac nerves when the heart was in a condition of either partial or com-
plete heart-block; indeed the cardiac nerves exert less effect than upon the
^pnn^^^^
1:1 CUmpiug
2:1
Stoppage
Undamped
FIG. 272. — Effect of gradually tightening the clamp. (After Erlanger ami Hirschfelder.) Shows
2 : 1 rhythm, finally stoppage of the ventricles with complete block. After this the ventricles can be seen
to contract at an independent rhythm.
uninjured heart. Erlanger and Hirschfelder investigated the subject still
further, and found that stoppage of the ventricles occurred when the clamp
was tightened rapidly and a complete block produced suddenly. It occurred
more rarely when the clamp was tightened slowly, and the heart was
allowed to pass through the various stages of partial block (2 : 1 and 3 : 1
rhythm). In only two experiments did it occur after the ventricles had
already taken on their independent rhythm. Whenever from any cause
(stimulation of the accelerators, application of heat, or rhythmic induction
30
466 . DISEASES OF THE HEART AND AORTA.
shocks) the rate of the auricles was increased, the degree of block was also
increased, a normal rhythm (1:1) passing to a 2 : 1, a 2 : 1 rhythm to a
4 : 1 or to complete block. When this occurred rapidly stoppage of the
ventricles sometimes set in. Conversely, slowing of the auricles from any
cause (stimulation of the vagus, application of cold, etc.) improved con-
ductivity and facilitated the passing off of the block.
In this respect the experimental heart-block differs greatly from the
clinical, since in a number of cases (Gibson, Thayer) it has been found that
stimulation of the vagus increases the degree of block while atropine re-
moves a partial but not a complete block. In other cases (Edes, Erlanger,
Schmoll) it has no such effect.
The duration of the period of " stoppage " (during which the ventricles
remained quiescent) varied greatly, and was greatest in those hearts which
could be inhibited longest by stimulation of the vagus. As in Gaskell's
tortoise, it seemed to be definitely "correlated to the rhythmicity " of the
ventricles, which is greater in some hearts and at some stages of the experi-
ment than at others. In general it has appeared to the writer that the
poorer the condition of the ventricular muscle the longer the period of
stoppage. Slight asphyxia, though it did not in itself bring about
stoppage of the ventricles, seemed to lengthen the period of stoppage
from clamping.
In some experiments the ventricle remained quiescent for so long
(more than 55 seconds) that the animal would have died at once had not
the heart been revived by mechanical stimulation.
In a subsequent paper Erlanger has shown that the condition of block
on clamping or injury depends upon the condition of the cells in the His
bundle. Each cardiac impulse leaves them in a condition of lowered irrita-
bility from which they recover gradually. When the injury is slight they
recover just too late for the next impulse from the auricle and are only
ready to receive the second stimulus (a 2 : 1 rhythm resulting). When
they are injured a little more they recover in time for every third or every
fourth impulse, and finally the stimulus always remains below the threshold
of irritability and complete block sets in. Similarly, the more rapid the
rhythm the less time the cells have had to recover and the less the intensity
of impulse from the auricles, hence the greater the block.
As regards the ventricle, the greater its irritability and rhythmicity
the sooner it will respond to its own internal stimuli with a contraction
and the shorter the stoppage and the more rapid the rhythm. A low ven-
tricular rhythm (under 25 per minute) is therefore often a sign of poor
condition of the ventricle and of a tendency to stoppage during the period
of complete block in spontaneous attacks.
The experiments of Erlanger and Hirschfelder have been confirmed
by v. Tabora under Hering's direction. The latter has found that stimu-
lation of the vagus may under certain circumstances increase the degree
of heart-block and facilitate the onset of stoppage, especially when digi-
talis has been administered. The apparent discrepancy between their
findings is probably due to the presence of the different nerve-fibres
in the vagus, so that sometimes conductivity, sometimes irritability is
most affected.
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 467
RELATION OF HEART-BLOCK TO ADAMS-STOKES SYNDROME.
It cannot be too strongly emphasized that: (1) heart-block (complete)
and Adams-Stokes syndrome are by no means synonymous; the former
represents merely the dissociation of rhythms, while the Adams-Stokes
syndrome brought on by cerebral anaemia during ventricular stoppage is
a totally different matter; (2) heart-block may persist for months or years
without the occurrence of the syndrome, as in the case about to be described.
Attacks of the Adams-Stokes syndrome may occur in three ways:
(1) at the transition from normal rhythm to complete block; (2) in the
midst of complete block; (3) probably also from stimulation of the vagus
in certain cases where conductivity is already diminished.
In the cases where the Adams-Stokes syndrome (ventricular stoppage)
appears at the transition from normal rhythm to complete block, the attacks
are usually preceded by quickening of the pulse; and the block passes off
and reappears suddenly. When the complete block becomes permanently
established, the Adams-Stokes syndrome may disappear, as is well shown
by the following case,1 seen by the writer in consultation with Dr. H. G.
Beck. The Adams-Stokes syndrome may be present only in the initial
and not the later stages of the heart-block.
CASE OF HEART-BLOCK, WITH ADAMS-STOKES SYNDROME ONLY AT ONSET OF BLOCK.
J. L., aged 72, had been perfectly healthy all his life except for attacks of malaria
when between 14 and 40 years of age, and pneumonia about ten years ago. Denies syphilis
and gonorrhoea; drinks little, but smokes considerably. Has been a blacksmith until
July, 1907. At this time he was struck on the head by a railroad gate, became unconscious
for one or two minutes, after which he recovered at once except for a slight transitory
weakness of the right arm and slight transitory aphasia. He remained well until Novem-
ber, 1907, pulse being 60 to 64. In the latter part of November he began to
have weak spells in which he fell but did not lose consciousness. He was seen by
the writer on January 12, when he had been having numerous attacks for about a week.
Fi<;. 273. — Tracing from jugular vein and carotid artery, in a case (J. L.) of complete heart -block,
after the syncopal attacks had subside* 1.
Patient was a fairly nourished man of good rosy color, pupils reacting normally; no signs
of intracranial disturbance nor of lues. Chest clear. Heart not enlarged; action regular;
p ii 1 se- ra t e :W |>er minute. Sounds accompanying the beats are loud and tin- first
sound is accompanied by a flowing systolic murmur not transmitted to axilla. Second
sound clear. Between these in the long pause there can l»c heard two or three
very soft distant sounds like the ticking of a watch, accompanying which
small undulations may be seen over the jugular vein, and on 1110*1 delicate
palpation of the radial a slight impulse can be felt there fci
1 A study of this case has been reported by Dre. H. G. Beck and \\ 15. Btoket,
Int. Med.. Chicago, 190S.
468 DISEASES OF THE HEART AND AORTA.
well, due to the beating of the auricles against the root of the aorta. The venous
tracing (Fig. 273) showed complete heart-block. At this time he had no attacks. On
January 17, however, he was again seen. His attacks had been very numerous, the pulse-
rate rising and falling with great rapidity. Tracings from the jugular vein and carotid
arteries, taken as an attack came on, show the following sequence events: At first a period
of complete heart-block lasting a few minutes. This then passed off and was
succeeded by a few moments of 2:1 rhythm. The 2 : 1 rhythm passed suddenly
into a 1 : 1 rhythm at a rate of about 90 per minute and began to quicken.
It was then prophesied that an attack was imminent, and in an instant the ventri-
cles suddenly ceased to beat. The patient cried out, became ashy pale, and a
convulsion set in, during which the auricles continued to beat at the old rate. In
about 11 seconds the ventricles began to beat, and soon resumed their regular independent
FIG. 274. — Diagram representing the conditions found in the tracing Fig. 273. A, auricular
contractions ; V, ventricular contractions ; 1, 2, first and second heart sounds ; a, a, sounds due to
contractions of the auricles.
rate of 28 to 30 per minute in complete block. After a few more seizures an
hour or so passed without further change in rate or further symptoms. When seen in the
afternoon and again on the next day the pulse-rate had not varied. It was then prophesied
by the writer that no more attacks were imminent, but the patient was
kept in bed for several weeks afterwards. A few weeks later he had a sinking spell with
weakness of the pulse, but no change in rate and regularity and no unconsciousness or
convulsions. This he also recovered from and remained free from symptoms and attacks
until his death two months later. He died rather suddenly but was conscious to the last;
his pulse-rate had not changed, and he died not from the Adams-Stokes syndrome but
from his coronary sclerosis. The lesion found in the His bundle will be discussed below.
In this patient the Adams-Stokes syndrome passed off as the com-
plete block became established.
Variations in Pulse=rate. — This case is no isolated example of such a
condition. Even Burnett's case (1824) furnishes an example, for he says,
"the pulse beats at the rate of 74 in the minute for the space of about a
minute, then intermits for 7, 8, or 10 seconds In the evening I
found that he had been attacked many times but was then much better.
.... He complained, however, of more pain about the precordia and
his pulse beat only 20 in the minute/' A similar tendency to improvement
after heart-block set in has been noted in Stokes's first case (1846), in that
of Alfred Webster (1900), in one of the cases reported by Edes (1901), and
in one of Erlanger's cases (1905).
Stoppage of the Ventricles during Complete Heart=block. — Unfortu-
nately, the Adams-Stokes syndrome does not always end with the estab-
lishment of permanent complete block. Just as in the two experiments
of Erlanger and H^rschf elder mentioned above, stoppage of the ventricles
sometimes occurs in the midst of a complete block when the pulse-rate is
slow and without preliminary variations in rate. This took place in the
case reported by His and in Erlanger's first case. The influences producing
this stoppage act directly upon the ventricles, the auricular rate being
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 460
Fio. 275. — Heart of a patient (J. L.) showing calcifications which produced Adams-Stokes disease.
(Drawn from the specimen.) A, B, C, D, E. Sections through the interventricular septum, .-howing the
ratification pressing upon the auriculov.-ntnrular bundle. (After Beck and Stokes.) F. Section through
a. iPhotomicrograph by Dr. C. S. B«>n<lJ
470
DISEASES OF THE HEART AND AORTA.
unchanged or quickened, but the nature of these influences is not well
understood. Erlanger has shown that the plugging of a coronary artery
in animals does not bring stoppage from complete block. On the other
hand, slight asphyxia, such as holding the breath after slight exercise",
FIG. 276. — Diagram showing the two types of ventricular stoppage producing the Adams-Stokes
syndrome. 1. Ventricular stoppage only at the moment when conduction ceases. 2. Stoppage of the
ventricles setting in during the periods of complete block. A, auricular contractions; V, ventricular
contractions; A—V, conduction of impulses from auricles to ventricles.
brought them on regularly. However, it cannot be said that the prognosis
is much if any more unfavorable in these than in the other group of cases,
since Erlanger's case at least lived several years after observation, and
this point has not been noted in most of the reported cases. Prof. Thayer
has recently reported a case in which the block has passed off.
LESIONS OF THE AURICULOVENTRICULAR BUNDLE.
These two groups represent cases in which the block appears to be
myogenic; and pathological evidence indicates that such is the case. Al-
though Adams (1827) mentions fatty degeneration of the ventricular septum
in his case, and many other au-
topsies had been performed, the
first case in which a lesion of the
auriculoventricular (or atrioven-
tricular) muscle bundle was
demonstrated was that of Luce
in 1902 in which a sarcoma was
found involving the auriculoven-
tricular bundle. Luce, however,
did not regard this as a causal
factor for the Adams-Stokes syn-
drome, and the first case in which
this connection was definitely
established was reported by Sten-
gel, of Philadelphia, in 1905, with
excellent figures showing fibrosis
of the bundle. Soon after this
Schmoll reported a case in which
no lesion could be discovered
macroscopically, but fibrosis of
the His bundle was demonstrated with the microscope.
In the case of J. L. reported above, autopsy showed extensive atheroma
of the aorta; the coronary arteries were converted into pipes of bony hard-
INF.
FIG. 277.— Section of a luetic infiltration of the
auriculoventricular bundle. (After Ash ton N orris and
Lavenson.) INF., area of round-cell infiltration.
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 471
ness. Large calcifications were present upon the mitral valve and in the
upper part of the interventricular septum, in which a long tongue of calci-
fication can be seen to intercept the auriculoventricular bundle. This was
beautifully shown in the sections which were made by Stokes under Retzer's
direction, and thoroughly explain the clinical features observed.
In the past two years a considerable number of cases have been studied
both histologically and physiologically, lesions in the His bundle being
uniformly found. The following represent some of the lesions reported:
Gumma, 7: Handford (1904), Keith and Miller (1906), Grunbaum (1906), Ashton,
Morris, and Lavenson (1907), Heineke (1907), Fahr (1907), Rendu (1895).
Calcified patches involving the bundle, 4: Stengel (1905), Hay and Moore (1906),
Beck and Stokes (1908), Heineke, Muller, and Hoesslin (1908).
Fibrosis of the bundle, 6: Schmoll (1906), Gibson, G. A. (1906), Fahr (1907), Gibson,
A. G. (1908), Dock, G., Vaquez and Esmein.
Tumors in the septum: Fibroma: Sendler (1892). Round-celled sarcoma: Luce.
Anaemic infarction of the auriclo(atrio) ventricular bundle: Jellinek, Cooper, Ophuls
<1906), MacCallum (1908).
Simple round-celled infiltration of the auriculoventricular bundle, 1: Heineke,
Muller, and Hoesslin (1908).
Mural ulceration involving the auriculoventricular bundle (ulcerative endocarditis) :
James (1908).
Fatty degeneration: Butler (1907).
Arteriosclerosis of artery supplying auriculoventricular bundle: D. Gerhardt (1908).
Absence of demonstrable lesion, macroscopic or microscopic: Heineke, Muller, and
Hoesslin (1908).
CASES OF ADAMS-STOKES SYNDROME NOT DUE TO LESION OF THE
AURICULOVENTRICULAR BUNDLE.
Although the overwhelming majority of cases of the Adams-Stokes
syndrome (persistent bradycardia, complete heart-block, and syncopal
attacks) have been proved to be due to lesions of the auriculoventricular
bundle, a few cases in the literature remain which must still be regarded
as due to over-stimulation of the vagus.
The most typical of these attacks is described by Thanhoffer (1875). A colleague was
compressing his own vagi in the neck, when suddenly he "stared at me with glassy eyes,
without releasing his grip and without answering. I could remove his hand from his throat
only with the greatest force and they still remained clenched. Consciousness did not
immediately return even after removing his hands."
Another case was reported by Neuberger and Edinger in 1898: The patient was a
neurasthenic man, aged 46, who had been repeatedly examined by various physicians but
no signs of organic nervous disease discovered. He suffered from severe constipation.
From Nov., 1896, to January, 1897, he occasionally fainted when at stool. His pulse dur-
ing that period was usually 60 between attacks. On January 1, 1897, he fell in a faint while
having a desire to go to stool; his head and eyes were drawn to the left and the eyes twitched.
During that day he had several similar attacks, before each of which the pulse disappeared,
returning during the attack to a rate of 16 to 18 per minute. By evening the rate had
returned to 60. He died in one of these attacks on January 8. Autopsy, performed by
Carl Weigert, showed almost complete atrophy of the right half of the cerebellum and a
varicose dilatation of the ependymal vessels in the medulla. It is probable that at stool
or during effort the pressure in these varices rose and caused them to compress the medulla
near the vagus nucleus. In spite of a very careful search by Weigert, no myocardial lesion
could be found. It is, therefore, fair to assume that in this case the attacks and the prob-
ably existing heart-block were vagal in origin.
Dr. Walter James also reported a case in which recurrent groups of ineffectual extra-
jsystoles caused the circulation to become so slow at times as to produce syncopal attacks.
472 DISEASES OF THE HEART AND AORTA.
A somewhat similar case was that of Holberton (1. c.) (1841), in which the attacks
dated from a fall from a horse, and no myocardial lesion was found. On the other hand,
our case (page 467) illustrates the need of caution in reaching this conclusion, since there
the attacks dated from a blow upon the head, and yet autopsy proved the presence of a
most typical lesion of the auriculoventricular bundle. Since these lesions may be micro-
scopic (Schmoll, Gerhardt), it is evident that a neurogenic origin of the syndrome can be
diagnosed only when the bundle has been examined by serial sections. The writer has
also seen in consultation a case of complete heart-block associated with a tumor along the
course of the vagus.
Since it requires a very considerable lesion to produce the neurogenic
syndrome, and since death occurs from the latter cause as well as from
the syndrome, the prognosis is no better in these cases than in the myogenic,
except in cases where the causal factor (tumor, etc.) may be removed by
operation or by treatment. However, it must be added that even with
the most liberal interpretation neurogenic cases are extremely rare, and
the presence of the Adams-Stokes syndrome may almost always be regarded
as prima facie evidence of a lesion of the auriculoventricular bundle.
Atropine Test. — The origin of the block in these cases can be readily
demonstrated by paralyzing the vagi by the administration of atropine,
1 mg. ( g-V gr.) , which causes the block to pass off in the neurogenic cases
and the pulse-rate to become rapid, but does not affect it in the myogenic.
In most cases of the typical Adams-Stokes disease (Edes, Erlanger, Schmoll),
atropine does not affect the rate, and the organic nature is further proved.
In our own two rather exceptional cases the atropine test was, unfortunately,
not permitted. Gibson and Ritchie have reported a most interesting case
in which both neurogenic and myogenic factors seemed to be at work, since
the complete block disappeared promptly upon giving atropine and reap-
peared an hour later when the effect had worn off. However, conductivity
was always diminished (conduction time, a-c interval, being 0.6 second
instead of 0.2) even when the vagi were paralyzed, so that the auriculo-
(atrio) ventricular bundle was probably injured as well. Professor Thayer
and Dr. F. W. Peabody have found that atropine caused the partial block
(4 : 1 rhythm) to pass off, but had no effect when the block was complete.
This observation harmonizes well with the other experimental and clinical
evidence regarding complete and partial blocks.
CONTRIBUTING FACTORS.
The Adams-Stokes syndrome is more common in men (84 per cent,
of Edes's cases), of which 48 per cent, occurred between the ages of 50
and 70. This, as well as the autopsy series mentioned above, establishes
the importance of coronary sclerosis as an etiological factor. It is quite
striking that in two cases of this small series (that of Cooper, Jellinek, and
Ophiils and one of those mentioned by Dietrich Gerhardt) gonorrhoeal
infection was the etiological factor. Mackenzie describes cases of partial
heart-block (2 : 1 rhythm) as a result of influenza and pneumonia, and the
writer has seen a similar depression of conductivity during the course of
the latter. Powers has reported a case with partial halving of the rate
after pneumonia. Saigo has found extensive vacuolization, fatty and paren-
chymatous degeneration, and cellular infiltration in the Purkinje fibres
of the conduction system following acute rheumatism and other diseases.
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 473
These were especially marked in the left branch of the auriculoventricular
bundle. The importance of infectious diseases as directly causal factors
is further shown by the case of Butler, in which the bradycardia dated
from an attack of typhoid fever, and also in Dunn's case, in which a radial
pulse (18 per minute) and typical Adams-Stokes syndrome occurred in a
boy of 1 1 on the ninth day of diphtheria. There can be no doubt that many
of the sudden deaths from pneumonia and diphtheria are due to heart-block.
Cardiac overstrain may also be a factor, as in the case of a boy of 15
reported by Striibing, who when otherwise healthy ran a considerable
distance, fainted, then walked home, and had several other syncopal attacks
with convulsions. His heart was enlarged, and the pulse 16 to 18 per minute.
Rest and proper treatment brought about some improvement, and his
pulse finally rose to 44, but he died soon afterwards.
It is possible that ptomaine poisoning or autointoxication due to severe
gastro-intestinal upset may give rise to the syndrome.
CASE OF ADAMS-STOKES DISEASE WITH SUBSIDENCE AND RECURRENCE OF SYMPTOMS,
AND WITH ATTACKS DURING COMPLETE BLOCK.
Recently the writer, with Professor Thayer and Dr. H. M. Thomas, examined a gentle-
man who had lately suffered from a severe acute gastro-enteritis with vomit-
ing and severe diarrhrea lasting several days. During this time he had fainted several
times while at stool, and his physician found him with a pulse-rate of 20 per
minute. With the improvement in digestion this bradycardia passed off within a few days,
and he had no further syncopal attacks. When examined ten days later his pulse-rate was
60, increasing normally upon slight exercise. There was no sign of heart-block, and con-
duction time (a-c interval) was normal (0.2 second). No signs of nervous disturbance
were present. After a few weeks of good health the fainting spells and bradycardia returned,
and lasted for several months. Prof. Thayer informs the writer that during this period
the rhythm varied from 1:1 to 2:1 and 4:1, returning to normal
rate when atropine was administered. Syncopal attacks also
occurred frequently in the midst of complete heart-block, and
during the periods of complete heart-block the rate was very slow and irregular. In
complete block the rate was unaffected by atropinu.
After some months conductivity gradually returned, and at the time of writing the
patient has remained quite well and has had a normal pulse-
rate for several months.
The presence of a hemorrhage in the auriculoventricular
bundle or its vicinity (apoplexy of the bundle) would account
for the occurrence and the subsidence of these symptoms. An
infiltration or fatty degeneration of the bundle might account for the occurrence and
subsidence of the first attack, but scarcely for the sudden recurrence during a period in
which the patient had been in excellent health.
Prentiss also mentions a case brought on by heavy lifting, in which
either hemorrhage or myocardial degeneration may have been the cause.
Partial heart-block has been reported from over-
doses of digitalis (Mackenzie, Hewlett, A. G. Gibson) (page 179),
but these have never given rise to complete block or Adams-Stokes
syndrome.
PHYSICAL SIGNS AND DIAGNOSIS.
As the Adams-Stokes syndrome may occur in cases having valvular
lesions, the physical signs over the heart may vary, and all forms of mur-
murs and of cardiac insufficiency may occur. Those which are character-
474 DISEASES OF THE HEART AND AORTA.
istic of the condition, as observed by Stokes and Chauveau, are the very
slow pulse disappearing entirely before the onset of the attack; the presence
of small visible pulsations in the jugulars, of more than double the number
of the pulse in the carotids, with the small jugular pulsations and occurring
at a regular rhythm which is more rapid than that of the ventricles; a faint
sound like the ticking of a watch may often be heard near the left sternal
margin, i.e., the right auricle; and a slight pulsation or shock may at the
same time be seen or felt over the apex. On most careful palpation a faint
shock of the same rhythm may also be felt in the radial pulse. This corre-
sponds to the small auricular wavelets upon the pulse, which, as Franc,ois-
Franck has shown, are due to the beating of the auricles against the root
of the aorta.
All these signs may usually be made out in cases of heart-block, and
the diagnosis should therefore be made by any clinician in the ordinary
physical examination.
In X-ray examination the independent contraction of the auricles
may be readily seen (Deneke), and this of course settles the diagnosis. Sim-
ilarly G. A. Gibson and Einthoven, as well as Barker, Bond, and the writer,
have demonstrated heart block by the electrocardiogram.
The usual and the most satisfactory method of diagnosis is by com-
parison of the venous pulse tracing with that from the carotid artery or
the apex, by which means the exact relation of auricular to ventricular
contraction, the degree of block, and the variations of conductivity are
readily shown.
Difficulties in diagnosis may occur from the following causes:
1. The pulse-rate may be so slow that heart-block may be suspected.
This occurs especially in old persons, in athletes when at rest, and in con-
valescents from infectious diseases. For the absolute exclusion of heart-
block a venous tracing may be necessary, in which the absence of a wave
midway between the normal a waves excludes the presence of a heart-
block. The writer has seen a number of cases whose pulse-rate was 44 to
48 per minute with no sign of heart-block on the venous tracing. (Figs.
48 and 106.)
2. The early diastolic wave (h wave of Hirschfelder, b wave of Gibson)
may sometimes occur midway between auricular waves, and may thus
simulate a 2: 1 rhythm. Moreover, the "third heart sound" is usually
present in these cases, and may easily be taken for the sound of auricular
contraction. The presence of the h wave may be differentiated from that
of partial block by increasing the heart-rate, by rapid respiration, mild
exercise, etc., upon which the h wave is no longer found midway between
a waves, but maintains its old interval from the v wave and approaches
the second a, whereas in partial heart-block it would maintain the mid-
position. This point is of great importance, since the presence of heart-
block is a grave sign, and it should not be diagnosed without due care.
The writer has seen a number of cases in which heart-block might have
been diagnosed had this precaution not been exercised, as for example the
patient whose phlebogram is shown in Fig. 106.
Slow pulse of vagal origin may also occur in brain tumor,
fracture of the skull, meningitis, etc., and, especially in the first, may be
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 475
accompanied by syncopal attacks. In these cases there is rarely any degree
of heart-block between attacks, and the site of the cardiac disturbance
can readily be determined by its disappearance after the administration
of atropine.
A slow pulse with occasional attacks of vertigo may also occur as the
result of extrasystoles too weak to open the aortic valves, and thus
give rise to a rhythm which is too slow to nourish the brain (W. James),
and a true Adams-Stokes syndrome arises without heart-block. The diag-
nosis is, however, readily made on ausculation, from the fact that between
effective beats a single loud sound is heard (whole rhythm being lub dub
1 121
lub, pause, lub dub lub) and not the feeble ticking auricular sound
of auricular contractions. The venous pulse and electrocardiogram char-
acteristic of extrasystoles (see page 68) establish the diagnosis.
In occasional cases, paroxysms of tachycardia are accom-
panied by fainting spells, the pulse between attacks being quite normal
or even very slow.
CASE OF PAROXYSMAL TACHYCARDIA WITH SYNCOPAL ATTACKS, SUGGESTING
ADAMS-STOKES DISEASE.
A few years ago the writer examined such a case in consultation with Professor Barker
and Dr. I. P. Lyon of Buffalo. The patient was a man past middle age, had a pulse-rate
of 60, and had been subject to attacks of palpitation with fainting spells. The case had
been seen by several specialists in various cities, who had diagnosed it Adams-Stokes
syndrome. Physical examination was negative except for a slight grade of arteriosclerosis.
Tracings of the venous pulse, however, showed conductivity to be normal (a-c interval
0.2 second), and this continued to be the case even when, upon exercise, the pulse-rate
rose to 120 per minute without dropping a beat. The Adams-Stokes syndrome was thus
excluded. From the sudden onset and the fainting spells during the attacks, it was con-
cluded that the condition was most probably paroxysmal tachycardia. The patient was
subsequently seen in a typical attack, with sudden approximate doubling and sudden
halving of the rate, and the diagnosis was thus verified. Dr. Lyon informs the writer that
the patient is much improved and has now only mild attacks of tachycardia.
There may occasionally be difficulty in differentiating the Adams-
Stokes syndrome from epilepsy and brain tumor. Heart-block is, however,
never present in the former, very rarely in the latter; so that the diagnosis
can usually be made from simple inspection of the jugular vein. If neces-
sary, venous tracings, supplemented by the atropine test, may be resorted to.
PROGNOSIS.
The course of cases suffering from the Adams-Stokes syndrome is
veiy variable. It is probable that many cases die in the first attack, but
the condition remains undiagnosed or is ascribed to coronary sclerosis.
It is not unlikely that histological examination of many cases of sudden
death would reveal lesions in the bundle of His or its artery. In some
cases death occurs within a few weeks or months after the first attack, but
in very many the heart-block may last for many years, with or without dis-
appearance of the syncopal attacks. Many cases of Edes's series lived seven
or eight years after the first attack. Osier's case lived thirty years after
the onset of bradycardia, and seven years after the first syncopal attack.
476 DISEASES OF THE HEART AND AORTA.
It is stated that the pulse-rates of Julius Caesar and of Napoleon were
abnormally slow (Napoleon's being sometimes 40, but at Elba 50 to 55),
and that the epilepsy of the latter was a sign of the Adams-Stokes syndrome,
but this is not proved. However, it is certain that the presence of com-
plete heart-block is compatible with ability to do a considerable amount of
work. Vigouroux had under observation a laborer with complete heart-
block who during five years did hard work, driving a cart with six oxen in
the hottest weather. His heart always beat at a rate of 20. Dr. Archibald
Hewan was able to climb a mountain several thousand feet high when his
pulse ranged from 32 to 40 and never rose above the latter. Most of the
cases die in the attacks (Edes), but death from coronary sclerosis without
Adams-Stokes syndrome, as in our case, is not uncommon. Gerhardt has
recently reported three cases in which not only the syncopal attacks but
also the heart-block completely disappeared, owing to subsidence of the
pathological process in the auriculoventricular bundle which was not
totally destroyed. Prof. Thayer's case, quoted above, probably belongs to
this group.
TREATMENT.
As regards treatment it must be frankly admitted that there is no
drug at our disposal which either improves conductivity, prevents stoppage
of the ventricles, or increases the ventricular rate.
General experience has shown that digitalis is either without
effect or positively harmful, and v. Tabora has shown experi-
mentally that it both decreases conductivity and increases the period
of stoppage.
Caffeine, theobromine, strychnine, strophanthus, and amyl nitrite
are equally without effect upon either of these phenomena in both clinical
usage and, as the writer has found, in experimental heart-block in dogs.
Atropine is usually without effect, but may be of temporary benefit
in certain cases with a neurogenic element (as in those of Gibson and
Ritchie and Thayer) . August Hof mann reports a case in which inhalations
of oxygen were of distinct benefit, but in the writer's experience this is
not often the case. Ammonium carbonate, with which Burnett claimed
to have aborted attacks, has not been much used in recent years.
In the syphilitic cases, however, antiluetic treatment —
inunctions of mercury and administration of large doses of
potassium iodide, ascending to 4 Gm. (5j) t.i.d., by mouth — has
been known to bring about a cure by absorption of the gummatous
lesion (Schmaltz, Erlanger), and should be tried whenever there is a
suspicion of lues.
Peculiar postures sometimes help in warding off syncopal attacks
by improving cerebral blood flow until the ventricular rhythm has become
established. Stokes (1846) writes that his patient "had two threatenings
of fits since his admission, and warded both off by a peculiar manoeuvre : as
soon as he^perceives symptoms of the approaching attack he directly turns
on his hands and knees, keeping his head low, and by this means he says
he often averts what otherwise would end in an attack." This was the
patient's physiological therapy to prevent cerebral anaemia.
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 477
It is evident that we have no specific remedy or procedure for the
relief of the Adams-Stokes syndrome. Nevertheless, since most cases
live several years after the first attack, a good deal can be done for the
patient. The two aims to be kept in view are, first, to avoid anything
which brings on rapid changes of pulse-rate (excitement, emotion, exertion,
straining at stool), and, second, to enable the ventricles to gain their inher-
ent rhythmicity and thus obviate stoppage. As has been seen from Schuster
and Prentiss's case and from the effect of exercise in Erlanger's case, exer-
cise is a particularly potent factor in bringing on attacks in the early stage
of the disease. Absolute rest is therefore indicated as long as the pulse-
rate is at all unstable (i.e., when there is transition from partial to complete
block) and vice versa.
When complete block has become permanent (for at least several
weeks) the condition is quite different. The ordinary influences (emotion,
mild exercise, etc.) affecting auricular rate now no longer play a role, and
the attack seems to be chiefly due to the action of CO2 upon the ventricular
muscle, as in holding the breath after exercise, or in the similar phenomena
when straining in order to lift, void, or defecate. In the stage of complete
block the patient may therefore be gradually allowed exercise which does
not cause him exertion. He must learn to avoid the latter, since it may
bring him sudden death.
In all stages of the disease the bowels should be kept open and the
stools fluid, but excessive purgation and straining at stool should be avoided.
Moreover, it should not be forgotten that in a certain number of cases,
like that of J. L. (page 467) and those of Gerhardt mentioned above, the
entire process may be due to acute toxic ormyocarditic changes
and may be transitory, so that if the patient be kept at rest during the
acute period the whole inflammatory process in the auriculoventricular
bundle may subside and perfect health may return, whereas strain upon
the heart may prevent the inflammatory process from subsiding and may
cause the attacks to continue.
BIBLIOGRAPHY.
HEART-BLOCK AND THE ADAMS-STOKES SYNDROME.
Adams, Robert: Cases of Disease of the Heart, Dubl. Hosp. Rep., 1827, iv, 448.
Burnett, Wm.: Case of Epilepsy attended with Remarkable Slowness of the Pulse, Trans.
Med. Chir. Soc., Lond., 1827, xiii, 202.
Morgagni: De sedibus et causis morborum, Venet., 1761.
Holberton, T. H.: A Case of Slow Pulse with Fainting Fits, Trans. Med. Chir. Soc., Lond.,
1841, xxiv, 76.
Pletnew, D.: Das Morgagni- Adams-Stokes'sche Symptomenkomplex, Ergeb. d. inneren
Med. u. Kinderhk., fieri., 1908, i.
Stokes, Wm.: Observations on some Cases of Permanently Slow Pulse, Dublin Quart. J.
M. Sci., 1846, ii, 73. Diseases-of the Heart and Aorta, Philad., 1854, p. 305.
Chauveau, A.: De la dissociation du rhythme auriculaire et tin rhythme ventriculaire,
Kcv. de M£d., Par., 1885, v, 161, whose observations on the same case appeared earlier
in the thesis of Figuet, Etude du rhythme couple du coeur, Lyon, 1882.
Wooldridge, L.: Ueber die Funktion der Kammernerven des Saugethierherzens, Arch. f.
Physiol., Leipz., 1883, 522.
Tigerstedt, R.: ibid., 1884.
Gaskell, W. H.: On the Rhythm of the Heart of the Frog and the Nature of the Action of
the Vagus Nerve, Phil. Trans., Lond., 1882, 993. On the Innervation of the Heart,
478 DISEASES OF THE HEART AND AORTA.
with Especial Reference to the Heart of the Tortoise, J. Physiol., Camb. and Lond.r
1883, iv, 43. The Meaning of the Heart-beat, Schaefer's Text-book of Physiol., Edinb.
and Lond., 1900, ii, 169.
Kent, A. F. Stanley: Researches on the Structure and Functions of the Mammalian Heart r
J. Physiol., Camb. and Lond., 1893, xiv, 233.
His, W., Jr.: Die Thatigkeit des embryonalen Herzens und deren Bedeutung fur die Lehre
von der Herzbewegung beim Wrwachsenen, Arb. a. d. med. Klinik zu Leipz., 1893r
14. Demonstration, Centralbl. f. Physiol., Leipz., Wien, 1895, ix, 469.
Retzer, R.: Musculose Verbindung zwischen Vorhof und Ventrikel, Arch. f. Anat., Leipz.,.
1904, 1. Some Results of Recent Investigations on the Mammalian Heart, Anat.
Rec., Phila., 1908, ii, 149.
Humblet, M.: Allorhythmie cardiaque par section du faisceau de His, Arch, internal
de Physiol., Liege et Par., 1905-6, iii, 330.
Hering, H. E.: His'sche Uebergangsbundel-immittelbare Wirkung der Accelerans und
Vagus, Arch. f. d. ges. Physiol., Bonn, 1905, cviii, 267.
Tawara, S.: Das Reizleitende System des Saugethier-herzens, Jena, 1906.
Erlanger, J.: Zentralbl. f. Physiol., Leipz. u. Wien, 1905, xix. A Report of some Obser-
vations on Heart-block in Mammals, Bull. Johns Hopkins Hosp., Bait., xvi. On the
Physiology of Heart-block in Mammals, with Especial Reference to the Causation of
Adams-Stokes Disease, J. Exp. Med., N. Y., 1905, vii; 1906, viii. Further Studies
on the Physiology of Heart-block. Effect of Extrasystoles upon the Dog's Heart and
upon Strips of Terrapin's Ventricle in the Different Stages of Block, Am. J.
Physiol., Bost., 1906, xvi, 161. Recent Contributions to the Physiology of the Cir-
culation, J. Am. M. Asso., Chicago, 1906. Irregularities of the Heart resulting from
Disturbed Conductivity, Am. J. M. Sc., Phila. and N. Y., 1908.
Erlanger, J., and Hirschfelder, A. D.: Eine vorlaufige Mittheilung ueber weitere Studien in
bezug auf den Herzblock in Saugetieren, Zentralbl. f. Physiol., Leipz. u. Wien, 1905r
xix, 270. Further Studies on the Physiology of Heart-block in Mammals, Am. J.
Physiol., Bost., 1906, xv, 153.
Erlanger, J., Blackman, J. R., and Cullen, E. K.: Further Studies on the Physiology of
Heart-block in Mammals, ibid., 1908, xxi, p. xviii.
Dunn, A. L. : Atrioventricular Dissociation following Diphtheria, J. Am. M. Asso., Chicago,.
1908, 1, 1985.
Luce, H.: Zur Klinik und pathologische Anatomic des Adams-Stokes'schen Symptomen-
complexus, Deutsch. Arch. f. klin. Med., Leipz., 1902, Ixxiv, 370.
Stengel, A.: Fatal Case of Stokes- Adams Disease, with Autopsy, Am. J. M. Sc., Phila. r
1905, cxxx, 1083.
Schmoll, E.: Adams-Stokes Disease, J. Am. M. Asso., Chicago, xlvi, 361. Zwei Falle
von Adams-Stokes'scher Krankheit mit Dissoziation von Vorhof und Kammerrhyth-
mus und Lasion des His'schen Biindels, Deutsch. Arch. f. klin. Med., Leipz., 1906,.
Ixxxvii, 554.
Handford: Brit. M. J., Lond., 1904, ii, 1745.
Keith, A. and Miller, C.: Lancet, Lond., 1906, ii, 1429.
Grunbaum, also reported by Keith and Flack (I.e.).
Ashton, T. G., Norris, G. W., and Lavenson, R. S.: Adams-Stokes Disease (Heart-block)
due to a Gumma in the Interventricular Septum, Am. J. M. Sci., Phila. and N. Y.r
1907, cxxxii, 28.
Heineke: Drei Falle von Adams-Stokes'scher Krankheit, Berl. klin. Wchnschr., 1907r
xliv, 1125.
Fahr: Ueber die muekulare Verbindung zwischen Vorhof und Ventrikel (das His'sche
Biindel) im normalen Herzen und beim Adams-Stokes'schen Symptomenkomplex,.
Arch. f. path. Anat., etc., Berl., 1907, clxxxviii, 562.
Rendu: Soc. med. d. hop., 1895. Quoted from James, W. B.: A. J. M. Sci., Phila. and
N. Y., 1908, cxxxvi, 469.
Hay, J., and Moore, S. A.: Stokes- Adams Disease and Cardiac Arrhythmia, Lancet, Lond.,
1906, ii, 1271.
Gibson, G. A: Heart-block, Brit. M. J., Lond., 1906, ii, 1113.
Gibson, A. G.: The Heart in a Case of Stokes- Adams Disease, Quart. J. M. Sci., Oxford,
1908, i, 183.
Vaquez and Esmein : Presse med., 1907, xv, 57.
HEART-BLOCK AND ADAMS-STOKES SYNDROME. 479
Sendler: Beitrag zur Frage ueber Bradycardie, Centralbl. f. innere Med., Leipz., 1892,
xiii, 642.
Jellinek, Cooper, Ophiils: The Adams-Stokes Syndrome and the Bundle of His, J. Am. M.
Asso., Chicago, 1906, xlviii, 955.
MacCallum, W. G.: Stokes- Adams Disease with Infarction. Read before the Johns Hoj>-
kins Medical Society, Nov. 4, 1907.
Heineke, A., Mtiller, A., and v. Hoesslin, A.: Zur Kasuistik des Adams-Stokes'schen Symp-
tomenkomplexes und der Ueberleitungsstorungen, Deutsch. Arch. f. klin. Med.,
Leipz., 1908, xciii, 459.
James, W. B.: A Clinical Study of some Arrhythmia of the Heart, Am. J. M. Sci., Phila.
and N. Y., 1908, cxxxvi, 469.
Butler, G. R.: Heart-block (Adams-Stokes Disease), Am. J. M. Sci., Phila. and N. Y.,
1907, cxxxiii, 715.
Gerhardt, D.: Ueber Riickbildung des Adams-Stokes'schen Symptomenkomplexes,
Deutsch. Arch. f. klin. Med., Leipz., 1908, xliii, 485.
Edes, R. T.: Slow Pulse, with Especial Reference to Stokes- Adams Disease, Trans. Asso.
Am. Phys., Phila., 1901, xvi, 521.
Thanhoffer: Centralbl. f. d. Med. Wissensch., 1875, 405. Quoted from His.
Neuburger, Th., and Edinger, L.: Einseitiger fast tot aber Mangel des Cerebellums, Varix
oblongatae Herztod durch Accessoriusreizung, Berl. klin. Wchnschr., 1898, xxxv, 69.
Gibson, G. A., and Ritchie, W. T.: Further Observations on Heart-block, Practitioner,
Lond., 1907, i, 587.
Mackenzie, James: New Methods of Studying the Affections of the Heart, Brit. M. J.,
1905, i, 519, 587, 702, 759, 812.
Powers. Quoted from Edes.
Saigo, Y.: Die Purkinjeschen Muskel fasern bei Erkrankungen des Myokards, Verh. d.
Deutsch. path. Ges., Jena, 1908, xii, 165.
Dunn, A. D.: Atrioventricular Dissociation following Diphtheria, J. Am. M. Asso., Chicago,
1908, 1, 1985.
Strubing: Deutsch. med. Wochnsch., Leipz., 1893. Quoted from Edes.
Hewlett, A. W.: Digitalis Heart-block, J. Am. M. Asso., Chicago, 1907, xlyiii, 47.
Gibson, A. G.: The Action of Digitalis on the Human Heart, Quart. J. M. Sc., Oxford,
1907, i, 173.
Deneke: Zur Rontgendiagnostik seltener Herzleiden, Deutsch. Arch. f. klin. Med., Leipz..
1906, Ixxxix, 39.
Einthoven, W. Quoted on page 61.
Schreiber, E.: Ueber Herzblock beim Menschen, ibid., 1906, Ixxxix, 277.
Vigouroux: Gaz. d. hop., Par., 1876. Hewan, A. Quoted from Edes.
Schmaltz: Zur Kenntniss der Adams-Stokes'scher Krankheit, Miinchen. met!. Wchnschr.,
1905, lii, 1120.
XII.
PERICARDITIS.
Historical. — The presence of changes in the pericardium in animals
was known to Galen, and Senac in 1749 described the condition in man.
Auenbrugger and later Corvisart were able to make out changes in dul-
ness due to pericardial effusions. Laennec detected the murmur of fibrin-
ous pleurisy, and described it as resembling the creaking of a new saddle,
but its diagnostic significance was positively established by Colliri and by
Devilliers in 1824.
ETIOLOGY.
The frequency with which pericarditis occurs varies greatly according
to various observers, and particularly according to the age of their patients.
It seems to be considerably more common in children than in adults with
cardiac disease, as stated by Poynton, as it accompanied endocarditis
and myocarditis in 94 per cent, of Sturges's cases of heart disease (carditis)
from the Great Ormond Street Children's Hospital. This is in accordance
with the somewhat exaggerated statement of Cadet de Gassicourt that all
children who are killed by rheumatism die from pericarditis; but it applies
more to children of the second decade than of the first, since death from
rheumatic affections is most common in the second decade. Pericarditis
was found in 19 of Osier's 73 autopsies upon cases of chorea. Pericar-
ditis occurred in 230 (1 per cent.) of the cases admitted to the medical
service of the Johns Hopkins Hospital. Of these 53 were associated with
endocarditis; 8 with myocarditis. Other factors were pneumonia 39;
rheumatism 31; nephritis 33; tuberculosis 25; pleurisy 17; gonorrhoea 3;
aneurism 2; leukaemia 2; syphilis 1. Rheumatism occurred in 51 per cent,
of the 100 cases reported by Sears from the Boston City Hospital. This
relationship between pericarditis and rheumatism has been proved experi-
mentally by Wasserman, Triboulet, Poynton and Paine, Walker, Cole and
Beattie (page 301).
Pneumonia is also one of the common causes of pericarditis (18 per
cent, of Sears's series), and usually ranks next to the rheumatic cycle as an
etiological factor. Pericarditis was present in 4.66 per cent, of the cases of
pneumonia at the Johns Hopkins Hospital (Chatard), and in 2-3 per cent,
of Preble's series in Chicago. According to the latter observer its relative
frequency is about proportional to the extent and severity of the disease.
This claim is also borne out by Chatard's statistics (frequency of 15.7 per
cent, in the cases coming to autopsy). Moreover, the appearance of an
acute pericarditis in the course of the disease is a very grave sign, for
only two cases (6.5 per cent.) of Chatard's series recovered.
480
PERICARDITIS. 481
Pericarditis is also common in scarlatina (especially with strepto-
coccus infection), in severe measles, and in smallpox. In the latter it is
frequently purulent.
Tuberculous pericarditis is quite common (8 per cent, of Breitung's
autopsies), and in contrast to the rheumatic form rarely subsides. It often
ends in effusion.
The pericarditis of chronic nephritis and uraemia constitutes a frequent
termination of this disease, though it is by no means always fatal. It is
usually due to an intercurrent infection, and the pyogenic cocci can often
be cultivated from the exudate.
Pericarditis may also result as* a secondary infection in septicaemia and
in puerperal infections as well as in gonorrhoea, especially when there is
accompanying arthritis. It is rare in typhoid fever (3 times in McCrae's
1500 cases) ; occurs occasionally in influenza; and sometimes results from
septicaemias due to B. coli, B. aerogenes cap^ulatus, B. pyocyaneus, etc.
Trauma without direct injury of the pericardium or viscera was the
cause of pericarditis in Blancard's case in 1688, and a large number of cases
due to this cause were collected by Bernstein in 1896. Blows upon the chest,
wagon running over the body, etc., are the common causes.
FORMS OF PERICARDIAL EXUDATION.
The exudate into the pericardial cavity may assume various forms.
In simple venous stasis and asphyxia of the endothelial cells (hydro-
pericardium) a clear thin fluid of low specific gravity, relatively poor in
proteid and especially in fibrinogen, is secreted. When there is true inflam-
mation of the pericardium, the exuded fluid is rich in fibrinogen and of rela-
tively high specific gravity (over 1015) and contains nucleo-albumen
(clouding with acetic acid). Samuel has shown that when the exudate is
poor in fibrin ferment it remains fluid (pericarditis with effusion) , whereas
when this is present the fibrinogen coagulates (fibrinous pericar-
ditis). According to Opie, the enzymes are derived chiefly from the
leucocytes, especially the polymorphonuclears, and hence the amount of
fibrin deposited depends largely upon the number of these cells present.
Moreover, since these cells pass out from the blood-vessels, the fibrin is first
and most thickly deposited in the vicinity of the latter, — i.e., along the
epicardium above the circumflex and descending rami of the large coronary
arteries, where it begins in the form of strands passing out from about
the leucocytes, and hence gives the heart a shaggy appearance (cor villosum,
Fig. 279). This layer of fibrin usually has the appearance and consistency
of a yellow batter. When fresh it is not very adherent to the heart, and
may reach a thickness of an inch or more. There may be no fluid in the
pericardial cavity, but, as a rule, both fibrin and fluid are present, the
latter often in large quantities. The fluid is usually thick, containing
uncoagulated fibrinogen as well as small flaky masses of fibrin, which may
render it too thick to be removed by aspiration. WThen the exudate is
extremely rich in bacteria and leucocytes, the proteolytic enzymes are
given off, which digest the fibrin, and the fluid becomes purulent.
When the fibrinous exudate of a simple pericarditis is absorbed rapidly,
it leaves no traces and the pericardium again becomes clear. But when it
31
482
DISEASES OF THE HEART AND AORTA.
lasts for some time and the resolution is slow, organization takes place,
and white patches of pericardial thickening ("milky spots") are found
over the surface of the heart.
These may, however, result from small perivascular foci like those of
chronic myocarditis, without ever giving rise to the clinical picture of
pericarditis.
FIG. 278. — Acute fibrinous pericarditis.
Fm. 279. — Tuberculous pericarditis (cor villosum).
Organization and Adhesion. — The strands of newly formed connective
tissue may penetrate the fibrin between the two layers of pericardium and
completely bridge the cavity with fibrous strands (Fig. 286). In many
cases the tug of the heart in systole stretches these out into fibrous cords
an inch or more in length; in other cases, or over other parts of the same
heart, the adhesions are denser, the two surfaces may be completely glued
together and the cavity obliterated (adherent pericardium) .
The division into these forms of pericarditis is, therefore, an arbitrary
one, but, as will be seen, is made necessary by the absolute difference in
both diagnostic signs and mechanical effects upon the circulation, and
thus as regards indications for treatment. Their relative frequency is
shown in the following table, which Gibson quotes from Breitung's autop-
sies at the Berlin Charite Hospital (Virchow;s Department).
Cases.
Serofibrinous 108
Hemorrhagic 30
Purulent 24
Tuberculous (secondary) 24
Tuberculous (primary) 2
Partially adherent Ill
Totally adherent 23
Ossified. . 2
324
Per cent.
33.3
9.2
7.5
7.5
0.7
34.3
7.3
0.7
100
PERICARDITIS. 483
Although the pathogenesis is the same, the clinical manifestations of
fibrinous pericarditis, pericardial effusion, and adherent pericardium are
different; hence they are discussed separately.
SIMPLE FIBRINOUS PERICARDITIS.
PATHOLOGICAL PHYSIOLOGY.
The friction due to the presence of the fibrinous exudate imposes a
slight increase in the resistance to both contraction and filling of the heart.
The exudate itself takes up a certain amount of space in the pericardial
cavity and may thus somewhat diminish the filling of the heart; but
these factors rarely suffice to embarrass the circulation.
Either as a result of the accompanying injury to the heart muscle or
from irritation of the depressor nerve, the peripheral vessels are dilated
and the blood-pressure is low. The pulse also becomes small and rapid,
but is usually regular.
SYMPTOMS.
Precordial pain, palpitation, shortness of breath, and weakness are
the common complaints, as well as occasional chilly feelings. Fever, with
which these are associated, is generally, but not always, present.
The onset is very often insidious, and the disease may not be recog-
nized at all by the patient. Precordial pain is the most striking
symptom. Sibson estimates that it occurs in 70 per cent, of the cases.
Henry Head calls attention to the fact that the pain of pericarditis is not
a referred pain, but a true local pain, often limited to the area over which
the friction is audible and associated with tenderness on pressure and on
percussion. It does not radiate from this site, and differs in this respect
from the anginal pain. The other symptoms, shortness of breath and palpi-
tation, manifest no special peculiarity.
Occasionally, especially when the pericarditis affects the posterior
wall of the pericardium, there is pain on swallowing. This pain
is in every way similar to the tenderness of the interspaces in front, and
occurs when the bolus of food presses upon the pericardium as it passes
down the oesophagus.
When the recurrent laryngeal nerve is affected by the inflammation,
aphonia or change in the voice results. Involvement of the phrenic
often produces hiccough.
PHYSICAL SIGNS.
The patients are usually quite pale, occasionally cyanotic. Except
for accompanying joint involvement, fibrinous pleurisy, or pulmonary
consolidation, there are few signs outside the heart. (Edema of the extremi-
ties is rare unless there are accompanying valvular lesions. Over the heart
there may be some precordial bulging, especially in children, but the cardiac
impulse may be less marked than usual, weak, diffuse, and wavy. On
palpation there is sometimes a slight superficial scratching felt, especially
between the left parasternal line and the sternum ; but this is by no means
as marked, as frequent, or as regular as in valvular lesions.
484 DISEASES OF THE HEART AND AORTA.
The area of cardiac dulness and flatness may or may not be increased
in one or both directions, dependent upon the amount of the exudate as
well as upon the degree of dilatation of the heart, but the outlines char-
acteristic of pericardial effusion are not present when the exudate
is plastic.
The pathognomonic sign of fibrinous pericarditis is the superfi-
cial scratching or churning murmur or friction sound
described by Laennec as resembling the rubbing of a new saddle. It
can be imitated more or less closely by placing the palm of the hand over
the ear and then scratching to and fro upon the back of the hand with the
finger-nail. The pericardial friction is exactly similar in character to the
friction heard in pleurisy, but its time is coincident with the cardiac cycle.
It does not, however, coincide sharply with either systole or diastole, but
is usually heard during portions of both. It is usually louder during systole
than during diastole, probably because the two surfaces are moved across
one another with greater force. A short pause usually occurs between the
systolic and the diastolic portion
of the friction. The diastolic
friction is softer than the systolic,
occurs rather early, and ceases
during the latter half of this
1 * A * " * * A A A A AA — period, or in other words as ven-
tricular filling diminishes. It
FIG. 280.— Diagram showing the relations of the may also be heard again at the
pericardial and pleural frictions to the cardiac and time of auricular SVStole, giving
respiratory movements. The pericardial friction is . , , , ' c
indicated by narrow zigzag line, the pleural friction a triple SOUnd tO tne
the heart S°unds by the usual (Broadbent). Sometimes, espe-
cially when the pericarditis is just
beginning and the friction very soft, it is not heard at all during diastole.
The friction, as a rule, does not replace the normal heart sounds, but
these, as well as loud endocardial murmurs, may be heard simultaneously
with it. Their more distant quality tends to accentuate the superficiality
of the friction sound. Moreover, the latter is considerably accentuated
by moderate pressure of the stethoscope in the interspaces. As Emerson
has shown, this is also true of certain endocardial sounds, but the latter
are quite different in quality from a fresh pericarditis.
As the exudate is absorbed, the friction softens gradually into a barely
distinguishable roughening of the first sound, and, finally, disappears
altogether.
When portions of the exudate become organized and remain as thick-
enings of the endocardium, they may still give rise to some roughening
of the first sound, which may be very difficult to interpret, and this is
especially true when they remain in the form of fibrous strands and loose
adhesions (see page 500).
The friction is usually first heard over the third and fourth left inter-
space near the sternum, over the area at which the exudate first appears.
In the cases which are secondary to pneumonia and pleurisy there is often
a "pleuropericardial" friction, with respiratory accentuation
heard over a considerable strip along the left margin of the heart where
PERICARDITIS. 485
the pleura overlies the pericardium. The pleurisy exists in the layers of
pleura in front of the pericardium. The two processes exist simultaneously
in separate cavities whose walls are in contact. Sears has pointed out
that in recurrent attacks of pericarditis the friction may be heard only
at the back in the left interscapular region. This occurred in a case in
which the anterior portion of the pericardium was adherent. The pulse
in acute pericarditis is usually small and rapid, the blood-pressure low
(100 mm. or under), and the pulse-pressure small (10-25 mm.), but this is,
at least in part, due to the loss of vasodilator tone, and in part to the myo-
cardial weakening brought about by the same process.
DIAGNOSIS.
Diagnosis is usually simple, and the murmurs are rarely mistaken for
endocardial, although Osier mentions one case in which a to-and-fro aortic
murmur was mistaken for a pericardial rub.
When a certain amount of fluid is present in the pericardium the
friction may disappear if the heart is pushed backward; and, as a small peri-
carditial effusion is often overlooked, the whole condition may escape
diagnosis.
CASE OF SIMPLE FIBRINOUS PERICARDITIS.
F. G., a colored hod-carrier, aged 50, entered the Johns Hopkins Hospital on July 22,
1904, complaining of pain around the heart. Except for the fact that one son died of gal-
loping consumption, the family history is negative.
The patient has been a healthy man, but had measles, chicken-pox, whooping-cough,
mumps, scarlet fever as a boy, and rheumatic fever at 38. He is not subject to sore
throat. He had a cough with pain in the chest twenty years before admission, but
has had no recurrence. He has had several attacks of gonorrhoea. He has always
done hard work.
He was perfectly well until six weeks before admission, when he had severe
pain in the right thigh and h i p which lasted five weeks, but he kept at work
in spite of the pain. Four days before admission he began to cough, and two days later
felt a cutting pain around the heart, which was especially severe on drawing
a deep breath. This has persisted. He did not notice any special shortness of breath, and
kept at work for three days after 'the precordial pain had set in.
The examination note by Dr. Cole states that the patient is a well-nourished colored
man, mucous membranes of fair color, no glandular enlargement. Lungs clear throughout
on auscultation and percussion. Over the heart a feeble impulse is seen in the fifth left
interspace 8.5 cm. from the midline. The impulse is localized. There is no bulging of the
interspaces. On percussion the area of cardiac dulness is found to extend
11.5 cm. to the left of the midline in the fifth interspace, 3.0 cm. to the right opposite
the fourth rib. The cardiohepatic angle is 90°.
The heart sounds are distinctly heard at the apex, but there is also aloud
rough pericardial friction which is not exactly synchronous with the heart
sounds and is increased by pressure with the stethoscope. There are no endocardial mur-
murs. The friction increases in intensity toward the base of the heart,
where the heart sounds are distant and the second pulmonic is louder than the second
aortic. The pulse is of fair volume, moderate tension, regular, 88 per minute.
The sputum is mucopurulent, but. contains no tubercle bacilli and no elastic fibres.
Urine, 450 c.c., amber colored, acid, containing a considerable amount of albumin
a n< 1 numerous hyaline casts. Blood count shows: red blood-corpuscles 3,500,000; haemo-
globin 50 per cent.; leucocytes 7100. Temperature ranges from 101° to 102.5° F.
An Ice-bag was kept continuously over the precordium, and he was given strychnine,
1.5 mg. (TV gr.), every four hours.
486 DISEASES OF THE HEART AND AORTA.
On the second day after admission the temperature fell to normal and the patient
felt better. The pain in the chest had gone. The pericardial friction was still heard, but
less intense than before, and by the following day could be heard only over a
small area in the fourth left interspace near the sternal margin.
It disappeared entirely during the course of the following week, and he became entirely
well. There were no signs of pericardial adhesion. The patient left the hospital on August
8, in the third week after his admission, and has not sought admission since then.
TREATMENT.
Absolute rest in bed is necessary, since the heart must be spared as
much as possible, and, moreover, cardiac strain and venous stasis tend to
increase the exudation. The diet should be light or should consist of milk
alone during the acute stages. If there is much pain, morphine may be
freely given to relieve it, since this symptom is not likely to become chronic;
and, on the other hand, it is important to keep the heart's action as quiet
as possible. For this purpose an ice-bag is usually applied to the precordium.
Silva has shown in dogs that by this means the local temperature
within the pericardium may be lowered 1° or even 3.5° C. (1.8°— 7.3° F.).
Buxbaum states that the use of the ice-bag in pericarditis is now quite
general throughout the world. In American clinics this is certainly the
case. The clinial experience of the writer has been one of uniform satis-
faction in its use. The fact that Rubino was able to produce pericarditis
in animals by the intravenous injection of cultures of pyogenic cocci only
when ice was simultaneously applied to the chest, has
probably little bearing upon the therapeutic use of the latter, since
Rubino probably chilled his animals severely, while in the therapeutic
application the cooling, especially of the deeper layers, is both localized
and mild. No doubt the local temperature of the inflamed pericardium
is reduced to normal, but not much below it.
Other methods of counterirritation are also useful and devoid of this
possible objection. Head cites a case in which relief of the pain within five
minutes was brought about by the application of three 1 e e c h e s to the
precordium, and Biers's suction cups or the old-fashioned dry or wet
cupping may be resorted to with equal satisfaction. This may also be said
of hot or warm poultices, hot-water bags, and the modern electrical heating
pads whose temperature can be kept regulated with great accuracy. Blis-
ters (cantharides) , mustard plasters, Paquelin cautery, and Finsen light
may also be used with great satisfaction, or even a ''light b a t h ' ;
from a single small incandescent lamp with reflector placed near the pre-
cordium.
Medicines seem to be of little value. Caton recommends potassium
iodide. Broadbent states that digitalis should be avoided in the early
stages, but Romberg recommends its use in the cases with nephritis. It
should be used at once and should be preceded by intravenous strophanthin
if signs of acute cardiac failure manifest themselves.
The pain is not relieved by salicylates, so that codeine, .03 Gm. (J gr.) ,
heroin, .005 Gm. (TV gr.),.dionin, .02 Gm. (J gr.), or morphine, .016 Gm.
(£ gr.), must often be given.
The bowels should be kept moving easily with saline purgatives.
PERICARDITIS. 487
PROGNOSIS.
Osier states that "simple fibrinous pericarditis never kills," but peri-
carditis is frequently seen as a terminal event in other conditions, espe-
cially in pneumonia, tuberculosis, gout, and nephritis. In any of these it
is a grave but not always fatal sign.
The main dangers accompanying fibrinous pericarditis are the develop-
ment of effusion on the one hand or of pericardial adhesions on the other.
Sometimes all three conditions occur successively in the same case, the
fluid collecting within a few days after the fibrinous exudate, is removed
after a few weeks by aspiration or absorption, and is followed by organi-
zation of the exudate with adhesions which usually last throughout one or
several years and finally terminate the life of the patient. Fortunately,
these complications are by no means the rule, and in many cases fibrinous
exudate is absorbed without further trouble.
It is evident from both the pathological and the clinical stand-point
that the fresher the exudate the cleaner will be its absorption. Hence the
importance of vigorous treatment.
PERICARDITIS WITH EFFUSION.
Frequently during the course, and especially in the second or third
week, of an acute pericarditis fluid collects within the pericardium. Under
normal conditions there are from twenty-five to fifty cubic centimetres
of serous fluid present. In pericardial effusions from 500 c.c. to 1 litre is
frequent; as much as 4000 c.c. has been found at autopsy by Verney. A
pericardial membrane of the usual size could not accommodate so large
an effusion, and stretching of the former usually goes on simultaneously
with increase in the latter. Hence it follows that the actual size of the
effusion may be of little import, and a small rapidly exuded effusion may
produce signs of intrapericardial pressure sooner than a large one arising
slowly.
The character of the fluid may vary as much as its quantity. It may
be thin and serous and free from coagula, especially when poor in leuco-
cytes, or it may contain small gelatinous coagula forming here and there
about masses of leucocytes ; or this process may be so generalized that the
whole mass may be converted into a very thin jelly. Diapedesis of corpus-
cles through the injured vessel walls may cause it to become bloodstained,
a condition which is especially frequent in carcinomatosis or sarcomatosis
of the pericardium.
PATHOLOGICAL PHYSIOLOGY.
. Franc. ois-Franck, Lagrolet, and Cohnheim have shown that the injec-
tion of fluid into the pericardial cavity hinders the entrance of blood into
the auricles, and thus causes "stasis of blood in the venae cavae and fall in
the blood-pressure. Their experiments were repeated by Starling, who
found that on injecting successive amounts of 20 c.c. and 10 c.c. of oil
into the dog's pericardium, the pressure in the vena cava rose gradually,
while that in the aorta and pulmonary vein remained constant for some
time. That is to say, the rise in venous pressure compensated for the
488
DISEASES OF THE HEART AND AORTA.
increased pressure within the pericardium, and although some venous
stasis occurred the circulation was not retarded. As much as 60 c.c. of oil
could thus be injected into the dog's pericardium without producing any
other change. But when 10 c.c. more were injected the
condition changed suddenly and completely. The small excess
of fluid in the pericardial cavity had caused the pressure within it to rise
considerably above that in the veins, and above the level to which the
venous pressure could rise during stasis. The walls of veins and
auricles, therefore, collapsed under excess of pressure
(Fig. 281), and, since but little blood could enter the ventricles, the blood-
FIG. 281. — The circulation in cases with pericardial effusion. (Diagrammatic.) I. Normal. II.
Small effusion, showing the rise in venous pressure and the increased difficulty in the filling of the heart.
III. Great increase in intrapericardial pressure, showing the complete cutting off of venous inflow and
fall in arterial pressure. The area shaded with horizontal broken lines indicates the height of the pressure
within the pericardium.
pressure in the aorta fell. The same change occurred in Franyois-Franck's
experiments when the intrapericardial pressure was raised from 10 mm. to
20 mm. Hg. When the pressure was not relieved death ensued, the heart
beating for a short time after the circulation had ceased. On the other
hand, when the small excess of fluid was removed, the
blood-pressure quickly rose again and the circulation returned
to normal. This experiment exactly reproduces the condition in man when
a pericardial effusion is collecting, illustrates the mechanism of death in
that condition, and also illustrates the beneficial effect obtained from par-
acentesis when even a small amount of fluid is removed.
SYMPTOMS AND COURSE.
•
Pericardial effusion is somewhat less frequent in children than are
the other forms of pericarditis, its subjects being usually adults and often
persons past middle age. The symptoms of pericardial effusion are more
insidious than those of the fresher fibrinous inflammation, pain being
somewhat less common and less intense, dyspnoea and weakness being
more intense. The patients are very much more comfortable in the vertical
than in the horizontal position, the difference being even more striking
than in the ordinary forms of heart disease. Few clinicians indeed can
concur in James Mackenzie's statement that the presence of fluid in the
PERICARDITIS.
4S<)
pericardium does not give rise to symptoms of circulatory embarrassment.
Fainting spells and sudden death are very common, occurring when the
inflow into the auricle is obstructed.
PHYSICAL SIGNS.
The patients are usually pale and weak with rapid respirations. The
veins of the neck and extremities may be prominent
(high venous pressure), and this is especially marked when the intraperi-
cardial pressure is approaching the danger point. There may be i n s p i r a -
tory distention of the veins.
Inspection of the thorax usually shows a fulness of the inter-
spaces over the precordium, and frequently a very diffuse wavy impulse
which is lacking in the definiteness usually seen in both systolic impulse
and systolic retraction over and about the normal or enlarged heart.
Neither this nor the presence
of a cardiac pulsation outside
the apex is of real value in
establishing the diagnosis of
pericardial effusion.
Palpation, as a rule, reveals
nothing of importance, except
that the cardiac impulse is
usually very feeble or absent.
Changes in Cardiac Outline.
-The pathognomonic sign is
revealed by the alteration
of dulness on percus-
sion. Auenbrugger in his first
diagnostic efforts was able to
demonstrate a great increase in
Hiilnp«<a in TV>rip«rrliti«j FIG. 282.— Area of cardiac dulness from pericardial
effusion, showing Corvisarfs triangular area of dulness
and Sibson's pear-shaped area of flatness; Ilotch's area
of dulness (R) in the fifth right interspace; Ebstein's
obtuse cardiohepatic angle (EB).
with effusion, and this obser-
vation was confirmed by Cor-
visart, who recognized a large
area of flatness in the form of
however, was also encountered
a triangle with base downward. This,
in numerous cases of dilated heart and
led to many errors in diagnosis, until T. M. Rotch, of Boston, in 1878,
demonstrated that flatness was p resent in the fifth right
interspace early in the disease and constituted an almost diagnos-
tic feature. He was able to prove this upon the cadaver by injecting
various quantities of cocoa butter into the pericardial cavity. Flat-
ness in the fifth right i n te r spa ce appeared whenever more
than 200 c.c. of cocoa butter had been injected. Less than 200 c.c.
could not be recognized.
Rotch's observations were confirmed by W. Ebstein in 1893, who
laid stress upon the obtuseness of the angle formed by cardiac and liver
dulness (cardiohepatic angle). This dulness is particularly
marked when the patient leans forward and toward the right, so that the
490 DISEASES OF THE HEART AND AORTA.
fluid gravitates to this point. The right border of an enlarged heart, on
the other hand, always forms an acute, or at most a right, angle with the
liver dulness, and flatness rarely extends to the fifth right interspace,
being most marked in the fourth. The matter has been still further investi-
gated by Aporti and Figaroli, who found that with the subject in the ver-
tical position as little as 150 c.c. of fluid showed itself by pushing the area
of dulness downward and outward at both its lower angles — at both cardio-
hepatic angle and at the apex. The lower border of flatness is, therefore,
the arch with concavity downwards which had already been
described by Concato. When more fluid collects, the pericar-
dium becomes more tense, all the surfaces become convex, and Concato's
arch disappears. As a diagnostic sign the variations in dulness about the
apex are much less definite than in the fifth right interspace, and hence
they are of little importance.
At the upper border of dulness the usual slight resonance behind the
sternum gives way to a tongue of absolute flatness when the exudate is
large, so that the d u 1 n e s s assumes the form of a pear hang-
ing from its stalk (Sibson). ,X
Moreover, the pericardium presses upon the lungs about its borders,
causes them to relax and give rise toSkodaic tympany and tubu-
lar breathing not only in front but also at the angle of the
left scapula (Ewart.) Flatness may also be observed
over the spines of the vertebrae, especially from the fifth
to the tenth, where, as found by Koranyi, the note is normally resonant.
This sign may also be present when the left auricle is greatly dilated, as
in mitral insufficiency.
Position of the Heart in Pericardial Effusion. — The signs on auscultation
may vary. Most commonly, as found by Pirogoff and subsequent writers,
the heart sinks in the pericardial fluid and comes to lie against the vertebral
column and away from the chest wall, from which it is separated by a
thick layer of fluid. This fluid muffles the heart sounds, which may be
totally absent, disappearing first about the apex, later at the base.
Aporti and Figaroli have shown that with 650 c.c. of exudate a very
small area of heart wall near the base will still remain free from fluid, and
over this the heart sounds and friction rub may be heard.
On the other hand, the heart sounds and friction may persist even
when a large amount of fluid is present, as in the case reported below, in
which the pericardium contained 1200 c.c. of fluid. The sounds were faint
at the apex, but became more distinct as the base was approached, where
the friction was also well heard. An aspirating needle introduced in the
sixth left interspace came at once against the heart. At autopsy the heart
was found lying against the chest wall. This anterior position, though
not the usual one, is, according to Schaposchnikoff, often assumed by the
heart of a cadaver when fluid or paraffin is injected into the pericardium.
Schaposchnikoff believes that the heart is held in this position in spite of
the force of gravity by the elasticity of the great vessels.
Abdomen. — The liver may be both enlarged from the venous stasis
and pushed down by the pericardial effusion, so that its lower edge is fre-
quently palpable, sometimes even as low as the umbilicus. The spleen
PERICARDITIS.
491
may also be somewhat enlarged. Ascites and movable dulness are some-
times present.
Over the extremities the veins may appear distended, and there is
often oedema.
Blood-pressure. — The blood-pressure is usually rather low, except in
the cases with nephritis, in which it may be above normal.
The pulse is usually small, frequently collapsing, and often of the type
of pulsus paradoxus — fall of blood-pressure during inspiration, with de-
crease in the size and frequency of the pulse, and, on the other hand, inspi-
ratory swelling of the veins. This condition is due to traction on the walls
of the vena cava producing stasis during inspiration.
Fio. 283. — Positions of the lieiirt in pericarditis with effusion. I. The fluid is in front of the heart,
as described by Pirogoff. II. The heart is floated up against the chest wall, as described by Schaposchni-
koff. ST, sternum; OE, a-sophagus; PV, pulmonary veins; 8, eighth thoracic vertebra. The arrows
indicate the compression of the auricles. The broken line indicates the outline of the uncollapsed auricle.
X-ray Examination. — Examination with the fluoroscope shows the
exact size, form, and position of the effusion (Fig. 283), and both before
and after paracentesis may be of great help in locating pockets of encapsu-
lated fluid. The relations to the diaphragm and the presence of mediastinal
adhesions may sometimes be diagnosed by this means, and particularly
by means of permanent radiographs made with a tube of low vacuum.
CASE OF PERICARDITIS WITH EFFUSION.
The following typical case was under the writer's care in the Johns Hopkins Hospital.
It lias been previously reported in considerable detail by Professor Thayer.
R. C. W. B., a (ierman saloon-keeper, aged 59, was brought to the hospital at 12.30
I-.M. on Sept. 1, 1903, barely able to speak, owing to shortness of breath and
weakness. He was too ill to give a history, except for the statement that for several
years he had been troubled with shortness of breath, which has gradually increased until
the past few days, when it suddenly became very much aggravated
Examination note by Dr. Cole was as follows: Patient is a moderately well-nourished
man. muscles flabby. At time of the examination he is lying flat with head slightly propped
up and looks very ill. Respiration 40 per minute. Pupils are small, re"act readily to lijrht.
Tongue dry. slightly coated. No marked pyorrhoea; teeth not good. Veins of the
neck are very full; no marked pulsation of the deeper vessels. No general glandular
enlargement. Chest: Expansion fairly good; equal; considerable respiratory distress.
Resonant throughout ritrht front ami axilla and left upper front, but note is markedly
impaired in lower left axilla and at lower rijrlit back, much more markedly in lower left
492
DISEASES OF THE HEART AND AORTA.
back up to the angle of the scapula. On auscultation. — Left: Breath sounds are
clear throughout upper front and upper back except for a few mucous rales in interscapular
space. Below they are very distant, practically absent at the extreme base, except just
at the angle of the scapula, where they are a little harsher (Ewart's
sign). Right side: Breath sounds are quite clear throughout except in the lower back
where there are mucous rales and breath sounds are distant.
Heart. — There is no impulse visible or palpable. There is a wide area
of cardiac d u 1 n e s s extending above to the middle of the third rib 16.5 cm.
to the left of the midline in the fifth interspace when the patient lies on his right side.
When on his back, however, the dulness is difficult to make out, as it extends directly to
the dulness in the axilla. On the right
dulness extends apparently 7 cm. to
the right of the midline in the fourth
interspace. The angle between the upper
limit of liver dulness and the cardiac dul-
ness is very obtuse. There is quite
definite precordial bulging, though
the intercostal spaces seem no fuller than
on the right. At the apex and over the
entire precordium the heart sounds
are barely audible until one reaches
almost to the costal margin in the fourth
and fifth left interspace, where the sounds
are heard faintly with a to-and-fro mur-
mur, which is also heard over the sternum
from the third to the fifth rib. This
murmur is quite superficial and
is louder during expiration than
during inspiration, apparently not increased
by pressure of the stethoscope. It sounds
suspiciously pericardial in charac-
ter, but not definitely so. The heart's
action is almost fetal in rhythm (pulse-
rate 138 per minute). Heart sounds are
heard more loudly in the second left inter-
space; neither aortic nor pulmonic second
is specially accentuated. Pulse is very
small and can hardly be counted.
The abdomen is full. There is no
movable dulness in the flanks. The feet
and legs are markedly cedematous.
At 5.45 P.M. the patient was prepared
for paracentesis pericardii by the method
of Delorme and Mignon under aseptic precautions. An incision was made in
the fifth left interspace at the sternal margin, the pericardium ex-
posed, and a trocar inserted through it. By means of a Potain aspirator 25-50 c.c. of thick
serosanguineous fluid were removed, after which no more could be removed.
Another puncture was immediately made in the costoxiphoid angle and a small amount
of fluid again removed. The patient's pulse and general condition did not change. He
became delirious and died at 7.30 P.M.
The autopsy findings confirmed the clinical observations. There were, how-
ever, still 1200 c.c. of pericardial fluid which lay behind the heart
both to the left and to the right. The heart lay directly against the
chest wall, and therefore had come against the point of the needle and prevented the
removal of the fluid. As Dr. Cole remarked in a subsequnet note, "the fact that the heart
sounds were heard loudest over the sternum and along the left sternal margin should have
led me to insert the needle either to the right of the sternum or far to the left — outside the
mammillary line", (preferably the latter). The pericardium was lined with a yellow
fibrinous exudate. The heart muscle showed cardiosclerosis. The coronary
FIG. 284. — Radiograph of a patient with pericar-
dial effusion, taken with the tube in front of the
patient. (Kindness of Prof. C. M. Cooper.) The
figure shows the overflowing of the pericardial cav-
ity. The spots over the surface of the lungs are
artefacts due to the presence of air-bubbles in the
developer.
PERICARDITIS. 493
arteries were tortuous. There were thickening of the aortic valves and adhesions of the
cusps, which gave rise to slight aortic stenosis. The left pleura contained 700 c.c. of slightly
turbid straw-colored fluid. Both lungs contained small areas of tuberculous broncho-
pneumonia.
PURULENT PERICARDITIS.
The effusion in many cases is purulent and associated with more or
less severe septic symptoms, septicaemia, chills, extreme pallor and weak-
ness, and, as a rule, a septic fever, though in some cases the temperature
remains normal.
The condition may follow exposure to bad weather, empyema, or
trauma to either the front, sides, or back of the chest. The staphylococci,
streptococci, pneumococci, gonococci, and a great variety of other bacteria
may be the infective agents.
The symptoms and physical signs are very similar in both simple
and purulent effusions. The history of trauma and the presence of empyema
or other foci of pus speak in favor of a purulent effusion. Leucocytosis
may be present in both conditions. The aspirating syringe usually gives
the diagnosis.
HYDROPERICARDIUM.
Hydropericardium, or simple serous effusion into the pericardium,
may occur along with ascites, hydrothorax, and general anasarca in chronic
heart failure or in nephritis, or it may occur alone as a result of local venous
stasis from the pressure of mediastinal growths, glands, or aneurisms, or
from strangulation of the veins by adhesions. In this case an afebrile
course is run. Leucocytosis is often absent (or may be due to simultaneous
bronchitis or bronchopneumonia), and the diagnosis rests upon the signs
of the intrathoracic condition which is the causal factor.
The differential diagnosis is made from the fluid obtained on para-
centesis, which is clear, thin, serous, of low specific gravity (under 1018),
and gives no clouding with acetic acid indicative of nucleo-albumin. It
is poor in leucocytes and fibrin ferment, and there is not much albumin
(shown by Esbach's method). The presence of a pericardial friction at
any time during the course of the disease is sufficient to exclude a simple
hydropericardium.
HjEMOPERICARDIUM.
Haemopericardium is produced by the effusion of pure or almost pure
blood into the pericardium, and occurs especially as a result of direct or
indirect trauma, stab or gunshot wounds penetrating the cavity, or rupture
of the heart or of an aneurism. It may also occur from erosion of a blood-
vessel by a malignant growth.
Hemorrhage into the pericardium takes place much more rapidly
than the other exudations, so that the pericardium has less opportunity
to stretch and accommodate itself to its contents. The intrapericardial
pressure, therefore, rises more rapidly than in the other conditions, and
symptoms, signs, and danger develop more rapidly. Death may occur
at once. When possible operative procedures must be begun promptly
in order to save the patient.
494 DISEASES OF THE HEART AND AORTA.
PNEUMOPERICARDIUM.
When air or gas enters or develops within the pericardial cavity (as
from perforation after trauma or tuberculosis or infection with Bacillus
aerogenes capsulatus Welchii in a case reported by Nicholls), the condition
is termed pneumopericardium. Usually this is associated with the pres-
ence of purulent or serous fluid (pyopneumopericardium, pneumohydro-
pericardium) . Since there is normally a negative pressure ( — 3 to — 5 mm.
Hg) within the cavity, it follows that air will enter, just as into the thorax
(pneumothorax) , whenever there is a free perforation to the outside or to
the air-passages. This is most frequent in perforating wounds, but occa-
sionally occurs as the result of tuberculosis or perforation of a purulent
pericarditis.
The signs of pneumopericarditis are very characteristic. The percus-
sion note over the cardiac area may vary from a bell-like tympany
to an absolutely wooden flatness, or when there is an open-
ing of medium size a cracked-pot note may be heard. With a free communi-
cation to the outside such as results from operation upon the pericardium,
however, the air within the pericardium is not set into vibration by the
percussion stroke and does not alter the note at all.
On auscultation, except in the latter condition, a loud c h u r.n i n g
•'mill-wheel'' murmur is heard, but when the communication is a free
one this may be totally absent.
TUBERCULOUS PERICARDITIS.
Tuberculous pericarditis is a common and severe condition. The
fibrinous stage is somewhat more chronic than in the other forms of peri-
carditis, lasting several weeks or months, and often resulting in the forma-
tion of deposits of fibrin (Fig. 256) an inch in thickness, with or without
the presence of fluid. Gray tubercles of various size may be visible within
and upon the surface of the exudate, but frequently they may not be pres-
ent, and the bacilli must be sought for histologically or by guinea-pig
inoculation.
The fluid in pericardial effusion is frequently blood stained. It is
occasionally purulent (Kast). Tuberculous pericarditis is most commonly
associated with other tuberculous processes, especially involvement of
the pleurae, but it may also occur as a " primary" manifestation by spreading
from caseous mediastinal lymph-glands.
The course, though more chronic than other pericardial processes,
is quite similar, but the exudate is not absorbed completely and goes on
to either fluid or adhesive pericarditis. Frequently both conditions occur
and encapsulated effusions result. There is usually a considerable rise of
afternoon temperature.
The physical signs and therapy of tuberculous pericarditis are about
the same as in the other forms, plus the general management of a case of
tuberculosis — rest, fresh air, very liberal diet (when cardiac symptoms have
subsided) , and sustaining measures. The prognosis is bad.
PERICARDITIS. 495
TREATMENT OF PERICARDITIS WITH EFFUSION.
Palliative treatment of fluid within the pericardium must be limited
to the periods in which intrapericardial pressure is well below the range
of venous pressure, and must be pursued with full cognizance of the fact
that death may ensue whenever the pressure exceeds this limit.
The palliative measures consist of counterirritation, with ice-bag or
poultices, etc., blisters, and especially application of Bier's suction cups
or leeches. Diuretics, — theocin, diuretin, — combined with digitalis or
strophanthus, and free purgation may be resorted to, and the liquid intake
restricted to below 1000 c.c. per day, in the hope of reducing the pericardial
fluid by these means. However, these methods are at best but feeble
palliatives, and often more risk is entailed in their use than in the more
radical procedures.
Paracentesis Pericardii. — The idea of removing fluid within by tapping
the pericardium was first suggested in 1646 by Riolan, who advised tre-
phining the sternum one inch above the xiphoid.1 He did not attempt,
however, to carry it out, and the first operation upon the pericardium was
performed in 1819 by Romero, of Barcelona. Romero operated upon three
cases of pericarditis, with two recoveries, a percentage which is above the
average even for the present day.2
Puncture of the pericardium by means of a trocar was first performed
by Jowett, of Nottingham, in 1827. It was brought into more general
repute by Schuh, of Vienna, under Skoda's direction (1839), in France
by Trousseau (1854) and by Aran (1855), and in England by Clifford
Allbutt (1866). Paracentesis pericardii should, of course, be undertaken
with all possible asepsis of skin, hands, and instruments.
The instrument used has varied from a thick trocar several millimetres in diameter
to the finest aspirating needle. The ideal cannula is one which has a bore (about 1 mm.)
sufficient to aljow a viscous liquid to escape easily, and yet not so great as to permit the
entrance of air through the perforation. A trocar and cannula, especially one ending in
a T and stop-cock, is the best form of apparatus, since it permits the operator to clear the
lumen of the cannula at will and at the same time to remove the fluid by suction through
an aspirating bottle.3
Various sites for the paracentesis are recommended, with four ends
in view:
1. To obtain the fluid.
2. To avoid infecting the pleural cavity and puncturing the lungs.
3. To avoid puncturing the heart.
4. To avoid injuring the internal mammary artery.
1 "Si non passis exhaurire istud serum per hydragoga, licet ne terebra sternum aj>erire,
intervallo pallicis a cartilagine xiphoide."
2 It is interesting that this method has recently been advocated by J. H. Bacon (A
Procedure for Opening the Pericardium, Am. J. M. Sc., IMiila. and X. York, 1905, cxxx,
652) as a result of a series of experiments upon the cadaver. Bacon does not mention the
work of these pioneer surgeons.
3 Dr. Chas. S. Bond has found a curved aspirating needle with lumen about
1 mm. in diameter very useful in tapping the pericardium when the fluid lies back or is
encapsulated. The needle which he uses has a radius of about 10 cm. following the curve
of the heart and enabling him to pass around the latter without injuring it. The danger
of entering the ventricle by a straight push is also much less with an instrument of this form.
496
DISEASES OF THE HEART AND AORTA.
Sites for Paracentesis. — Trousseau (1854) recommended introducing the needle in the
fourth interspace just below the mammilla; Dieulafoy (1873) in the fifth about six centi-
metres from the sternal margin. Puncture at these sites or at the outer border of absolute
dulness (flatness) has the disadvantage of always traversing and often infecting the pleural
cavity, so that occasionally the patient may be caused gratuitous empyema or even a fatal
pneumonia.
In order to avoid entering the pleural cavity, Baizeau (1868) and Delorme and Mignon
advocate puncturing the pericardium as near as possible to the
sternal margin in the fifth, or if possible the sixth, left inter-
space. In order to render the procedure more certain, the latter investigators advise
making an incision through the skin with a bistoury. The needle (of medium diameter)
is then introduced into the sixth interspace if possible, and otherwise into the fifth along
the edge of the sternum, pushed in for a centimetre or two, and then the point directed
downward and inward by a slow con-
tinuous movement until the liquid
emerges. In order to empty the peri-
cardial cavity the needle should be
connected with an aspirator bottle and
the fluid collected by gentle aspira-
tion.1 When the instrument is inserted
slowly in the manner described, the
risk of injuring the heart (right ven-
tricle) is minimal, for the beating of
the latter against the point can be felt
as soon as it is touched and long
before it can be penetrated. Even
if through lack of care the
right ventricle be penetrated,
harm rarely results. For
example, Hulke mentions a case in
which he penetrated the right ventricle
and a few jets of blood spurted out,
but the patient's condition improved!
and he cites several other similar cases.
Only one case of death (from laceration
of the right ventricle) due to para-
centesis is on record (West). Unques-
tionably when all goes well the technic of Delorme and Mignon is the most satisfactory,
since the danger of injuring both heart and pleura is minimal. On the other hand, the
chance of a "dry puncture" is great. At the place selected the point of the needle may
penetrate a great deal of dense fibrous tissue and even periosteum and the lumen may thus
become plugged. Should the fluid not appear, this source of error may be obviated by
carefully inserting a wire through the whole length of the needle after it has been pushed
into the cavity and then withdrawing the wire. Another difficulty may lie in the position
of the heart itself, as occurred in the above-mentioned case of the writer's, in which the
heart instead of lying behind the fluid lay directly against the chest wall in the position
described by Schaposchnikoff. When the needle was introduced by Dr. Cole, it encountered
the heart at once, and the rubbing of the latter against the point could be readily felt.
This might have been prophesied from the fact that the heart sounds were well heard over
the precordium. With the exception of a few cubic centimetres of clear fluid the puncture
was a dry one, in spite of several successive insertions of the needle both at this point and
in the costoxiphoid angle. The patient's condition became very bad, and he died before a
second paracentesis could be undertaken. Autopsy showed the heart lying directly against
the chest wall with 1200 c.c. of fluid above and to the left. In this case, as in all those in
which the heart sounds and pericardial friction are well heard at the time of paracentesis,
FIG. 285. — Sites for paracentesis pericardii and peri-
carditomy. Ri, Riolan (1646), trephining the sternum;
D & M, Delorme and Mignon (1895), paracentesis;
R, Romero (1819), pericardiotomy; E, v. Eiselsberg's
pericardiotomy; Tr, Trousseau (1854); Di, Dieulafoy
(1873), paracentesis; W, West, pericardiotomy (1883).
1 Sew&ll, J. Am. M. Asso., Chicago, 1909, advises aspirating the fluid into the aspirator
bottle by sucking out the air with the mouth instead of with a mechanical aspirator. The
procedure is simpler and mistakes and failures of the pump are impossible.
PERICARDITIS. 497
it would have been better to have introduced the needle at the outer border of cardiac flat-
ness in spite of puncturing the pleura, and to have risked empyema to save the patient.
Drainage of the Pericardium. — Prof. Pearson, of Cork, punctures the pericardium,
with a large trocar, withdraws, and then introduces a fine rubber
catheter into the pericardial cavity through the tube of the trocar. The rubber catheter
follows the curves of the pericardium without danger of rupturing it, and thus enables him
to reach exudates which, as in the case of R. C. W. B. cited above, are located behind
the heart. He also withdraws the metal tube and leaves the rubber tube in place as a
permanent drain for several days at a time, and states that in this way he has been able
to cure a number of stubborn cases of chronic pericarditis with effusion which had resisted
all other methods of treatment.
The fact cannot be too greatly emphasized that cases with pericardial effusion are
usually desperate cases, and the fluid should be gotten out at all hazards. It is true that
all the fluid need not be removed to effect recovery, since the removal of a small amount,
just as in Starling's experiment, allows the circulation to re-establish itself and often per-
mits the rest to be absorbed.
Resection. — As has been seen, paracentesis pericardii, even in cases
of simple serous pericarditis, may be far from satisfactory. In purulent
pericarditis and haemo- and pneumopericardium it is still less so. In such
cases paracentesis is inadequate and the pericardium must be opened
freely. Radical as this procedure may seem, its satisfactory performance
by Romero antedates paracentesis. Romero made an incision in the fifth
intercostal space at the level of the costochondral articulation, introduced
his finger into the wound, palpated the pericardium with his finger, and
then seized it with forceps and opened it with curved scissors. The opera-
tion is best performed under light chloroform anaesthesia. Though this
must be carefully administered on account of the cardiac weakness, it is a
significant fact that most of the patients have stood the anaesthetic well.
The site for free incision has varied with different operators. Rosen-
stein made a free incision in the fourth left interspace close to the sternum
and then inserted a rubber-tube drain. West operated in the fifth left
interspace in the nipple line, having previously introduced an aspirating
needle, which he used as director for a long narrow-bladed sharp-pointed
bistoury, subsequently enlarging the opening with a probe-pointed bistoury.
V. Eiselberg resected the fourth costal cartilage and then opened the peri-
cardium. Delorme and Mignon perform what is probably the least danger-
ous and most satisfactory operation. They disarticulate the fifth and sixth
costal cartilages from the sternum with a pointed bistoury, draw them
forward one by one, and fracture them about 4 cm. from the sternum.
They then dissect down to the pericardium, which they pull forward with
forceps, and then slit it up with scissors for several centimetres.
Many observers, from Aran to the present, supplement the simple
drainage with irrigation of the pericardium. Aran injected
a dilute tincture of iodine at 100°, a procedure which in his case (though not
in all others) did not cause pain; West used warm 1 per cent, carbolic
acid; others used simple salt solution. The importance of irrigation can-
not be too freely emphasized, since the treatment should aim not only at
recovery but also at reducing the exudate and the resulting adhesions to
a minimum.
Delorme and Mignon operated upon all forms of pericardial effusions.
Their conclusions are summed up in the following: " 100 observations
32
498 DISEASES OF THE HEART AND AORTA.
— 82 paracentesis, 18 incision: 82 paracentesis — mortality 65 per cent.;
18 incisions — mortality 38 per cent. Let us do for the pericardium what
we have done for the peritoneum."
The relative merits of palliative therapy, paracentesis, and free incision
are well shown in West's case of purulent pericarditis:
A van boy, aged 16, was struck in the back by a truck and knocked down. No symp-
toms for two months, then shivering and pain in the left side and precordium. Pain sub-
sided in a few days. Three weeks later he went out for a short walk; became very faint
and almost fell down. Pain seized him in the pit of the stomach. Became cyanotic, dys-
pnceic, and nauseated. Admitted Sept. 7. Pulse 78; paradoxic, losing 2-3 beats at each
inspiration. Precordial bulging and oedema. Dulness from right nipple line to three inches
outside left nipple line. Cardiac sounds almost inaudible. Liver pushed down and felt in
epigastrium. Slight oedema of feet.
Twelve leeches applied to the precordium followed by poul-
tices. Palliative treatment for a week. Pulse and general condition feebler.
Sept. 14. Paracentesis pericardii — fourth left interspace below nipple;
90 c.c. 1 per cent, carbolic acid at 100° then introduced through the needle and used to
wash out pericardial cavity. No pain. Patient much relieved.
Sept. 17. Patient's condition again bad. Paracentesis fails to remove fluid. Free
incision under chloroform, as above described, in fifth left interspace; at least
two quarts of pus removed. Immediate improvement. Uneventful recovery.
Left hospital Feb. 23, and the following September was perfectly well and had been
following his usual work for the past six months as well as ever.
Rosenstein's case and those of Delorme and Mignon show similar
results.
. West gives the following statistics for paracentesis:
Number. Recovery. Death.
Phthisis 13 4 9
Rheumatic fever 11 7 4
Scurvy 9 6 . 3
Pleurisy 6 5 1
Injury 3 2 1
Pneumonia 2 . . 2
General dropsy:
Morbus cordis 2 . . 2
Nephritis 2 2
Chronic bronchitis 1 1
Mediastinal tumor 1 ... 1
Unassigned 17 7 10
67 34 33
In spite of the comparative harmlessness and brilliant results obtained
by the radical operation in purulent pericarditis, it is not probable that
this procedure can be extended to the milder exudates, since, just as in
joints, free prolonged drainage is followed by complete obliteration of the
cavity. Irrigation of the cavity through an aspirating needle or trocar,
after tapping, is possible only when the diameter is large 'and the outflow
is a free one.
PERICARDITIS. 499
BIBLIOGRAPHY.
PERICARDITIS.
Historical data are taken from G. A. Gibson, Diseases of the Heart and Aorta, Edinb. and
Lond., 1898.
Poynton, F. J.: Heart Disease and Thoracic Aneurism, Lond., 1907.
Sturges. Quoted from McPhedran, A.: Pericarditis, Osier's Mod. Med., Phila., 1908, iv.
Cadet de Gassicourt. Quoted from Hochsingers in Pfaundler and Schlossmann's "Diseases
of Children," translated by Shaw and La Fetra, Phila., Lippincott, 1908.
Sears. Quoted from Osier, Principles and Practice of Medicine, 4th edition, N. Y., 1901.
Chatard, J. A.: Acute Pericarditis complicating Acute Lobar Pneumonia, Johns Hopkins
Hosp. Bull., Balto., 1905, xvi, 334.
Breitung: Ueber pericarditis tuberculosa, Berl., 1877.
Head, Henry: On Disturbances of Sensation, with Especial Reference to the Pain of
Visceral Disease, Brain, Lond., 1896, xix, 153.
Emerson. C. P.: Bull. Johns Hopkins Hosp.
Silva. Quoted from Buxbaum, B.: Lehrbuch der Hydrotherapie, Leipz., 1903.
Rubino, A.: Les pericarditis expe>imentales et bacte>iques, Arch. Ital. de Biol., 1892,
xvii, 298, and Rif. Med., 1892, viii.
Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttgart,
1906.
Verney: Gaz. hebd. de meU, Par., 1856, iii, 793. Quoted from Thayer, W. S.: Observa-
tions on Two Cases of Pericarditis with Effusion, Bull. Johns Hopkins Hosp., Balto.,
1904, xv, 149.
Frangois-Franck, A.: Recherches sur la mode de production des troubles circulataires
dans les epanchements abandons du pericard, Gaz. hebd. de me"d., Par., 1877.
Lagrolet: De la compression du cceur dans les epanchements du pericard, These, Paris,
1878.
Cohnheim, J.: Vorlesungen ueber allgemeine Pathologic, Berlin, 18X2.
Starling, E. H.: Some Points in the Pathology of Heart Disease, Lancet, Lond., 1897, i,
569, 652, 723.
Bolton, C.: The Experimental Production of Uncomplicated Heart Disease, with Especial
Reference to the Pathology of Dropsy, J. Path, and Bacteriol., Edinb. and Lond.,
1904, ix, 67.
Auenbrugger, L., and Corvisart. Quoted from Ebstein.
Rotch, T. M.: Absence of Resonance in the Fifth Right Interspace diagnostic of Pericardial
Effusion, Bost. M. and S. J., 1878, xcix, 389, 421.
Ebstein, W.: Zur Diagnose der Flussigkeitsansammlung im Perikarcliuni, Virchow's Arch.,
1893, cxxx, 418.
Aporti, F., and Figaroli, P.: Zur Lage der akutentstandenen Ergiisse im Herzbeutel,
Zentralb. f. inn. Med., 1900, xxi, 737; from whom Concato, Riv. clin. di Bologna,
Anno vii, Fasc. 4, is quoted.
Sibson: Article on Pericarditis in Reynolds's System of Medicine, Lond., 1877.
Koranyi, F.: Ueber den Perkussionsschall der Wirbelsaule und (lessen diagnostische Ver-
wentung, Ztschr. f. klin. Med., Berl., 1906, Ix, 295.
Thayer, W. S.: Observations on Two Cases of Tuberculous Pericarditis with Effusion,
Johns Hopkins Hosp. Bull., Baltimore, 1904, xv, 149.
Pirogoff. Quoted from Schaposchnikoff.
Schaposchnikoff, B.: Zur Frage ueber Perikarditis, Mittheil. a. d. Grenzgeb. <1. Med. u. d.
Chir., Jena, 1897, ii, 86.
Riolan and Romero. Quoted from Schaposchnikoff, Delomr and Miirnon.
Jowett. Quoted from S. West.
Dieulafoy: Traite" de 1'aspiration des liquides morbides, Par., 1873.
Delorme, E., and Mignon: Sur la ponction et incision du pericarde, Rev. de Chir., Par.,
1895, xv, 797, 987. and 1896, xvi, 56.
West, S.: A Case of Purulent Pericarditis treated by Paracentesis and by Free Incision,
with Recovery, Statistics of Paracentesis pericanlii. Mod. Chir. Trans., Lond., 1883,
Ixvi, 235.
500
DISEASES OF THE HEART AND AORTA.
ADHERENT PERICARDIUM.
(Adherent pericardium, — adhesive pericarditis, synechiae pericardii,
concretio pericardii cum corde, chronic mediastinopericarditis.)
Whenever a pericardial exudate, fibrinous or fluid, is absorbed slowly
a certain amount of organization takes place in it and adhesions form just
as after pleurisy or peritonitis. The form of these adhesions varies consid-
erably, from long thin strands stretching like cords across the pericardial
cavity to short bands of dense fibrous tissue, or even to a firm tissue which
LONG
DENSE
FIG. 286. — Specimen showing the two layers of pericardium united in some parts by long strands
and in others by short bands of dense adhesions. (From a specimen in the Army .Medical Museum,
Washington, D. C.)
knits the two surfaces together and completely obliterates the cavity. All
these forms may be present in different areas of the same pericardium, so
that the process need not be considered as perfectly homogeneous.
Moreover, not only the adhesions within the pericardium but particu-
larly the extrapericardial adhesions which are formed simultaneously on
the outer surface, are of clinical importance, since it is the latter which
form the, tightest lines in the harness and determine the strain upon the
heart. As shown by Manges' case cited below, complete obliter-
ation of the pericardial cavity may cause no symptoms
as long as the extrapericardial adhesions remain unimportant.
PERICARDITIS.
501
The main adhesions do not always occupy the same position, but may
be divided into the following groups (Fig. 288) :
1. Chondropericardial — fixing the heart to the costal cartilages and chest wall in front.
2. Pleuropericardial — gluing it to the pleurae and fixing the edges of the lungs.
3. Mediastinopericardial — fixing its posterior surface and especially harnessing
the auricles.
4. Phrenopericardial — fixing it to the diaphragm.
FIG. 287. — Sections showing adherent pericardium. (Photomicrographs by Dr. C. S. Bond.)
A. Seen with low power. B. Same specimen under high power. C. Another specimen, showing the
extreme vascularity of pericardial adhesions.
Each of these gives rise to a distinct group of physical signs; and, since
these may occur separately, it is important that they should be consid-
ered so.
PATHOLOGICAL PHYSIOLOGY.
The mechanical effects upon the circulation due to pericardial adhesions
may be twofold: 1, the work of the ventricle is increased by the tug upon
the adhesions; 2, the filling of the heart may be hindered by strangulation
of the vena cava. At each contraction the heart must not only drive out
the blood, but must pull on its harness of adhesions. The additional work
which it thus has to perform depends both upon the tightness of the
502
DISEASES OF THE HEART AND AORTA.
adhesions and upon the weight or rigidity of the structures
pulled. The latter factor depends upon the position of the adhesions,
whether it is the ribs, pleura, mediastinum, or the diaphragm and liver that
are tugged upon, being greatest for adhesions to the ribs and diaphragm.
3. The emptying of the heart and the flow through the aorta may, as
claimed by Kussmaul, be hindered by the tugging of the adhesions upon
the arch of the aorta. This can readily be shown experimentally if such
traction be made in a dog whose chest has been opened. The pulse may
be made to disappear absolutely in spite of the fact that the heart rate
remains unchanged and the heart dilates from overfilling; enough blood
flows in from the venae cavse to dilate the heart.
r^
H ' '/ '
RLE. P.
FIG. 288. — Anterior and posterior pericardial adhesions. (Semi-schematic.) A. Anterior adhe-
sions showing the stumps of adhesions to the ribs. B. Mediastinal adhesions, showing a side view of the
heart. PLE. P., pleuro-pericardial adhesions; C, P., costo- (or chondro)-pericardial, P. P., phreno-peri-
cardial, M. P., mediastino-pericardial adhesions.
When this additional work is imposed upon a heart already weak, it
may succumb to the strain, and death may occur with all the manifesta-
tions of broken compensation. The importance of adherent pericardium
in causing death from heart disease is shown by the fact that it was present
in almost all the cases of Sturges' series.
Usually, however, the ventricles gradually recover from the strain and
simply undergo a gradual work hypertrophy proportional to the additional
strain, and an additional amount of work may be done at each systole
sufficient to balance the amount required. During exercise, emotion, dis-
ease, or other strains, however, not only the work of the heart in the circu-
lation is increased, but with the increased systolic output and systolic
excursion of the walls the tug upon the adhesions is increased enormously,
and the heart is thus readily overstrained. The heavy beating of the heart
under emotional excitement is especially likely to bring this about.
Moreover, the process of hypertrophy is not a pure one. With the
fibrosis of the pericardial adhesions outward, the process of fibrosis also
PERICARDITIS. 503
extends inward into the somewhat injured myocardium, and this process
goes on progressively with each moment of overstrain until the myofibrosis
cordis is advanced and the heart failure complete.
The site of the adhesions determines not only the degree but the char-
acter of the heart failure. If the densest adhesions are over the left ven-
tricle, the effect is to inhibit the action of the latter alone. Nature performs
the experiment of Welch, and gives rise to the clinical picture of broken
pulmonary compensation with dyspnoea, cardiac asthma,' or pulmonary
oadema.
If the chief adhesions are over the right ventricle, on the other hand,
broken systemic compensation sets in with venous stasis, tricuspid insuf-
ficiency, enlargement of the liver, and collection of fluid at various sites,
but particularly in the peritoneal cavity (cf . Pseudocirrhosis, page 509) .
On the other hand, the tugs of the adhesions on auricles and ventricles
may act as mechanical extrastimuli and produce an extrasystolic arrhyth-
mia, which in itself hinders the circulation.
SYMPTOMS.
Since the actual formation of the adhesions really represents the sub-
sidence of the acute pericardial process, it is not surprising that the onset of
the pathological lesion is insidious, and indeed may coincide with the sub-
sidence rather than the onset of symptoms. This is well illustrated by cases
of purulent pericarditis like that reported by Manges, in which obliteration
of the pericardial cavity accompanied the curve of the healing of the incision.
The patient was free from symptoms, and a year later was working as a
messenger boy. In most cases the process continues insidiously during
months or years before cardiac symptoms and heart failure set in, during
which the patient may be apparently well or may suffer only upon over-
exertion, over-indulgence in venere et potu, or emotional excitement.
Sooner or later the pump wears out and symptoms become marked.
The symptoms of adherent pericardium are mainly those of chronic
heart failure — palpitation, weakness, etc. Precordial pain localized about
the apex or the base of the sternum is common (65 per cent. -70 per cent,
of cases) . As stated above, the other symptoms may fall into the category
of cardiac dyspnoea or that of venous stasis and dropsy, dependent upon
whether the failure of compensation is in the pulmonary or systemic circu-
lation. In the former case there are attacks of coughing and acute dyspnoea,
sometimes with smothering sensations. The latter often begins insidiously
with weakness, enlargement of the liver and spleen, swelling of the abdomen
(Pick's pericarditic pseudocirrhosis of the liver, or pericarditic polyse-
rositis), and swelling of the feet. These symptoms may also set in more
acutely as in the form of simple heart failure.
Delirium occasionally occurs with adherent pericardium, perhaps due
to disturbed cerebral circulation. In one case under the writer's care the
patient was subject to hallucinations of vision during the periods when his
cardiac condition was bad. These were probably due to congestion of the
retinal capillaries, so that he saw lions and tigers jumping over one another
at the foot of his bed, even though he realized it was a physiological hallu-
cination.
504 DISEASES OF THE HEART AND AORTA.
PHYSICAL SIGNS.
Corresponding to the variations in the site of adhesions, the physical
signs of adherent pericardium are both multifarious and interesting. The
patients are often pale and pasty, the haemoglobin being low and the ca-
pillaries rather empty of blood. Sometimes the opposite holds true, and
plethoric cyanosis prevails. Inspection of the veins of the neck may
show filling of the latter during inspiration (Kussmaul's
sign), accompanied by inspiratory diminution in the size of
the pulse or even omission of some beats during inspiration (pulsus
paradoxus, Kussmaul) (see page 506) . The sounds over the heart during
this period may become weaker, but usually still continue.
The so-called Friedreich's sign (diastolic collapse of the vein), now
known to represent merely a weak positive venous pulse (see page 57) ,
is common to many weak hearts and has no diagnostic or prognostic value.
C. M. Cooper has recently added what seems to be a valuable accessory sign of ad-
herent pericardium. He determines how long the patient can hold the breath in inspira-
tion, and, five minutes later, the same for holding the breath in expiration. In normal
insp.= 40-70 25 .
individuals ~ : m cardiac lesion -—; in persons with mediastmal and pen-
exp. =20-25 15
cardial adhesions - — — (paradoxical ratio). Patients with bronchial asthma also
exp. = Zo
showed — r (paradoxical ratio); so that its chief value is as confirmatory
exp. =25-35
evidence. The presence of a paradoxical ratio may prove very useful in confirming, and
a normol ratio in excluding, mediastinopericarditis.
Broadbent' s Sign. — The chest usually shows marked precordial bulging,
especially in children. Walter Broadbent in 1895 called attention to a
"visible retraction, synchronous with the cardiac
systole, of the left back in the region of the eleventh
and twelfth ribs," and " in less degree of the same region of the
right back " (Broadbent's sign) . Such retractions of the interspaces
have also been recognized in many cases of cardiac hypertrophy by the
Broadbents as well as by other observers (Tallant). J. H. F. Broadbent
has lately (Heart Diseases, 4th edition) stated the facts more definitely
and more accurately in the following words: "The systolic recession of
spaces alone is, however, not a trustworthy indication, as it may be due
to atmospheric pressure, especially when the heart is much hypertrophied.
When the costal cartilages or lower end of the sternum
are dragged in, there can be little doubt as to the diagnosis, as this could
not be effected by atmospheric pressure." This sign is often most marked
in deep inspiration when the diaphragm is tense.
Broadbent also states that systolic retraction over the apex is a valuable-
sign, but only when the impulse is forcible on palpation, as it may otherwise
be due to atmospheric pressure (over the right ventricle; cf. page 91).
This is certainly true in many cases, but in the writer's experience there
are frequent exceptions to this rule, and it is of value chiefly as a cor-
roborating sign.
Percussion. — The area of cardiac dulness is usually but by no means
always enlarged, owing to the hypertrophy which usually takes place,
PERICARDITIS.
505
though fixation of the lung borders may cause the area of flatness and area
of dulness on the left to almost coincide. The characteristic features on
percussion are: Absence of the usual change in the left
border of flatness between deep inspiration and deep expiration.
This movement of the border of the lungs, which is normally 2-3 cm.,
may be reduced to less than 1 cm. or may absolutely disappear. The
position of the apex, as determined by palpation, auscultation,
and percussion, also becomes fixed, and may not change
at all when the patient turns from lying on his right side to lying
on his left. However, both these
fixations may be present with
simple pleural adhesions and no
actual involvement of the peri-
cardial cavity. This was well
exemplified in the case of a
little girl who had been a pa-
tient in the Johns Hopkins
Hospital several times during
the last couple of years, and
who presented signs interpreted
as adherent pericardium. At
autopsy the pericardial cavity
was free from inflammatory
processes, but the pleurae were
everywhere bound down tightly
around it. Practically the effects
were nearly the same as if the
pericardial cavity had been in-
volved, Broadbent's sign and
pulsus paradoxus being present
to a slight degree. Such cases
are, however, extremely rare, and difficult to diagnose when they occur.
Palpation. — Sir William Broadbent has called attention to the im-
portance of an exaggeration of the diastolic shock or rebound
(accompanying the second sound) over the greater part of the pericardium
as characteristic of adherent pericardium. This is certainly a useful aid
especially in corroboration of other signs, but, unless the distinctness of
the shock is far greater than would be warranted by the loudness of the
sound at the base, it is of little value. Nevertheless, the writer recalls a
case in which the diagnosis of adherent pericardium (accompanying a well-
defined aneurism) was based upon this sign alone and was verified at
autopsy. Professor Thayer has found that there is often in addition a
protodiastolic shock accompanying the third heart sound, which may be
the most intense shock in the whole cardiac cycle. Apparently this is
distinctive of adherent pericardium.
Thrills, especially presystolic in time, are occasionally felt, probably
owing to tugs upon strands of adhesions, but these alone are not typical.
Auscultation.— Since pericarditis is frequently (34 per cent, of Sears's
cases) accompanied by various forms of valvular disease, the presence of
FIG. 289. — Cardiac outline in adherent pericardium.
The broken line indicates the fixation of the left border
of the heart (apex) and of the left border of cardiac
flatness (anterior margin of the left lung). The small
diagram at the left shows the relation of the heart sounds
to the cardiac cycle, indicating the unusually loud thin!
heart sound. BR BR indicate areas of systolic retrac-
tion of the ribs, xiphoid, and interspaces; R 1, 2,
gastric sounds in adherent pericardium.
506
DISEASES OF THE HEART AND AORTA.
all varieties of valvular murmurs, especially of mitral origin, is not sur-
prising. A presystolic rumble, probably due to the stretching of strands
of adhesions by the contraction of the auricle, is occasionally heard in
cases of adherent pericardium in which aortic, mitral, and tricuspid valves
are normal. Sewall also reports several cases with reduplication of the
first sound, which was shown at autopsy to be due to old peripheral adhe-
sions. Professor Thayer finds the third heart sound and the corresponding
protodiastolic shock and wave very distinct in adherent pericardium.
This may be due to the fact that they are more easily transmitted to the
chest wall, or perhaps because the filling of the heart causes sudden stretch-
ing of the adhesions.
RESP.
RIEGELS R
PHENOMENON
VEN.
CAROT.
PULSUS
PARADOXUS
JW
\\f*
V
/uvLjvlA/
COSTOPERIC
MEDIASTINO
PER1C
FIG. 290. — Inspiratory and expiratory dropping of beats (Riegel's pulse and the pulsus paradoxus)
in adherent pericardium, showing the position of the adhesions which bring the condition about. VEN.,
jugular pulse; CAROT., carotid pulse; RESP., respiration (downstrokes represent inspiration; upstrokes
represent expiration). In cases with Riegel's phenomenon (anterior costo-pericardial adhesions) the
conditions are as shown in the diagram (upper respiratory tracing, venous pulse, carotid pulse); those
with pulsus paradoxus correspond to the conditions shown by venous pulse, carotid pulse, and lower
respiratory tracing.
Riess' Gastric Sounds. — A very interesting sign was described by Riess
in 1879, and, since it has been verified by so excellent an observer as Fran-
9ois-Franck, merits attention. On listening over the stomach in some
cases of adherent pericardium, observers have been able to hear the heart
sounds loud and metallic in quality. These sounds are not much influenced
by changes of position, by respiration, nor by inflation or filling of the
stomach. They are probably due to adhesions to the diaphragm only, and
hence, as originally stated by Riess, are not present in all cases of adherent
pericardium.
Variations in the Pulse. — The pulse in adherent pericardium is usually
small and rapid, generally regular, but often showing an extrasystolic
irregularity which is probably due to tugs upon the strands of adhesions.
The striking and characteristic feature is the marked diminution of
the pulse-wave during inspiration, amounting sometimes to the dropping
of a beat during that phase. This was first noticed by Griesinger in 1854
in a case in* which autopsy showed strands of adhesions about the arch of
the aorta, causing kinks and stenosis in its lumen when pulled upon by the
descent of the diaphragm. The vena? cavse were also caught in dense
PERICARDITIS. 507
adhesions which strangulated them in similar manner during inspiration.
Both inflow and outflow of blood were therefore hindered in that phase,
hence the diminution of the pulse. The same condition was studied by
Hoppe and later by Kussmaul (1873), since whose report it is known as
the p u 1 s u s p a r a d o x u s . It is not entirely pathognomonic of adhe-
rent pericardium or even of pericarditis in general, occurring with open
ductus arteriosus Botalli (Franc,ois-Franck, see page 450) and in many
normal or neurasthenic individuals (Reichmann), though in these the dimi-
nution does not amount to complete dropping of beats during inspiration.
ADHES-
FIG. 291. — A. Radiograph of a case of adherent pericardium. (Kindness of Prof. C. M. Cooper.)
B. Diagram illustrating the condition seen in A, showing the pericardium pulled outward to the right and
a portion of the diaphragm pulled upward by the adhesions (ADHES).
The occurrence of exactly the opposite condition of the pulse, namely diminution
of the wave and impulse during expiration, has been described by Riegel in cases
in which autopsy showed pleuropericardial adhesions upon the anterior surface of the
heart. Riegel believes that the relaxation of the lung during expiration pulls the heart
upward and produces a fall of pressure from displacement of the latter.
Rosenbach has been able to show experimentally that when the heart was displaced
by an inflated rubber bulb the venae cavse became kinked and the pulse became smaller
and blood-pressure fell. When this displacement occurs during inspiration from downward
traction, a pulsus paradoxus results; when it occurs during expiration, Riegel's phenom-
enon occurs.
Apart from these respiratory variations the blood-pressure shows no
special features, being usually low in uncomplicated cases; but it is fre-
quently normal from compensatory vasoconstriction and increased cardiac
effort, and occasionally high in the nephritic and uracmic cases.
X-ray Examination. — The demonstration of pericardial adhesions
by means of the Rontgen rays was first made by Moritz Benedikt in 1897.
Some question was thrown upon his methods by the criticism of F. Moritz
(1900), showing that normal shadows along the edge of the cardiac and
liver shadows may simulate adhesions. These objections were obviated
by Stuertz, who reported five cases in which the presence of adhesions was
demonstrated not only by suspicious shadows through the lungs and along
the edge of the pericardium, but also by the fact that the margin of the
pericardium at these points was pulled downward or outward when the
structures were rendered tense in inspiration. Some areas were also shown
508 DISEASES OF THE HEART AND AORTA.
to be quite fixed during respiration. Stuertz's observations have been
confirmed by Lehmann and Schmoll and by Dr. C. M. Cooper, to whom
the writer is indebted for the X-ray shown in Fig. 291.
The special value of the X-ray examination lies in the fact that it
reveals the mediastinal and diaphragmatic adhesions with accuracy, and,
by demonstrating the points at which the fixation and tension are greatest,
points out the path for operative interference.
Abdomen. — The abdomen is often negative, but enlargement of the
liver and spleen and ascites are frequent, as has been shown by Weiss in
1876.
CASE OF ADHERENT PERICARDIUM.
The following very typical case was under the writer's care in the City and County
Hospital of San Francisco. (As the original history was lost, these notes are taken from
the article of Lehmann and Schmoll, who have previously published the case.)
*L. A., engineer, 23 years old, entered the hospital complaining of headache, nausea,
and shortness of breath. He had had rheumatism six years before admission, and then had
pain over the heart. Since then he had had two attacks. During the past few years he
has been subject to periods of heart failure with dyspnoea, during which he is frequently
depressed and sometimes even maniacal.
The patient's lips, ears, and extremities are deeply cyanotic. The pulse is irregular,
with numerous extrasystoles, many of them ineffectual. The apex impulse (systolic pro-
trusion) is visible in the sixth interspace 3 cm. outside the mammillary line, beyond which
there is a well-marked systolic retraction of the interspaces in front and back. There is
also systolic retraction of the ribs and costal margin (Broadbent's sign). The apex is
fixed and does not move with change of position, but the area of flatness changes during
respiration (movement of the lung border). There is well-marked pulsation over the right
ventricle. Dulness extends above to the third rib and 3 cm. to the right of the right para-
sternal line. A loud presystolic rumble and a loud systolic murmur are heard over the apex.
The second pulmonic is markedly accentuated. Both sounds are heard with the extra-
systoles.
The lungs are clear except for dulness and bronchovesicular breathing at the left
base behind.
The liver is greatly enlarged and readily palpable, but there is no pulsation. There
is some oedema of the feet.
Clinical diagnosis: Left-sided pleurisy, adhesion of the pericardium with the pos-
terior surface of the heart, mediastinum, and diaphragm, mitral stenosis and insufficiency.
Examination with the fluoroscope showed the heart to be dilated to right and left.
There was a marked angular protrusion along the right border of the cardiac shadow.
In this region the outlines of the shadow are less sharply defined than usual, merging into
the liver and vertebral shadows. The diaphragm is equally high on left and right, moving
less on the latter.
The patient's condition did not improve under rest and digitalis. He often had in-
tense precordial pains. On one occasion he was subject to definite hallucinations, imagin-
ing that he saw lions, tigers, and other brightly colored wild animals springing to and fro
upon the floor of the ward and over his bed, though he was at the time otherwise rational,
and even realized that it was an hallucination. He was placed in a solitary cell for twenty-
four hours at his own request, for fear of doing personal violence to the persons about him.
His condition became so much worse that cardiolysis was decided upon as a last
resort and was performed by Professor Stillman. The ribs were resected over the pre-
cordium and the pericardium opened in exploration. The heart was everywhere covered
with adhesions, which over the anterior surface of the heart consisted of strands about an
inch long. There was no fibrinous exudate and no fluid. The patient took the ether badly
and became extremely cyanotic. The shock of the operation did him evident harm, for
during his entire sojourn after that he felt even worse than before. The wound itself caused
him no trouble and healed per primum. The patient left the hospital three weeks after
the operation, in spite of advice.
PERICARDITIS.
509
Fro. 292. — Case of pericarditic p.«eudocir-
rhosis. (After Cabot. Boat. M. and ,S. J ., 1898,
cxxxviii.)
Pericarditic Pseudocirrhosis of the Liver (Pick), and Polyserositis from
Adherent Pericardium (Cabot). — Hutinal in 1895 described a form of
liver cirrhosis of cardiac origin (cirrhose cardiaque). Friedel Pick (1896)
in Pribram's clinic called attention to a very interesting clinical condition
which is not infrequently encountered, but whose nature is often over-
looked. This is seen in certain cases which run the course of a primary
hepatic cirrhosis, beginning with asci-
tes, enlargement of the liver, slight
jaundice, general weakness and
dyspnoea, but devoid of any special
cardiac features. Occasionally there
were also enlargement of the super-
ficial veins of the abdomen and oedema
of the feet. The first and second
cases were considered clinically to be
primary cirrhosis of the liver, and the
discovery of adherent pericardium at
autopsy came as a surprise. In his
third case adherent pericardium was
carefully sought for and found, and
the diagnosis was correctly made.
Death occurred in two to four years
after onset of symptoms. The peri-
cardia in these cases were found to
be completely or almost completely adherent, the rest of the heart normal.
The livers showed both interlobular cirrhosis and chronic perihepatitis
(iced liver, Curschmann), the peritoneum was thickened, and chronic
perisplenitis was present. An example of this condition is found in the
case of J. M. C. cited on page 272, in whom the presence of adherent pericar-
dium was not suspected during life.
In 1898 R. C. Cabot described a similar case. Flesch and Schossberger find the con-
dition not infrequent in children, presenting the superficial manifestations of a primary
cirrhosis without the presence of alcohol and syphilis as etiological factors. On careful
examination the presence of adherent pericardium is readily detected by its usual signs.
Flesch and Schossberger were able to reproduce the condition experimentally in dogs.
They produced pericarditis by injections of tincture of iodine into the pericardial cavity
and allowed the animals to recover, during which period adherent pericardium occurred.
After a few months ascites and oedema set in and the animals died. Their results have
been confirmed by O. Hess, who has also produced cyanosis and cirrhosis of the liver by
suturing the inferior vena cava to the diaphragm.
Another point in the differential diagnosis from true primary cirrhosis is the fact that
the veins of the arms and neck are usually enlarged to almost the same extent as those of
the portal system, showing that the stasis is not confined to the latter. There is no
caput medusae.
TREATMENT.
The treatment of adherent pericardium may be both palliative and
operative. The palliative treatment is simply the general treatment for
cardiac weakness: rest, diet, and cardiac stimulants, strychnine and digi-
talis, during the onset and acute stages; careful graduated exercises and
training during the period of relative freedom from symptoms.
510 DISEASES OF THE HEART AND AORTA.
It is impossible to remove the condition, and the therapy must be
simply so directed that that which cannot be cured may best be endured.
Ansemia should be treated with iron, exposure to infection avoided,
and general hygienic conditions maintained. For reasons mentioned above,
these precuations should be carried out even more carefully than for simple
valvular disease.
Surgical Treatment (Cardiolysis) . — In 1902 Brauer, of Heidelberg,
introduced a simple method of treatment which promises to revolutionize
the therapy of adherent pericardium. Brauer proposed ''to relieve
the heart functionally by breaking the strong bony
ring of ribs, not by a severe operation with the breaking up of exten-
sive adhesions but only by substituting a soft covering for the natural bony
covering of the heart On account of the tremendous strain upon
the heart, due to traction on the chest wall, we foresaw a danger in opera-
tion under narcosis. .... The operation was tried upon a patient with
adherent pericardium, broken compensation, ascites, and oedema. Seg-
ments of the third, fourth, and fifth ribs 7 to 9 cm. in length were resected
under light narcosis, the periosteum being carefully removed. The patient
made an uninterrupted recovery. His pulse soon became stronger and
more regular, the ascites and oedema disappeared, and he was able to do
heavy work without symptoms. The pulse still remained irregular."
Brauer reported two other cases with equally good results, and these
have been confirmed by Beck, Umber, Meyer, Westfeld, Wenckebach,
and others. Brauer particularly states that he does not attempt to break
up the adhesions, as Delor.me and Carl Beck have proposed, since he believes
that this operation is too severe and that the adhesions would form again
too rapidly, although he states that, in individual cases, this might be
done besides his operation.
As regards the indications for cardiolysis, it would appear that, since
the adherent pericardium cannot otherwise be relieved, this operation is
worthy of trial whenever symptoms of cardiac weakness occur and recur
in a patient with well-marked adhesions to the chest wall (tugging in of
the lower ribs, fixation of the left border of flatness on inspiration, immo-
bility of the apex) and recur in spite of general cardiac hygiene. It is not
necessary to wait for the complete cardiac break-down to prophesy that
this must sooner or later occur in such a case, and to see that the sooner
the work of the heart is relieved the longer will be the life of the patient.
Moreover, it is evident that if the operation is performed between attacks
of cardiac overstrain, the patient is in better condition to withstand the
shock of the operation and the clanger of the latter is diminished. If the
cardiolysis is not performed until the patient's heart has almost completely
given way, as in the case of the patient with the visual hallucinations
referred to above, he can scarcely fail to suffer from the shock of the opera-
tion; but even in such cases Brauer's results have been striking, and, since
there is no other mode of relief, operation is warranted.
It must be confessed that in such cases the manner in which the anaes-
thesia is administered determines a large part of the shock from the opera-
tion, and may prove a decisive factor in the outcome. The selection of the
anaesthetist constitutes no small part in the management of the case.
PERICARDITIS. 511
The question also arises whether operation should be advised in chil-
dren or adolescents whose pericardia are adherent to the chest wall, but in
whom, owing to the flexibility of the latter, the symptoms do not as yet
demand operative interference. In this regard each case must of course
be decided upon its own merits, but it is evident that as age advances the
rigidity of the ribs is bound to increase and the strain upon the heart pro-
portionately. If the case remains relatively free from symptoms as age
advances, it should be left alone ; but if the progress of the second or third
decade brings with it increasing cardiac symptoms or the signs of pericardi-
tic pseudocirrhosis, the question of early cardiolysis should be seriously
considered. Since there is no hope that children will " outgrow " an adhe-
rent pericardium, it should be relieved as much as possible before the strain
has ruined the heart muscle. When valvular lesions are present, especially
mitral stenosis, the danger from operation is of course greater, but in the
hands of a skilful surgeon this is much less than might be expected and is
probably less than that in pericardiotomy for purulent pericarditis.
BIBLIOGRAPHY.
ADHERENT PERICARDIUM.
Manges, M.: Adherent Pericardium, Internal. Clin., Phila., 1905, 15 ser, i, 1.
Hoppe, F.: Ueber einen Fall von Aussetzen des Radialpulses wahrend der Inspiration und
die Ursachen des Phanomens, Deutsche Klinik, 1854, No. 3.
Kussmaul: Ueber schwielige Mediastino-pericarditis und paradoxen Puls, Berl. klin.
Wchnschr., 1873, x, 433, 445, 461.
Friedreich, N.: Ueber den Venenpuls, Deutsches Arch. f. klin. Med., Leipz., 1865-6, i, 241.
Cooper, C. M.: The Respiratory Ratio; a Preliminary Note, J. Am. M. Assoc., Chicago
1909, lii, 1182.
Broadbent, Walter: An Unpublished Physical Sign, Lancet, Lond., 1895, ii, 200.
Broadbent, Wm. H.: Adherent Pericardium, Trans. M. Soc., Lond., 1897-8, xxi, 109.
Broadbent, Wm. H. and J. H. F.: Heart Disease and Aneurism of the Aorta, New York,
4th ed., 1906.
Camac, C. N. B.: Broadbent's Sign, Johns Hopkins Hosp. Bull., Balto., 1898, ix, 271.
Tallant, A. W.: Some Observations on the Occurrence of Broadbent's Sign, Boston M.
and S. J., 1904, cli, 457.
Sewall, H.: On a Common Form of Reduplication of the First Heart Sound due to Extra-
cardiac Causes, Contrib. Sci. Med., Vaughan, Ann Arbor, 1903, 29.
Riess, L.: Ueber ein neues Symptom der Herzbutelverwachsung, Berl. klin. Wchnschr.,
1878, xv, 751. Weitere Beobachtungen ueber einer die Herztone begleitende Magen-
consonanz bei Herzbeutelverwachsungen, ibid., 1878, xvi, 333.
Francois-Franck, A.: Des bruits extracardiaques in g£n£ral, en particulier des bruits
gastrique rhythmes avec le coeur; contribution au diagnostic de I'adh6rence au p£ri-
carde, Gaz. hebd. de Mckl., Par., 1885, 2 se>., xxii, 757.
Griesinger's observation (1854), reported by A. Widenmann, Beitrag zur Diagnose der
Mediastinitis, Diss., Tubingen, 1856.
Hoppe, F.: Ueber einen Fall von Aussetzen des Radialpul.so wahrend der Inspiration.
u.s.w., Deutsche Klinik, 1854, No. 3.
Reichmann, E.: Die inspiratorische Verkleinerung des Pulses (sogen Pulsus Parad<>
Ztschr. f. klin. Med., Berl., 1904, liii, 112.
Riegel, F.: Ueber extrapericardiale Verwachsungen, Berl. klin. Wchnschr., 1877, xiv, 657.
Rosenbach, O.: Experimentelle Untersuchungen Ueber die Einwirkung von RaumbeM-h-
rankungen in der Pleurahohle auf den Kreislauf apparat, Arch. f. path. Anat., etc.
Berl., cv, 215.
Benedikt, M.: Wien. med. Wchnschr., 1897.
Moritz, F.: Miinchen med. Wchnschr., 1900. Quoted from Lehmann and Schmoll.
512 DISEASES OF THE HEART AND AORTA.
Stuertz: Zur Diagnose der Pleuraadhasionen aus Pericard und Zwerchfell, Fortschr. a. d.
Geb. d. Rontgenstr., Hamb., 1904, vii, 215.
Lehmann and Schmoll: Pericarditis adhesiva im Rontgenogramm, ibid., 1905, ix, 196.
Cooper, Charles Miner: Personal communication.
Pick, F.: Ueber chronische unter dem Bilde der Lebercirrhose verlaufende Pericarditis
(pericarditische Pseudolebercirrhose), Ztschr. f. klin. Med., BerL, 1896, xxix, 385.
Cabot: Bost. M. and S. J., 1898.
Flesch and Schossberger: Diagnose und Pathogenese der in Kindesalter, haufigsten Form
der Concretio Pericardii cum Corde, Ztschr. f. klin. Med., Berl., 1906, lix, 1. Con-
firmed also by Hess, O.: Diagnose und Pathogenese der im Kindesalter haufigsten
Form der Concretio Pericardii cum Corde, Ztschr. f. klin. Med., Berl., 1906, Ix, 174.
Brauer, L.: Cardialyse, Mlmchen. med. Wchnschr., 1902, xlix, 982. Untersuchungen an
Herzen Cardiolysis und ihre Indikationen, Arch. f. klin. Chir., Berl., 1903, Ixxi, 258.
Beck. Quoted from Brauer.
Umber: Perkiarditis und mediastinale Verwachsungen und Cardiolysis, Therap. d. Gegen-
wart., 1905.
Wenckebach, K. F.: Remarks on Some Points in the Pathology and Treatment of Adherent
Pericardium, Brit. M. J., Lond., 1907, i, 63. Ueber pathologische Beziehungen zwi-
schen Atmung und Kreislauf, Samml. klin. Vortr , Leipz., 1907, No. 465, 466.
For a review of the subject see also Delatour, H. B.: Surgery of the Pericardium
and Heart. Am. J. Surg., N. York, 1909.
XIII.
WOUNDS OF THE HEART AND CARDIAC TRAUMA.
Hippocrates and Celsus, Paul of ^gina, Roland, Lanfranc, and other
writers of antiquity taught that wounds of the heart were followed immedi-
ately by death; but Ambroise Pare (1552) saw a gentleman of Turin "who,
although wounded in the heart during a duel, was able to pursue his antag-
onist 700 feet before he dropped to the ground and died." Muler (1641)
treated a soldier who lived for fifteen days after sustaining a wound of the
heart, — an observation so unheard of at the time that he had the autopsy
protocols signed by the commander of the garrison! Aprilis (1680) de-
scribes a wound of the right auricle, after receiving which the man had lived
for five days.
The results of modern times were summed up by G. Fischer in 1867
(351 cases) and Loison (1899) (277 cases). Fischer found the wounds
occurring with the following frequency:
Death within a few
minutes. Recovery.
Right ventricle 107 — 21 . 9 per cent. 6
Left ventricle 95 — 25 . per cent. 6
Both ventricles 24 — 34 . per cent. 2
Right auricle 28 — 25 . per cent.
Left auricle 13 — 38 . per cent.
Apex 12 4
Base 1 1
Septum ventriculorum 6 1
Whole heart 15—62 . per cent. 1
Left heart 5
Right heart 3 11
Coronary artery 1 1
Pulmonary artery 1
Not specified 40 17
351 "soTn.2%)
In 452 cases there were 50 (12 per cent.) of spontaneous recovery.
EXPERIMENTAL SURGERY.
Elsberg in 1899 made a very careful study of wounds experimentally
produced in the rabbit's heart. He found that those produced during
systole, when the heart fibres are shortened, become enlarged during dias-
tole and hence bleed more than wounds of corresponding size produced
during the latter phase. Wounds that completely penetrate the heart wall
bleed more than those which do so partially. Those which enter perpen-
dicularly bleed more than those which penetrate obliquely, for in the latter
case the walls form a valve-like approximation during systole. Indeed
Prof. Barker and the writer have produced oblique wounds penetrating the
entire wall of the dog's ventricle, which scarcely bled at all.
33 513
514 DISEASES OF THE HEART AND AORTA.
Even the smallest incised wounds made by Elsberg in the rabbit's
auricle were always fatal unless sutured, while those of the right ventricle
were more fatal than those of the left. Wounds of 2 mm. or less in the left
ventricle frequently healed spontaneously. However, when suture was
employed a large part of the ventricles could be cut through and the ani-
mal's life saved.
The size of the instrument producing the injury plays little role, for,
although in general large wounds bleed more and are more uniformly fatal
than small ones, nevertheless large and fatal wounds have been produced
by even ordinary needles. For example, Thiemann describes the case of a
man who in pressing against a heavy beam accidentally drove a sewing-
needle through his chest wall, where it became imbedded and stuck into the
FIG. 293. — Wounds of the left ventricle. (From specimens in the Army Medical Museum, Wash-
ington, D. C.) A. Bullet wound in the heart of a soldier who lived for two days after. B. Stab wound in
the left ventricle ; death within two hours.
heart wall, ripping one hole 1.5 cm. long in the wall of the right auricle and
another smaller hole in the wall of the right ventricle. His life was saved by
operation four and one-half hours later.
A single small puncture of the heart wall with a needle with prompt
withdrawal of the needle and no laceration, as is occasionally done in para-
centesis pericardii, as a rule causes no marked disturbance and does not
require operative interference.
Death from penetrating wounds of the heart results either from bleed-
ing, or, as was already shown by Morgagni and by Cohnheim, from accumu-
lation of blood within the pericardium (see page 487), compressing the
auricles and preventing the entry of blood into the heart.
It is possible that in the rare cases of instantaneous death the
trauma may cause the ventricles to pass into a state of fibrillation and
the circulation abruptly cease. There is no proof that this is frequent,
however, and the cases of instantaneous death from wounding the heart
are less common than might be expected.
WOUNDS OF HEART AND CARDIAC TRAUMA. 515
SYMPTOMS.
The symptoms accompanying a wound in the thorax which suggest a
wound of the heart (intrapericardial pressure) are those of angina pec-
toris — pain down the left arm, a feeling of precordial oppression and
precordial pain, especially marked on expiration. Pressure upon the pre-
cordium increases these pains. There is shortness of breath. Occasionally
there are abdominal pain and spasm of the abdominal muscles (Rehn). A&
Fischer pointed out, pain is also felt about the external wound, but as a
rule not in the heart itself. Even probing of the heart wound,
while it maygive rise to weakness and syncope, is not
accompanied by pain. Thus, one patient whose left ventricle had
been wounded thought that the knife had only gone through his clothes.
Blood is often found spurting from the wound with a well-defined pulsa-
tion. Sometimes it is foamy and mixed with air, indicating that the lung
has been penetrated.
PHYSICAL SIGNS.
The area of cardiac dulness is increased or is replaced by tympany
(pneumo-hiemopericardium) . The heart sounds are replaced by loud
churning or water-wheel murmurs. The blowing murmur caused
by the jet of blood passing out of the heart may also be distinguished.
The pulse becomes small, weak, rapid, and finally imperceptible.
Whenever time warrants, an X-ray examination should be done at
once, and the bullet or foreign body located. This may sometimes be very
exactly done by means of stereoscopic pictures and greatly simplifies the
operation.
TREATMENT.
Operative interference in the treatment of wounds of the heart was first
proposed by Rose, who confined himself to opening the pericardium and
removing the blood that compressed the auricles. This procedure was often
of benefit and even effected cure in cases where bleeding ceased spontane-
ously, but when the heart continued to bleed it was of no avail.
Up to this time it had been thought, in spite of the experiments of
physiologists, that suture of the heart wall itself would be accompanied by
instant death. But in 1895 Salomoni and Del Vecchio demonstrated that
wounds in the heart of the dog could be successfully treated in this manner;
and in 1896 Cappelen, Farina, and Rehn sutured the heart wall in man.
The passing of the sutures had no ill effects. Cappelen's and Farina's
patients died a few days later from secondary causes, but Rehn's patient,
who had received a stab wound in the right ventricle, operated on forty-
eight hours after the injury, recovered, and thus a revolution in cardiac
surgery was made. Rehn had demonstrated that wounds of the heart
could and should be successfully explored and sutured like wounds of
other viscera.
If the patient is in severe collapse from loss of blood, an intravenous
infusion of warm salt solution (37° C.) should be begun at once while the
operators are hastily cleaning and disinfecting the field of operation. As
a last resort a direct arteriovenous transfusion into the veins of the arm
516 DISEASES OF THE HEART AND AORTA.
may be made from another individual by the method of Crile, Buerger,
or Hartwell while the operation on the heart is going on, and some exsan-
guinated patients may thus be saved.
Operative Procedure. — The incision should be sufficiently large to
admit of a satisfactory exposure. A flap is made in the chest wall over
the point of penetration, usually including two ribs and three interspaces.
The flap adopted by most operators is horizontal U shaped with bifurca-
tions pointing to either left or right, the connecting bar passing through
either sternochondral or costochondral articulations. Occasionally the
Fio. 294. — Exposure of the heart for suturing a wound. (After G. T. Vaughan, J. Am. M. Assoc.,
1909, lii.) 1, heart; 2, deep sutures; 3, superficial sutures; 4 and 5, retractors on the pericardium; G,
left pleural line; 7, flap of chest wall including the fourth, fifth, and sixth ribs; 8, heart, outlined by
broken outline.
form is that of an upright or an inverted U, a H , or an H. If the wound
is near the sternum and has not already penetrated the pleura, that cavity
should not be opened, and the cj or H shaped flap is the best; but if the
wound has pierced the pleura, any convenient exposure may be adopted.
The incision through the pectoralis major should be parallel to its fibres
which may be retracted. The sternochondral or costochondral articula-
tions are cut through, the ends of the incision prolonged along parallel to
the ribs, and the flap forcibly reflected back, fracturing the costal cartilages
to permit a wide opening. If the pleura has not been penetrated, it
should be pulled toward the outer edge of the wound with retractors. A
free incision should be made into the pericardium, the pericardial cavity
emptied of clots, the wound in the heart located, and sutured with a fine
curved needle and silk thread. In passing the sutures the heart wall may
WOUNDS OF HEART AND CARDIAC TRAUMA. 517
be grasped with forceps without danger, the irregularity which accom-
panies the passing of the needle representing merely a few extrasystoles
resulting from the irritation, and passing off rapidly. Elsberg never ob-
served sudden stoppage of the heart and fibrillation following the inser-
tion of sutures. The writer, after several hundred experiments upon ex-
posed dogs' hearts, is able to confirm these statements of Elsberg. Elsberg
states that the interrupted suture is preferable to the continuous, for,
though it takes longer to apply, it injures fewer muscle fibres and is more
certain to hold. The sutures should be tied during diastole; these
do not tear out as readily as sutures tied during systole. In tightening the
sutures the two serous surfaces of the wound should be pushed in so as to
be brought into apposition. The surfaces unite by the usual growth of
fibrous tissue. The nuclei of the muscle cells near the wound seem to be
increased in number, and there is some amitotic and mitotic division but
no definite regeneration of muscle.
Control of Hemorrhage. — When the bleeding was so profuse that
death seemed imminent, Elsberg found it necessary to adopt provisional
means for stopping bleeding while putting in the sutures. For this he used
a hastily placed tobacco-pouch suture, or even a ligature about the whole
heart just above the wound. (This does not apply, of course, to wounds
in the upper half of the ventricles.) He was then able to place the sutures
bloodlessly, after which the provisional ligature was removed. In this
way he was able to suture tremendous wounds (2 cm. in a rabbit's heart,
corresponding to about 10 cm. in the human heart), with 66 per cent,
of recoveries.
Large wounds of the auricle may be more difficult to control. Sauer-
bruch recommends stopping the bleeding by gently compressing the auricle
between the middle and ring fingers while grasping the point to be sutured
between the index finger and thumb. Rehn finds that with some care a
ligature may be placed about the auricle to still the bleeding while the
sutures are rapidly put in, but there is danger of death from fibrillation if
the circulation is completely cut off. The writer has been able to control
the hemorrhage from quite large wounds in the dog's heart for over ten
minutes by holding his finger gently against the wound. The heart's action
was not weakened by this procedure, nor did it become irregular; and suffi-
cient time was gained to lay the sutures carefully. This was found to be
more bloodless, and for large wounds more convenient, than Elsberg's
method of laying temporary sutures.
If possible the bullet should be removed unless it is too deeply imbedded
in the cavity of the heart. Under these circumstances it may be left at
least for a subsequent operation, as it often becomes encapsulated and may
do no further harm. All operators agree that operation in the Sauerbruch
negative pressure chamber or with Brauer's positive pressure lessens the
danger of pneumothorax, and is therefore advisable when it requires no
delay. It is particularly useful when the wound is about to be closed, to
prevent the continuance of the pneumothorax.
As regards the question of drainage, each individual case must be de-
cided on its own merits. It is, of course, important to prevent sepsis,
purulent pericarditis, and pyopneumothorax. When the pleura has not
518 DISEASES OF THE HEART AND AORTA.
been pierced, the pericardium may be closed in a large number of cases
without drainage (Rehn's statistics show 4 cases — 3 cures, 1 death — with-
out drainage of pericardium; with drainage, 5 cases — 5 deaths; perhaps,
however, drainage was used in only the more severe cases). When the
pleura has been pierced, it should usually be drained. Whenever bits of
cloth, dirt, etc., have entered the wound, it should always be drained.
Before closing the wound the pericardial cavity should again be
explored to see that no other wounds in the heart wall or vessels have
been overlooked.
Occasionally large branches of the coronary arteries are found to be
pierced and must be ligatured. This is necessary, and, as shown by Porter
and Baumgarten (see page 280), is not always fatal, as there is a certain
amount of collateral circulation, but sudden death may result during
subsequent excitement, so that in such cases more prolonged rest is advisa-
ble than in cases of simple suture. It is worthy of note, however, that
this complication is not mentioned in the twelve cases of late results com-
piled by Rehn.
After closure of the wound, with or without drainage, administration
of urotropin is probably advisable, since Crowe has found that it is excreted
in the pleural and pericardial fluids in a concentration sufficient to inhibit
the growth of bacteria; and Bernheim believes that its use increases the
resistance of these membranes (in dogs at least) to infection. It has,
moreover, no harmful effects.
Results of Operation. — Since Rehn's first operation a large number of
cases have been reported. In 1907 he was able to collect statistics of 124
cases — 49 recoveries (39.5 per cent.), 75 deaths (60.5 per cent.). In this
series there were only 15 cases of gunshot wound, but in a series of 30
cases of the latter compiled from the series of Ricketts, Borchardt, and
Rehn, there were 14 recoveries (46.6 per cent.) and 16 deaths (53.4 per
cent.). Of the 75 deaths in Rehn's series 16 died on the operating table,
17 died of loss of blood and collapse within two days, 30 died of infection
(purulent pericarditis and empyema) . In many cases the haste of operation
prevented disinfection of the field. One patient (Gerzen's) died of sudden
hemorrhage on the fifty-third day. Rehn also collected reports of 12 cases
from nine months to ten and one-half years after operation. In nine exam-
ination of the heart was negative; in three there was slight dilatation.
There were costopericardial adhesions in 5; 9 were absolutely free from
symptoms; 2 had pains down left arm; 1 precordial pain. Only one had
symptoms of definite cardiac weakness.
G. T. Vaughan has recently summarized and tabulated 150 cases
operated on between 1896 and 1909, of which 51 (34 per cent.) recovered,
a striking contrast to the 12 per cent, of recoveries in the earlier years from
which Fischer's series was taken.
NON-PERFORATING INJURIES.
Injuries of the chest wall which do not enter the pericardium, such as
blows upon the chest, frequently produce secondary lesions of the heart
and pericardium, which have been mentioned in previous chapters.
WOUNDS OF HEART AND CARDIAC TRAUMA. 519
The first case of cardiac disease from contusion was recorded by Blan-
< aid in 1688 and is very typical. The patient was a peasant 45 years of
age, previously healthy, who was run over by a hay-cart. He did not
sustain any fracture, but suffered from pain in the chest, dyspnoea, then
fever, delirium, and died 11 days later of purulent pericarditis and myo-
carditis. Similar cases were recorded by Bonetus (1700), Akonside (1766),
and numerous other writers both ancient and modern.
Bernstein in 1896 was able to collect 126 cases from the literature.
In autopsies upon 42 of these cases there was found
Endocarditis alone 16 times
Myocarditis " 0
Pericarditis " .10
Endo- and myocarditis 4
Peri- and myocarditis 5
Endo- and pericarditis 5
The signs and symptoms appeared :
Immediately after the trauma 67 .6 per cent.
Within one month 17.5 " "
Within one year 4.7 '
Later than one year 7.1 '
Time not given 3.1 " "
G. Fischer gives a list of the causes of traumatic rupture of the heart
in his series:
Run over by or crushed between wheels of wagon 21
Crushed by machinery 4
Falls from considerable heights 13
Falls from heights of 10 feet or less 7
Struck by falling objects 6
Kicked in chest 4
Hurled against wall 2
Kiilbs has recently investigated the subject experimentally. The
results in 23 animals within 12 days of the injury were:
Hemorrhages into the heart valves 17 times
(1 rupture of an aortic valve)
Subendocardial or subpericardial hemorrhages 10 times
extensive hemorrhage into the septum 3 times
Pericardial hemorrhages 10 times
Hemorrhages from lungs 6 times
There was polymorphonuclear infiltration and disintegration of muscle fibres in the
vicinity of the hemorrhages.
The symptoms and signs of these conditions following trauma do
not differ from those in similar lesions due to other causes, and have
been considered under those heads.
520 DISEASES OF THE HEART AND AORTA.
BIBLIOGRAPHY.
WOUNDS OF THE HEART AND CARDIAC TRAUMA.
For historical data see —
Ricketts, B. M.: The Surgery of the Heart and Lungs, New York, 1904.
Borchardt, M.: Ueber Herzwunden und ihre Behandlung. Pfahlungs verletzungen von
Herz und Lunge, Samml. klin. Vortrage, No. 411-412; Chir. No. 113-114, Ser. xiv,
Heft 21-22, Leipz., 1906.
Elsberg, C. A.: An Experimental Investigation of the Treatment of Wounds of the Heart
by Means of Suture of the Heart Muscle, J. Exp. Med., N. Y., 1899, iv, 479.
Fischer, G.: Die Wunden des Herzens und des Herzbeutels, Arch. f. klin. Chir., Berl.,
1868, ix, 571.
Loison, E.: Des blessures du pericarde et du coeur et de leur traitement, Rev. de Chir.,
Paris, 1899, xix, 49, 205, 774; 1899, xx, 37.
Rehn, L.: Zur Chirurgie des Herzens und des Herzbeutels, Arch. f. klin. Chir., Berl., 1907,
Ixxxiii, 723.
Rose: Deutsch. Ztschr. f. Chir., xx. Rosenthal: Deutsch. med. Wchnschr.,, 1895. Del
Vecchio: Rif. Med., 1895; Zentralbl. f. Chir., 1895, 574. Salomoni: ibid., 1896.
Farina: ibid., 1896, 1224. Quoted from Rehn.
Rehn, L.: Ueber penetrirende Herzwunden und Herznaht, Arch. f. klin. Chir., Berl.,
1897, Iv, 315.
Buerger, L. A: Modified Crile Transfusion Cannula, J. Am. M. Asso., Chicago, 1908, li, 1233.
Hartwell, J. A. : A Simple Method of Blood Transfusion without Cannula, ibid., 1909, lii, 297.
Thiemann: Nadelstichverletzung des rechten Herzventrikels und Vorhofs, Arch. f. klin.
Chir., Berl., 1907, Ixxxiii, 565.
Sauerbruch, E. F.: Die Verwendbarkeit des Unterdruckverfahrens bei der Herzchirurgie,
ibid., 1907, Ixxxiii, 537; also The Present Status of Surgery of the Thorax and the
Value of the Sauerbruch Negative Pressure Procedure in the Prevention of Pneumo-
thorax, J. Am. M. Asso., Chicago, 1908, li, 808.
For discussion of the positive pressure methods see Robinson, S.: Artificial Intrapul-
monary Positive Pressure; Experimental Applications in the Surgery of the Lungs,
ibid., 1908, li, 803; and Green, N. W., and Maury, J. W. D.: The Positive Pressure
Method of Artificial Respiration, with its Experimental Application to the Surgery of
the Thoracic (Esophagus, ibid., 1908, li, 805.
Vaughan, G. T.: Surgery of Wounds of the Heart, J. Am. M. Asso., Chicago, 1909,
lii, 429.
Bernstein: Ueber die durch Kontusion und Erschutterung entstandenen krankheiten des
Herzens, Ztschr. f. klin. Med., Berl., 1896, xxix, 519.
Kiilbs: Experimentelle Untersuchungen ueber Herz und Trauma, Verhandl. d. deutsch.
path. Gesellsch., Jena, 1908, xii, 172.
XIV.
ANEURISM.
Aneurism (aneurysm) (Greek avevpiafia a widening out) = a dilatation of artery or
veins (Galen).
An aneurism is a blood-containing tumor whose walls are formed by the
walls of a blood-vessel and whose cavity is in direct connection with the
blood-vessel from which it arises (Osier).
Historical. — Hippocrates (430 B. C.) and the early Greek writers do not seem to have
been familiar with aneurism, but its occurrence and nature were well known to Rufus and
Galen (A.D. 131-201), who recognized two forms: "one from dilatation, the other from
wounding of a vessel," usually from venesection followed by sepsis.
Fio. 295. — Specimen of a large aneurism. (After Hough.)
"Vesalius (1543) was the first to recognize aneurisms within the thorax and abdomen
and was even able to make the diagnosis of thoracic aneurism during life. Ambroise Pare"
(sixteenth century) recognized the existence of "aneurism by anastomosis, rupture, erosion,
and wound, along with the frequency of thrombosis within the sack." He was also the first
to suggest that venereal disease was a factor in the genesis of aneurism. The r61e of syphilis
was demonstrated definitely by Lancisi (1728). The next great step was made by Scarpa
(1805), who demonstrated that the most important mechanical factor was weakening of the
middle layer of the arterial wall, a fact which has furnished a basis for the more modern
pathology of aneurism.
CLASSIFICATION OF ANEURISM.
. It is extremely difficult to make a satisfactory classification of aneu-
risms, but the following, which is based upon that of Osier, may suffice for
most purposes:
521
522 DISEASES OF THE HEART AND AORTA.
1. True aneurism (aneurysma verum, aneurysma spontaneum), in which one or
more of the coats of the artery form the walls of the tumor.
A. Dilatation aneurism.
(a) Saccul ate d , in which the bulging or out-pocketing of the walls does not
embrace the whole circumference of the artery and is sharply localized.
(6) Fusiform (or cylindroid) aneurism, in which the dilatation occurs over a
larger area of artery whose entire circumference is involved in the dilatation.
2. Dissecting aneurism, in which the coats of the artery are separated and a
new cavity (sometimes lined with endothelium) is formed between these layers (usually
between media and adventitia).
3. False aneurism, following wound or rupture of an artery, consisting of a peri-
arterial hsematoma, all the coats of the artery having been penetrated.
4. Cirsoid aneurism or telangioma, a tumor consisting of a large number of
tortuous arteries which are continuous with the artery from which they arise.
5. Arteriovenous aneurism, a communication between artery and vein, either
direct, aneurismal varix, or with the intervention of a sac, varicose aneurism.
ARTERIES AFFECTED.
By far the most common forms are the true aneurisms, fusiform and
sacculated. The relative frequency in the various arteries is shown in the
following statistics of 530 cases (Crisp) :
Thoracic aorta 175
Popliteal artery 137
Femoral artery 66
Abdominal aorta 59
Carotid artery 25
Subclavian artery 23
Axillary artery 18
External iliac artery 9
Cerebral artery 7
Common iliac artery . 2
Posterior tibial artery 2
Gluteal artery 2
Pulmonary artery 2
Brachial artery 1
Subscapular artery 1
Ophthalmic artery 1
OCCURRENCE.
According to a large set of statistics compiled by Richter and by Arn-
spcrger, aneurism of the aorta represents one of the not infrequent causes
of death, 0.6 per cent, of total mortality (Emmerich), Brodier 1.2 per cent.,
Miiller 1.49 per cent.; in American cities 0.6 per cent., Philadelphia 0.6 per
cent., St. Louis 0.2 per cent.
According to Gibbons and Richter the percentage of deaths from aneurism in San
Francisco from 1866 to 1870 (1.35 per cent.) was much greater than elsewhere in the
United States. Dr. Gibbons has informed the writer that aneurism at that time was par-
ticularly common among stevedores, who formed a considerable percentage of the popula-
tion, and in whom syphilis, alcohol, and hard work were ever-present factors. With the
passing of the adventurer and the stevedore as important elements in the population, the
percentage of aneurism in San Francisco has diminished, being 0.90 per cent, in 1880-1884,
0.42 per cent, in 1890-1894, 0.33 per cent, in 1900-1904 (Gibbons).
On the other hand, in communities where syphilis is common the fre-
quency of aneurism increases. Thus, it is eleven times more common in the
British Army in India than in the civilians at home, and much more common
ANEURISM. 523
in the British than in the Austrian and German armies, where venereal dis-
ease is five times less prevalent.
Aortic aneurism is much more common in men than in women.
Crisp 67 women out of 551 cases
Agnew • 26 women out of 269 cases
Lisfranc 13 women out of 154 cases
Richter. . . 58 women out of 736 cases
164 women out of 1810 cases
9.05 per cent., or 1 in 11.
On the other hand, 48 per cent, of cases of carotid aneurism and 66 per
cent, of dissecting aneurisms occurred in women.
As regards age Crisp's cases were distributed as follows:
1 to 10 1 50 to 60 65
10 to 20 71 60 to 70 25
20 to 30 51 70 to 80 8
30 to 40 198 80 to 90 2
40 to 50 129 90 to 101 1
59 per cent, between the ages of thirty and fifty.
As regards site Lawson gives the following figures :
Ascending aorta 34 . per cent.
Arch of aorta 34 . 8 per cent.
Descending aorta 17.4 per cent.
Abdominal aorta 13 . 8 per cent.
Hare and Holder find in 953 cases collected indiscriminately :
Ascending 570 = 60 . per cent.
Transverse arch 104 = 10.6 per cent.
Descending 110 =11. 5 per cent.
Unclassified 169 = 17. 5 per cent.
figures which are certainly unusually high for the ascending portion.
Aneurisms are by no means always single, but may sometimes be mul-
tiple. Two, three, " or even a score " may appear along the course of the
aorta, or numerous aneurisms may be present in the peripheral arteries.
The condition is simply the manifestation of the generalized action of the
factors of sclerosis and blood-pressure on the arterial walls, and multiple
aneurism formation is one of the features of experimental adrenalin
aortitis (Erb, Jr.).
The symptoms, signs, and diagnosis present no specific features, except
the ease with which the other aneurisms may be overlooked after one is
diagnosed. Careful examination and especially fluoroscopic examination
will prevent this error.
PATHOLOGICAL ANATOMY AND PATHOGENESIS.
No change of pressure that can occur during life is sufficient to dilate
an artery to the proportions of even the smallest aneurism. According to
the elasticity curve of Roy, the dilatation occurring between the blood-
pressure of 120 and 170 mm. Hg is about 20 per cent, of the diameter of the
artery, and the results of (Irehant and Quinquaud show that very little fur-
ther dilatation occurs if pressure is raised until the artery ruptures (at a pres-
=im- of Kiso to MM) mm. Hg; 10 to 20 times the blood-pressure during life).
524
DISEASES OF THE HEART AND AORTA.
FIG. 296. — Aneurism arising just above a sinus
of Valsalva. (From a specimen in the Army Medi-
cal Museum.Washington, D. C.) OR., orifice through
which the aneurism is connected with the aorta;
AN., aneurismal sac.
FIG. 297. — Aneurism of the ascending arch and
innominate artery. (From a specimen in the Army
Medical Museum.) *
FIG. 298. — Aneurism of the transverse portion
of the aortic arch penetrating through the sternum.
(From a specimen in the Army Medical Museum.)
JNNOM., innominate artery; L. CAR., left carotid
artery; L. SUB., left sublavian artery; D. AOR.,
descending aorta.
FIG. 299. — Aneurism of the descending aorta eroding
the vertebrae. The sac con tains a laminated clot.
ANEURISM. 525
Changes in Arterial Wall in Aneurism. — On the other hand, as was
first shown by Scarpa (1805), aneurismal dilatation is always preceded by
changes in the arterial coats and especially by weakening of the media.
In 1875 Koester showed that this was due to localized degeneration of the
elastic fibres as the result of certain inflammatory changes in the vasa
vasorum of the media. "The inflammatory process begins in the vasa
vasorum on the exterior of the blood-vessel, follows them perpendicularly
into the muscularis (media) , and distributes itself within this layer, being
most intense at the places where the vasa vasorum break up into capillaries.
As a result of this chronic multilocular mesarteritis, the media (muscle
fibres and elastic fibres) degenerate. The intima (which may be thickened)
and the adventitia unite to form a thick and very vascular membrane
which forms the wall of the aneurism." Since these studies of Koester,
writers are practically agreed that the degeneration of elastic tissue result-
ing from mesarteritis is the underlying cause of aneurism formation.
WALL
FIG. 300. — Sections through the wall of an aneurism. (Photomicrographs made by Dr. C. S. Bond.)
A. Section through the wall of an aneurism showing the clot unorganized. B. Orcein stain showing the
destruction of elastic tissue in the aneurism wall. Elastic tissue (ELAS) stained dark.
Simple arteriosclerosis in which thickening of the intima is the essential
feature does not weaken the wall of the artery and plays no r61e unless the
media be destroyed. This fact is further borne out by the experimental
changes in the artery produced by injection of adrenalin (see page 257).
The resulting lesion is a mesarteritis without changes in the intima, quite
dissimilar to the ordinary arteriosclerosis of man; but aneurisms, and even
multiple aneurisms, are present in a large percentage of the animals. Other
toxic substances, bacterial toxins, lead, alcohol, nicotin, lactic and other
acids, etc., produce these changes.
Fabris has also produced aneurisms by external cauterization of the
arterial wall with silver nitrate. A local inflammation was thus set up in
the adventitia and media, which resulted in degeneration of the fibres of
the latter and their replacement with young fibrous tissue devoid of elastic
526 DISEASES OF THE HEART AND AORTA.
fibres. In a few cases there was slight intimal thickening. The resistance
of such a fibrous tube is less than that of an elastic tube, and aneurismal
dilatation, sometimes localized, sometimes fusiform, took place in from
20 to 25 days.
Etiological Factors. — In man the etiological factors of aneurism are
those that produce mesarteritis. Chief among these is syphilis, which, as
first noted by Ambroise Pare and Lancisi, is concerned in a very large per-
centage of the cases (Klemperer 25 per cent., Fraenkel 36 per cent., Puppe
36 per cent., Trier 40.5 per cent., Heiberg 41.87 per cent., Bramwell 50 per
cent., Thieberge 50 per cent., v. Noorden 54 per cent., Gerhard! 56 per cent.,
Schutz 64.7 per cent., Welch 66 per cent., Etienne 69 per cent., Malmsen
80 per cent./ Hanpeln 82 per cent., Backhaus 85 per cent., Heller 85 per
cent., Rasch 92 per cent.). This is especially true of aneurisms occurring
in young men and women, when the other factors of arteritis play a rela-
tively less marked role than in later life; so that, as stated by Professor
Osier, the presence of an aneurism in a man or woman under thirty is
almost to be regarded as presumptive evidence of syphilis. Moreover,
syphilitic aortitis is often most intense in the first part of the ascending-
aorta, hence the commonness of the lesion at this site (Heller). It must
be added, however, that, though the careful researches of Ophiils have
failed to substantiate this general belief, a positive Wassermann reaction
is usually obtained in such cases.
Other factors are alcohol, hard work, lead poisoning, tobacco, gout,
nephritis, and especially the infectious diseases. Trauma (blows, gunshot
and knife wounds, etc.) furnishes a frequent cause for aneurisms of the
peripheral arteries and abdominal aorta, but is much rarer in thoracic
aneurisms. Cases like that described by Hirsh and Robins show, however,
that it is a factor to be reckoned with. The relative importance of these
factors -is shown by the figures of Etienne, who found syphilis as a cause
of 166 out of 230 aneurisms, while alcoholism was present in only 28. More-
over, according to Hamilton, aneurisms are extremely rare in sanitaria
for alcoholics. They are, however, most important contributory causes,
not only increasing the arteriosclerosis but, by raising the blood-pressure,
increasing the liability to dilatation. Thus, aneurisms, according to most
writers, are particularly common in syphilitics who perform hard work.
This is exquisitely shown in the colored patients at the Johns Hopkins
Hospital, in whom syphilis is very common and who, as a rule, perform
hard work. Among these persons aneurisms are between five and ten times
as common as in the patients in the white wards of the same hospital. The
sudden rise of blood-pressure which occurs during lifting and heavy strains
(cf. page 132) is a particularly important predisposing factor, and the
patient often notices that his first symptoms occurred at the time of a
heavy muscular strain or began just afterwards.
EMBOLIC AND MYCOTIC ANEURISMS.
A somewhat rarer form of aneurism, described by Tufnell (1853), Ogle
(1866), Church (1870), Smith (1870), Ponfick (1873), and Weinberger
(1907), is the so-called embolic or mycotic aneurism, which arises especially
ANEURISM. 527
during the course of acute septicaemias, of puerperal, arthritic, and influen-
zal origin. Septic emboli become lodged astride of the bifurcation of the
smaller arteries, causing necrosis of the neighboring portions of the arterial
wall, which may protrude or form a true aneurism, or may rupture into
the surrounding tissues, forming a false aneurism. These arise acutely
during the course of the febrile diseases. They are usually multiple and
are confined to the smaller arteries, while the sclerotic aneurisms are more
common in the larger arteries.
DEVELOPMENT OF THE ANEURISM.
Once formed, the aneurismal sac expands progressively, usually pushed
outward from the artery along the lines of the least resistance until it
meets with some obstruction. The higher the blood-pressure the more
rapid is the dilatation. When pointing freely into the thoracic cavity, it
may expand until it fills almost the entire half of the cavity before ruptur-
ing. On the other hand, if the proliferation of connective tissue in the wall
of the aneurism does not keep pace with its growth, or if local necrosis
from infection, pressure, or irritation takes place, a secondary bulging will
take place at this point, and it finally ruptures there. A rupture is especially
precipitated by high blood-pressure, such as occurs on exertion, and sud-
den deaths from this cause are quite common in aneurism.
When the wall of the sac presses upon neighboring tissues it begins
to erode them. The pressure acts in the following way: First, it cuts off
the blood supply to the neighborhood because the pressure within it (aortic
pressure) is greater than that in the smaller blood-vessels. Secondly,
necrosis of these tissues results from this compression. Thirdly, the products
of necrosis are absorbed by the cells in the tissues of the very vascular wall
of the aneurism as fast as they are produced. Bone tissue too is absorbed
by the activity of the osteoclasts, and the wall of the sac thus advances
gradually through the chest wall very much as a tumor might do, though
without the intervention of abnormal cells. Thus, the aneurism eats its
way through muscle, cartilage, bone, nerves, and skin, and also through
the walls of the other vessels (pulmonary artery, vena cava, etc.), bronchi,
and oesophagus, always forced onward in a straight line by the arterial
pressure in the aorta. Hence, aneurisms usually point in the direction
given them by the impact of the blood stream ; those of the ascending aorta
pointing to the right, those of the arch pointing upward, those of the
descending arch pointing backward and to the left (Fig. 301). However,
resistance of surrounding tissues, and especially local thinning of the aneu-
rismal wall, may cause its course to be deflected somewhat from these
typical directions.
Rupture. — The excessive thinning which results in perforation fre-
quently occurs when the sac has just penetrated the wall of one of the sur-
rounding structures, — bronchus, oasophagus, etc., — no doubt from the pres-
ence of local infections within their lumina, and sudden death may result
from hemorrhage. Or, on tin- other hand, small hemorrhages may occur
from the erosion of smaller bronchial or oesophageal arteries (see page .")
or through t ho wall of the aneurism without any such immediate results.
528
DISEASES OF THE HEART AND AORTA.
The growth of an aneurism after penetrating the chest wall is well
shown by the outlines in Fig. 302. The sac becomes larger and larger,
secondary sacculations appear upon its surface (Fig. 302), and over these
the thinned skin becomes smooth, tense, glossy, and finally of a reddish
FIG. 301. — Composite figure showing the relations of various aneurisms to surrounding structures.
(Schematic.) OES, oesophagus; AN SUBCL, aneurism of the subclavian artery; SUP. V. C., superior
vena cava; AN INNOM, aneurism of the innominate artery, pointing through the skin; AN TR, aneu-
rism of the transverse portion of the arch; PHREN, phrenic nerve; REC LAR, recurrent laryngeal;
L. VAG, left vagus; DA, ductus arteriosus (Botalli); A N. P.A., aneurism of the pulmonary artery; LBR,
left bronchus; AN. SIN VALS, aneurism arising from a sinus of Valsalva; AN. R. COR and AN. L. COR.,
aneurism of right and left coronary arteries; AN RA, aneurism of right auricle; AN. L.V., aneurism of left
ventricle. The arrows show the directions in which the aneurisms usually point.
or brawny hue. The whole process usually requires a few months, but it
may occur more rapidly. On the other hand, in a case described by Hirsh
and Robins the pulsating tumor upon the chest remained practically
unaltered in size for twenty-five years, during which the patient continued
to do heavy work. Finally, however, a stage is reached at which a small
perforation appears, oozing blood, and soon after, with a rush of blood like
ANEURISM. 529
the bursting of a dam, the aneurism ruptures and the patient bleeds to
death within a few minutes.
The rupture into the bronchus, trachea, or oesoph-
agus proceeds in the same way. There is usually a slight premonitory
haemoptysis. This generally occurs a few days before death, but may not
occur until a few hours before the final rupture; or, as in the case reported
by Clarke, it may be present for months. At the final rupture the blood
spurts out of the patient's mouth and nose and may even be projected
several feet away from the bed.
On the other hand, when the aneurism ruptures inter-
nally into one of the cavities of the body, the symptoms are quite differ-
ent. The patient feels something giving way within. Sudden collapse,
asthmatic attack, and gradual exsanguination mark rupture into the
pleura. Rupture into the pericardium is attended with intense pain,
breathlessness, collapse, an anginal attack, and occasionally a con-
vulsion. In rupture into the pericardium
death is accelerated by cutting off the
venous inflow, just as in simple pericar-
dial effusion, only within a minute or two.
Of course, under these circumstances no
blood appears externally.
Rupture of the aneurism into
the pulmonary artery, vena cava,
A . . •; • i_ -i FlG- 302.— Tracings of the outlines
Or Tight auricle Or right Ventricle SOme- Of an aneurism of the innominate artery,
times occurs. The symptoms are usually showing the progress of its growth and
J J the formation of secondary prominences
Sudden Onset Of dyspnoea, Weakness, Often upon its surface. (Tracings made on
collapse, and extreme cyanosis, which ends *£j !!$*£'£ "
in death after a period varying from sev-
eral hours to several months, the heart being unable to accommodate
itself to the sudden changes in the distribution of blood.
However, in a large percentage of cases (863 cases — 47 per cent. — of
Arnold's 1829 cases) death from aneurism is not due to rupture
of the sac but " from pressure of the sac upon important nerves and blood-
vessels, or from secondary changes which take place in these tissues and in
other vital organs, as a direct or indirect result of such pressure." In 154
cases without rupture the causes of death were :
Obstruction to air-passages 66
Exhaustion 50
Affections of lungs and pleura 28
Pericardial affections 8
Pressure on the vena cava superior. 1
Collapse 1
Clotting within an Aneurism. — The healing of an aneurism occurs by
clotting within the sac. Since the latter is lined by arterial intima, there
is under ordinary circumstances no more reason for clotting to take place
there than elsewhere in the artery. As shown by Mall and Welch, arterial
thrombosis occurs quite suddenly when the circulation is slowed and pulsa-
tion disappears, especially if there is some injury to the wall of the artery,
and this is a most important factor in bringing about thrombosis within
34
530 DISEASES OF THE HEART AND AORTA.
an aneurism, though some fibrin ferment must be present. As a rule, in
fusiform aneurisms the circulation is too strong and rapid for coagulation
to set in, but in sacculated aneurisms a certain amount of fibrin collects
along the wall. Each layer of fibrin serves as a filter for leucocytes, from
which more fibrin ferment is generated and a second layer laid down, and
so on until occasionally the entire aneurism may be filled spontaneously
by a laminated clot.
Owing to the large area and great thickness of the fibrin deposited,
and to the fact that the intimal endothelium is in most places still ifitact,
there is little entrance of fibroblasts into the clot and little organization
goes on. The aneurismal clot is, therefore, not converted into a solid mass
of connective tissue as in endarteritis or thrombo-angeitis obliterans, but
remains simply laminated fibrin. Deposits of calcium salts sometimes
occur upon them, however, and tend to convert the obliterated aneurism
into a solid tumor.
SYMPTOMS.
The signs and symptoms produced by aneurisms vary greatly, and
depend upon the site at which they occur along the aorta, so that Broad-
bent has been "led to divide thoracic aneurisms into two classes, — namely,
aneurisms of physical signs and aneurisms of symp-
toms, from the predominance of physical signs and symptoms respec-
tively,— the former term applying to aneurisms of the ascending aorta
and first part of the arch, the latter to aneurisms of the transverse and
descending portions of the arch."
The symptoms produced by aneurisms arise secondarily as the
result of pressure upon surrounding structures. Shortness of
breath is frequent, resulting both from pressure on the trachea and
bronchi and from concomitant disturbances in the circulation (embarrass-
ment of heart action, stasis from pressure on veins). Cough is a common
symptom, from pressure upon the recurrent laryngeal nerves as well as
from bronchitis as a result of pressure (occasionally from tuberculosis).
The pressure on -the laryngeal nerve causes paralysis of the corresponding-
vocal cord and gives the cough a peculiar metallic quality known as ' ' the
goose cough, brassy cough, stenotic cough, paretic cough,"
etc. It is really the cough characteristic of paralysis of one vocal cord, and
it is characteristic of aneurism only in so far as that the latter is the com-
monest circulatory disturbance in which laryngeal paralysis is a symptom.
Paroxysmal dyspnoea may occur, and especially in certain
postures in which the trachea and bronchi are pressed upon by the aneurism.
This ' ' a s t h m a ' ' is the most common symptom of patients presenting
themselves for treatment, and careless physicians often accept its presence
as the final verdict, remaining oblivious to the true nature of the disease.
Attacks of dyspnoea or suffocation very commonly come on during sleep
when the laryngeal muscles relax and narrow the laryngeal slit. They
occur especially when the patient falls into an unpropitious position, so
that he soon finds it most convenient to sleep bolstered upright and leaning
slightly forward with chin depressed. This position affords the maximum
space about the air-passages with the minimum of tension upon them.
ANEURISM. 531
Not infrequently a small aneurism of the arch pointing backward
and pressing upon the trachea or bronchi may cause actual suffoca-
tion, for which tracheotomy may be necessary. In some cases, however,
the aneurism may be situated so low that it may be impossible to do the
tracheotomy below the area compressed. The only possible means of relief
is then to dissect or pull the aneurism away from the trachea, or to intro-
duce a metal tube into the latter and thus hold the trachea open at the point
compressed. This procedure is, of course, extremely difficult, and under
all circumstances great dyspnoea from pressure on the trachea is in itself
a dangerous symptom.
P ai n is a common symptom in aneurism, and may be of three kinds:
1. Angina pectoris — reflex referred pain over the heart or down the arm.
This is especially common in early aneurism at the beginning of the ascending aorta and
from the sinus of Valsalva, and is probably due to changes in or pressure upon the aortic
plexus. After these changes have been long established this pain may disappear (Osier).
2. Sharply localized pain may arise in or about the aneurism itself when
its walls are pressed upon, or even spontaneously, and especially when it begins to erode
the chest wall.
3. A second form of referred pain arises without reflex mechanism directly
from pressure upon the intercostal nerves and those of the brachial plexus, especially in
aneurisms of the transverse and descending aorta. The latter may give rise to pain in the
back, shoulder-blades, and sides and also down the arm, and may for a while be mistaken
for intercostal neuralgia or for the pain of pleurisy. Pain down the arm is especially com-
mon when the aneurism involves the innominate or subclavian arteries, particularly when
the return of venous blood is interfered with by pressure on the veins.
Difficulty in swallowing and the feeling of a lump in the
throat may result from pressure upon the oesophagus, especially when the
aneurism is adherent to it or is infiltrating its walls. This is, of course,
characteristic of aneurisms of the descending portions of the arch and to a
less degree of the descending aorta. It is not at all a rare symptom, and
yet is by no means as common as might be expected even when the aneurism
is large.
PHYSICAL SIGNS.
1. The presence of a visible mass upon the chest wall or elsewhere
showing a pulsation of an elevation which begins about 0.05-0.10 second
later than the ventricular systole (or the first heart sound), and which on
palpation is felt to be forcible and expansile in character (i.e., presses
outward in all directions). The shock with the first sound is usually well
felt and often accompanied by a thrill; and a diastolic shock accompanying
the second sound is, when present, almost characteristic.1 On auscultation
there is usually a systolic murmur heard over the aneurism, and occasionally
a diastolic murmur when the blood flows back into the aorta during diastole,
especially through a narrow opening. This is, of course, most common
and most marked when aortic insufficiency is present, either organic or
relative, resulting from the general dilatation of the aorta.
Long before an aneurism perforates, and in many cases when it is
not pointing outward but upward toward the episternal notch or clavicles.
1 The writer has seen one case of hypernephroma of the thigh in which a diastolic
shock was palpable, but this is rare even in the most vascular tumors, such as the vascular
MHMliastinal sarcomata.
532 DISEASES OF THE HEART AND AORTA.
there may be seen a diffuse systolic lifting of the whole chest
wall or of the parts above the tumor. The localized heaving is, of course,
most marked when the aneurism is in the vicinity of cartilages or articu-
lations in the chest wall and in younger individuals; while the most diffuse
heaving occurs in the portions and persons where the ribs and sternum
are most rigid. The impulse thrill and shocks, systolic and diastolic, are
also frequently present when no heave or pulsation can be seen.
For discerning and timing slight pulsations the writer has fre-
quently found it convenient to hold the index finger a few millimetres
away from the chest wall, and watch for either a periodic narrowing of
the slit between the finger and the chest or for a visible movement of the
shadow cast by the finger upon the chest. For the latter purpose the light
should strike as nearly as possible paral-
lel to the chest so as to magnify the
movement of the shadow (Fig. 303).
When aneurism is suspected, it is
particularly important to ex-
amine the patient's back as
well as to inspect carefully the front of
the chest. This precaution was always
particularly emphasized by one of the
great teachers of medicine who also un-
Fio.303. — Method of inspecting for pulsa- r , ,. „ .„ , .,
tions. E, eye of observer looking down from intentionally illustrated its importance,
above; E', eye of observer upon level with Qn one occasion he and another pro-
pulsating area; nnger above pulsating area; ... ^ ^• •
S and 8', shadows thrown by the finger upon feSSOr, who Was VlSltmg the clinic,
the pulsating mass. Solid and dotted lines nn(5tratprl to tVm inninr «stiiHpTit<5 a
represent the outlines of the pulsating mass; OnStratCQ tO tne JU1
arrows indicate the extent of movement seen. of SUSpected aneurism, but Sent him to
the wards for X-ray examination with-
out having examined the back. The absolute diagnosis was at once made
by the house officer, who in the routine examination discovered a well-
marked pulsation at the back at the level of the third thoracic vertebra.
Dulness on percussion is of course present over an aneurism as
over other tumors, the note being flat when the tumor is near the surface,
slightly improved when it is deep. This improvement is often very slight
in deeply situated aneurisms of the arch, and percussion, especially in
the first right and left interspaces and over the manubrium, should be
very carefully carried out when aneurism is suspected. The exact outlining
of an aneurism by percussion may be very difficult. The area of dulness
on even the lightest percussion may be considerably greater than that of
the aneurism itself (just as is true of the cardiac dulness, see page 95).
The uniform dilatation of the aortic arch (to about twice its normal diame-
ter) which is so frequent in aortic insufficiency may give an area of dulness
over and on both sides of the sternum which may lead to a diagnosis of
aneurism (Fig. 311). The true nature of the condition can be shown only
by the X-ray (Fig. 308).
In large and in deeply situated aneurisms direct percussion of the ver-
tebral spines by Koranyi's method may show an unusual dulness over the corre-
sponding area (especially between the third and the sixth thoracic spines) and may prove
of assistance in establishing the diagnosis. It is, of course, of no value in those aneurisms
ANEURISM. 533
of the arch in which the trachea is interposed between vertebra and the tumor. The heart
is occasionally very much displaced by an aneurism which may itself come to occupy the
usual site of the heart, so that on casual examination it may be mistaken for the latter.
With careful auscultation, however, this error may be excluded.
Pressure upon the sympathetic on either side may give rise to inequality
of the pupils, usually with a dilatation upon the affected side. In
late stages, however, the sympathetic on that side may be completely
destroyed and the pupil then becomes smaller on the affected side.
The dilatation is best seen when there is moderate illumination, for in strong
lights the reflex pupillar constriction may overcome the dilator action of
the sympathetic.
Tracheal Tug. — W. S. Oliver, who described the sign in 1878, gave
the following directions: "Place the patient in the erect position and
direct him to close his mouth and elevate his chin to the fullest extent;
then grasp the cricoid cartilage between the finger and thumb and use
gentle upward pressure upon it; when if dilatation or aneurism exist the
pulsation of the aorta will be distinctly felt transmitted through the trachea
to the hand." This tracheal tug is no absolute sign of aortic dilatation.
It is as readily produced when solid mediastinal tumors or enlarged bron-
chial glands adhere to both aorta and air-passages as from aneurism.
Sewall finds that in a large percentage of tuberculous individuals
(91 out of 212 — 43 per cent.) a slight twitch of the trachea may be felt
during inspiration, due to contraction of the accessory muscles, but this is
not continuous, not synchronous with the pulse-beat, and should not be
mistaken for the true tracheal tug. Moreover, in his large series of obser-
vations this tracheal twitch of non-aneurismal origin was always confined
to inspiration, Sewall found it particularly common in cases of tuberculo-
sis or old pleurisies in which there was adhesion to the left pleura. Medias-
tinal adhesions anchoring the aorta to the air-passages can produce it.
Wenckebach has also called attention to the fact that it may occur in cases
of enteroptosis, in which the heart is pulled downward with the liver, and
the arch of the aorta thus made to pull upon the bronchi. (This is well
illustrated by the patient mentioned on page 602.) The tracheal tug is
most marked in inspiration.
Tracheal Percussion Shock (Smith).— H. L. Smith has found that if
one lightly taps the chest wall (direct percussion) over an aneurismal area
one feels a sudden increase in the impulse as soon as the aneurismal area
is reached, a shock resembling " the sensation experienced by one when a
rubber bag filled with water is simultaneously palpated and percussed " (semi-
fluctuation). The fact that he has been able to elicit it in 62 per cent, of his
cases of which only 46 per cent, gave a tracheal tug indicates the usefulness
of the sign. In certain cases it is undoubtedly of considerable assistance.
THE PULSATION AND ARTERIAL PULSE IN ANEURISM.
The pulsation over the aneurism resembles the form of the arterial
pulse except that owing to the elasticity of the sac the rise and fall are
usually more gradual. It is sometimes of importance to determine whether
the pulsation corresponds to an aortic aneurism or an aneurism of the
ventricle. This requires the most carefully timed tracings simultaneously
534 DISEASES OF THE HEART AND AORTA.
from apex and tumor. If the pulsation in the aneurism begins .07-. 09
second later than the apex beat, the aneurism may be assumed to arise
from the aorta. If it arises from the ventricle, the two will, of course, be
synchronous. On the other hand, as occurred in a case still under the
writer's observation, the two pulsations may be absolutely synchronous
and yet X-ray and other signs may show that the aneurism arises from
the aorta.
Delay and Inequality of the Pulse. — Inequality of the pulse in cases of
thoracic aneurism was recognized by Harvey, who stated very correctly
that " the pulse in the corresponding arm was small in consequence of the
greater portion of the blood being diverted into the tumor and so inter-
cepted." The nature of this inequality was made the subject of a careful
clinical and experimental study by Marey and Fransois-Franck, who found
that when an aneurism with elastic walls occurred along the
aorta it served to damp the oscillations of pressure
in the arteries nearest to it and thus to make the pulse smaller
in these arteries. The pulse-wave thus
/l/l/l/) f\ f\ f\ A became smaller and its onset less sud-
VwJ\J\J\jl J\J\J \J\ den> the uPstroke becoming very
2 oblique (pulsus tardus).
/\y\/V/\ ^^fc^-^^^ Certain aneurisms, however, have
ART YZ iK no effect on the pulse, and it may be
A even larger upon the side of the aneu-
FIG. 304.— Effect upon the circulation of in- . ,, ~. , . ,
terposing (A) an inelastic, and (B) an elastic bulb HSHl than Upon the Unaffected Side.
along the course of an artery in a model of the Marey and Francois - Franck showed
circulation. (Modified from Francois-Franck.) J .
1, 2 3 represent successive time markings. Upon their models that if the Sac
VENT, pressure curve within the model of the w«q i n P 1 fl «? t i r> thp mil«5P-wavA
ventricle; ART, pressure curve within the model WaS pUlSC-Wave
artery. A, normal artery. The elastic sac dimin- was increased On the a f -
ishes the size of the pulse, delays the upstroke, ^ J • J J • + v.
and delays the transmission of the pulse-wave. lected Side, and its character
became collapsing.
Owing to this damping of the pulse-wave, the maximal and minimal blood-pressures
in the arteries nearest the aneurism tend to approach the mean pressure, so that the maxi-
mal pressure may be from 5 to 30 mm. lower than the maximal pressure in the opposite
arm, though there may be a considerable difference in the size of the pulses without any
marked difference in maximal or minimal pressures.. The minimal pressure, being already
nearer to the mean, is less affected than is the maximal, and often no difference can be noted.
Changes in the size and in the quality of the pulse in the two radial arteries are much more
marked to the palpating finger than to the instrument, for the slowed circulation may be
compensated by a local vasoconstriction which causes a smaller pulse without appreciable
change in the pulse-wave. The pulse is usually smaller and less sudden on
the side nearest the aneurism, and hence often appears to be retarded when
this is not actually the case, though in actual fact the onset of the pulse- wave is synchronous
and only the summit of the pulse- wave is belated (Franc, ois -Franck, Marey, v. Ziemmsen)
(Fig. 283). Francois Franck and Marey showed, however, that, both in man and in the
model, the presence of an elastic aneurismal sac along the aorta caused a general slowing
in the transmission of the pulse-wave (apex beat — radial pulse interval = 0.2-0.22 second
instead of 0.12-0.14 second)1 in all the arteries, so that the pulse-wave in both radial
arteries begins at exactly the same time. When the aneurism arises not from the aorta
but upon the innominate or the subclavian artery, the result is different. The pulse-wave
in the aorta now advances at the usual rate (apex — radial = 0.12-0.14 second), while the
1 In cases in which aortic insufficiency is present, especially with aneurisms of the
ascending arch, this delay of the pulse-wave is not present.
ANEURISM.
535
Fio. 305. — Effect of aneurisms at various sites upon the blood-pressure, rate of transmission, and
the form of the pulse-wave. (Schematic.) Bp, blood-pressure in mm. Hg ; RR, pulse in right radial
artery; LR, pulse in left radial artery. I. Aneurism upon innominate artery. II. Aneurism upon the
ascending aorta. III. Aneurism upon the transverse portion of the arch of the aorta. IV. Aneurism
upon the left subclavian artery. The first column of figures indicates blood -pressure in mm. Hg; the
second column indicates the transmission time of the pulse wave in seconds. The figures given are typical
though the differences are larger than are usually encountered.
transmission in the artery from which the aneurism arises is slowed. The pulse-wave is,
therefore, definitely retarded (0.05 to 0.07 second later than in the other radial), in some
cases even when there is no difference in the suddenness of the upstrokes. This dif-
ference in the time of the pulse-waves when present furnishes a
means of differentiating between aneurism of the innominate or
subclavian artery, and de-
monstrates that the aorta itself is
not involved (Frangois - Franck) .
This fact may be of great practical
importance in determining the oper-
ative treatment, especially where
the shadow cast by the aneurism lies
close to that of the aorta. How-
ever, this delay in the pulse does not
occur in all aneurisms, but only in
those whose walls are elastic, — the FIG. 306. — Radial pulse tracings from the right and left
greater number. It may also disap- "«lial "te/jf" of a !»«•«* with aneurism of the first part of
, ... , / t lie arch of the aorta. I he upstroke of the pulse-wave in tln>
pear as clotting occurs along the rit<ht radial arterv whi,.h is Iiwirpr (0 (he aneurisni tnnn tll«.
walls of the aneurism, and the elas- left, is more gradual than that in the latter.
ticity of the sac is thus lessened.
In view of these facts, it is evident that the form of the pulse tracing
is of no more value than the simple palpation of the pulse in the diagnosis
of aneurism, and the only graphic method of practical importance is thai
• it' taking simult ancous tracings from both radial or both carotid arteric-
536
DISEASES OF THE HEART AND AORTA.
in cases where it is necessary to determine whether an aneurism is confined
to the innominate, subclavian, or carotid artery, or whether it also involves
the aorta. These relations often cannot be shown by the X-ray and rest
upon this differentiation alone.
X-RAY EXAMINATION.
Most of the things which are inferred from physical examination
can be actually seen with the fluoroscope, and an exactness of diagnosis
can be reached which is utterly impossible with the ordinary methods. In
104 cases of aneurism thus examined by Baetjer, the clinical diagnosis had
been correctly made in 70 per cent. ; there had been tentative diagnosis of
aneurism in 20 per cent. ; and an unsuspected aneurism had
been discovered with the X-ray in 10 per cent. These
findings are particularly important,
since it is just in these early cases
when the physical signs are still
indefinite that treatment may be
profitably instituted.
However, unless certain precau-
tions are taken in the examination
an aortic shadow may be seen which
may be diagnosed an aneurism even
though none be present. This
rounded shadow is cast by the arch
of the aorta just to the left of the
sternum, and it may be specially
marked if the aorta is somewhat
tilted, as sometimes takes place in
enteroptosis ( Wenckebach) . Holz-
knecht has shown, however, that
this error will not be made if the
patient is also turned so that the
rays pass from left back to right front (Fig. 81). The normal aorta thus
lies in a plane parallel to the rays and is seen as a narrow nearly vertical
band, with the light spaces of anterior and posterior mediastinum in front
and behind it. The uniformly dilated aorta appears as a wide but uni-
form band. The aneurism of the ascending aorta appears as a battledore
or tennis racket with handle up, the aneurism of the arch as a racket with
handle down. Aneurisms of the innominate are separated from the aortic
shadow by a clear space which is bridged by the narrow shadow of the
artery.
As Baetjer states, it is most important to examine the chest for mal-
formations and for misplacement of the aorta which might be mistaken
for aneurism. Persistence of the ductus arteriosus (Botalli) must also be
considered in shadows near that of the descending arch. The shadow of
enlarged mediastinal glands is usually speckled or blotchy with occasional
lighter areas, rather than uniformly dark, while the edges of sarcomata
and other solid tumors are often irregular and may fade away gradually
FIG. 307. — Radiograph of a patient with a large
aneurism of ascending aorta and the arch, viewed
from behind. (Kindness of Prof. C. M. Cooper.)
ANEURISM. 537
into the surrounding tissues. Moreover, unless there is a considerable
degree of intrasaccular clotting, an aneurism will be seen to expand during
systole and to contract in diastole,1 whereas a solid tumor will at most
rotate upon its axis.
CHARACTERISTIC FEATURES OF ANEURISMS AT DIFFERENT SITES.
Characteristic features of thoracic aneurisms are given in .the table
below. It must be borne in mind, however, that these represent the con-
ditions only while the aneurisms remain relatively small, for with their fur-
ther growth they may press upon other structures and so present the picture
of an aneurism affecting a different part of the aorta. Large aneurisms also
displace the heart, and may even occupy the usual position of the latter.
FIG. 308. — Radiograph of a patient with dif- FIG. 309. — Diagram of the radiograph shown
fuse dilatation of the arch of the aorta. (Kind- in Fig. 308. The broken lines indicate the nor-
ness of Prof. C. M. Cooper.) The figure also shows mal outlines. A O, aorta; OES, O3sophagus; LV,
dilatation of the left ventricle and slight dilatation left ventricle,
of the left auricle.
Aneurism of the Heart. — Symptoms. — Indefinite signs of cardiac weak-
ness. Physical signs. — Two points of maximal impulse over which tracings
show exactly synchronous pulsations (this point is far from pathogno-
monic). Irregular outline of cardiac dulness (encapsulated pericarditis,
pleurisy, and tumors must be excluded) . Sometimes systolic and diastolic
murmurs over heart and aneurism not present over aorta. Pulse. — Feeble
but equal and not delayed. X-ray. — Bulging of shadow of ventricle or
auricle with 'enlargement of shadow synchronous with systole of correspond-
ing chamber. Rupture. — Into pericardium. Death often from cardiac
weakness or coronary sclerosis.
Aneurism of Coronary Arteries. — Symptoms. — No characteristic symp-
toms. Occasional cardiac pain. Physical signs. — Arteriosclerosis. No
characteristic signs or even signs of illness. (Aneurism usually size of
pigeon's egg.) X-ray. — No abnormal shadows. Rupture. — Into peri-
cardium in 19 out of 21 cases. In one case into pulmonary artery.
Ascending Aorta; Intrapericardial (Aneurism of Symptoms). — Symp-
toms.— Angina pectoris. Attacks of cardiac asthma. Precordial pains.
1 Holzknecht particularly emphasizes the importance of using the lead diaphragm
in examining the edges of the shadow for pulsation.
538 DISEASES OF THE HEART AND AORTA.
Pain down right or left arm. Shortness of breath. Symptoms of cardiac
failure predominate. Physical signs. — Distention of veins of head, neck,
upper chest, arms; oedema of these parts. Tracheal tug absent while
aneurism is small. Pupils equal if aneurism is small. Aneurism usually
small, situated in second and third right interspaces. Pulsation in second
and third right interspaces. Often signs of aortic insufficiency. General
oedema from aortic insufficiency. Pulse. — Delay of pulse-wave uniform.
Pulses may be equal in both radials or may be smaller in either. X-ray.—
Inverted racket-shaped shadow in left post, to right ant. illumination.
Arch of aorta clear. Rupture. — Into pericardial cavity. Pulmonary artery.
Right auricle. Superior vena cava. (Esophagus. Left auricle. Right
ventricle. Left lung. Right lung. Other causes of death. — Dyspnoea.
Exhaustion. Hydrothorax. Hydropericardium. Bronchitis and pneu-
monia. Pulmonary infarction. Suffocation.
Aneurism of the Ascending Aorta between Pericardium and Innominate
Artery (Aneurism of Physical Signs). — Symptoms. — Slight dyspnoea. Pain
when aneurism presses on or erodes chest wall. Often an accidental finding.
Physical signs. — Flushed face with dilated veins; sometimes oedema. Di-
lated veins of arms. Pulsation in second, third, and fourth right interspaces
(occasionally shifting). Dulness to the right of the sternum, not over the
manubrium. Systolic, sometimes diastolic murmur, thrill and diastolic
shock over aneurism. Tracheal tug, if aneurism is large. Pulse. — Uni-
form delay of pulse, both sides synchronous. Right radial usually smaller
than left. X-ray. — To right of sternum in second to fourth interspaces;
best made out in post. -ant. or right post, to left ant. illumination. In left
post, to right ant. illumination inverted racket-shaped shadow. Compli-
cations.— Often aortic insufficiency. Bronchitis. Tuberculosis of right
lung. Hemorrhage. Right hydrothorax. Rupture. — Into pericardium.
Right pleural cavity. Right bronchus. Right auricle. Superior vena cava.
Aneurism of the Innominate Artery. — Symptoms. — Like those of an-
eurism of arch except that there is no dysphagia in small aneurisms. Pain
and numbness down right arm and to right shoulder. Physical signs. —
Dilated veins and swelling over right arm and right side of face. Dulness
extends out under right clavicle. Pulsating tumor may be felt under the
right clavicle. Paralysis of right vocal cord. Right pupil in early stages
larger than left. Pulse. — Right radial pulse smaller and definitely
later than left. X-ray. — A ^-shaped shadow is seen upon the left
arm of the V which the shadow of the innominate artery makes with that
of the aorta on left post, to right ant. illumination. Complications. — Right-
sided bronchitis. Bronchopneumonia. Tuberculosis. Hydrothorax.
Rupture. — Usually points upward and outward toward the clavicle, but
may point downward to pleura or bronhci.
Aneurism of the Arch of the Aorta (Aneurism of Symptoms). — Symp-
toms.—Change in voice, especially high notes. Brassy cough. Difficulty
in swallowing. Pain in throat. Dyspnoea, sometimes amounting to suffo-
cation. Physical signs. — Inequality of pupils. Usually dilatation of left
pupil. Dilated veins, flush, and sometimes swelling over left side of face,
chest, and left arm, or changes bilateral. Tracheal tug early. Pulsation
palpable in suprasternal notch. Pulsation in suprasternal and supraclavic-
ANEURISM. 539
ular fossae. Lifting of manubrium; later perforation of manubrium or
sternoclavicular articulation. Palpable heaving, systolic and diastolic
.shocks, and often thrill over manubrium. Heart sounds: usually systolic
murmur and sometimes diastolic murmur over the tumor. In aneurism
beyond the innominate, the systolic murmur may be heard in the left car-
otid and brachial but not in the right. Bronchoscopy may show tumor per-
forating bronchus. X-ray. — Shadow racket shaped, especially seen in left
post, to right ant. illumination. Post. -ant. or ant. -post, illumination seen
as massive shadow above that of the heart. Complications. — Bronchitis.
Tuberculosis. Suffocation (asphyxia). Inanition. Rupture. — Externally
(anteriorly through manubrium or above clavicle). Into left bronchus.
Trachea. (Esophagus. Lungs and pleural cavity, pericardium, mediasti-
num. Pulmonary artery. Other causes of death. — Exhaustion. Pericarditis.
Collapse. Suffocation. (Edema of larynx. Pneumonia. Tuberculosis.
Aneurism of the Descending Aorta.1 — Symptoms. — Lancinating and bor-
ing pains in back, left shoulder, left side, and left side of abdomen. Stiffness
of back. Shortness of breath. When the aneurism is near the diaphragm,
abdominal pains may be present and the condition may be considered to be
abdominal. Physical signs. — Visible pulsation just to left of spinal column.
Dulness on percussion. Heart sounds and corresponding shocks over
aneurism and tenderness over corresponding spines. Areas of hyper-
a'sthesia or analgesia in corresponding spinal segments. Pulse. — Pulses
synchronous; smaller and more gradual in left than right. X-ray.—
V-shaped shadow to left of sternum, especially in right posterior to left
anterior illumination. Complications. — Left-sided bronchitis, broncho-
pneumonia, tuberculosis, hydrothorax, paraplegia from erosion of vertebrae.
Rupture. — Backward and externally; into oesophagus, left pleural cavity,
right pleural cavity, bronchi and lungs, pulmonary artery. Other causes of
death.— Pressure on trachea and bronchi, exhaustion, pneumonia, and
tuberculosis.
The following histories illustrate typical cases of aneurism :
ASCENDING ARCH ABOVE PERICARDIUM (ANEURISM OF PHYSICAL SIGNS).
D. N. L., aged 45, married. Except for a well-compensated aortic insufficiency for
the past eight years, with slight shortness of breath, he has been quite healthy. In
November, 1903, his aneurism was discovered accidentally by his
brother, who is a physician.
Examination by Dr. Osier revealed a well-nourished man who does not appear ill.
1 ace a little congested, veins of neck and arms full; pulse 48 per minute, both apparently
-\ nchronous, a little larger on left than on right (maximal pressure: left arm 140; right
arm 125). There is no tracheal tug. Over the thorax a wavy impulse is seen in all
the right interspaces above the liver, and an area of dulness as outlined in Fig. 310, A. Rela-
tive cardiac dulness in fourth interspace extends 16.5 cm. to left and 15 cm. to
right of midline. Over the aneurismal area there is a marked systolic thrill and murmur;
over the heart a svstolic and diastolic murmur.
1 In 120 cases of aneurism of the descending aorta collected from the literature Milanoff
found pain in 72. dysphairia in 20, liaematemesis 13, haemoptysis 21, left-sided pleural effu-
sion in a fe\v cases. Andreef found only s cases of paraplegia from aneurism in the litera-
ture. The duration is often from 10 to 15 years; longer than that of aneurisms elsewhere.
The condition is very well discussed in Kn«rli>h by Osier and more recently by Hewlett
and Clark, who give excellent radiographs and a very useful summary of the literature.
540
DISEASES OF THE HEART AND AORTA.
X-ray examination by Dr. Baetjer showed the pulsating shadow of an aneurism of
size corresponding to the area obtained on percussion, arising from the ascending arch of
the aorta.
Patient left the hospital, and one month later died without warning while asleep.
The only signs of the approaching end were fifteen minutes of stertorous breathing.
Autopsy revealed a large aneurism corresponding to that diagnosed clinically, as well as
arteriosclerosis and aortic insufficiency. There is no note of rupture of the aneurism.
FIG. 310. — Cardiac dulness in cases of aneurism. A. Ascending aorta (D. N. L.). B. Subclavian
artery (J. B.): the shaded area indicates the tumor, the curve indicates the pulsation. C. Second part
of the transverse portion of the arch (K).
ANEURISM OF INNOMINATE ARTERY.
J. B., aged 44. Had syphilis 13 years ago, otherwise healthy.
Two years ago complained of aching in right shoulder and right side of
neck down arm to hand. No pain in chest. There were swelling of feet and ankles and
shortness of breath. About this time he began to have troublesome paroxysms of
coughing. In May, 1903, noticed that his v o i c e was "cracked." In August,
1903, he noticed a pulsating swelling above the right clavicle. This was
diagnosed as aneurism of the innominate, and the right carotid was ligated
above the tumor. The subclavian could not be ligated, as the patient took chloroform
ANEURISM. 541
badly. After the ligation the tumor rapidly increased in size. When he entered the Johns
Hopkins Hospital two months later, his voice was husky, the right pupil was larger than
the left (irritation of the right sympathetic ganglia), and a large rounded pulsating tumor
was seen occupying the position of the manubrium and extending out along the right
clavicle (Fig. 310, A, B). The prominence of this tumor is shown in Fig. 302. Over the
tumor a well-marked systolic and diastolic shock may be felt. The two heart sounds are
heard over the tumor. There is some resonance on percussion between the tumor and the
heart. The area of cardiac dulness is not enlarged, but a soft diastolic murmur is heard
at apex and base. The right radial pulse is smaller than the left and a little delayed. The
blood-pressure varied, at first being 160 in left arm, 140 in the right brachial, later reach-
ing 150 in right and 130 in left.
Patient was seen by Dr. Finney, but wiring and other operative procedures were
considered impracticable. He was kept at rest in bed on restricted diet, but nevertheless
the aneurism grew rapidly, as shown by the successive elevations in Fig. 302.
On Dec. 2, at 4.00 A.M., he felt a severe throbbing in the aneurism, and a couple of
smaller bulgings (Fig. 302) appeared upon its surface, which had not been present the
day before, and the whole aneurism appeared to be definitely larger. The patient insisted
upon leaving the hospital at once to return to his home in South Carolina.
ANEURISM OF THE FIRST PART OF THE TRANSVERSE ARCH OF THE AORTA.
J. D., an unmarried sailor, aged 37, entered the Johns Hopkins Hospital on Jan. 5,
1909, complaining of pain in the chest and inability to sleep. He had had no infectious
diseases except gonorrhoea, denied spyhilis, and gave no history of secondaries. Except for
occasional sprees, he uses alcohol in moderation. As a sailor he has always done heavy work.
He was well until about four months before admission, when he had an attack of
"heavy pressure" and tightness across his chest at night, and some weeks later stinging
pains in his chest 3-4 cm. above the xiphoid process, which seemed to radiate to both
sides of the chest and to pass through to the back. The pressure kept him from sleeping.
Upon examination the veins upon the left side of the neck were found to be dilated,
and the veins were much more prominent than on the right. There was no t radical tug.
There was an area of dulness behind the medial end of the right clavicle, the manubrium,
and the medial half of the left clavicle, which was continuous with the upper border of
cardiac dulness. The left radial pulse was somewhat smaller than the right and seemed
to be a trifle retarded. Maximal pressure in the right radial ranged from 115 to 130 mm.
Hg, in the left from 85 to 110 mm. Hg.
Fluoroscopic examination by Dr. Baetjer showed a pulsating tumor about the size
of a hen's egg projecting almost entirely to the left of the sternum opposite the first and
second interspaces (transverse portion of the arch of the aorta).
The patient was discharged somewhat improved after a short sojourn in the hospital.
ANEURISM OF THE LEFT SIDE OF THE TRANSVERSE ARCH.
H. D. K., brush-maker, aged 49, admitted to the surgical service of the Johns Hopkins
Hospital on March 14 , 1908, complaining of aneurism. Family history was negative. He had
been perfectly healthy all his life except for an attack of pleurisy six years before admis-
sion, an attack of gonorrlura at 19, and a chancroid, not followed by secondaries, at 25.
Two weeks before admission he felt a burning pain in the left chest :m<l
had some shortness of breath, both of which have become worse since then. He sometimes
is awakened with shortness of breath and precordial pain. For the past year his voice has
been husky, a condition which set in suddenly after violent exertion while splitting wood.
He is a well-nourished man of Father anxious expression. The pupils are equal and
react to light and accommodation. There is a well-marked tracheal tug. Chest expansion
is slight on respiration. There is a definite pulsation over the first left interspace and
sternoclavicular junction, in which area the shocks accompanying the two sounds are
readily palpable.
Note by Dr. Bnggs. — H e a r t : Maximal impulse in fifth left interspace 11 cm. from
midsternal line; dulness extends to this point on left, reaches above to middle of third
rib, and on right 2.5 cm. in third left interspace. Cardiohepatic angle is normal. There
is dulness behind the m a n u b r i u m , ext«-n«iinir to left, as per diagram, 8.5 cm.
542 DISEASES OF THE HEART AND AORTA.
in first interspace and below to second interspace, on the right to just beyond the sternal
margin. On palpation over the dull area there is a strong lifting pulsation,
maximal at a point 5.5 cm. to left and definitely expansile. No thrill felt. Diastolic shock
well marked. At apex and inward toward the base there is a very short systolic murmur,
which is not transmitted beyond the border of the heart. First sound is rather tapping
at apex. Along the left sternal border this murmur increases in intensity and is maximal
over the mass above the heart at the point of greatest pulsation, where there is a well-
marked systolic bruit followed by a ringing second sound. A very faint systolic murmur
is heard at the aortic ring, and the second sound is clear. No diastolic murmur. The
second pulmonic is louder than the second aortic. The pulse is of good volume, regular,
rather high tension, and not collapsing. Vessel wall definitely thickened. Some cyanosis
of finger-tips and lips. The volume of the pulse on the right side is
decidedly larger than on the left. There is a circumscribed area of
dulness in the left interscapular region in which percussion note has
a peculiar wooden tympany like that over consolidated lung. Over this area the breath
sounds are rather more intense than over the rest of the lung but they are not tubular
in character.
On January 20 the aneurism was wired, under Schleich solution anaesthesia, by Dr.
Finney, with twelve feet of silver-copper wire, through which a 10-MA current was passed
(Moore Corradi method). Clotting took place promptly. The patient stood the opera-
tion well. The patient was considerably relieved as regards pain, but the pulsation soon
returned.
ANEURISM OF THE DESCENDING AORTA.
Notes of the following case are taken from the records of the Johns Hopkins Hospital :
Ch. L., colored laborer, aged 48, was first admitted to the Johns Hopkins Hospital
on October 14, 1898, complaining of pain in the back, left side, and abdomen.
His family history was negative. He had always been healthy, but had measles,
whooping-cough, tertian malaria, and at 17 had syphilis which was not adequately
treated. He has done a great deal of hard work on a farm, has drunk a great deal of whiskey,
and smoked heavily.
His present trouble began suddenly about four years ago, when he was seized with
a severe pain in the lower left abdomen. This lasted a couple of weeks. It was
always relieved when his thighs were flexed upon the abdomen, and was always increased
after exposure to bad weather. Four years after this a pain in the left side of the
back appeared, which has gradually increased. This also is relieved by flexing the thighs.
For the past six years he has passed blood in the stools during periods when the pain in
the left flank was worse.
A note by Dr. Futcher at that time states, that " the patient was found lying in bed
on the left side with the knees flexed. Pupils are of normal size, equal, and react to light
and accommodation. The lung expansion and vocal fremitus are diminished over the
entire left lung, and the breath sounds were exaggerated in front and in the axilla. There
were a few moist rales in the third and fourth left interspaces. Behind, the breath sounds
are very indistinct below the angle of the scapula. The percussion note was found to be
impaired over the entire left front as far down as the fifth rib and over the entire left
back, being flat below the angle of the scapula.
Heart. — The maximal impulse was seen in the fifth interspace 7.5 cm. from the mid-
line, but dulness extended 3 cm. to the left of this point. Both the first and second sounds
were reduplicated.
The liver was slightly enlarged; the spleen just palpable. There were no masses nor
areas of tenderness in the left flank to account for the pain.
On Oct. 21 Dr. Futcher noted a definite heaving of the entire body of the sternum
and a well-marked systolic retraction in the eighth, ninth, and tenth left interspaces be-
hind. A tracheal tug was present, but the vocal cords were not paralyzed. The pulse was
equal on the two sides.
In spite of rest, restricted diet, and potassium iodide and repeated gelatin injections,
his pain in the back gradually became worse, compelling him to seek relief by lean-
ing over tbe back of the chair. It became so severe that it was not relieved
by 30 mg. (gr. ss) of morphine. However, later in his stay his condition gradually became
better and the pain became a little less frequent and less intense.
ANEURISM.
5-13
There was very little change in his condition between that time and March, 1902,
when for the first time there was noted a definite systolic pulsation in the left
interecapular region which gradually increased until it involved three ribs and interspaces.
His condition gradually became worse. Respiratory movement almost entirely disappeared
upon the left side and a scoliosis developed with concavity toward the right. The area
of cardiac dulness increased to the right, where pulsation was particularly well marked
and a superficial scratchy systolic murmur was heard over the precordium. His pain
became so intense that he could but rarely lie down. An area of absolute analgesia devel-
oped in the sixth and seventh left interspaces, impaired sensibility to heat, cold, and pain
being found in the fifth interspace as well. About this time he began to feel pain on swal-
lowing, referred to the middle of the sternum.
During the night of Oct. 25 he complained of pain and intense shortness of breath,
and suddenly vomited about 50 c.c. of bright red blood. Ten minutes later he
vomited 25 c.c. more blood. He was quieted with morphine during the night, but in the
early afternoon of the twenty-fifth he vomited about 500 c.c. of blood within three minutes,
became pulseless, and died.
At autopsy the heart was found to be displaced to the right (extending 8 cm. to
the right of the midline) by a tremendous aneurismal sac 18X14X9 cm. This sac was
fusiform with sacculations at its upper and lower ends. It arose from the descending
part of the arch and the descending aorta itself and pointed backward,
eroding the bodies of all the thoracic vertebrae from the fifth to the tenth as
well as the seventh, eighth, and ninth ribs. The erosion of the intervertebral disks was
much less marked. The aneurismal sac also compressed the oesophagus at the level of the
bronchial bifurcation, where it eroded through the oesophageal wall, making
an opening 2.5 cm. in diameter. "The edges of this aperture were ragged and necrotic:
the tissue about it dark gray-green in color."
The aneurismal sac was partly filled by a large lamellated clot.
The ascending aorta was dilated and atheromatous; the descending aorta below the
aneurism likewise.
The heart was much enlarged; the walls hypertrophic ; the valves normal.
There were many pericardial adhesions, especially firm over the left auricle and the
coronary veins, and there were tortuous
patches over both ventricles.
The stomach contained a litre of
clotted blood. Other organs normal.
SIMPLE DILATATION OF THE ARCH.
L. D., gardener, aged 55, native
of Ireland, came to the Johns Hopkins
Hospital Dispensary on July 13, 1909,
complaining of pain on swallowing and
trouble in passing water.
The family history was negative.
The patient had smallpox at 18, gon-
orrhoea at 35 and again at 48, and
a chancre at 35 followed by definite
secondary manifestations, for which
he had been given medicine by mouth.
He has drunk whiskey in excess and
has done a good deal of heavy work.
He was perfectly healthy until the past ten days, since when he feels food passing
down his resophagus and has a little pain which is referred to the level of the cardia. He
vomits immediately after eating, but can swallow liquids without difficulty.
Examination reveals :i fairly nourished man of ruddy complexion with some dilated
venules. The left pupil is somewhat larger than the right, though both react to light and
accommodation. There is a slight but definite tracheal tug; no trucheal percussion shock.
There is no glandular enlargement. The lungs are clear except for a few widely scattered
piping rales.
Fir,. 311. — Area of cardiac dulness in a patient (L. D.>
with dilated arch i>f the aorta.
544 DISEASES OF THE HEART AND AORTA.
The heart is not enlarged; apex in fifth left interspace 10 cm. from the midline. Dul-
ness extends 4.5 cm. to the right. The relative dulness is continuous above with a strip
3.5 cm. upon either side of the sternum, over which the percussion note is very slightly
impaired. This area extends up as far as the upper border of the second rib, and is shown
by the fluoroscope to correspond with a uniform shadow of the dilated aortic arch. The
heart sounds are clear; the second aortic distinct; no diastolic murmur present. Pulse
is of good volume, not collapsing.
Abdomen shows no masses; no visible peristalsis. There are no tenderness and no ab-
normalities palpable. The stomach tube is passed into the stomach without difficulty,
and a very small amount of clear fluid, free from HC1, obtained; lavage fluid clear. Des-
moid test negative. He was given alkaline gentian tincture + strychnine (1 mg. = -fa gr.)
before meals, under which treatment his symptoms rapidly diminished.
Diagnosis : Chronic alcoholic gastritis, anacidity, dilatation of the aortic arch.
ANEURISM OF THE ABDOMINAL AORTA.
M. P., machine agent, aged 30, was first admitted to the Johns Hopkins Hospital
on Oct. 31, 1899, complaining of kidney and stomach trouble. The family his-
tory was negative.
The patient had had measles, chicken-pox, mumps, and whooping-cough, typhoid
fever at 23, followed by pain in the ankles and knees. He had gonorrhoea two years before
admission (about one year before the onset of the present trouble), but denies lues. He
worked on a farm until his attack of typhoid fever, since when he has not been strong.
He does not drink nor smoke and is a hearty eater.
The present illness began six months before admission, with some soreness and pain
in the abdomen, which had no relation to the taking of food except that it was
more intense after a large meal. He vomited occasionally but rarely. The pain was at
first a sharp throbbing pain in the left side. It was so severe as to
cause him to remain in bed for a period of three months, during which he
had to be given morphine. After the three months' sojourn in bed the pain became less,
and he was almost free from symptoms for about six weeks, when he was taken with a
sudden sharp cutting pain in the right side just under the ribs, running
around toward the right and down toward the testicle.
On examination he was found to be a well-nourished man of rather sallow color.
There was no glandular enlargement. The lungs were clear on auscultation and percussion.
The heart was not enlarged; the heart sounds clear.
In the abdomen there was a very well-marked pulsation visible in the epi-
gastrium. There was dull tympany over this area, and inflation of the stomach showed
that the pulsating mass was covered by the latter. There was considerable tenderness
over the pulsating area; Dr. Osier was able to make out a definite soft systolic mur-
mur, and on Nov. 5 with the deepest possible palpation could make out a definite mass
with expansile pulsation. The case was diagnosed as abdominal aneurism
and wiring was advised. This was performed by Dr. Finney two months later.
Note by Dr. Finney. — An incision was made 2.5 cm. befow the xiphoid. The stomach
was retracted downward; the lesser peritoneum was opened. The pancreas
covered the lower surface of the tumor. Attempt was made to dissect the pan-
creas. This was abandoned on account of profuse and persistent hemorrhage.
The incision was then enlarged upward, the edge of the liver elevated, and the tumor
exposed above and to the right of the pancreas. A needle was inserted at this point to a
depth of 3-4 cm. and 8-9 feet of silver and copper alloy wire introduced. Ten milliamperes
of current were passed for one hour. The needle was withdrawn, the wire cut close to the
aneurismal sac and turned in with a clamp. No bleeding. One or two bleeding points
about the pancreas were tied with fine silk. The incision was closed. The patient made
an uneventful recovery and experienced considerable relief from pain, so that nine
months later it gave him little trouble, though the aneurismal pulsation was still
expansile. There was now aloud systolic murmur over the mass.
The pain, however, gradually returned and never left him. It was so severe that he
was a frequent visitor at the hospital and was compelled to use a good deal of morphine.
He was admitted to the writer's ward in Jan., 1904, somewhat worse than at any time
previously. The aneurismal mass now extended from the ensiform to within 3
ANEURISM. 545
centimetres of the umbilicus. Its surface was smooth and no areas of bulg-
ing could be made out.
On Jan. 7 the leucocytes were 5000: the hsemogolobin 90 per cent. He was quite well
(when given morphine) until the night of Jan. 21, when he had asudden attack of
most intense pain in the lower back and abdomen, "causing him to cry out and toss
about, arching his back and stiffening all his muscles in his attempts to bear the pain in
silence." There was no objective change in the abdomen, but the tenderness over the
aneurism was more marked than before.
The next day he had several attacks of pain and vomiting. At 4.00 P.M. the vomit-
ing was very severe and was accompanied by intense pain and sudden collapse.
His color became a ghastly pallor. He became almost pulseless before any one could
reach him. He was still conscious and complained of great pain in the back and
right side of the abdomen, to relieve
which .15 Gm. (gr. iiss) of morphine
were necessary, given within an hour.
At 5.45 P. M. a small saline infusion
was given and caused the pulse to
improve slightly. Strychnine, 2 mg.
(sV gr-), + digitalin (German), .15mg.
(iV gr-)> had n° effect. The maximal
blood-pressure before the collapse was
130 mm. Hg, after it was 70 mm. Hg.
The next day there was dulness
throughout the right flank extending
up to liver dulness (due to outpouring
of blood into the peritoneal cavity).
The systolic murmur over the tumor
disappeared, but the aneurismal mass
still pulsated. The haemoglobin was
found to have fallen to 55 per cent.;
the leucocytes rose to 17,500.
During the next few days the
patient's condition seemed to improve. **
The pulse became stronger; the maxi-
mal blood-pressure rose to 120 mm.
Hg. However, his kidneys absolutely ceased secreting. He did not void at all spon-
taneously, and 50 c.c. of clear reddish liquid, of neutral reaction and with a specific
gravity of 1030, was all that could be obtained on catheterization on the evening of
Jan. 24. It contained a large amount of albumen, no sugar, no casts, a few red blood-
corpuscles, and a large number of pus-cells. This was the last urine obtainable, even by
catheter.
From this time on the patient's condition became worse. He complained of
sudden shocks like electric shocks through his nervous system, to which he responded
by sudden single twitches. He had no general convulsions. His mind remained
perfectly clear, his pulse good until the morning of Jan. 26 (five days after the rupture),
when his pulse gradually became weaker, he lapsed into unconsciousness, and died at
10.30 P. M.
Autopsy confirmed the clinical diagnosis, showing a large saccular
aneurism of the abdominal aorta which had ruptured into the retroperi-
toneal tissue and lesser peritoneal cavity, causing infarction of the left kidney and oblitera-
tion of the vessels to the right. There was thrombosis of all renal vessels and a tremendous
hemorrhage into the greater peritoneal cavity as well. This rupture had evidently occurred
at the time of the collapse on Jan. 22. There was an island of clot within the coil
of silver wire within the sac, but a wide free blood channel between this clot
and the aneurismal wall, so that the clot had not strengthened the latter
in the least.
It is probable that during the months following the wiring, while he was free from
pain, the clot filled the entire aneurismal sac, and that the eddy currents dissected it free
from the aneurismal wall about the time that the pains returned.
35
546
DISEASES OF THE HEART AND AORTA.
FIG. 313. — Tortuous subclavian artery, simu-
lating a small aneurism. The tumor which it
formed above the clavicle is indicated by the
shading.
DIAGNOSIS.
The diagnosis of thoracic aneurism is, as a rule, easy, especially with
the aid of the X-ray. Most of the conditions with which it can be confused
have been mentioned above. The most important of these are simple
dilatation of the aorta, mediastinal tumors, pulsating empyema or encapsu-
lated pericarditis, and enlarged mediastinal or branchial glands. Any of
these may cause the dulness, the tracheal tug, the inequality of pupils
and pulse. The systolic thrill and murmur may also be communicated by
a very solid tumor or may arise in a very vascular sarcoma, aberrant thy-
roid with stroma, or metastasis from
a medullary carcinoma or hyperne-
phroma. A diastolic shock is scarcely
ever felt over even the most vascu-
lar tumors, but is, of " course, well
marked over a dilated aorta. The
presence of a forcible expansile
pulsation in the interspaces is suffi-
cient to exclude tumors; but in the
first and second interspaces when
there is no actual bulging it may
be due to a simple dilatation of the
aorta. The tracheal tug may further
be due simply to displacement of the heart or aortic arch or to enterop-
tosis, while the inequality of the pulse may arise from the presence of adhe-
sions or arteriosclerotic plaques about the origin of the subclavian arteries.
The absolute diagnosis can almost always be made by X-ray exam-
ination, but even then a tumor may be encountered whose shadow shows
no expansile pulsation and whose nature remains in doubt. The homogene-
ous shadow, with its regular spherical or oval form and its connection
with the aorta, is usually evidence of aneurismal nature.
In doubtful cases the greatest care is necessary, for the physician should
always bear in mind that the earlier the aneurism can be treated the greater
the chance of cure, and this stage of hope is usually the stage in which the
physical signs are still far from definite.
Occasionally a tortuous carotid or subclavian artery presenting its
convexity in the supraclavicular fossa may simulate an aneurism, so that,
as in the case seen in Fig. 313, it is necessary to outline the supposed aneu-
rism with the tip of the little finger. In this case, which had once been
diagnosed aneurism, it was possible to reach below the convexity and to
feel the outline of a narrow but tortuous subclavian artery. Of course,
the X-ray examination in such a case would at once clear up the diagnosis,
even if the outline of the artery could not be felt.
Another condition which may simulate aneurism of the subclavian
artery is a dilated jugular bulb, which appears as a pulsating sac above the
clavicle. This is especially marked when tricuspid insufficiency is present.
In such cases the arterial blood-pressure may be low and the arterial pulses
weak; nevertheless, the pulsation is so feeble and the connection with the
dilated veins so evident that it should never be mistaken for an aneurism.
ANEURISM.
547
DISSECTING ANEURISM.
Shakelton in 1822 gave the first descriptions of dissecting aneurisms,
which were soon confirmed by Hope (1833) and Henderson (1843). In
this condition the coats of the aorta are split longitudinally into two sleeves,
— an outer, originally formed by the adventitia, and later lined by new-
formed intimal endothelium; and an inner sleeve representing the original
tube of the aorta, composed of the original intima and media, and later
also covered with new-formed endothelium.
PATHOLOGY.
The condition is not an extremely rare one, so that Bostroem in 1887
was able to collect reports of 177 cases. It usually arises in the aorta,
especially at the beginning of the descending arch, and not infrequently
is formed as the continuation of a simple aneurism of the arch. From
this region it commonly extends along the whole length of the aorta to
Fio. 314. — Dissecting aneurisms. A. Specimen of a dissecting aneurism (partial clot formation)
in a man with only two aortic cusps. (From the Army Medical Museum, Washington, D. C.) B. Dis-
secting aneurism of I.. 1! ., involving the arch and the descending aorta. (After MacCallum; kindness
of the Johns Hopkins Hospital Bulletin.)
the bifurcation, the arteries sometimes arising from the inner, sometimes
from the outer tube. Occasionally the split occurs between the layers of
the media, so that both sleeves have a wall of media. Very infrequently
the outer tube ruptures into the inner tube near its lower end, so that the
blood passes back into the latter.
The most satisfactory explanation for this remarkable lesion seems
to be the following (v. Moller, Flockemann, Schede) : As long as the lumen
of the artery is uniform, the blood exerts only a lateral pressure upon the
548 DISEASES OF THE HEART AND AORTA.
arterial walls, which acts " across the grain " of the arterial coats. However,
when calcified plaques project into the lumen, these tend to impede the
blood-current so that the longitudinal pressure of the latter acts as well.
As Bostroem has shown, the resultant force acts in a parabola pointing
outward and downward. When this is acting upon an area where the media
is thinned or absent, it tends not only to split the coats "with the grain"
but also to push the adventitia outward. The wall gives way, the split
lengthens, and the outer sleeve is formed. Whether or not the aorta then
ruptures depends upon the ability of the adventitia alone to withstand
the blood-pressure.
The coagulation of the blood within the sac depends upon the formation
of fibrin ferment in the tissues of the adventitia and the rapidity of the
blood-flow within the new-formed sac. It is quite frequent for extensive
and even total coagulation of the contents to take palce.
SYMPTOMS AND SIGNS.
A considerable proportion of the cases of dissecting aneurisms give
no outward manifestation during life and are accidental findings at autopsy.
A large number give the usual signs of ordinary aneurism, especially when
they arise as a continuation of the latter. This is well exemplified by the
following case, which was under the writer's observation during his last
admission to the hospital. (The pathological findings and clinical notes
are taken from the report of Professor MacCallum.)
L. R., negro, aged 30, had been treated in the Johns Hopkins Hospital one year
previous to his final admission, at which time the diagnosis of aneurism of the aorta
had been made. At the final admission the patient was found to be suffering from an
arthritis with symptoms of general fever, sweating, etc. The heart was enlarged, dulness
extending 13.5 cm. to left and 3 cm. to right of midline. There was visible impulse and
heaving in second, third, fourth, fifth, and sixth interspaces, far out in first and second
left interspaces. Heart sounds were clear, dull, and ringing; second sound followed by
soft diastolic murmur in third left interspace, not heard in neck.
Patient died in delirium with high fever.
Autopsy showed general streptococcus septicaemia, hemorrhagic nephritis, acute
purulent arthritis, obliterative pericarditis, aneurism of ascending aorta, dissecting aneu-
rism of the descending aorta. The aortic orifice is not dilated (8 cm. in circumference). A
large aneurismal sac (7 cm. in diameter) lies behind the pulmonary artery; it extends
upward in the aorta to the arch, beyond which the tube becomes double, the inner tube
(the original lumen of the aorta) having for its walls the original intima plus media,
the outer tube media plus new-formed endothelium. Numerous trabeculae jut out
transversely into its lumen. Some of the intercostal vessels arise from the new, some from
the old lumen. The left renal artery arises from the old lumen; the right has been torn
and arises from the outer. At the lower end above the bifurcation the outer tube has
ruptured back into the original lumen.
Another type is exemplified by a case under the care of Professor
Halsted; also reported by MacCallum.
Patient, aged 60, subject to mental disturbance and epileptiform attacks, complained
on May 28 of intense pain over the whole body, which he could not locate. On May 28 his
abdomen was much distended and he was jaundiced. There was pain in the region of
the appendix. His temperature was 100°. Leucocytes 20,000. Exploratory laparotomy
showed an extremely distended colon which was relieved by colostomy. Patient died
the next day.
ANEURISM. 549
Autopsy showed a dissecting aneurism along the whole aorta, splitting
the media. The outer sleeve of the descending arch perforated into the posterior mediasti-
num, giving rise to a tremenduous haematoma which distended that space down to the
diaphragm. The rupture had evidently given rise to the pain; the disintegration of red
corpuscles in the clot had caused the hcematogenous jaundice. Both these phenomena
are common in cases of this type.
ANEURISM OF THE PULMONARY ARTERY.
Aneurisms of the pulmonary artery are very rare as compared with
those of the aorta. Henschen (1906) has recently summed up the reported
cases. In contrast to aortic aneurism, he finds that there is no close rela-
tionship to hard work; 18 out of 34 cases (50 per cent.) were in men, 16 (47
per cent.) in women; 39 per cent, occurred under the age of 30 (as com-
pared with 18 per cent, of aortic aneurisms). Acute infectious diseases
and lues seem to be the main etiological factors. The ductus arteriosus
Botalli was frequently found open (17.5 per cent.), which would indicate
that some disturbance during fetal life or soon after birth had been a pre-
disposing factor. Frequently there is a certain degree of narrowing of the
pulmonary artery (32 per cent.). In 8 cases (20 per cent.) there were also
marked arteriosclerotic changes in the pulmonary artery.
Among 40 cases there were the following complications: pulmonary
stenosis 2; relative pulmonary insufficiency 5; organic pulmonary insuffi-
ciency; other valvular lesions 3.
The subjective symptoms are not pathognomonic and are very similar
to those of congenital heart disease; palpitation, dyspnoea and cardiac
asthma, constriction of the chest, cough, often cedema of the lungs and
blood-tinged expectoration, intense cyanosis, cedema, anasarca, ascites,
hydrothorax. Death sometimes results suddenly from rupture, sometimes
from intercurrent pericarditis and endocarditis, sometimes from diseases
of the respiratory tract.
DIAGNOSIS.
According to Henschen, the diagnosis is justified when the following
signs are all present simultaneously:
1. Intense cyanosis and other signs of stasis, constriction, and bloody
expectoration, sometimes sternal pain.
2. Prominence of second and third left costal cartilages or second left
interspace and well-defined dulness or X-ray shadow in this area.
3. Pulsation and well-defined thrill and murmur in second left inter-
space.
4. Loud superficial rasping systolic murmur.
5. Hypertrophy of the right heart.
6. Absence of dilatation or hypertrophy of left heart (apex dulness
not outside the mammillary line)!
7. Absence of other signs of aortic aneurism.
The X-ray shadow furnishes the most important aid in diagnosis.
However, the correct diagnosis was made intra vitam only once or
twice in his 40 cases.
550 DISEASES OF THE HEART AND AORTA.
ANEURISM OF THE ABDOMINAL AORTA.
Owing to its frequency (10-14 per cent, of aneurisms) and its surgical
accessibility, aneurism of the abdominal aorta is of great importance. Owing
to its exposed situation, trauma is a more frequent cause than in thoracic
aneurism. As Sibson has shown, it is usually (133 out of 171 cases) situated
just below the diaphragm and above the coeliac axis, in the place where it
gives the greatest number of symptoms and is most inaccessible to operation.
The most important symptom of aneurism of the abdominal aorta
is abdominal pain, — epigastric or in the regions of kidney and gall-
bladder, sometimes in the flanks, sides, and back. The pain is usually
more marked on one side than the other, but may be bilateral. Until the
appearance of a palpable tumor the condition may be readily mistaken
for renal calculus, gastric ulcer, or other abdominal disease, or for psoas
abscess. The pain may be so intense as to require morphine, even in large
doses, though acetanilid, antipyrin, aspirin, etc., may be of use at first.
Palpitation is also commonly felt in the aneurism.
All these symptoms are common in neurasthenic women who have
vigorously pulsating abdominal aortas, especially associated with enterop-
tosis. It is probable that in this condition the peritoneal moorings of the
aorta are rather loose. When the arterial pressure rises at systole, the angle
curves of the abdomnal aorta and common iliac arteries tend to straighten
themselves and thus throw the aorta forward toward the abdominal wall,
at the same time giving a painful tug upon the abdominal nerves as they
emerge from the vertebral column. The looser the moorings of the aorta
the greater its excursion and the greater the pull upon structures other
than those which normally hold it. Arteriosclerosis of the abdominal
vessels may also give rise to similar symptoms.
Mere pulsation of the aorta in the epigastrium and elsewhere, even
when associated with quite intense pain, is therefore not necessarily a sign
of abdominal aneurism. In doubtful cases it is most important
to outline the whole course of the aorta by pressing the
fingers of the two hands down on either side of the vessel so as to include
the abdominal aorta between them. The expansile nature of the pulsation
can be felt by pressing downward and inward. Any irregularity or bulging
along its course may be felt readily in this way. For the diagnosis
of an aneurism it is necessary to outline a tumor with
expansile pulsation arising from the abdominal aorta, limited in
extent above and below, and spherical or oval in shape. There is usually
a well-marked thrill over an aneurism. The pulse-wave in the femorals is
usually much retarded in aneurism (apex beat— femoral pulse interval =
0.24+ sec.) but not in simple aortic pulsation. The early diagnosis may
sometimes be made with the fluoroscope, care being taken to empty the
bowels by a day or two free purgation and preliminary milk diet, and then
to examine the abdomen with a "compression diaphragm" (Kompres-
sionsbletide) so as to push the other structures aside. Oblique illumina-
tions and inflation of stomach and colon with air may be helpful.
As the aneurism grows it may press upon the renal arteries and veins
and may cause albuminuria, cylindruria, haBmaturia, or even anuria
ANEURISM. 551
and death from this cause. It may press upon the intestines and cause
intestinal paralysis, with death from obstruction, or may give
rise to many symptoms from pressure. Erosion of the vertebrae
and pressure on the cord or cauda equina may lead to paraplegia
(flaccid) and may cause most intense pain.
Abdominal aneurisms may rupture the retroperitoneal tissue into
the peritoneum, especially the lesser peritoneal sac into the stomach,
intestines, or vena cava. They rupture externally in the epigastrium. The
rupture is attended with excruciating pain and often collapse, but death
may not ensue for some time thereafter, as the clotting of blood in a small
space may prevent further outflow from the vessels. Thus, in the case
cited below, the aneurism ruptured into the retroperitoneal tissue, com-
pressing the renal vessels. The pain accompanying and following rupture
was excruciating, probably owing to stretching of the solar plexus.
PROGNOSIS AND TREATMENT OF ANEURISM.
In spite of the fact that aneurisms occasionally cease to develop or
even undergo spontaneous cure by thrombosis, this procedure is to be re-
garded as a rarity, and it is not, under any circumstances, to be expected.
By far the greater number of aneurisms cause the death of the patient
within from one to five years, though occasionally they remain stationary
for twenty-five or thirty. It is, therefore, necessary to attempt to modify
the course by treatment. As the intrathoracic aneurisms were not well
known to the ancients, their therapy for aneurism was confined to ligature
of the peripheral arteries.
Valsalva (1666-1723) recommended lessening the force of the heart-
beat by absolute rest in the recumbent posture, "starvation diet." and
frequent removal of small quantities of blood by venesection. The two
former procedures were revived by Tufnell in 1874. Tufnell reported a
number of cases, especially of aneurism of the abdominal aorta, cured by
restriction of the daily intake to ten ounces of solids and ten ounces of
liquids for several weeks.
f Bread and butter ........ . . .60 Gm. (3ii)
Breakfast ............. \Milk ....................... 60c.c. (3H)
j Meat ...................... 60-100 Gm. (3H-iii)
......... I Milk ....................... 75-125 c.c. (3«i-iv)
f Bread ..................... 60 Gm. (3")
{ Milk ....................... 60 c.c. (3ii)
The patient is given no water, and is not allowed to rise from the horizontal position
even for an instant. As a result of this the blood-pressure falls and the pulse-rate also.
In his first case the pulse-rate fell from 104 to 69 per minute, equalling a diminution
of 50,400 beats in twenty-four hours. The wall of the aneurism is spared just this amount
of strain, the volume of blood diminishes, and the aneurismal sac may gradually contract
down, facilitating clotting.
Tufnell's results (cure of two abdominal and one popliteal aneurism)
are rather striking, but the treatment imposes the greatest hardship on
the patient and few have the hardihood to give it an adequate trial. That
the restriction of fluid to ten ounces daily may be harmful is suggested by
552 DISEASES OF THE HEART AND AORTA.
the fact that his first case developed uraemia at the end of the treatment
and died from that about as soon as he would probably have died from the
natural progress of the aneurism.
Alonzo Taylor has made very careful studies of the blood in three patients under
Tufnell treatment, who were also receiving potassium iodide 1 Gm. (gr. xv) and calcium
chloride 2 Gm. (gr. xxx) daily, and who were being bled (250 c.c.) every eighteen days.
He found no change in the concentration of the blood or in calcium in the blood, and only
slight fall of red corpuscles. The coagulation time was unchanged in one patient, slightly
shortened in another. The aneurisms became somewhat smaller, but no cures resulted.
At the Johns Hopkins Hospital the method was tried very assiduously for many years,
supplemented by subcutaneous gelatin injections as suggested by Lancereaux. Later
calcium lactate has been used. There have been but few satisfactory results (Futcher),
though Professor Osier stated that he had seen several cases of cure in his extensive
experience.
Potassium iodide was used in aneurism by Bouillaud (1859)
and Chuckerbutty (1862), and especially by Balfour, who found that it
caused great relief from the pain, and claimed that the aneurism also dimin-
ished considerably in size. Subsequent experience demonstrates the cor-
rectness of the claim that aneurismal pains are often relieved by potassium
iodide, but few, if any, cures of well-defined thoracic aneurisms can be ob-
tained by its use. Its modus operandi is still obscure, but it may cause a
retrogression of the luetic mesarteritis which is so often present. Gibson
thinks that "we may admit it to be extremely probable that under the
influence of iodide of potassium the nutrition of the walls of the sac, as
well as of the whole of the arterial system, undergoes improvement."
Wiring. — The reason that an increased coagulability of the blood
and a slowed circulation do not of themselves produce intrasaccular clot-
ting is that the latter, like the vessels, is lined with endothelium and does
not furnish fibrin ferment. As stated by Moore in 1864, "the first indis-
pensable condition for the cure of a thoracic aneurism is to provide means
of eliciting fibrin from the blood" (producing fibrin ferment in situ), and
the "second .... to extend the surface within it on which the fibrin
may coagulate." In order to supplement these deficiencies, Moore sug-
gested the introduction of fine wire into the aneurismal sac. Murchison
submitted to him a case of aneurism of the ascending aorta which pointed
on the surface of the chest. Moore slowly introduced twenty-six yards
of fine iron wire through a fine needle. The pulsa fell from 116 to 92, the
pulsation of the tumor almost ceased, but the patient died in collapse two
days later.
Previously to Moore, Guerarcl (1821), Petrequin (1845), and Ciniselli
(1847) induced clotting by passing weak electric currents between the tips
of two needles introduced into the sac (galvanopuncture) . Corradi com-
bined the two methods by using the wire as one pole of the battery. As
now performed, the wire (silver alloy) is attached to one pole of the battery.
It is introduced through a needle which is covered with lacquer to prevent
stimulation of the intercostal muscles, etc., and a weak current (10 milli-
amperes) is passed through it. This accelerates clotting and gives a
firmer clot.
The details of technic, as well as an excellent report of the literature,
are given by Hunner. Hunner cites 14 cases treated by wire alone (Moore's
ANEURISM.
553
method), with cure in 2 cases of abdominal aneurism (Morse and Langton) ;
with the combined (wire plus electricity) method (Moore-Corradi), 23
cases — 17 thoracic, with 3 cures (17.7 per cent.) (Dr. Rosenstirn informs
the writer that his patient is still alive and well twenty years after the
operation), and 6 abdominal aneurisms. Finney's case, who was appar-
ently cured in 1900, died in 1903 of rupture of the aneurism after intense
suffering for several years.
Unfortunately, the number of cases in which the Moore-Corradi
method can succeed is a limited one. Its usefulness, as already pointed
out by Moore, is limited to sacculated aneurisms of the aorta and to aneu-
Fio. 315. — Diagram showing the various methods for the operative treatment of aneurism. Arrows
indicate direction of the blood stream. A. Ligature above and below the sac (Antyllus). B. Ligature
above and below the sac; removal of the sac (Hueter). C. Ligature above and at some distance from
the sac (Hunter). V. V. represent vasa vasorum. D. Ligature below the sac (Brasdor, Wardrop).
E. Metal band (Hatsted). F. Obliteration of the sac (Matas). a, laying the sutures in the sac; b, arterial
tube left patent after tightening sutures; c, entire lumen obliterated by sutures. G. Successful wiring of
a sacculated aneurism by the Moore-Corradi method, showing the electrodes ( f , — ) in place. H. Wiring
of an aneurism with wide mouth, showing the action of eddy currents in penetrating between the clot
and the aneurism wall. (Compare with Fig. 310.)
risms of arteries which have already been ligated below the aneurism (Bras-
dor's ligature, — e.g., wiring of an innominate aneurism after ligature of
the right carotid and right subclavian arteries), so as to convert them into
blind sacs.
The narrower the opening of the sac the greater the chance of per-
manent cure, for the clot then completely fills the sac and the blood passes
by it without entering the old sac. However, if the sacculation has a wide
mouth the condition is different. The whole sac may be filled by clot at
the time of operation,, but the irregularities about the edges of the clot
give rise to eddy currents which gradually dissect the clot loose from the
aneurismal wall, and leave as an end result an unaltered aneurism with an
island of wire containing clot floating in the centre (Figs. 315, H, and 316).
In an individual case the treatment will, of course, be more likely to succeed
if preceded by a prolonged period of absolute rest, restricted diet and liquids,
554
DISEASES OF THE HEART AND AORTA.
WIRE
CLOT
and vigorous use of potassium iodide, so that the blood-pressure may be
as low, the size of the sac as small, and its neck as narrow as possible. The
same treatment should follow the operation to give a chance for the most
compact adhesion of the clot to the aneurismal wall.
In fusiform aneurisms the wiring method is worse than useless, since
it merely gives rise to a clot in mid-blood stream from which emboli are
readily dislodged.
Compression. — Aneurisms of the peripheral arteries, and especially
of the abdominal aorta, are sometimes cured by compressing that vessel
above the aneurism. This was done successfully by Murray in 1864, who
obliterated the aneurism and
the femoral pulse by means of
a tourniquet wound around
the body above the tumor. A
number of similar successful
cases have been reported since
Murray's, especially when the
aorta is compressed with the
fingers. The operator cannot
continue digital compression
longer than five or ten min-
utes at a time, so that it is
often the custom to obtain
the assistance of a whole
class of medical students
FIG. 316. — Specimen of wired abdominal aneurism, working in relaVS. In this
showing an island of clot within the coils of wire sur- oi_ i_ i i J.T- i_
rounded by a free blood-channel. Way Shepherd and Others have
been able to keep the aorta
occluded for twenty-four hours, and have brought about recovery.
On the other hand, the prolonged pressure may bring about necrosis
of the abdominal wall, intestine and pancreas, or secondary peritonitis,
and intestinal obstruction may result (Bryant, Lunn and Benham, Moxon
and Durham) . The method is therefore still a daring one, and is probably
more severe and less certain than Halsted's metal band method. Moreover,
Sibson found 133 out of 177 abdominal aneurisms (75 per cent.) above
the level of the coeliac axis where they could not be reached by pressure.
Ligature and Partial Occlusion. — Double Ligature. — The oldest method
of treating aneurisms of the peripheral arteries is to ligate them above
and below the sac (Antyllus) (Fig. 315, A), after opening the latter to
remove the blood. A more modern modification of this method is that of
Hueter, who dissected out the entire sac after ligating, thus removing a
large mass of tissue which would otherwise become gangrenous.
Proximal Ligature. — Ambroise Pare (sixteenth century) departed from
the procedure of Antyllus by merely ligating the artery close above the
aneurism (proximal ligature — close to the aneurism). This cut off the
blood supply to the walls of the latter and to its vicinity, inducing necrosis
and suppuration, so that Anel (1710), Desault (1785), and John Hunter
(1785) were led to adopt the proximal ligature at a considerable distance
above the aneurism (ligature of brachial for aneurism of the radial artery;
ANEURISM. 555
ligation of femoral below the adductors for popliteal aneurism; ligation of
femoral above the adductors — in Scarpa's triangle — for popliteal aneurism).
Distal Ligature. — In the eighteenth century Brasdor and later Wardrop
practised ligation of the artery below the aneurism (distal ligature) in
cases like aneurism of the innominate in which the proximal ligature was
impossible. As a result of the procedure, a fusiform aneurism of the innomi-
nate becomes practically a sacculated or flask-shaped aneurism of the aorta,
the innominate artery being converted into a blind sac with narrowed
neck, and coagulation is thus facilitated. This operation is still the one
most commonly performed for aneurisms of the innominate, carotid, and
first part of the subclavian artery. Sheen has collected statistics of 36
cases of innominate and subclavian aneurism, 22 before 1880 with 1 recov-
ery, 14 after 1880 with 8 recoveries, 7 after 1890 with 5 recoveries and 5
cures. To this list might be added 2 cases of Haltsed and 1 of Finney
with recovery and cure. The deaths before 1880 were usually due to sepsis
and hemorrhage. In operating upon the innominate artery it is most im-
portant that both the carotid and subclavian arteries should be ligated,
for if one of these arteries be left open (as in the case of J. B.) the pressure
in the sac is increased without stopping the blood-flow through it, and the
growth of the aneurism is actually favored.
Moore in his first paper suggested the combination of this form of
ligation with wiring for aneurisms of the innominate. This double proced-
ure has not attracted much attention, as in the absence of sepsis the simple
ligature is often satisfactory, but it is no doubt applicable in a certain
number of cases where ligation is not quite adequate.
The chief objection to the simple ligation of arteries
lies in the fact that the permanent results are often unsatisfactory, for
either the ligature may be so tight as to produce necrosis of the tissues
under it and thus bring on rupture of the artery, or, as Halsted has shown,
the arterial lumen may be re-established in spite of the ligature. In many
of Halsted's experiments upon ligating the larger arteries, the lumen of the
artery gradually dilated above and below the ligature, so that the latter
was left surrounded by a thin membrane or septum of scar tissue. This
septum then perforated in one or two places.
Occlusion with Metal Bands. — To obviate this and for other reasons
Halsted has devised a very ingenious procedure, which consists in the occlu-
sion of the vessel by surrounding it with wide metal bands. These metal
bands take the place of the ligature; but when properly applied, do not
occlude the vasa vasorum, and hence permit the proper nourishment of the
arterial wall. Their effect is more certain than that of ligatures, since they
do not allow the lumen to be re-established. The chief advantage, how-
ever, lies in the ability of the operator to obtain a partial occlusion of the
vessel sufficient to reduce pulsation in the aneurism to any desired degree,
without obliterating the circulation below before a collateral circulation
has been established. This renders it the operation par excellence in ab-
dominal aneurisms and aneurisms of the iliac and femoral arteries, in which
the other procedures are likely to be dangerous.
The bands are made of No. 33 sheet aluminum of a width varying from 5 to 15 milli-
metres according to diameter of the artery which is to be occluded. The strip is cut a little
556 DISEASES OF THE HEART AND AORTA.
longer than the circumference of the artery (as shown by a tape passed around the artery).
All the sharp edges must be carefully filed off until they are smooth and round, lest they
cut into the walls of the artery. The strip is then inserted into a specially devised holder
(Fig. 315, E), where it is held in a slot; from this it may be extruded by pressing upon the
rammer above; and as it is extruded below it is curled by the curve at the foot of the slot.
The faster the strip is extruded the more tightly it is curled. The curved foot of the holder
is placed beneath the artery, which is held just tightly enough against the instep of this
foot to almost occlude the lumen. The strip is extruded by pushing the rammer just fast
enough to give the desired curl. Tension on the artery is then relaxed. The pulse can be
felt in the artery below the band, accompanied by a well-defined thrill. The band is then
tightened by rolling it gently under the fingers of one hand while palpating the artery below
it with the other. The degree to which the band is tightened depends upon the artery
affected. In the case of the abdominal or descending thoracic aorta it should be rolled until
the thrill has greatly diminished but not disappeared; in the larger branches of the aorta
the pulse may be made to disappear absolutely. In a few minutes a regurgitant pulse
may mark the appearance of a collateral circulation. When this operation is performed
successfully, the artery becomes gradually occluded at the point of constriction, and a
rich collateral circulation formed, so good in fact that in one case in which Professor Halsted
had occluded the descending thoracic aorta Erlanger found the blood-pressure in the femoral
(eight months afterward) only thirty millimetres below that in the brachial. For practical
purposes this exactly duplicates the conditions in the adult type of stenosis of the isthmus
of the aorta (see page 452), except that the anastomoses take place later and hence are
not quite as extensive.
Professor Halsted has now operated upon a number of cases with very
promising results, and the operation gives promise that in the hands of a
surgeon who has practised the technic, it may completely supersede the
methods of ligature and compression.
Arteriorrhaphy (Matas Operation). — R. Matas in 1905 introduced an
entirely new technic in treating the aneurism of peripheral
arteries exactly in accordance with the principles of
treating inguinal herni a — by obliteration of the sac. The opera-
tion is performed bloodlessly.
The limb is elevated, an Esmarch rubber bandage put on, or bleeding from the main
artery prevented by compression with a traction loop, adjustable clamps (Crile's), padded
forceps, or digital compression. A free incision parallel to the long axis of the sac is then
made down to the sac to expose its whole length. Any important nerves or veins should
be dissected away from it. The sac is then freely opened and emptied.
It is then ready for closure. In most cases it will be decided to obliterate the sac completely,
but in some cases of fusiform aneurism it may be preferable to leave a lumen the size of
the original artery.
When the sac is to be completely obliterated, the lining of the sac
is thoroughly scrubbed over its whole extent with sterile gauze soaked with salt solution
to remove the endothelial layer of the intima, and thus accelerate union. The sutures
(chromicized gut) are then applied very much like Lembert's intestinal sutures. The
most important point is to approximate carefully intima to intima. The sutures
are laid in three layers in such a way that the cross-section of the sac after suture is made
to form a Y; the first and deepest layer of sutures shutting off the sac from the artery at
the Y, and the third layer obliterating the cavities in each arm of the Y (Fig. 315, F).
In suturing a fusiform aneurism the lumen of the artery is preserved by placing the
first layer of sutures over a rubber tube which is inserted into the artery. After the new
lumen is thus provided for, the rest of the sac is scrubbed and the sutures laid in the usual
way. Care must be taken to preserve the blood supply and nutrition of the sac, and all
portions of it which have been dissected away from their vascular surroundings should be
excised.
In 1908 Matas reported the results of 86 such operations, including
aneurisms of the femoral, the iliofemoral, tibial, gluteal, external carotid,
ANEURISM. 557
axillary, brachial, and subclavian arteries, as well as the abdominal aorta
(the latter both fatal): 78 recoveries; 8 deaths; 4 cases of gangrene; 4 re-
lapses, all in operations where the lumen was restored. In view of the fact
that these 86 operations were performed by fifty-two different operators
the excellent results obtained are a striking argument in favor of the feasi-
bility of the operation.
BIBLIOGRAPHY.
ANEURISM.
More complete historical accounts are given by
Lobker: " Aneurysma," Eulenburg's Realencyclopaedie der ges. Heilk, Wien u. Leipz.,
1894, i, 560; and Osier, W.: Aneurism, Mod. Med., Phila. and N. Y., 1908, iv, 448; also
Gibson, G. A.: Diseases of the Heart and Aorta, Edinb. and Lond., 1898; to which the
writer acknowledges his indebtedness.
Arnsperger, H.: Die Aetiologie und Pathologic der Aortenaneurysmen, Deutsch. Arch. f.
klin. Med., Leipz., 1903, Ixxviii, 387.
Crisp: On the Structure, Diseases, and Injuries of the Blood-vessels, Lond., 1847.
Hare, H. A., and Holder: Some Facts in Regard to Aneurism of the Aorta, Am. J. M. Sci.,
Phila. and N. Y., 1899, cxviii, 399.
Gibbons, H. W., Jr.: Proc. San Francisco Med. Soc., Sept. 8, 1868; Pacific M. and S. J.,
N. S., ii, 213.
Richter, C. M.: Zur Statistik der Aneurysmen, u. s. w., Arch. f. klin. Chir., Berl., 1885,
xxxii, 524.
Lawson, and others quoted from Richter, Arnsperger and Lobker.
Le Boutillier, T.: A Case of Aneurism of the Transverse Portion of the Aortic Arch in a
Girl of Nine Years, with Table of Reported Cases under Twenty Years of Age, Am. J.
M. Sci., Phila. and N. Y., 1903, cxxv, 778.
Helmstedter: Du mode de formation des aneurismes spontajies, Strassburg, 1873.
Roy, C. S.: The Elastic Properties of the Arterial Wall, J. Physiol., Camb. and Lond., 1881,
iii, 125. Note on the Elasticity Curve of Animal Tissues, ibid., 1888, ix, 227.
Grehant and Quinquaud: M£sure sur la pression necessaire pour determiner la rupture des
vaisseaux sanguins, J. de 1'Anat. et Physiol., Par., 1885, xxi, 287.
Koester: Ueber die Enstehung der spontanen Aneurysmen und die chronische Mesarteritis,
Berl. klin. Wchnschr., 1875, 322.
Fabris, A.: Experimentelle Untersuchungen ueber die Pathogenese der Aneurysmen, Arch.
f. path. Anat., u. s. w., Berl., 1901, clxv, 439.
Ophiils, W.: Some Notes on Arteriosclerosis of the Aorta, Am. J. M. Sc., Phila. and N. York,
1906.. cxxxi, 978.
Hirsch, J. L., and Robins, M. C.: A Case of Aneurism of the Aorta of Twenty-five Years'
Duration, Maryland M. J Baltimore, 1903, xlvi, 93.
Weinberger, M.: Ueber die Diagnostik und klinischen Verlauf der mycotisch-embolischen
Aneurysmen und Gefassrupturen, sowie der Influenzaendokarditis, Ztschr. f. klin.
Med., Berl., 1907, xlii, 457.
Libman, E.: Cases of Mycotic Aneurisms, Trans. N. Y. Path. Soc., April, 1905; and Mt.
Sinai Hosp. Rep., N. Y., 1905, 481. A Case of Embolic Aneurisms, Mt. Sinai Hosp.
Rep., N. Y., 1905, 488.
McCrae, J.: A Case of Multiple Mycotic Aneurysms of the First Part of the Aorta, J. Path.
and Bacter., Edinb. and Lond., 1905, x, 373.
Clarke, T. W.: Repeated Copious Haemoptoysis from an Aortic Aneurism Extending
into the Right Lung and finally Rupturing, Bull. Johns Hopkins Hosp., Bait., 1905,
xvi, 98.
Arnold, H. D.: Cause of Death in Aneurisms of the Thoracic Aorta which do not rupture;
Report of five cases, Am. J. M. Sci., Phila. and N. Y., 1902, cxxiii, 72.
Hare, H. A., and Holder, C. A.: Some Facts in regard to Aneurism of the Aorta, ibid., 1899,
cxviii, 399.
Broadbent, W. H. and J. H. F.: Heart Disease and Aneurysm of the Aorta, 4th edition,
N. Y., 1906.
558 DISEASES OF THE HEART AND AORTA.
Oliver, W. S.: Physical Diagnosis of Thoracic Aneurism, Lancet, Lond., 1878, ii, 406.
Sewall, H.: Some Considerations other than Aortic Aneurism which determine the Occur-
rence of the Tracheal Tug, Am. J. M. Sci., Phila. and N. Y., 1901, cxxii, 150.
Wenckebach, K. F. : Ueber pathologische Beziehungen zwischen Athmung und Kreislauf
beim Menschen, Samml. klin. Vortrage begr. v. R. Volkmann, Leipz., 1907, N. F. Inn.
Med., 140-141.
Smith, H. L.: A New Sign in Thoracic Aneurysm, Am. Med., Phila., 1902, iii, 814.
Franc. ois-Franck: Recherches cliniques et experimental es sur la valeur compared des
signes fournis par 1'examen du pouls radial dans les aneurysmes du tronc brachio-
cephalique de 1'aorta et de 1'artere sous claviere. Importance du retard du pouls,
J. de 1'anatomie et de la physiol. norm, et path, de 1'homme at des anim., Par., 1878,
xiv, 113. Recherches sur la diagnostic du siege des aneurismes de 1'aorta, ibid., 1879,
xv, 97.
Marey, E. J.: La circulation du sang a 1'etat physiologique et dans les maladies, Paris, 1881.
V. Ziemmsen, A. : Ueber den Pulsus differens und seine Bedeutung bei Erkrankungen des
Aortenbogens, Deutsch. Arch. f. klin. Med., Leipz., 1890, xlvi, 288.
Baetjer, F. H.: The X-ray Diagnosis of Thoracic Aneurysms, Bull. Johns Hopkins Hosp.,
Bait., 1906, xvii, 24.
Holzknecht, G.: Die Rontgenologische Diagnostik der Erkrankungen der Brusteingeweide,
Fortschr. a. d. Geb. d. Rontgenstr., Hamb., 1901, Erganzungsheft, 6.
Milanoff: Etude de la douleur et de quelques autres symptomes des aneurismes de 1'aorte
thoracique descendente, These, Par., 1900.
Andreef : Contribution a 1'etude des aneurismes de 1'aorte descendente, These, Toulouse, 1904.
Osier, W.: Aneurism of the Descending Thoracic Aorta, Internat. Clin., Phila., 1903,
xiii ser., i, 1.
Hewlett, A. W., and Clark, W. R. P.: The Symptoms of Descending Thoracic Aneurism,
Am. J. M. Sc., Phila. and N. Y., 1909, cxxxvii, 792.
Bostroem: Das geheilte Aneurysma dissecans, Deutsch. Arch. f. klin. Med., Leipz., 1887,
xlii, 1.
Schede, Fr.: Zur Aetiologie, Verlauf, und Heilung der Aneurysma dissecans der Aorta.
Arch. f. path. Anat. u. s..w., Berl., 1906, cxcii, 52.
MacCallum, W. G.: Dissecting Aneurism, Bull. Johns Hopkins Hosp., Bait., 1909, xx, 9.
Henschen, S. E.: Das Aneurysma Arteriae pulmonalis, Volkmann's Samml. klin. Vortrage,
Leipz., 1906. No. 422-423.
Albertini and Valsalva. Quoted from Gibson.
Tufnell, J.: The Successful Treatment of Aneurism by Consolidation of the Contents of
the Sac, Lond., 1875. The Successful Treatment of Aneurism by Position and Re-
stricted Diet, Trans. Med. Chir. Soc. Lond., 1874, Ivii, 83.
Taylor, A. E. : The Effects upon the Blood of the Tufnell Method and the Calcium Salts
in the Treatment of Aortic Aneurism, J. Exp. Med., N. Y., iii.
Lancereaux and Paulesco: Du traitement des anevrismes en general et de I'aneVrisme de
1'aorte en particulier par injections sous-cutane"es d'une solution gelatineuse, Bull,
de 1'Acad. de MeU, Par., 1897.
Futcher, T. B.: The Treatment of Aneurisms by Subcutaneous Gelatin Injections, J. Am.
M. Asso., Chicago, 1900, 204.
Bouillaud: Gaz. des hop., Par., 1859, 61.
Chuckerbutty: Brit. M. J., Lond., 1862, ii, 61, 85. Quoted from Balfour.
Balfour, G. W.: On the Treatment of Aneurism by Iodide of Potassium, Edinb. M. J., 1869,
xiv, 33. Further Observations on the Treatment of Aneurism with Iodide of Potas-
sium, ibid., 1870, xv, 47.
Moore, C. H.: On a New Method of Procuring the Consolidation of Fibrin in Certain Incur-
able Aneurisms, Trans. Med. Chir. Soc., Lond., 1864, xlvii, 129.
Murchison, C.: Report of a Case of Saccular Aneurism of the Ascending Aorta projecting
through the Anterior Wall of the Left Side of the Chest, ibid., 136.
Pe"trequin: Suite et fin du me"moire concernant une nouvelle me"thode pour gue"rir certains
aneurismes sans operation a 1'aide du galvanopuncture, Rec. d. trav. Soc. med. d.
Indre-et-Loire, Tours, 1845, 117; also Compt, rend, de 1'Acad. d. Sc., Paris, 1845,
xxi, 992.
Ciniselli, L. : Osservazione di aneurismi dell' aorta trattati coll elettropuntura, Gior. d. r.
Accad. di med. di Torino, 1872, 35, xii, 418; Gazz. Med. di Milano, 1847, vi, 9.
ANEURISM. 559
Hunner, G. L.: Aneurism of the Aorta treated by Insertion of a Permanent Wire and
Galvanism (Moore-Corradi Method), Bull. Johns Hopkins Hosp., Bait., 1900, xi, 263.
Rosenstirn, J. : The Surgical Treatment of a Case of Aneurism of the Arcus Aortae, with a
Case cured by the Loreta-Barwell Method, Am. J. M. Sci., Phila. and N. Y., 1891, ci, 55.
Murray, W. : An Account of a Case of Aneurism of the Abdominal Aorta which was cured
by Compression of that Artery immediately above the Tumor, Trans. Med. Chir. Soc.
Lond., 1864, xlvii, 187.
Shepherd, F. J.: Digital Compression for Aneurism, Montreal M. J., 1903, xxxii, 70.
Bryant, Lunn and Berham, Skerritt, Paget. Quoted from Pringle, J. J.: A Case of Aneu-
rism of the Abdominal Aorta treated by Laparotomy and the Introduction of Steel
Wire into the Sac, Trans. Med. Chir. Soc. Lond., 1887, Ixx, 261.
For details of the various ligatures see
Lobker: Aneurisma, Eulenberg's Realencycl. d. ges. Heilk., Wien und Leipz., 3d ed., 1894,
i, 560, or Ref. Handb. Med. Sc., or various text-books of surgery.
Sheen, W.: Results of Ligature of the Innominate Artery, Ann. Surg., Phila., 1905, xlii, 1.
Halsted, W. S.: Partial, Progressive and Complete Occlusion of the Aorta and other Large
Arteries in the Dog by Means of the Metal Band, J. Exp. Med., N. York, 1909, xi, 373.
The Partial Occlusion of Blood-vessels, especially of the Abdominal Aorta, Bull.
Johns Hopkins Hosp., Bait., 1905, xvi, 346.
Matas, R. : An Operation for the Radical Cure of Aneurism based upon Arteriorrhaphy,
Ann. Surg., Phila., 1903, xxxvii, 1903. J. Am. M. Asso., Chicago, 1906. Statistics
of Endoaneurismorrhaphy, or the Radical Cure of Aneurism by Intrasaccular Suture,
ibid., 1908, li, 1667.
PART IV.
i.
PAROXYSMAL TACHYCARDIA.
COTTON in 1867 described a peculiar condition in which attacks of
extreme tachycardia were present, leaving the heart quite normal in the
interim. Similar cases were reported by Bensen, Nothnagel, Proebsting,
Priesendorfer, Pribram, and Bristowe> who considered them to be due to
a sort of vagus neurosis. Bouveret, however, regarded the condition as
a distinct clinical entity, of which he was able in 1889 to collect over
twenty cases from the literature, and which he designated as " essential
(or idiopathic) paroxysmal tachycardia (tachycardie paroxystique essen-
tielle)". According to Bouveret, this condition is characterized by
attacks in which the pulse suddenly attains a rapidity
(200 to 300 per minute) which is never seen in any other con-
dition, even in the gravest heart failures. These attacks last from
several minutes to several days or even weeks, and subside as sud-
denly as they come. They sometimes recur for years and often for
decades without seriously interfering with life and general health of the
patient; or, on the other hand, an attack sometimes ends in death.
Bouveret's clinical description was so complete that, though many
cases were subsequently reported, little that was essential was added until
Aug. Hoffmann in 1900 called attention to the fact that the paroxysms of
tachycardia began and ceased with extreme suddenness, and showed by
excellent tracings that the complete change of rate often occurred within
the period of a single cardiac cycle. Moreover, he showed that this
change of rate was an exact doubling, trebling, or quad-
rupling of the previous rate, and ended by halving, quartering or drop-
ping to one-third. For example, the normal pulse-rate being 70, the rate
during an attack might be 140, 210, 280 per minute, and vice versa. Hoff-
mann regarded this sudden complete change of rate as
characteristic of the essential or idiopathic paroxys-
mal tachycardia, in contrast to the simple tachycardia
of exercise, excitement, or convalescence, in which the
change of rate is due to loss of vagus tone and comes
on by a gradual increase of rate during a period of from one
to several minutes. Such a tachycardia rarely exceeds 120 to 140 per min-
ute. Even though it may give rise to sharp attacks coming on more or
less suddenly and accompanied by palpitation, it is not to be regarded
as idiopathic (essential) paroxysmal tachycardia, but will be considered
under the simple nervous affections of the heart (Chapter III).
560
PAROXYSMAL TACHYCARDIA.
561
As will be seen, one cannot lay too much stress upon
the importance of distinguishing between "paroxysms
of tachycardia" and "idiopathic paroxysmal tachycar-
dia." Only those cases should be considered in which the mode of
onset and cessation of the attack is carefully given, if possible with venous
pulse tracings. The mechanism involved in the attacks should also be
noted. It is only in this way, and not by indiscriminate analyses of cases
in which the heart occasionally becomes rapid, that an accurate knowledge
of the condition can be acquired. The accurate knowledge of paroxysmal
tachycardia, therefore, dates from Hoffmann's analysis of pulse tracings.
FIG. 317. — Venous pulse in a case of paroxysmal tachycardia (G. D. R.). (Kindness of the Johns
Hopkins Hospital Bulletin.) A. During the attack (pulse-rate 144 per minute). Ventricular type of
venous pulse, no a wave discernible, c, carotid wave. Time of the carotid wave. B. Tracing taken five
minutes later, just after cessation of the attack. Pulse-rate 80. Venous pulse of the normal auricular
type, conduction time (n-c interval) normal. C. Tracing from the same case taken during a period of
irregularity a few days later, showing extrasystoles with shortened conduction time. The intervals are
measured in millimetres upon a uniformly running drum.
Still more accurate knowledge came with the analysis of venous tracings as
well, and of tracings obtained at the moments when the attacks began
and ceased.
Types of Paroxysmal Tachycardia. — By this means several types of
venous tracings have been recorded:
1. Attacks of tachycardia in which the auricular type of venous pulse
remains, and in which, at the cessation of the attack, the auricles continue
for a while at least at their old rhythm, the rate of the ventricles falling to
half or less by the onset of a partial auriculo(atrio) ventricular block and
a 2 : 1 rhythm (cases reported by Hoffmann, Gerhardt, Rihl, and Schmoll).
There may be periods of irregularity between, especially just before and
just after, attacks due to the occurrence of partial block for occasional
beats. The partial block even in these cases does not persist indefinitely,
but the rate of the auricles finally also becomes slow, and a 1 : 1 rhythm at
the slow (normal) rate is resumed.
36
562 DISEASES OF THE HEART AND AORTA.
2. Attacks in which the venous pulse is of the ventricular type (see
page 57) with no wave due to auricular contraction, and which subside sud-
denly with approximate halving or quartering of the rate without signs of
auriculo(atrio) ventricular block, the venous pulse between attacks show-
ing only a single auricular wave for each ventricular contraction. Between
attacks there may be an irregularity due to the presence of extrasystoles
with shortened conduction time. Cases of this type have been studied by
Mackenzie, Hirschfelder, Hay, and others.
A careful analysis of the pulse-rate during and between attacks shows
that the rate is by no means always a definite multiple, but varies within
FIG. 318. — Diagram showing the various types of tachycardia. I. Simple non-paroxysmal tachy-
cardia, showing the gradual increase and gradual decrease in rate. JUG, venous pulse; A, auricular
impulses; V, ventricular impulses; A-V, auriculoventricular conduction. II. Paroxysmal tachycar-
dia, with persistent auricular contraction and ending in auriculoventricular heart-block (2 : 1 rhythm).
III. Paroxysmal tachycardia with auricular fibrillation and ventricular type of venous pulse.
considerable limits (as for example, from 1.7 to 2.1 : 1; 88 to 140 and vice
versa 70 to 160) even when tracings are obtained from the instant of onset
or of cessation of an attack.
OCCURRENCE AND ASSOCIATED LESIONS.
Paroxysmal tachycardia is equally common in both sexes (Bouveret,
Hoffmann). It occurs at all ages, frequently beginning in early childhood
and persisting for decades. On the other hand, it frequently occurs in old
persons, as in G. R. who was 72 years of age. It is not usually associated
with valvular or organic disease of the heart, though the occasional attacks
of sudden tachycardias often seen in aortic insufficiency may belong to
this group.
Sometimes, as in the cases reported by Romberg, there is associated
coronary sclerosis — a group which seems to be particularly common. This
seems to correspond to the experimental observation that shortly before
death the auricles of the exposed dog's heart sometimes pass into fibrillary
contractions for a short period upon the slightest mechanical irritation, as
well as to the experiments of T. Lewis. The writer has encountered a num-
ber of cases associated with mitral stenosis.
The autopsy findings of Mackenzie and Keith, patches of fibrous myo-
carditis in the vicinity of the His bundle and coronary sinus, are of great
interest, but await further observations before they can be accepted as the
PAROXYSMAL TACHYCARDIA.
563
pathogenetic lesion. On the other hand, tumors, patches of fibrosis, and
arteriosclerosis in the vicinity of the vagus nucleus in the medulla, adhesions
along the course of the vagus (Reinhold, Hoffmann, Pitres, Oppenheimer,
Schlesinger, Pal), multiple sclerosis (Miiller), early tabes (Hirschberg) are
sometimes found. However, S. Hyman, in Sir Victor Horsley's laboratory,
has produced permanent lesions of the vagal nuclei in a series of dogs
and monkeys without ever giving rise to paroxysms of tachycardia.
Nevertheless, it is conceivable that continued reflexes from irritation of
nerves through pressure of tumors from hernias, intestinal parasites, etc.,
may increase the irritability of the heart muscle just as they often increase
that of the cerebral cortex. Indeed, paroxysmal tachycardia bears certain
superficial resemblances to a condition of "epilepsy of the heart," and is
occasionally associated with idiopatfyic epilepsy (Nothnagel, Schlesinger).
In a number of cases 'collected by Hoffmann disturbances of the digestive
and pelvic organs. fyere found, in some, cases floating kidney. In some
IS
FIG. 319. — Experimental paroxysm of tachycardia produced by faradization of the dog's auricle.
(Kindness of the Journal of the American Medical Association.) ST 1, 2, 3, 4, 5, faradic stimulation of
the right auricular appendix; A, auricular systoles; V, ventricular systoles. Time in seconds.
cases the attacks date from an acute cardiac overstrain; in others from
an attack of rheumatism, with or without other cardiac complications.
However, the writer can confirm the statement of Hoffmann, that in
many cases neither the underlying condition nor the factors bringing
on the attack can be discovered.
Onset. — The attacks themselves often occur at the moment of awak-
ing from sleep, after or during defecation, during conditions of fatigue,
and are sometimes brought on by nervous excitement, as was the case in
the second attack of one of our patients. Mere percussion of the precordium
has been known to bring on an attack (Bouveret). Change in the position
of the body from the horizontal to the vertical may bring on an attack
(orthostatic paroxysmal tachycardia).
NATURE OF FUNCTIONAL DISTURBANCES.
The nature of the functional disturbance is still obscure, though
several theories have been advanced. Hoffmann, Lommel, Gerhardt,
and Mackenzie at first believed that it consisted in the interpolation
of an extr# systole between each two regular systoles,
calling attention to the fact that the arterial pulse often showed an alterna-
tion of large and small beats; but Bayliss and Starling, Hirschfelder, and
others have been able to show that this indicates that the rate is a little
564 DISEASES OF THE HEART AND AORTA.
too fast for the optimum contractions of the ventricles rather than that
the small systoles are of abnormal origin.
Hoffmann (1904) suggested that the sudden change of rate (to approxi-
mate multiples or fractions of that pre-existing) represented the coming
on or the passing off of a block between the site at which the cardiac im-
pulses arise (remains of embryological sinus, the area bounded by the vena?
cavse, coronary sinus, and septum auriculorum and in front by the Eusta-
chian valve) and the auricular muscle tissue — a true sino-auricular
block. Just as in the cases of atrioventricular block above mentioned,
the attacks would thus correspond to the periods when the block has passed
off, the return to normal pulse corresponding to the onset of block. How-
ever alluring this theory may be, it must be admitted that there is at pres-
ent little evidence to support it.
More plausible is the theory of Mackenzie (1903-04), that these attacks
are brought about by a condition in which the (Purkinje) cells of
the His auriculo- (atrio-) ventricular bundle initiate
the rhythm of the beat instead of the sinus. This theory
is founded not only upon the above-mentioned venous tracings, but also
upon the statement of Gaskell that, if one "touch the auriculoventricular
ring of muscle (in the frog) with the slightest stimulus, immediately a
series of rhythmical contractions occurs/' while touching the auricular
and ventricular muscle causes only a single contraction in each case. In
mammals, however, the evidence upon this point is very flimsy, for it
has been impossible to stimulate the fibres of the atrioventricular bundle
alone without including fibres of the auricles and ventricles. Lohmann,
it is true, stimulated the region of the auriculoventric-
ular bundle (including the auricular and ventricular muscle) and
obtained simultaneous contractions of the auricles and ventricles, which
outlasted the period of stimulation. Erlanger has obtained somewhat
similar results, but does not regard them as conclusive. Hering and
Rihl obtained extrasystoles with shortened conduction time and assumed
that they arose in the bundle of His. Mackenzie and Keith, however,
claim to have found deposits of cells whose cicatrization "irritates the
bundle and renders it more excitable than the sinus. The contraction
of the heart then originates from this more irritable part. Somewhat
analogous changes follow in cardiosclerosis and in degeneration of the
coronary arteries."
Hi rschf elder, however, has been able to duplicate exactly
the findings of Lohmann and Hering by faradic stimulation of
the exposed dog's auricle, not in the vicinity of the auriculoventricular bundle,
but far out upon the auricular appendix. Under these conditions he obtained the follow-
ing results: Very weak faradic stimuli caused the occurrence of ordinary auricular
extrasystoles with normal conduction time, slightly stronger stimuli caused the
auricles suddenly to assume a rapid regular rhythm approximately double the previous
rhythm (the ratio varying from 1.7 to 2.1 to 1). The ventricles usually followed perfectly.
Conduction time was prolonged. Long continuance or repetition of this stimulation
or increase in the faradic stimulus increased the irritability of the auricular
muscle (perhaps also that of the Purkinje fibres). The first effect was shortening
of the conduction time. With still more increased or more frequently repeated
stimuli the auricles went into fibrillary contractions (delirium) upon
slight stimulation, the fibrillation, at first lasting only during the period of stimulation;
PAROXYSMAL TACHYCARDIA. 565
later or with stronger stimuli, outlasting the period of stimulus. When the stimulus and
the abnormal auricular contractions were only instantaneous, extrasystoles with shortened
conduction time were present (auriculo(atrio)ventricular extrasystoles), just as in the
writer's case of paroxysmal tachycardia. When the fibrillation was prolonged, a
long period of ventricular tachycardia accompanied it, sometimes lasting for many minutes,
and ending by a sudden return to the original rhythm with nor-
mal auricular rate, force, and normal conduction time. In the
less irritable hearts these attacks may be brought to a stand-
still by stimulation of the vagus, but as irritability increases the tachy-
cardia returns. It is found that the whole heart may be stopped by vagus stimulation,
but the tachycardia is resumed as soon as vagus stimulation ceases! Moreover, Cushny
and Edmunds who have investigated paroxysmal irregularities with tachycardia in man
and animals have found that, just as in the cases of paroxysmal tachycardia, the venous
pulse assumes the ventricular type during fibrillation of the auricles. This condition repre-
sents the nearest approximation to paroxysmal tachycardia which has been produced ex-
perimentally, and has led the writer to the hypothesis that " true (idiopathic) paroxysmal
tachycardia is usually caused by some one of a number of conditions which bring about a
state of increased irritability of the heart muscle, especially of the auricles, which may
pass into a state of fibrillation." It is possible that cells of the atrioventricular bundle
may either primarily or secondarily give rise to the impulse.
CAROTID PRESSURE ^yV-
VOLUME OF VENTRICLES
VENOUS PRESSURE
FIG. 320. — Diagram showing the effect of a paroxysm of tachycardia upon the circulation. The under-
lined portion indicates the paroxysm.
Whether the stimulus originates in the Purkinje fibres or elsewhere
seems for the present to have little practical importance. More important
is the fact that Reid Hunt, Cushny and Edmunds, Garrey and Hewlett,
and the writer have observed that such paroxysms may occur not only
spontaneously or from direct stimulation of the heart muscle, but also
upon stimulating the cardiac nerves, either accelerator or vago-sympa-
thetic, in hearts whose irritability is already abnormally high. Hence it
is natural that when the cardiac irritability is high, small reflex stimuli
bring about an attack.
Stimulation of Cardiac Nerves. — That something more than mere
neurogenic influences is essential was shown by Gerhardt and Hirschfelder.
These observers paralyzed the vagi of such patients with
atropine and yet produced no attack. Hirschfelder found
that slight stimulation of the accelerators, by exercising his patient to the
point of giddiness twenty-four hours after an attack and while his vagi
were paralyzed with atropine, caused a slight gradual increase of pulse-rate,
but nothing resembling an attack of paroxysmal tachycardia. The con-
dition of extreme irritability of the cardiac muscle had evidently passed off.
Paroxysmal Tachycardia from Coronary Ischaemia. — Quite recently T. Lewis
(Paroxysmal Tachycardia, Heart, Lond., 1909, i, 42) has succeeded in producing
paroxysms of tachycardia in cats and dogs by ligating one of
the coronary arteries, especially the right. These attacks come on
even after section of both vagosympathetic nerves, and hence were not neuro-
genic in origin. He has been able to obtain four types of abnormal cardiac cycles
566 DISEASES OF THE HEART AND AORTA.
during such paroxysms: 1. Approximate doubling of the rates of both auricles and ven-
tricles, with normal or slightly diminished conductivity; 2. Approximate doubling of
these rates of these chambers, but the auricles and ventricles contract simultaneously
(nodal rhythm?); 3. Fibrillation of the auricles with approximate doubling of rate in
the ventricles; 4. Approximate doubling of rate in both auricles and ventricles, but the
ventricles contract before the auricles (ventricular tachycardia). The writer has also
obtained all of these four types during faradization of the auricles, so that it would
appear that they may all be traced to a common cause, most probably over-excitability
of the heart muscle. Moreover, Rothberger and Winterberg have obtained electrocardio-
grams with small irregular waves, suggestive of auricular fibrillation, from a patient with
paroxysmal tachycardia, and Professor Barker, Dr. Bond, and the writer have recently
obtained a similar tracing from a patient between paroxysms, though electrocardiograms
from another patient in the midst of a severe paroxysm showed apparently normal
contractions of the auricles. Rothberger and Winterberg have obtained exactly similar
electrocardiograms from animals with exposed hearts in which they produced a state of
auricular fibrillation by faradization of the auricles.
This coronary form of paroxysmal tachycardia is exactly similar to the cases of
Romberg and Barker (page 283), but it is by no means certain that this factor is the
causal one in all cases of paroxysmal tachycardia.
EFFECTS ON CIRCULATION.
The effect which these paroxysms of tachycardia exert upon the circu-
lation is primarily due to the deficient filling of ventricles during the short
diastoles. As Yandell Henderson has shown, the ventricles fill to their
normal extent only when the pulse-rate is moderately slow. When the
pulse becomes rapid, the ventricles do not have time to fill, and, since the
period of systole is never much less than 0.2 second, it is evident that when
the heart-rate is much above 200 the period during which filling can take
place is very short and little blood can enter the ventricles. The volume
of the heart remains small. As a result of this condition, blood stagnates
in auricles and veins, venous pressure rises (to 30 cm. H2O in one case
examined by Eyster and Hooker), and with it there come engorgement of
the liver and oedema of the extremities. Stasis also occurs in the pulmonary
veins, ushering in oedema and dyspnoea, and sometimes these symptoms
of broken pulmonary compensation dominate the scene (see page 139).
On the other hand, the arterial pressure falls, because, as the filling
of the ventricle is small, the amount which is driven out into the arteries
is diminished correspondingly. This fall in blood-pressure is usually accom-
panied by pallor and often by symptoms of cerebral anaemia, exactly as
occurs in hemorrhage, surgical shock, or other conditions in which the
amount of blood in the arteries is diminished. Other organs also suffer
from anaemia, and finally also the heart itself, which may give signs of weak-
ening, first evinced by lowered tonus and dilatation. It is evident that hearts
whose coronary arteries are sclerotic would suffer more readily than those
with normal blood supply.
PHYSIOLOGICAL SUMMARY.
The pathological physiology of paroxysmal tachycardia may therefore
be suirfmed up as follows;
Underlying causes: Increased irritability of cardiac muscle.
Predisposing factors for an attack: Slight reflex stim-
ulations of cardiac nerves.
PAROXYSMAL TACHYCARDIA. 567
Condition during attack: "Doubling" or multiplication
of pulse-rate, with or without auricular fibrillation.
Mechanical effects on the circulation, to which these
symptoms are referable:
1. Systemic stasis, high venous pressure.
2. Pulmonary stasis, high pressure in pulmonary veins.
3. Anaemia of brain, kidneys, and heart, from low arterial pressure.
SYMPTOMS.
Although attacks of tachycardia sometimes run their course without
the patient's knowledge, it is more common for them to be accompanied
by symptoms. These symptoms may be grouped as follows:
1. Symptoms of cardiac excitability.
2. Those due to engorgement of systemic veins (failure of right ven-
tricle) .
3. Those due to engorgement of pulmonary veins (failure of left
ventricle) .
4. Those due to cerebral anaemia.
1. Palpitation, a feeling of discomfort or oppression in the pre-
cordium, and weakness are the most common symptoms. This is often
worse just at the end of the attack, and may, as in Hay's case, resemble
the symptoms of angina pectoris. In this case there was also hyperaBsthesia
of the precordium and neck. The latter may be due to engorgement of
the cervical veins, as in angina pectoris it may be referred from the heart
(Mackenzie).
2. Besides the above-mentioned feeling of fulness in the
neck, the patient often has a similar feeling in the abdomen from dis-
tention of the liver, and swelling of the feet commonly appears before the
end of the attack.
3. Dyspnoea is frequent. It is striking that this may occur with-
out any change in the rate of respiration, even in cases with severe myo-
cardial changes (Romberg). No doubt this is associated with engorgement
and high pressure in the pulmonary veins. It is often accompanied by
cough and the expectoration of mucus, sometimes containing large endo-
thelial cells with blood pigment (Herzfehlerzellen). Occasionally there is
actual hemoptysis (in three of Bouveret's eleven cases) during the attack.
Actual pulmonary oedema may indeed set in, as in Pribram's case, — a
young woman otherwise healthy, whose attacks were so severe that "the
pulse became barely palpable. The patient fell into a state of collapse,
and finally redema appeared in the lower part of the lungs. At the moment
when death seemed imminent, when collapse was at its height, she gave
a cry of anguish; it seemed to her as though something were taken out of
her neck, and the scene suddenly changed. The pulse fell to 76, became
large and full, and the collapse disappeared."
On the other hand, this sudden change does not always occur, and
death sometimes supervenes during the attack.
The venous stasis also leads to albuminuria, though in the milder
attacks the urine may be increased and of low specific gravity.
568 DISEASES OF THE HEART AND AORTA.
4. The fall in arterial pressure usually brings about symptoms
of cerebral anaemia; weakness, vertigo, and even extreme nerv-
ousness is the rule during the attacks, accompanied by restlessness, loss
of appetite, and inability to sleep. Even syncope may occur. In a gentle-
man whom the writer examined some years ago these syncopal attacks
had led several prominent physicians to diagnose Adams-Stokes syndrome ;
when, as was shown by the examination and subsequent observation,
the cerebral anaemia resulted not from bradycardia but from tachycardia.
Fortunately, these attacks have a tendency to become milder. Dr. Lyon
writes, three years after the first examination, that this patient "is now
able to play cards, go fishing, and do almost anything in a quiet way during
attacks/'
PHYSICAL SIGNS.
Physical signs are absent between attacks of par-
oxysmal tachycardia. During the attacks the face is usually
pale, the expression anxious, the pupils are equal, the veins of the neck
are seen to be engorged and often to show a positive ''single'
pulsation accompanying each systole (sometimes due to transitory
tricuspid insufficiency), perhaps due to the feebleness of the auricular con-
tractions. The tumultuous heart action is often seen in a precordial heav-
ing and well-marked apex beat. The area of cardiac dulness is rarely
increased except toward the end of the attack. It is usually un-
changed or decreased in size, corresponding to the diminished
filling of the ventricles. This diminution in the size of the heart
during an attack has been seen with the fluoroscope by Hoffman, Dietlen,
and others, and it can be demonstrated in the experimental paroxysms.
Towards the end of severe attacks dilatation sets in from cardiac weakness.
The heart sounds may be unchanged, but usually become short and
somewhat muffled. There is often embryocardia. It is very common to
hear a soft systolic over the right ventricle and apex, perhaps due to a,
mitral or tricuspid insufficiency of the papillary type.
Sometimes the cardiac rhythm is irregular, owing to inability of the
ventricles to follow all the impulses from the sinus and auricles or to the
presence of extrasystoles. The liver often is felt to be enlarged, and often
shows a systolic pulsation during attacks (tricuspid insufficiency), but
ascites rarely occurs. (Edema of the ankles and feet is very frequent.
CASE OF PAROXYSMAL TACHYCARDIA.
G. D. R., a hotel-keeper aged 72, was admitted to the Johns Hopkins Hospital on
Feb. 22, 1906, complaining of palpitation of the heart. The family history and personal
history were negative. The patient had always been a robust man, had had no infec-
tious diseases and no other cardiac manifestations.
The first attack of palpitation and tachycardia came on suddenly after
retiring one evening twenty years before admission. It caused him great
fear, but no pain. The attack lasted six hours and left him weak but other-
wise well. Attacks similar in character recurred once a month until the winter of
1905-1906, when they became more severe and began to occur once or twice a week.
During the attacks he passed large amounts of urine. He never noticed palpitation
between attacks of tachycardia.
PAROXYSMAL TACHYCARDIA. 569
The patient was a large well-nourished man of good color. His pupils were equal
and reacted well to light and during accommodation. The thorax was rather barrel-
shaped; the percussion note was hyperresonant, and the breath-sounds were clear, though
distant. The cardiac impulse was neither seen nor felt, but the apex, as made out by per-
cussion and auscultation, was situated in the fifth left interspace 11 cm. from the midline.
The cardiac dulness extended up to the upper border of the third rib, but could not be
made out to the right of the sternum. The sounds were distant, but clear. The pulse-
rate between attacks was 64 per minute. It was usually regular in force and rhythm,
of good volume and rather high tension; the blood-pressure ranged from 165 to 190, the
minimum from 100 to 115.
The abdomen was large and flabby, with considerable panniculus. Liver and
spleen were not palpable. The examination was otherwise negative. The venous pulse
between attacks was usually normal.
On Feb. 23 and March 1 and 15 the patient had attacks of tachycardia,
in which his pulse-rate rose suddenly from 80 to 88 per minute
to a height of 144 to 160 per minute. The attack of March 15 began just
after returning from the closet, where he had passed a soft fluid stool. Tracings made
from the patient during this attack showed what is probably a ventricular type of venous
pulse during the attack. When the latter ceased, however, the pulse
resumed the normal auricular type. There was no sign of auriculoven-
tricular block. Excitement incident to being shown at the clinic precipitated a second
attack on March 15, which was not relieved by the application of an ice-bag, yawning,
deep breathing, pressure on the vagus, in front of the sternocleidomastoid, nor by admin-
istration of spiritus aetheris nitrosi, amyl nitrite, or digitalin. The attack ceased spon-
taneously within an instant, at 3.10 p.m.
On March 21 his pulse was irregular, due to the presence of numerous extra-
systoles with shortened conduction time (auriculo ventricular?). These
subsided, however, leaving his pulse regular. On March 24 his pulse remained at 76 in
spite of the administration of 2mg. atropine. Even rapid walking while he was under
the influence of the atropine did not bring on an attack, nor did the administration of
amyl nitrite on March 24.
A very well-defined case of tricuspid insufficiency resulting from the
cardiac overstrain of a prolonged paroxysm of tachycardia is exemplified
by the following patient seen in consultation with Professor Barker.
CASE OF LONG-STANDING PAROXYSMAL TACHYCARDIA.
W. W. C., clerk in the U. S. Patent Office, aged 29, had always been healthy except
for a very severe attack of gonorrhoea six years before admission. He had no cardiac
disturbance until seven years ago (one year before the attack of gonorrhoea), when he had
symptoms of slight cardiac weakness which was said to be valvular ( ?), but these ,
soon disappeared under treatment, so that1 he was able to dance and take all kinds of exer-
cise without symptoms. Two years before admission he awoke one morning,
after an emission, with severe palpitation and a very rapid
weak pulse. He was kept quiet, an ice-bag put to his chest, and he was given strych-
nine, 1.5 mg. (?V gr-)> also tincture of strophanthus. His pulse-rate dropped
to 72. Three weeks later he had another emission and another attack, and since then had
a large number. The attacks often come on after emissions, which leave him feeling very
much depressed. They subside very suddenly and the pulse returns
to normal at a bound, remaining between 70 and 100 per minute between attacks.
In the present attack, however, t h e p u 1 s e - r a t e has been rapid continu-
ously for over a year (since April, 1908), and this has been accom-
panied by palpitation and great weakness, occasionally by n a u s e a and vomit-
ing. It has not been relieved by strophanthin, digitalis, strychnine, nitroglycerin,
belladonna, or potassium bromide.
The patient is a pale, nervous-looking young man. The pupils are rather wide, but
there are none of the ocular signs of Basedow's disease. The thyroid is not enlarged. There
is no glandular enlargement. His chest is long and rather flat, but shows nothing of
importance.
570 DISEASES OF THE HEART AND AORTA.
The heart is much enlarged, the apex being located in the sixth left inter-
space 10.5 cm. from the midline. It is very movable within the chest, site altering 5 cm.
as the patient turns from side to side. There is a heaving impulse over the precordium,
with systolic retraction of the interspaces over the right ventricle and marked systolic
retraction in the epigastrium. Dulness extends above to the second inter-
space at the left sternal margin, and to the right reaches 5 cm. from the
midline. Longitudinal diameter, 20 cm. The area of flatness extends from the apex to
the level of the fourth rib and just beyondthe sternal margin in the fifth
right interspace. The heart sounds are heard at the apex, the first being accom-
panied and followed by a slight soft systolic murmur not transmitted to the axilla, while
the second is fairly distinct. The second pulmonic is accentuated, the second aortic clear.
There are no diastolic murmurs. The striking feature is a loud superficial
blowing systolic murmur heard over an elliptical area bounded
above by the level of the fourth interspace, to the left by a
point 9 cm. from the midline, below by the middle third of the
ensiform cartilage, and to the right by a point 1 cm. to the right of
the sternal margin. This represents the tricuspid area. The heart's
action is extremely rapid, about 180 per minute, and is irregular; the pulse still more so, as
about 40 beats per minute are ineffectual and do not open the aortic valves. The radial
pulse is therefore 140 per minute. The right jugular vein is rather full and shows a defi-
nite ''single'' systolic pulsation coincident with the apex beat. This is
borne out by the tracing, upon which there are no waves of auricular con-
traction. The pulse is small, of rather low tension, and very irregular. The vessel
wall is not sclerotic.
Blood-pressure with the Erlanger apparatus: Maximal varies from 100 to 110
mm. Hg: minimal varies from 70 to 80 mm.
The liver is much enlarged and extends almost to the level of the umbilicus.
Its surface is smooth, the edge round and fairly soft, but it does not pulsate.
His venous tracing is shown in Fig. 74, page 74.
The patient improved somewhat during his stay in the hospital; but his pulse
remained rapid, he was bedridden, and died two months later.
DIAGNOSIS.
In the cases in which the pulse-rate is above 160 per minute the diag-
nosis rarely presents any difficulty, for the tachycardias of simple nervous
origin, on the one hand, and those of organic cardiac disease rarely reach
that height. But in the border-line case in which the tachycardia is about
140, the diagnosis may be difficult. The crucial point in the differentiation
lies in the suddenness of the change of rate, and for this it is important
to have observed the beginning and the end of an attack, the sudden rise
to maximum rate within a few seconds indicating idiopathic paroxysmal
tachycardia, while a gradual step-like or progressive rise indicates a simple
tachycardia. Thus while the patient G. R. exemplifies the idiopathic con-
dition, the following case is typical of the simple tachycardia.
CASE OF SIMPLE EMOTIONAL TACHYCARDIA RESEMBLING IDIOPATHIC PAROXYSMAL
TACHYCARDIA.
The patient, a biological student at the University of Virginia, aged 20 years, had
recovered from an attack of typhoid fever about a year before. Previously to
this he had been strong and free from cardiac symptoms; but since convalescence
he is troubled with attacks of palpitation and tachycardia in
which the pulse-rate rises from about 60 to about 120 per minute. Slight mental
excitement and even the mere mention of taking a pulse tracing suffices to bring on
an attack. Before the apparatus could be applied he felt his pulse begin to rise. I n t he
successive quarters of a minute the pulse-rate was 15, 21, 26,
PAROXYSMAL TACHYCARDIA. 571
3 0 , having doubled itself within a single minute. But the change of rate was
not sudden!
Physiological examination was negative, heart not being enlarged and sounds normal.
The case was therefore considered a simple tachycardia. A favorable prognosis was given,
which was verified by the subsidence of tachycardia and palpitation within a few months.
TREATMENT.
Drugs. — As regards the treatment of paroxysmal tachycardia various
methods have been employed. The first essential is to put the patient
into the best possible physical condition, to treat any anaemia, digestive
disturbance, constipation, disturbance of vision, heaving, enteroptosis,
or other conditions which may bring about reflex irritations; to stop the
use of tea, coffee, tobacco, and alcohol, and so to arrange the life of the
patient as to do away with mental excitement, worry, over-exertion, and
fatigue. If necessary, a "rest cure" may be resorted to. These measures
may do much to diminish the frequency of the attacks, but often the latter
do not disappear altogether. Small doses of digitalis or aconite may be
tried in the interim between attacks, in the hope of keeping them down
by increasing the action of the vagus: or potassium bromide or valerian
may be given, in the hope of quieting the nervous system; but the desired
result is only occasionally obtained.
To quiet the attack after its onset drugs are of little avail.
Morphine, bromides, etc., and other sedatives may diminish the in-
tensity of the symptoms, but do not slow the heart-rate.
The administration of a few whiffs of chloroform, of amyl nitrite, nitro-
glycerin, Hoffman's anodyne, strychnine, digitalis and its derivatives
(digitalin, digalen), is without effect. Though large doses of strophan-
thin sometimes stop auricular fibrillation in animals, intravenous injection
of strophanthin has not given satisfactory results in three cases of par-
oxysmal tachycardia to whom it has been administered in the Johns Hop-
kins Hospital. Aconite also, though the best stimulant for the vagus,
was without clinical effect in the one case in which the writer used it.
The application of an ice-bag to the precordium sometimes relieves
the symptoms, but only rarely is a sufficient cardiac sedative to stop
an attack.
Mechanical Methods for Stopping the Attacks. — A novel method has recently been
suggested by Fairbrother based on experiments upon himself. He has found that he can
cause his own attacks to stop by any sudden or violent exercise during the attacks,
such as running, jumping, skipping rope, etc. Needless to say, these methods, if resorted
to in any individual case, should be superintended by the physician and used with the
utmost caution.
The paroxysms themselves may sometimes be stopped by various
mechanical methods which stimulate the vagi; deep inspirations (Noth-
nagel), especially yawning, "squeezing arms and elbows tightly against
the chest while holding breath and compressing abdomen" (Valsalva's
experiment with elbows compressed against chest) (Hay), swallowing,
especially of ice-water, or belching, may be successful.
Max Herz has found it possible to suppress many troublesome attacks in his patients
by bringing about belching in the following manner: The patient is made to sit down, fill
572 DISEASES OF THE HEART AND AORTA.
his mouth with water, bend his head backward as far as possible, and swallow. This not
only brings about a desire to belch, but also facilitates the eructation of a large amount of
gas, and frequently brings the attack to a close. Needless to say, care should be taken that
the belching does not pass over into continuous air swallowing and that the patient does
not acquire this pernicious habit (see page 604).
When belching fails to stop the attack, vomiting may be resorted
to, and frequently proves an effectual though unpleasant method. Tick-
ling the pharynx with the finger is usually sufficient to bring it about,
especially after swallowing some water. Emetics need not be used.
One of the oldest and best procedures (Bensen, 1880) is pressure
upon the vagus just to the left of the thyroid cartilage. The nerve
which is just behind the carotid artery is pressed very firmly against the
vertebrae and held tightly for two or three minutes. In a considerable
number of cases this stops the attack, but in many it fails, or succeeds for
a moment and then the tachycardia is resumed (Priesendorf er) , just as
is the case in the experimental auricular fibrillation.
However, when the results of all methods of treatment have been taken
into account, one is inclined to share the feelings expressed by Mackenzie
when he wrote: "In my early days I, too, thought I knew how to stop
attacks, but more extended experience has shown me that when they
stopped it was from some cause unknown to me and which was independent
of any means I employed."
BIBLIOGRAPHY.
PAROXYSMAL TACHYCARDIA.
Bouveret, L.: De la tachycardie paroxystique essentielle, Rev. de Med., Par., 1889, ix,
753, 836.
Hoffmann, Aug.: Die paroxysmale Tachycardie (Anfalle von Herzjagen), Wiesb., 1900.
Pathologic und Therapie der Herzneurosen, u.s.w., Wiesb., 1901. Neue Beobachtungen
ueber Herzjagen, Deutsch. Arch. f. klin. Med., Leipz., 1903, Ixxviii, 39. Ueber Ver-
doppelung der Herzfrequenz, Ztschr. f. klin. Med., Berl., 1904, liii, 206.
Rihl, J.: Analyse von fiinf Fallen von Ueberleitungstorungen, Ztschr. f. exp. Path. u.
Therap., Berl., 1905, ii. 83.
Schmoll, E.: Paroxysmal Tachycardia, Am. J. M. Sci., Phila. and N. Y., 1907, cxxxiv, 662.
Mackenzie, J.: On the Inception of the Rhythm of the Heart by the Ventricles, Brit. M. J.,
Lond., 1904, i, 529. New Methods in the Study of Affections of the Heart, ibid., 1905,
i, 813. Abnormal Inception of the Cardiac Rhythm, Quart. M. J., Oxford, 1907, i,
39. The Extrasystole: A Contribution to the Functional Pathology of the Primitive
Cardiac Tissue, ibid., 1908, i, 182 and 481. Diseases of the Heart, Lond., 1908.
Hirschfelder, A. D.: Observations upon Paroxysmal Tachycardia, Bull. Johns Hopkins
Hosp., Balto., 1906, xvii, 337.
Hay, J.: Paroxysmal Tachycardia, Edinb. M. J., 1907, N. S. xxi, 40.
Romberg, E.: Lehrbuch der Krankheiten des Herzens und der Blutgefasse, Stuttg., 1906.
The complete bibliography of cases will be found in the monograph of Hoffmann
and the articles of Reinhold, Schlesinger, and Schmoll.
Gerhardt, D.: Beitrage zur Lehre von den Ext rasy stolen, Deutsch. Arch. f. klin. Med.,
Leipz., 1905, Ixxxvii, 509. Lommel, F.: ibid 1905, Ixxxii, 495.
Bayliss, W. M., and Starling., E. H.: On some Points in the Innervation of the Mammalian
Heart, J. Physiol., Camb., 1892, xiii, 407.
Gaskell, W. H.: Schaefer's Text-book of Physiology, Edinb. and Lond., 1900, ii.
Lohmann, A.: Zur Automatic der Briickenfasern des Herzens., Arch. f. Physiol., Leipz.,
1904, 431, and Suppl., 265.
PAROXYSMAL TACHYCARDIA. 573
Bering, H. E., and Rihl, J.: Ueber atrioventrikulare Extrasystolen, Ztschr. f. exp. Path.
u. Therap., Berl., 1906, ii, 510. Experimentelle Untersuchungen ueber Herzunregel-
massigkeiten an Affen, ibid., 1906, ii, 525.
Hirschfelder, A. D.: Contributions to the Study of Auricular Fibrillation, Paroxysmal
Tachycardia, and the so-called Auriculo- (atrio-) ventricular Extrasystoles, Bull.
Johns Hopkins Hosp., Bait., 1908, xix, 323.
Cushny, A. R., and Edmunds, C. W.: Paroxysmal Irregularity of the Heart and Auricular
Fibrillation, Am. J. M. Sc., Phila. and N. Y., 1907, cxxxiii, 66. Studies in Pathology,
Quart. Publ., Aberdeen Univ., 1907.
Hunt, R.: Direct and Reflex Accelerations of the Mammalian Heart, Am. J. Physiol.,
Bost., 1899, ii, 395.
Carrey, W. E.: Effect of Chemicals on the Heart Nerves, Calif. State M. J., San Francisco,
1907. Some Effects of Cardiac Nerves upon Ventricular Fibrillation, Am. J. Physiol.,
Bost., 1908, xxi, 283.
Henderson, Y. (with the collaboration of M. McR. Scarborough and F. P. Chillingworth):
The Volume Curve of the Ventricles of the Mammalian Heart, etc., Am. J Physiol.,
Bost., 1906, xvi, 325.
Pribram, A.: Wien. med. Presse, 1882. Quoted from Bouveret. Lyon, I. P.: Personal
communication.
Dietlen, H.: Orthodiagraphische Beobachtungen ueber Veraenderungen der Herzgrosse
bei Infektionskrankheiten, exsudativer Perikarditis und paroxysmaler Tachykardie,
Muenchen med. Wchnschr., 1908, Iv, 2077.
Nothnagel. Quoted from Bouveret.
Fairbrother, H. C. : A Remedy for Paroxysmal Tachycardia, J. Am. M. Asso., Chicago,
1909, liii, 300.
Herz, M.: Ein Kunstgriff zur Unterdriickung der Anfalle von Angina Pectoris und paroxys-
maler Tachykardie, Wien. klin. Wchnschr., 1908, xxi, 803.
Bensen: Berl. klin. Wchnschr., 1880.
II.
THYROID HEART.
The cardiac disturbances associated with thyroid disease were the
most striking features observed by Parry in 1815 in the first described cases
of exophthalmic goitre. His first case died of heart failure. Graves (1835) ,
Basedow (1848), Stokes (1854), and Trousseau (1856) were also impressed
by the cardiac features of this disease. Trousseau found them especially
important in the "formes frustes " or " atypical " forms to which he called
attention, likening such cases to a defaced ("fruste") coin.
The important role which these "formes frustes" of Basedow's1
disease play in many cases of so-called cardiac neurasthenia and hysteria
has, since Trousseau, been recognized with increasing frequency, and espe-
cially since Friedrich Kraus in 1899 called attention to them by introducing
the term "Kropfherz" ("goitre heart" or thyroid heart), which is now
widely used in Germany.
FORMS OF CARDIAC DISTURBANCE DUE TO THYROID DISEASE.
Strictly speaking, as shown by Rose, Schranz, and Minnich, there is
some cardiac disturbance with all forms of goitre. Four main forms of
cardiac disturbance may thus be distinguished, due to:
I. Pressure of the goitre upon the trachea, bronchi, veins, chest,
and sympathetic ganglia (in simple goitre) , pneumo-mechanical
goitre heart (Rose) .
II. Hypothyroidism (in myxoedema, cretinism, and achondroplasia) .
III. Hyperthyroidism (exophthalmic goitre and formes frustes).
IV. Goitre secondary to the cardiac disease (goitre cardiaque, "car-
diac goitre").
CARDIAC DISTURBANCES FROM PRESSURE OF THE THYROID.
Potain in 1863 and Rose in 1878 reported cases of heart failure and
more or less sudden death in cases in which large colloid goitres pressed
upon the veins and trachea. Such a goitre has several mechanical effects:
1. It may prevent adequate filling of the lungs and thus
produce emphysema, deficient aeration of the blood, and later asphyxia.
The chronically deficient aeration of the blood may lead to secondary car-
diac overstrain and finally to myocardial weakness. This will be enhanced
by all pulmonary infections.
1 Basedow (" Bas-e-do ") . Dock after a careful study of priorities advises the accept-
ance of this name, which was the first unobjectionable term given and is the one most widely
accepted.
574
THYROID HEART. 575
2. The goitre often presses on the sympathetic ganglia on
one or both sides of the neck, thus stimulating the accelerators and bringing
on a chronic tachycardia just as is produced in Basedow's disease. Miiller's
muscle in the orbit may also be stimulated and exophthalmos produced.
This exophthalmos is often unilateral. The condition of exoph-
thalmos and tachycardia from the pressure of a simple
goitre is known as pseudo-Basedow's disease.1
CASE OF SIMPLE GOITRE RESEMBLING BASEDOW'S DISEASE. •
Such a case is represented by that reported by Potain in 1863 :2 M. K., servant girl,
aged 50. Complains of palpitation, feeling of pressure in chest, attacks of suffocation,
irregular menstruation. She has had goitre all her life, unaffected by iodine treatment.
For some years her eyes have been larger than before. She has lost weight, has suffered
from dyspnoea especially on exertion, she has throbbing of the goitre, and her legs are
swollen. Her pulse is 152, irregular. Apex is in the sixth interspace 13 cm. from midline.
There is heaving of the entire precordium. At the apex and over the precordium there is
a meso-systolic murmur. The veins of the neck are dilated. There is a large goitre which
does not pulsate and no murmur is heard over it. Digitalis is without effect,
and the patient died from pulmonary cedema 11 days after admission.
Autopsy showed colloid cystic goitre with some hemorrhages from stasis, slight
infarction of the lungs, and a somewhat enlarged, very flabby heart.
The livor, orthopnoea, asphyxia, and sudden death, as in Rose's case,
are due to pressure upon the air-passages, and are to be regarded as cardiac
symptoms. The respiratory origin of this suffocation is seen in the very
marked inspiratory (not systolic) retraction of all the thoracic interspaces.
CARDIAC AFFECTIONS OF HYPOTHYROIDISM (CARDIOPATHIA
THYREOPRIVEA) (KRAUS).
In all the conditions in which there is atrophy of the glandular tissue
of the thyroid and diminution in the internal secretion of the gland, there
are symptoms of cardiac weakness. The patients get out of breath on very
slight exertion. The pulse is small and weak, but may be either slow or
slightly accelerated (Kraus). This is due to the fact that the physiological
vagus tone is largely due to the thyroid secretion (v. Cyon), and when it
is deficient there is an overstimulation of the accelerators. However, as
Kraus points out, the cardiac features in cachexia thyreoprivea are not
prominent features of the disease, and hence are of little importance in
connection with diseases of the heart.
Revilliod has, however, called attention to another effect of hypo-
thyroidism upon the circulation, namely, early arteriosclerosis with cal-
careous deposits. This effect has also been produced by v. Eiselsberg in
new-born lambs from which he removed the thyroid glands. In contrast
to other experimental arteriosclerosis, the arterial changes affected the
intima and not the media.
1 In some cases, however, this is not due to pressure on the sympathetic but to the
activation of thyreoglobulin by the iodine treatment. Occasionally, moreover, a goitre
shows in one part colloid degeneration, in another hyperplasia like that of Basedow's disease.
2 Bull, de la Soc. d'Anat. de Paris, 1863, p. 87, quoted from Minnich.
576
DISEASES OF THE HEART AND AORTA.
DISTURBANCES DUE TO HYPERTHYROIDISM.
Basedow's Disease (also "Formes frustes," and Accidental Hyperthyroidism
in the Treatment of Obesity) .
As stated above, these conditions present the most important cardiac
features which are due to disturbed thyroid metabolism.
PATHOLOGY, PATHOGENESIS, AND PATHOLOGICAL PHYSIOLOGY.
The veil of mystery has been lifted from diseases of the thyroid by the
hands of the physiological chemists. The surgeons Astley Cooper, Rever-
din, and Kocher had found that extirpation of the thyroid for goitre
led to myxoedema, and Pisenti Gley and Vassale had demonstrated
that these symptoms could be prevented by feeding the dried thyroid sub-
stance. But the accurate knowledge
elates from the studies of Baumann
and his pupils, Roos and Oswald.
Thyreoglobulin and lodothyrin.
— Baumann, Roos, and Oswald have
shown that the active principle of the
thyroid is a globulin (iodothyreo-
globulin) which contains all the
iodine of the gland. Thyreoglobulin
is at first formed within the cells
free from iodine and later
acquires its iodine from the
blood, becoming iodized thyreoglob-
ulin or iodothyreoglobulin. The cells
secrete thyreogiobulin more readily
after it is combined with iodine. In
cases of colloid goitre when the
blood content is low in iodine, the
cells become loaded with the iodine-
free thyreogiobulin and undergo col-
loid degeneration. Iodine-free
thyreogiobulin is physio-
logically inactive, and the
entire activity of the gland
is due to the iodized thyreogiobulin. Indeed, as Baumann has
shown, it is duetto a comparatively simple molecular group with which
the iodine is combined, and which can be split off from the rest of
the globulin molecule by hydrolysis with H2SO4 (iodothyrin).
Effect of Thyreoglobulin on Thyroid Structure. — According to Oswald,
it is the state of the thyreogiobulin which determines the histological
changes in the thyroid. When the iodine-free thyreogiobulin accumulates
in the cells, they become overloaded with colloid and gradually undergo
colloid degeneration, so that the acini are found surrounded with the original
single layer of flat epithelial cells in all stages of colloid degeneration, whose
disintegration adds -to the colloid within the lymph spaces and within the
acini. (Oswald, Huerthle.)
FIG. 321. — Photograph of a patient with
Basedow's disease. (Kindness of Prof. Blood-
good.)
THYROID HEART. 577
An excess of the iodized product, on the other hand, stimulates the
cells to hyperplasia, so that instead of a single layer of columnar epithelium
the cells about the acini are found to be several layers and protrude into
the lumen in irregular papillary masses suggesting adenomatous changes
(Halsted, Oswald, MacCallum, Wilson). The same hyperplasia takes place
as a compensatory process when a part of the gland is removed (Halsted,
Marine). The colloid gradually disappears from the lumen as glandular
activity and hyperplasia progress and as the symptoms become more
Fio. 322. — Photograph of a portion of the thyroid gland removed from the patient shown in Fig. 321.
(Kindness of Prof. Bloodgood.)
severe, and in very bad cases it may be entirely absent (Marine and Wil-
liams, Wilson). The arteries and veins are very much dilated (C. Ger-
hardt). When the iodine is administered in cases of colloid goitre, the
excess of thyreoglobulin may be suddenly iodized and by escaping into the
blood may give rise to symptoms of hyperthyroidism (palpitation tachy-
cardia, tremor, loss of weight, exophthalmos — Basedowification of a simple
goitre). When there is an excess of iodine-and iodized thyreoglobulin in
the blood, the symptoms are the same as arise from the administration
of thyroid substance (thyreoglobulin or iodothyrin, its split product).
PHYSIOLOGICAL EFFECTS OF THYROID SECRETION.
It has been shown that the effects of excess of thyroid secretion in
the blood are:
1 . An increase in metabolism, especially in the oxidation
processes and the breaking down of proteids in the tissues and bone,
giving rise to an increase in N and P2O5 (Fr. Miiller) excreted and in the
gas metabolism (Magnus- Levy) . In man this finds its concrete expres-
sion in the loss of weight, due especially to loss of muscle substance (Bau-
mann and Roos).
2. There is a general stimulation of the peripheral
nerves both medullated and sympathetic. V. Cyon, Roos, Oswald
and Kraus, and Friedenthal have shown that these substances have several
distinct actions on the circulation:
37
578
DISEASES OF THE HEART AND AORTA.
A. They stimulate the depressor or afferent nerves from the heart, giving rise on the
one hand to the cardiac sensations, palpitation, and anginal pains, and on the other hand
to the vasodilation and low diastolic blood-pressure which are often observed in these cases
B. They stimulate both the vagi and the accelerator nerves. The action upon the
accelerators predominates, however, and tachycardia is thus produced. The vagus still
remains irritable, however, and the heart can be slowed by pressure on it. The same
stimulation of the other fibres of the cervical sympathetic gives rise to the peculiar ocular
signs of Basedow's disease (see page 583) .
C. Cleghorn has shown that thyroid extract has a direct action on the cardiac
muscle, increasing the size and force of the contraction, which manifests itself in the
increased pulse-pressure, increased maximal pressure, and cardiac hypertrophy.
FIG. 323. — Drawing of a histological specimen from the same thyroid. The histological picture
of advanced thyroid hypertrophy observed in cases of Graves's disease in which the symptoms are most
marked. (Bloodgood, Surg. Gyn. and Obstcs., August, 1905, vol. i, p. 113.) This drawing was made in
June, 1903.
Biochemical Evidences of Hyperthyroidism. — Falta and Zuelzer, Kraus and Frieden-
thal have shown that thyroid extract directly antagonizes adrenalin in its pupillo-dilator
action on the frog's eye, and that this can be used as a test for hyper-
thyroidism in clinical cases.
Another important biochemical blood test for hyperthyroidism is that of Reid Hunt,
who has shown that the blood of such patients increases the resistance of mice to poisoning
with acetonitrile and morphine, so that the lethal dose is thus doubled.
All these investigations have proved without doubt that in Basedow's disease there
is an excess of thyroid secretion into the blood (as claimed by
Mobius), and that the secretion is indistinguishable from that of the normal thyroid,
representing a condition of hyper thyreosis (increased secretion) rather than of
dysthyreosis (altered secretion) . Whether they will be of practical value in the diag-
nosis of the puzzling " formes frustes" remains still to be determined, since the excess of
thyreoglobulin in the blood of these cases may be too small for chemical recognition.
THYROID HEART. 579
It is possible that this anti-adrenalin action may be responsible for
the brownish pigmentation (Jellinek's sign) which occurs in many cases
of hyperthyroidism, especially about the eyelids. This pigmentation some-
what resembles the pigmentation of Addison's disease (lack of adrenalin
secretion). Kraus and Friedenthal have also found that this antagonistic
action upon the frog's pupil is valuable in diagnosis, since it is given by
the blood of patients with Basedow's disease, but not by the blood of
neurasthenics and hysterical patients.1
V. Cyon has shown the very important fact that injection of
thyroid exact or iodothyrin causes an increased blood
flow through the thyroid gland, probably thus acting as a
hormone to increase its own secretion and to introduce a vicious circle:
Hyperthyroidism
(Basedow's disease)
t 1
Increased thyroid . Increased blood flow
secretion through thyroid
It is this increased dilatation of the arteries which gives rise to the
murmurs over the thyroid in Basedow's disease (Guttmann).
ETIOLOGICAL FACTORS.
Basedow's disease is more common in women than in men (805 women,
175 men in Buschan's 980 cases); 60 per cent, occur in the fourth decade
of life (Buschan). In Passler's 58 cases there were 4 under 15 years, 29 at
from 15 to 25 years, 18 at 25 to 45 years, 7 over 45 years.
Basedow's disease is very widespread, but is somewhat more rare in
regions where simple goitre is common than elsewhere,
perhaps owing to the lesser intake of iodine. Heredity plays some role;
mental and nervous disease, diabetes, and tuberculosis are often found in
the same family. In one famous family reported by Osterreicher eight
out of ten children of a hysterical woman had Basedow's disease, and one
of these daughters had three children with the same illness.
The following list gives the predisposing factors in the series of A.
Kocher and of Landstrom:
Cases.
Gradual onset with etiological factors unknown 28
Pregnancy 10
Chlorosis 7
At first menstruation 6
After fright, shock, or grief 5
After fatigue 8
Infectious diseases (influenza alone, 7) 13
Old simple goitre 5
Sojourn at high altitude 2
Heredity 1
Appendicitis 1
Total . . .86
1 It seems doubtful whether the blood of cases with mild formes frustes contains
enough excess of thyreoglobulin to give this test a hard-and-fast diagnostic significance.
580 DISEASES OF THE HEART AND AORTA.
It will be seen that infectious diseases and especially influenza con-
stitute the most common cause. De Quervain has found a subacute thy-
roiditis quite common in these conditions, especially in influenza, typhoid
fever, rheumatism (as in Parry's first case), and diphtheria, and this thy-
roiditis was followed by Basedow's disease within a few months in about
20 per cent, of the cases. Boggs and Sladen have found mild thyroiditis
present in most of the cases of typhoid fever in which the pulse is over
120 at the height of the fever. Tonsillitis may also be a forerunner; and
Engel-Reimers has found acute thyroiditis in secondary lues leading to
Basedow's disease. After pregnancy the hyperthyroidism which is normally
present in that condition may increase and lead directly into Basedow's
disease. The coexistence of puerperal infection, mastitis,
fright, grief, or shock undoubtedly predisposes to the disease,
as in the case of a girl under Friedrich Miiller's care, whose symptoms
began when she was suddenly deserted by her lover just after the birth of
an illegitimate child. In one of v. Graefe's cases the symptoms set in within
a few days following a night of sexual excesses. These factors
may act by producing a reflex dilatation of the vessels in the thyroid.
Thus, Trousseau writes of a woman of 53 who suffered deep grief from
the death of her father. " One night, after she had been crying for a long
time, she suddenly felt her eyes swell and lift up her lids, her thyroid gland
increase notably in size and throb in an unusual manner; she had at the
same time violent palpitation of the heart." The writer on one occasion
had the opportunity to observe a case of acute enlargement of the thyroid
in a man of thirty, associated with tremor, tachycardia, palpitation, slight
v. Stellwag's but no other ocular sign. The disturbance followed the inges-
tion of two cups of strong coffee at a time of great worry and was compli-
cated by a mild attack of "grippe." The enlargement of the thyroid was
sufficient to prevent buttoning the collar. It subsided entirely after 24
hours, and with it the symptoms of hyperthyroidism. It is probable that
the grippe (influenza or streptococcus infection) rendered the thyroid par-
ticularly sensitive.
SYMPTOMS.
The classical pathognomonic symptoms of exophthalmos are the
well-known triad of struma, tachycardia, and exophthalmos,
or the tetrad of struma, tachycardia, exophthalmos, and
tremor.
These are well described by Parry (1815) in his first case, a married woman, aged 37,
who had " caught cold in lying in, and for a month suffered under a very acute rheumatic
fever. Subsequently she became subject to more or less palpitation of the heart
very much augmented by bodily exercise, and gradually increasing in force and frequency
till my attendance, when it was so violent that each systole shook the whole thorax. Her
pulse was 196 in a minute, very full and hard, alike in both wrists, irregular
as to strength, and intermitting at least once in six beats. . . . Twice or thrice she had
been seized in the night with a sense of constriction and difficulty in breathing,
which was attended with spitting of a small quantity of blood. She described herself also
as having frequent and violent stitches of pain about the lower part of the
sternum. . . . About three months after lying in, while she was suckling her child, a
lump about the size of a walnut was perceived on the right side of her neck. This
THYROID HEART. 581
continued to enlarge till the period of my attendance, when it occupied both sides of her
neck so as to have reached an uncommon size, projecting forward before the lower angle
of the jaw. The part swelled was the thyroid gland. The carotid arteries on
both sides were greatly distended, the eyes were protruded from
their sockets, and the countenance exhibited an expression of agitation
and distress, especially on any muscular exertion, which I have rarely seen equalled.
Bowels were usually lax. . . . For a week she has had osdematous swelling of
her legs and thighs." (The patient died with symptoms of heart failure.)
Besides the pathognomonic triad, increased nervous excitability,
tremor, loss of weight, and pigmentation of the skin, especially about the
eyelids, are important accessory symptoms.
The chief symptoms of Basedow's disease may be grouped in the fol-
lowing categories, and arranged in what is approximately the order of
increasing severity.
Cardiac Phenomena. — Palpitation, continuous slight elevation of
pulse-rate, with occasional attacks of intense tachycardia brought
on by emotion, excitement, or exercise, or occasionally on awak-
ening; visible pulsation and dilatation of carotid arteries; pulse
collapsing; angina pectoris; hypertrophy of the heart; precordial
heaving and intense pulsation; irregularity of pulse; dilatation
of heart; heart failure; ascending oedema, etc.
Psychic Symptoms. — General nervousness, insomnia, restlessness,
mental exuberance alternating with depression and melancholia,
delusions and hallucinations.
Ocular. — Staring gaze without winking for considerable periods.
Widening of palpebral slit (Dalrymple, v. Stellweg's sign), lids
do not follow eyeballs perfectly, a white streak of sclera is seen
between lid and cornea, especially on glancing downward or
upward (v. Graefe's sign), inability to converge in looking at
near objects (Mobius' sign), exophthalmos, overflow of tears,
pain and feeling of tension in the eyeballs, corneal ulceration.
Peripheral Nerve Symptoms. — Fine tremor (from 8 to 10 per second),
especially of the finger tips, nystagmus, superficial and cog-
wheel breathing, astasia-abasia, hypera3sthesias and paraesthesias
occasionally, inability to frown or wrinkle forehead (Joffroy's
sign).
Cutaneous from vasodilation and anti-adrenalin action). — Feeling
of heat, continuous and intense; lowered electrical resistance;
sweating; color usually pale brownish — Addison-like pigmenta-
tion, especially about eyelids (Jellinek) ; flushes; localized transi-
tory 03dema, especially about eyelids; scleroderma.
Nutritional (increased rapidity of metabolic processes— loss of N and
P2Of). — Loss in weight; sometimes absolute anorexia, sometimes
excellent appetite; attacks of diarrhoea, often with slimy stools;
polyuria; glycosuria. Fever (varying from 99° to 104°).
Blood. — Slight leucocytosis without change in red blood-corpuscles
or secondary anaemia; polymorphonuclears 50-55 per cent., lym-
phocytes 20-25 per cent., large mononuclears 8-16 per
cent, (large mononulcear leucocytosis present in formes frustes).
(Barker, Caro.)
582 DISEASES OF THE HEART AND AORTA.
Psychic Manifestations. — The psychic symptoms in hyperthyroidism
have been very aptly compared to the well-known effects of over-indul-
gence in coffee, — increased activity of thought, restlessness, irritability,
insomnia, and in the more severe cases garrulity and delusions. As men-
tioned above, over-indulgence in coffee may sometimes be followed by
enlargement of the thyroid. There can be little doubt that many cases of
so-called neurasthenia and hysteria are due to a more or less- transitory
state of over-secretion of the thyroid. This is particularly true when the
symptoms are accentuated at the menstrual periods, for then the thyroid
secretion is increased. It is possible that, as suggested by Graves, the
"globus hystericus" may be due to an acute swelling (erectile expansion)
of the thyroid. Neurasthenic symptoms may, however, have a basis in
hyperthyroidism in cases when this would be least expected. For example,
a young physician in robust health recently complained to the writer of
having suffered from insomnia and palpitation for several months, during
which time he had been compelled to forego his accustomed daily exercise.
On closer observation, however, he observed that at about the time his
symptoms had begun he noticed a slight swelling of his thyroid which had
persisted ever since, although he had no tremor.
Cardiac Signs and Symptoms. — The cardiac symptoms also
have some similarity to those of an overdose of coffee, especially the pal-
pitation. This symptom is probably due to the direct stimulation of the
afferent nerves of the heart (depressor), which has been shown by v. Cyon
to result from injection of thyroid extracts, iodothyroin and thyreoglobulin.
Palpitation is the earliest and often the mort severe symptom.
The tachycardia, like most of the signs of Basedow's disease,
results from the stimulation of the accelerator nerves and from the degree
to which this outweighs the effect upon the vagus. The pulse-rate may
be continuously elevated (over 120), or the tachycardia may be latent
and attacks of rapid pulse may be brought out only by slight disturbance
of the equilibrium or by the administration of very minute doses of thyroid
extract (Emerson, quoted by Barker) . In these attacks the pulse-
rate rises gradually during a few minutes and falls gradually
(in contrast to idiopathic paroxysmal tachycardia), but in one case v.
Hoesslin has seen sudden doubling and sudden halving of the rate. Stru-
bing has found that pressure upon the vagus slows the rapid heart of Base-
dow's disease, showing that there is no paralysis of that nerve.
Although, as Cleghorn has shown, thyroid extract increases
the force and size of cardiac contraction (the increased
pulse-pressure shows increased cardiac output), the persistent over-stimu-
lation of this organ draws so much upon its reserve force that it may readily
suffer from overstrain and undergo acute dilatation. Afferent impulses
through the depressor nerves, which are already in a state of increased
irritability, may give rise to symptoms of typical angina pectoris, with
referred pain down the arms and precordial hypersesthesia. This thyroid
type of angina pectoris has been described on page 293. Prolonged
overstrain may result in failure of either the left or the right heart, and
symptoms of pulmonary or systemic decompensation (oedema, ascites,
etc.) set in.
THYROID HEART. 583
The irregularity is probably due to occasional extrasystoles,
though careful analyses of its nature are lacking. In one case reported by
v. Hoesslin there was definite paroxysmal tachycardia with sudden onset
and sudden cessation — approximate halving and doubling of rate, but
Hirschfelder finds that this condition is a rare one in Basedow's disease.
The attacks of tachycardia and palpitation most commonly begin and end
by a gradual, though rapid, change of rate, and indicate a simple exaggera-
tion of physiological variations.
The maximal blood-pressure is usually high, the minimal
normal; the pulse-pressure increased; this shows that there is an increased
systolic output with low peripheral resistance, and corresponds well with
the experimental results from injection of thyroid tissue juice (Pressaft).
In 10 cases of Basedow's disease Krause and Friedenthal found:
Lowest. Average. Highest.
Cm. H2O. Mm. Hg. Cm. H2O. Mm. Hg. Cm. H2O. Mm. Hg.
Maximal blood-pressure... 145 106 182 134 215 158
Minimal blood-pressure ... 85 62 89 . 5 65 . 8 90 66
This accords with the writer's experience, but in the early cases and
"formes frustes" the maximal pressure may not be elevated even when
there is tachycardia.
The heart is usually enlarged and hypertrophied, the apex impulse
forcible, and the large systolic excursions impart a heaving to the whole
chest. In periods of overstrain from exertion or excitement there may be
transitory dilatation of the heart, and this uniformly occurs during the
chronic heart failure. There is often a blowing systolic murmur heard
over both ventricles and at the apex, perhaps due to functional insuffi-
ciencies of the auriculoventricular valves.
Heart failure is the immediate cause of death in most cases of Base-
dow's disease.
Ocular Manifestations. — The ocular manifestations are peculiar and
very characteristic. V. Graefe (1857) called attention to the fact
that when the eyes moved upward and downward the lids
did not follow them perfectly, but a streak of white sclera could
be seen between lids and cornea (Graefe's sign) . Dalrymple and in
1867 v. Stellwag noted the widening of the palpebral
slits, the staring expression, the absence of winking. V. Stellwag's
sign is in most cases the earliest characteristic sign of Basedow's disease.
M 6 b i u s ' sign is the inability to converge the two eyes when
looking at a very near object.
The origin of these signs is very simple. Claude Bernard, when he first
stimulated the cervical sympathetic, demonstrated that widen-
ing of the palpebral slit and dilatation of the pupil resulted
and that the eyeball was pushed forward. Aran and Kaufmann (1860)
demonstrated that this exophthalmos resulted from stimulation of Miiller's
non-striated muscle in the eyelid, which is innervated by the cervical sympathetic.
These experiments were confirmed by a number of writers, especially MacCallum and Cor-
nell (1904). The exact course of the fibres of Miiller's muscle and their mode of operation
has been described by Landstrom. Landstrom finds that the fibres of smooth muscle
form a narrow cuff, or truncated cone, encircling the anterior portion of the orbit. The
fibres at the posterior border of the cuff pass backward and are inserted into the sclerotic
coat of the eyeball. The fibres forming the anterior margin of the cuff are inserted into the
584
DISEASES OF THE HEART AND AORTA.
upper or lower lids, in which they run obliquely toward the palpebral slit. The middle
portion of the cuff constitutes the fixed point from which the muscle acts, and is attached
by short fibrous bands to the bony wall of the orbit. Contraction of this muscle
therefore tends to draw the eye forward (exoph thalmos) as well
as to pull the lids apart (Dalrymple and v. Stellwag's sign).
The delicate coordination of lid movement and eye movement
is disturbed by this added traction upon the lid (v. Graefe's
sign). Moreover, the contraction of these fibres tends to keep
the axes of the eyes divergent, and thus antagonizes conver-
gence (Mobius' sign).
FIG. 324. — Diagram showing the relation of the various anatomical structures concerned in the
production of the ocular and cardiac manifestations of Basedow's disease. A. Distribution of the branches
of the cervical sympathetic to the heart, thyroid gland, and eyelids. The arrows indicate the direction in
which stimulation of the cervical sympathetic moves the eyelids and eyeball. SYMP N, sympathetic nerve
plexus; SUP. C. GANG, MID. C. GANG, INF. C. GANG, superior, middle, and inferior cervical ganglia.
B. Relation of Muller's muscle to the eyeball and structures within the orbit (schematic). Muller's muscle
(MULL) is shown in black. The arrows indicate the direction of its pull. TEND, tendinous attach-
ment of Muller's muscle to the orbit, septum orbitale (SEPT. ORB}. C. Section through the lateral
portion of the orbit (semi-schematic, modified from Landstrom). ORB, orbitalis; LEV, levator palpe-
brarum; CONJ, conjunctiva; SCLER, sclera; RECT MED, rectus medius.
Muscular Changes. — A fine tremor beginning in the fingers, with 8-10
contractions per second, has been shown by Marie to be almost common
enough to be included among the cardinal symptoms. It is probably due
to the overstimulation of the peripheral nerves, and finds its analogue in
the tremor from coffee and tobacco. Tremor of the tongue and sudden
movements of the tongue and lips are not as common as in alcoholism. It
is probable that the muscular weakness consequent upon the katabolism
of muscle proteid aids in the tremor.
Astasia abasia (giving way of the legs in standing and walking) is rare,
but has been reported. It represents an extreme grade of nervous disturbance.
The increased metabolism of N and P2O5, with destruction of muscle
tissue, fat, and to a lesser extent of the bones, is important and finds its
expression in the general loss of weight (often 25 to 50 pounds) . It is the
direct result of iodothyrin intoxication.
THYROID HEART. 585
Diarrhoea is common. There is often a good deal of mucus in the stools,
suggesting some relation to the so-called mucous colitis.
Changes in the Thyroid itself. — As regards the size and appearance of
the thyroid gland there is great variation. In spite of the common term
of "exophthalmic goitre," the thyroid may not be prominent nor even
palpable. Since there is great variation in the average size and weight of
the thyroid in different regions, — 25 to 33 Gm. in certain regions, 60 Gm.
in others, 100 Gm. in Switzerland (Oswald), — a merely palpable thyroid
need be of no diagnostic importance. Increase in the size of the thyroid
is equally difficult to interpret. The size of the thyroid bears a definite
relation to sexual activity, and increases regularly during menstruation
and pregnancy, often to a considerable degree. Indeed, in some cases of
formes frustes it is not unlikely that we are dealing with slight hyperthy-
roidism whose intensity is determined by these physiological factors.
Increased vascularity is of great importance in differentiating between
transitory and persistent hyperthyroidism. It can be demonstrated by
eliciting a murmur and thrill over the thyroid when the gland is pressed
upon (Guttmann). This cannot be produced in simple goitres or normal
glands.
SECONDARY HYPERTHYROIDISM.
Moreover, it is probable that in many neurotic, toxic, and organic
diseases the actions of nerves or of hormones arouse the thyroid to a second-
ary activity, which may, nevertheless, be of great importance in determining
the features of the case. For example, Holz has reported two cases of exoph-
thalmic goitre in children in whom the disease subsided on removal of the
adenoids; one case recurred and again subsided with the recurrence
and removal of the adenoids. Accordingly it is advisable not only to treat
the Basedow's disease but also to look for and treat the other foci of excita-
tion.
DIAGNOSIS.
It is evident that, though there can be little doubt as to the nature
of well-developed thyroidism, there may be room for much debate regarding
cases of formes frustes, for these cases must be differentiated from simple
physiological hypoactivity of the thyroid. Patients should be carefully
watched for the development of ocular signs, especially at menstruation,
since these are practically never present in persons whose thyroid activity
is normal.
In cases in which symptoms are so mild, however, it is still important
to bear in mind the possibility of a thyroid origin for the condition, at
least in so far as an increased thyroid secretion may arise
reflexly and perpetuate itself through the vicious
circle mentioned on page 579. It is probable that on this basis the
origin of many an obscure "cardiac neurosis" will be cleared up. Hyper-
thyroidism and hysteria, sexual neurasthenias, epilepsy, tobacco poisoning,
alcoholism, myocardial disease, and valvular diseases are frequently asso-
ciated, and when one of these conditions is present it still remains important
to look out for contributing roles on the part of the thyroid.
586 DISEASES OF THE HEART AND AORTA.
Each case of morbus Basedowii may be considered as an autointoxi-
cation due to the passage of more or less iodized thyreoglobulin from the
thyroid gland into the blood. When this is secreted in large quantities,
the condition is outspoken and presents many of the symptoms, among
them some of severe grade. When but little excess of thyreoglobulin
circulates in the blood, it may give rise to the " formes frustes" with but
few symptoms and those of the milder type predominating.
However, even in the most atypical cases of "forme fruste" o n e o r
more of these symptoms may reach excessive sever-
ity, and the disease may persist in the form of a cardiac neurosis, a psycho-
sis, a chronic enteritis, a progressive inanition, a diabetes, or even a mild
relapsing fever, for long periods. The cardinal suggestive signs may be
so slight in intensity as to be noticed only when the suspicion of Basedow's
disease has once been aroused in the mind of the examiner, and then the
coexistence of several unobstrusive features may make the condition defi-
nite; as, for example, a slight staring, anxious expression in a thin, nervous
woman who suffers from attacks of palpitation and precordial pain and
who manifests a slight fine tremor of the fingers and a tendency to diar-
rhoea. On closer examination it may be found that the lids do not follow
the eyeballs perfectly and there is slight fulness of the neck, but none of
these symptoms are striking.
CASE OF BASEDOW'S DISEASE WITH ANGINAL ATTACKS.
Mrs. K. M., housewife, aged 23. seen under treatment at the Johns Hopkins Medical
Dispensary on Dec. 29, 1906, when she complained of palpitation of the heart and
pain in the right chest going down the arm. She is quite nervous and sometimes has
crying spells.
She is a rather pale woman, fairly nourished. The gums and mucous membranes are
a trifle pale. The palpebral slit is wider than normal, but lids follow eyes. Convergence
is, however, not perfect. The outlines of the thyroid gland can be seen; the gland is readily
palpable, but not much enlarged. The lungs were clear on auscultation and
percussion.
The heart was not enlarged; sounds clear. Pulse of good volume, regular in force
and rhythm; blood-pressure apparently low.
She was given Blaud's pills and also tincture of aconite 0.3 c.c. (^Iv) and potassium
bromide, without relief. She was seen a number of times during the course of the next
year, during which she passed through a normal pregnancy and labor. Palpitation
continued. A well-marked exophthalmos developed and palpebral slits
became a little wider than normal.
During April, 1907, she had attacks of pain over the left side of the chest
and down the front (extensor surface) of the left arm, sometimes radiating to the shoulder.
During attacks there is often tenderness in the fourth left interspace, sometimes also in
the fifth, about the mammillary line. It never radiates to the right of the midline. These
attacks are accompanied by palpitation and the heart-rate is rapid. She also has a peculiar
fluttering sensation, and occasionally an irregular beat Tracings at this period showed
normal venous and carotid pulse. She was given small doses of ergotin without relief. A
week later she was given calcium lactate 0.6 Gm. (gr. x) after meals, after which
she began to feel better at once, though never relieved by any other medicine. The remedy
was, however, far from specific, and the old symptoms returned in spite of the calcium
lactate. During the course of the next six months various remedies were given, none of
them with marked effect. It seemed to both patient and physicians, however, that she
experienced a distinct improvement in symptoms whenever calcium
lactate was given and distinct retrogression when other drugs were substituted.
Operation was advised but not consented to, and the patient was lost sight of.
THYROID HEART. 587
One group of cases to which attention should be especially directed
are those of very acute Basedow's disease with fever, prostration, tachy-
cardia, profuse sweats, sometimes chills and slight jaundice — a clinical
picture very closely simulating acute endocarditis (W. G. Thompson).
These cases are rather rare, but very grave. The diagnosis depends upon
the cardinal symptoms aided by a negative blood culture.
PROGNOSIS AND TREATMENT.
Statistics regarding the mortality of Basedow's disease vary considera-
bly, as shown by the following list.
V. Dusch 12.5 per cent.
V. Graefe 12 per cent.
Mackenzie 12 . 5-25 per cent.
Cheadle 9.6 per cent.
Billingham 18 . 1 per cent.
Gaill 21.3 per cent.
Charcot 25 per cent.
Buschan (900 cases) 12 . 5 per cent.
Thompson 10 per cent.
Williamson 25 per cent.
These figures err, on the one hand, because only the serious cases reach
the literature, and, on the other, because most of the cases have been fol-
lowed for only short periods. Williamson, who followed his cases for some
years and found a 25 per cent mortality, probably approximates the truth.
J. Berry gives the following statistics of 56 cases treated without
operation :
Complete recovery 10
Considerable improvement 24
Little or no change 8
Fatal 14
Even after recovery recurrence is the rule, so that as ex-
cellent an observer as August Hoffmann states that in 23 outspoken cases
he has not seen a single permanent recovery!
It is evident, therefore, that at the onset of undoubted Graves's
disease therapeutic interference is necessary. The best principles in inau-
gurating treatment are those which may be deduced from the findings of
v. Cyon's experiments, — i.e., that the clinical manifestations are due to
hypersecretion of thyreoglobulin, that this is proportional to the blood flow
through the thyroid, and that the thyroid secretion in the blood tends
itself to increase this flow and to produce a vicious circle.
The first essential of any palliative treatment, therefore, is to reduce
the thyroid secretion to its lower ebb by the removal of the two stimulating
causes — exercise and excitement. In the mild cases a simple isolation cure,
with absolute rest in the horizontal position, can sometimes so lessen
the flow through the thyroid and the secretion of this gland by diminishing
the size and number of heart-beats that the thyreoglobulin content of the
blood falls to normal and symptoms subside. If the rest cure be prolonged,
588 DISEASES OF THE HEART AND AORTA.
the slight glandular hyperplasia of early cases may subside and a permanent
cure may result.
Various measures assist this process, especially those which act as
psychic sedatives. Psychotherapy and suggestion, in so far as
they tend to lessen the elements of worry, quiet the patient's mind, and
thus quiet his heart's action, may aid in tiding over a period of not too
intense excitement. Similarly Mobius, the apostle of serum therapy,
reports the cure of one case by hypnotism ! These are, however, exceptional.
Psychotherapy in Basedow's disease is to be classed among the valuable
sedative measures, but not among those of fundamental therapeutics.
Cold wet packs, especially before retiring, may be of considerable
assistance (Eichhorst), as also the bromides and the soporifics (veronal,
trional, etc.), though to a less degree. Calcium salts are often very
satisfactory as sedatives. The iodobromide of calcium was used by Guptill
(1874). In one case (K. M.) under the writer's care calcium lactate was
the only drug which caused any symptomatic relief, but even this was
not marked. Miiller and others have used quinine, especially as the
hydrobromate, but in many cases it is without effect.
Iodine as used by the earlier observers may sometimes exert
a positively harmful influence by activating (iodizing) still
more of the thyreoglobulin, and it may thus bring on an exacerbation of
the condition. The effect of potassium iodide is less certainly harmful
and is sometimes beneficial, but its action is uncertain.
Galvanization. — One of the oldest and best forms of treatment is
galvanization of the cervical sympathetic, with the
anode over the carotid artery and the cathode at the nape of the neck.
With currents of 2-3 milliamperes, as used by Chvostek, Benedikt, Car-
dew, and others, it uniformly gives a certain degree of improvement,
without effecting a cure. In early cases J. O. Hirschfelder has obtained
complete subsidence of symptoms in a considerable number of patients by
the use of strong currents (20-30 milliamperes), the negative pole being
applied over the sympathetic at the neck, the positive over the thyroid for
two or three minutes. After this it is applied over the heart. This vigorous
treatment seems to be the best method of applying electricity, but must
be continued for several months.
X=Rays. — Exposure of the thyroid to the Rontgen
rays was introduced by Pusey, Boggs, and Beck in America, and has had
in the main a favorable action. Schwarz (1908) collected reports of 40
cases, showing gain in 26, improvement in nervous symptoms in 40,
exophthalmos better in 15, but struma lessened in only 8.
Specific Sera. — Two forms of so-called specific sera are also in use:
(1) anti-thyreoidin (thyroidectin), the serum of thyroidectomized sheep
(Mobius), has been in use for some years, and in spite of numerous favorable
reports has been found absolutely without effect by Ewald, Mackenzie,
and Strumpell. (2) Beebe has prepared an antiserum for the nucleo-
proteid of the thyroid gland from animals into which the purified nucleo-
proteid thyreoglobulin had been injected, in the hope of bringing about
retrogressive changes in this gland. This serum has been used therapeu-
tically by Rogers and by W. G. Thompson, who report distinctly favorable
THYROID HEART. 589
results, especially in the very acute cases (90 cases : 23 cured, 54 improved,
1 1 failed, 4 died) ; but other observers state that the results are no better
than those in ordinary hospital practice, and further confirmation is needed.
Operative Treatment. — Thyroidectomy. — The physiological indication
for therapy in Basedow's disease is to lessen the amount of thyreoglob-
ulin secreted into the blood. If the various methods intended to affect
the gland as a whole are unsuccessful, the secretion may be diminished by
removing a large portion of the gland (thyroidectomy) . This operation
was first successful in the hands of L. Rehn (1884), and has now come
into quite general use, especially through the work of Mickulicz and the
Kochers in Europe, and Halsted and the Mayos in America.
The operation should be done under local cocaine anaesthesia. It may vary from
ligature of the arteries to one-half of the gland, or this may be combined with excision of
the latter; or, on the other hand, one-half of the gland may be excised and the arteries
supplying a portion of the other may be ligated. The technic and results in large series
of cases have been reported by A. Kocher, Landstrom, and C. H. Mayo, and many of the
important details by Halsted and Evans.
Kocher (1907) especially calls attention to the necessity of suiting
the extent of the operation to the condition of the patient, especially the
cardiovascular condition. "A systolic blood-pressure, even of 195 mm.
Hg, does not forbid operation; . . . but if we find the blood-pressure
below normal and the disease highly developed, we must study the condi-
tion and especially note the action of the heart after exercise or excite-
ment. Under these circumstances we might find a sudden, very marked
dilatation of the heart, irregularity of pulse, and a blood-pressure which
cannot be measured by our ordinary methods."
The patient should be given a preparatory period of rest and pallia-
tive treatment to prepare her for the operation, and two or more opera-
tions should be done on the same patient rather than too extensive an opera-
tion at one sitting. Kocher never ligates more than two arteries nor re-
moves more than one-half the gland at one sitting, but these measures
suffice in cases that are not too far advanced. Halsted has called particular
attention to the need of preserving the parathyroid gland
in order to avoid tetany. Hence he advocates tracing out the
branches to these small bodies and then ligating the main artery beyond
them. Both Kocher and Halsted insist upon the greatest care in
the ligation of all bleeding points during the opera-
tion and in draining off any small collection of serum
which may collect during the healing of the wound. This greatly diminishes
or obviates the intensification of Basedow symptoms which sometimes
result a few days after operation (probably from absorption of iodothyreo-
globulin upon the raw surface of the gland) and which may be dangerous.
Halsted also found that the continuous use of an ice-bag upon the neck
during a few days after the operation retards the absorption from the gland
and lessens the frequency of these symptoms.
As a result of this procedure in 254 patients (2 operations in 71 cases),
A. Kocher has obtained great improvement in every case, with abso-
lute and permanent cure in 83 per cent., and 3.5 per
cent, of deaths. In the last 91 operations, since the above precautions
590 DISEASES OF THE HEART AND AORTA.
had been observed, he has not had a single death! C. H. Mayo had 9
deaths in 176 cases, but only one in his last 75; and Professor Halsted's
results at Johns Hopkins are equally favorable.
In cases of long standing the exophthalmos never disappears, for the
depths of the orbit have become filled with fat which continues to push
the eye forward after the contraction of Miiller's muscle has subsided.
Hypertrophy of the heart and secondary myocardial changes also
remain, perhaps some cardiac weakness, but these are greatly diminished
when the continuous cardiac excitation is removed.
It must be admitted also that, as Tinker states, the operation requires
more skill and practice than most surgical procedures, and the prognosis
is therefore far better done by a man whose experience in this line is con-
siderable than by a surgeon of even excellent local reputation.
As regards the indication for operation, Kocher believes that ''dis-
tinct vascular symptoms (other than mere palpita-
tion and tachycardia) should at once induce surgical
treatment. ' '' Before these have set in, the palliative method may be
used for a while, and many cases may be relieved thereby or subject only
to occasional recurrences. Should the mental symptoms and tachycardia
persist or become more severe, the physician should recommend operation
while the patient's general condition is still good, and should not wait
until she is a complete physical wreck before turning over the responsibility
to the surgeon. The surgeon should be allowed to operate upon the early
but chronic cases which do not improve under palliative treatment.
These rules apply as well to the cases of "formes frustes" as to the
outspoken Basedow's disease. The persistence of psycho- and cardio-
neuroses gives the indications, whether all the. cardinal features are pro-
nounced or not, and spontaneous recovery is no more likely to occur after
the "forme fruste" has persisted than in cases where all the signs are well
marked.
Sympathectomy (Jonnesco's Operation). —Another operation, which
has been performed by Jonnesco, is the removal of the sympathetic ganglia
on both sides of the neck. The result of this is usually an immediate slow-
ing of the pulse, and often a cessation of other symptoms. Jonnesco reports
several cases of permanent cure, but in the hands of a considerable number
of later observers, among them Kocher, good results have been lacking or
transitory, and this method should therefore be cast aside.
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THYROID HEART. 591
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592 DISEASES OF THE HEART AND AORTA.
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Bernard, Aran and Kaufmann, and H. Miiller (Ztschr. f. wiss. Zool., 1858, ix, 541). Quoted
from Landstrom.
MacCallum, W. G., and Cornell, W. B.: On the Mechanism of Exophthalmus, Med. News,
N. Y., 1904, Ixxxv, 733.
Marie, P.: Contributions a 1'etude et au diagnostic des formes frustes de la maladie de
Basedow, These, Paris, 1883.
Holz: Berl. klin. Wchnschr., 1905, xlii, 91.
Thompson, W. G.: A Clinical Study of Eighty Cases of Exophthalmic Goitre, Am. J. M.
Sc., Phila. and N. Y., 1906, cxxxii, 835.
Williamson: Remarks on Prognosis in Exophthalmic Goitre, Brit. M. J., 1896, ii.
Berry, J.: Diseases of the Thyroid and Exophthalmic Goitre, Phila., 1901.
Hoffmann, Aug.: Pathologic und Therapie der Herzneurosen und der functionellen Kreis-
laufstorungen, Wiesb., 1901.
Eichhorst, H.: Physikalische Therapie der Stoffwechselkrankheiten, Physik. Therap.,
1906, i, 212.
Guptill, C. H.: Exophthalmic Goitre successfully treated by the lodobromide of Calcium,
Am. J. M. Sc., Phila., 1874, Ixvii, 125.
Chvostek, Fr.: Weitere Beitrage zur Pathologic und Elektrotherapie der Basedow'schen
Krankheit, Wien. med. Presse, 1871, 1872, 1875.
Benedikt, M.: Nervenpathologie und Elektrotherapie, Leipz., 1876.
Cardew, H. W. D.: The Practical Application of Electrotherapeutics in Graves's Disease,
Lancet, Lond., 1891, ii, 6, 64.
Pusey, Boggs, Beck. Quoted from Landstrom.
Schwarz, G.: Ueber Rontgentherapie der Basedow'schen Krankheit, Wien. klin. Wchschr.,
1908, xxi, 1332.
Mackenzie, H.: A lecture on Graves's Disease, Brit. M. J., Lond., 1905, ii, 1077.
Beebe, S. P.: Preparation of a Serum for the Treatment of Exophthalmic Goitre, J. Am.
M. Asso., Chicago, 1906, xlvi, 484. A Serum having Therapeutic Value in the Treat-
ment of Exophthalmic Goitre, ibid., 1906, xlvii, 661.
Rogers, J.: The Treatment of Thyroidism by a Specific Serum, ibid., 1906, xlvii, 655.
Rehn, L.: Ueber die Extirpation des Kropfes bei Morbus Basedowii, Berl. klin. Wschnchr.,
1884, xi, 11.
Kocher, A.: The Surgical Treatment of Exophthalmic Goitre, J. Am. M. Asso., Chicago,
1907, xlix, 1240. With discussion by Halsted and Mayo.
Halsted, W. S., and Evans, H. M.: The Parathyroid Glandules, their Blood Supply and
their Preservation in Operation upon the Thyroid Gland, Ann. Surg., 1907, xlvi, 489.
Jonnesco, Th.: The Enduring Results of Total Bilateral Resection of the Cervical Sym-
pathetic in Basedow's Disease, Intern. Clin., Phila., 1903, 13th Ser., 136.
III.
MISCELLANEOUS DISTURBANCES OF CARDIAC FUNCTION—-
THE SO-CALLED "CARDIAC NEUROSES"
AND "CARDIAC NEURASTHENIA."
GENERAL CHARACTERISTICS.
One of the largest groups of cases seen by the clinician is made up
chiefly of pale, anaemic-looking young patients, with hollow lustreless eyes
and sunken cheeks, who complain of symptoms which may be divided into
two categories:
Symptoms. — 1. Symptoms referable to sensory disturbances
about the heart: — palpitation, precordial tenderness, pain or constriction,
pains and sensory disturbances down the arms, and, in rarer cases, of
attacks resembling angina pectoris.
2. Symptoms referable to motor disturbances of the circulation,
and especially to the distribution of blood in the body: — cardiac arrhyth-
mia, weakness, lassitude and weariness, vertigo, muscae volitantes, fainting
spells, and an infinite variety of psychasthenic and nervous symptoms.
This same symptom complex has already been encountered in the
attacks of paroxysmal tachycardia (Chapter II.), where it has been seen
to result from " arterial anaemia/7 or the relative depletion of the arteries
through dilatation of the veins, especially in the splanchnic region. Y.
Henderson believes that under these conditions the viens are not overfilled,
but that they too have become depleted by transudation of fluid into the
lymph and tissue spaces. Mr. C. C. Cody, in the Johns Hopkins medical
clinic, has found a very low venous pressure (—2 to —7 cm. H2O) in a
number of cases of neurasthenia and post-operative asthenia in which the
above-mentioned symptoms were present. The arterial pressure in all
but one of these cases was about normal, ranging from 104 to 125 mm. Hg.
This same circulatory state seems to be present throughout the groups
of cases about to be discussed, although the mechanisms by which it is
brought about are various.
Changes in Rhythm. — Alterations of rhythm are very common in this
group of cases (Hoffmann, Mackenzie, Reissner). They are usually associ-
ated with respiration, with a slowing of the pulse during inspiration and a
quickening during expiration (Fig. 325). It will be noted that this exactly
corresponds to the normal centripetal action currents in the vagus (Eint-
hoven, Flohil and Battaerd) which occur with each inspiration, and it is
probable that in the condition of heightened excitability this (usually sub-
normal) reflex stimulation becomes active. Stadler and Hirsch have been
able to produce such irregularities by inflating the intestines of dogs and
rabbits, but find them only accompanying dyspnoea. These observers also
found that such inflations of the intestines were always accompanied by rise
38 593
594 DISEASES OF THE HEART AND AORTA.
of blood-pressure. The writer has been able to confirm these observations.
Moreover, McCaskey and Russell find that an elevation of 30 or 40 mm.
Hg in blood-pressure may occur in the course of gastro-intestinal troubles,
especially hyperchlorhydria and flatulence. Russell suggests that there is
a relationship between chronic gastric intestinal disturbances and sclerosis
of mesenteric vessels.
In the cases of enteroptosis and of bathycardia a true pulsus para-
dox us (diminution or dropping of beats during inspiration) may occur
from the tugging upon the mediastinum, aorta, and great veins when the
diaphragm is drawn down during inspiration. In rarer cases, and espe-
cially those of gastro-intestinal origin, small, early beats resembling
extrasystoles are present. In making the diagnosis of extrasystoles,
however, great care must be used, for it must be remembered that in the
RESP.
RADIAL
FIG. 325. — Respiratory arrhythmia in a young cigarette smoker.
usual rhythmic variations in rhythm the last beat of a series with increasing
rapidity may be followed by the pause due to maximal slowing, and thus
an extrasystole may be simulated. On the other hand, it must be remem-
bered that no experimenters have as- yet been able to produce extra-
systoles by stimulating the extrinsic cardiac nerves (Hering, Hoffmann, the
writer and others), and therefore each case of the sort should be carefully
studied with venous tracings and electrocardiograms. True ventricular
extrasystoles demonstrable with the electrocardiogram are often brought
on by flatulence, though many writers agree with Friedrich Miiller that
the presence of definite extrasystoles is indicative of myocardial disease.
Some years ago the writer had under observation a man forty years of age who was
subject to palpitation and an arrhythmia brought on whenever he developed gas in
the stomach or intestines. He himself was able to distinguish " large and small " beats
among the palpitations, and tracings with modified Erlanger apparatus from veins and
arteries bore out his impressions. It is, however, difficult to decide whether these small
beats represent auricular extrasystoles or whether there is simply a rapid rhythm inter-
rupted by long pauses of vagal origin. He stated that nevertheless he was able to " out-
walk his doctors" at hill climbing during periods when he was suffering from both palpita-
tion and arrhythmia. A moderate dose (£ mg. = gr. T^) of atropine caused dryness of the
mouth and some vertigo, but did not greatly alter the pulse-rate nor cause the arrhythmia
to disappear. The patient would not allow a larger dose to be given. If one could be certain
that this dose had paralyzed the vagus the extrasystolic nature of the arrhythmia would
be established, but it is most probable that the vagus was but little affected and that this
evidence cannot be regarded as conclusive.
It has long been customary to designate such cases as "cardiac
neuroses, or, from the neurasthenic symptoms which are most striking
to the physician, as "cardiac neurasthenia." On closer exami-
nation, however, it may usually be found that both the cardiac
and the neurasthenic symptoms are not primary, but
DISTURBANCES OF CARDIAC FUNCTION. 595
are secondary to some visceral displacement or irri-
tation, to some intoxication, or in rarer cases to some
primary intense emotional disturbance. The heart itself
is sound, but, owing to the distribution of blood, does not get a chance
to do the work of which it would be capable. The terms " cardiac " and
" neurasthenia " are therefore both misleading, and it might perhaps be
more satisfactory to designate such conditions by the adjective "pseu-
docardiac'' ("pseudocardiac enteroptosis," " pseudocardiac gastral-
gia," " pseudocardiac aerophagia," etc.).
CLINICAL GROUPINGS.
Most if not all of these " cardiac neurasthenias " are brought on by the
following conditions:
Alterations of the position of the heart in the thorax.
a. Kyphoscbliosis, narrowness or flatness of chest.
6. Cardioptosis or bathycardia (low heart),
(1) due to enteroptosis (low diaphragm),
(2) due to long thorax with diaphragm normal,
c. High diaphragm from
(1) flatus,
(2) fat,
(3) tight lacing.
Although many cases arise in which no site of origin can be found for
the symptoms, the following represent a few of the more common causes:
1. Abnormal position of the heart,
a. From curvature of the spine.
b. From pleural adhesions.
c. Owing to a low diaphragm.
2. Vi.sceral reflexes.
a. Gastric, oesophageal and intestinal.
(1) Air swallowing.
(2) Gastritis, gastralgias.
6. Sexual organs.
(1) Sexual excesses (male or female).
Female — At onset of menses and at menopause; at menstruation;
from myoma and other lesions of generative organs.
Males — Gonorrhosa, prostatitis, masturbation.
3. Intoxications.
Tobacco.
Alcohol.
Coffee.
4. Anaemia.
5. Intense emotional disturbances.
ALTERATIONS IN POSITION OF THE HEART.
DISPLACEMENT OF THE HEART FROM MALFORMATIONS.
The displacement of the heart which occurs in kyphosis and scoliosis
is often the cause of a true cardiac weakness, i.e., weakness and dyspnoea
on exertion as well as from nervous causes — a so-called constitutional heart
weakness as Kraus terms it.
596
DISEASES OF THE HEART AND AORTA.
The patients are usually pale, rather weak, and readily become ex-
hausted and cyanotic, and manifest all the cardioneurotic symptoms.
The actual cause of the trouble lies not so much in the heart as in the posi-
tion in which it is placed in the thorax. Pressure and tractions upon both
the vense cavae and the arteries render
both inflow and outflow difficult, and
thus bring about a high venous and
a low arterial pressure, with the
symptoms which follow in its wake.
Kraus and recently Herz have
called attention to the cardioneurotic
symptoms which occur in all narrow-
chested individuals. Herz calls atten-
tion to the fact that in such cases
there is a tremendous lifting of the
ribs and precordium with each sys-
tolic erection of the heart. This is
due to the short anteroposterior and
especially oblique diameter of the
chest, so that the heart pivoted
against the posterior chest wall must
push out the left anterior wall in order to complete its systole (cf. Fig. 326).
As will be noted, this condition is quite different from that which results
from the low diaphragm or from cardioptosis, for in those conditions the
heart either beats in the long axis of the thorax, or from its mobility can
adapt itself to a narrower chest.
FIG. 326.— Cross section of the thorax of
a flat-chested individual, showing the systolic
heaving of the chest wall (broken lines) and
the forces bringing it about. The outlines of
the chest wall and heart during the systolic
heaving are shown by the dotted lines and
obliquely shaded areas. The protrusions and
retractions are shown by the arrows.
LOW HEART.
Even when there are no malformations of the chest, conditions arise
in which the position of the heart within the thoracic cavity is altered,
and these give rise to cardioneurotic symptoms. These conditions are:
I. Cardioptosis (wandering or movable heart), in which the mediastinal
attachments are loose and the heart readily moves from side to side, as
well as up and down.
II. Bathycardia (low or unsupported heart), in which the heart lies
low in the thorax because the dome of the diaphragm is lower than normal.
This is sometimes due to hepatoptosis and sometimes to a congenitally
low liver.
III. The high heart (high diaphragm), from various causes, especially
flatulence, fat, lacing, and during pregnancy.
MOVABLE HEART (CARDIOPTOSIS) .
Cardioptosis, or extreme mobility of the heart as shown on change
of position, was first described by Glenard (1885) and by Cherchevsky
(1887). The latter observer noted that, while the borders of the normal
heart move 1-3 cm. when the patient turns from the left side to the right
(while lying down), a certain number of cases (2.4 per cent, of all cases,
according to Einhorn) are encountered in which it moves from 4-7 cm.
DISTURBANCES OF CARDIAC FUNCTION. 597
without any other changes or any enlargement of the heart. As a rule,
the symptoms date from some time when the patient has lost in weight,
perhaps because the disappearance of mediastinal and omental fat causes
the organs to become looser than before. Einhorn has found it much more
common in men (18 cases) than in women (4 cases) and always associated
with hepatoptosis; though in cases like that given below the element of
hepatoptosis may be absent.
CASE OF CARDIOPTOSIS.
This, as well as the other symptoms, is beautifully illustrated by a case which the
writer has recently seen in consultation with Dr. L. P. Hamburger. The patient, aged 31,
had been a trained nurse since 18. Her father had died of enlarged heart and her mother
died suddenly. Except for scarlet fever, whooping-cough, and measles as a child, she had
been perfectly healthy until the age of 19, when a dermoid cyst of the left ovary caused
profuse menstrual bleedings. This was removed and the wound drained. Adhesions
formed, causing headaches and backaches and finally a nervous break-down, so that a
second operation was done nine years later to relieve the adhesions. At the time of this
operation she lost 14 pounds and was very nervous, and during her early
convalescence had asyncopal attack during which her hands and forearms became
completely blanched. One year later the patient felt her first cardiac symp-
toms, suffering palpitation, and when lying down has a feeling "as though the heart
were turning over" or " like a rubber bulb or sponge being squeezed out." She then feels
sick and has a feeling of oppression in the chest.
Physical examination shows a fairly nourished young woman of good
color; pupils equal and no signs of Basedow's disease. The left lobe of the thyroid is slightly
hard, but that organ is rather small.
The thorax is quite well formed, not especially flat. Costal angle normal. Lungs
clear. The heart is not enlarged and the sounds are clear. On turning from side
to side, however, the heart moves 8 cm. The pulse is of good volume
and shows a well-marked respiratory irregularity of the type described above, but no
extrasystoles. The abdominal walls are soft but not especially lax; the liver does not
descend when the patient stands, but the right kidney is palpable.
Bromides, nitroglycerin, and strophanthus have been without avail; tincture
of belladonna has somewhat quieted her cardiac symptoms. The
intensity of the symptoms seems to vary with her general condition. Upon being
assured of the trivial nature of her complaint, her symptoms
immediately disappeared.
Several months later she reported, however, that they reappeared from time to time
during periods when she was fatigued or nervous. The presence or absence of symptoms
was always quite independent of the mobility of the heart. In spite of her gain in weight
and the improved condition under treatment, the cardiac borders moved at least 7 cm.
during the periods when she was free from symptoms.
Treatment. — The treatment of cardioptosis presents a number of dif-
ficulties. As seen from the case cited above, the symptoms depend not
only upon the actual mobility of the heart but also upon the general
condition of the patient's nervous system. It is the latter which deter-
mines whether or not the afferent impulses from the heart shall reach the
threshold of consciousness. Accordingly, the unpleasant cardiac sensa-
tions may be present only when the irritability of the nervous system is
increased by fatigue, anaemia, or other affections; so that relief of the
latter by general measures relieves the cardiac symptoms as well, without
affecting their underlying cause. The mobility of the heart itself cannot
be treated directly; but it is sometimes possible, by overfeeding, to
cause a sufficient deposit of fat in the mediastinum and pericardium
598
DISEASES OF THE HEART AND AORTA.
to diminish the movements a little. Even when unsuccessful in this
way, however, overfeeding often aids by improving the general condition
and nervous tone.
GENERAL SPLANCHNOPTOSIS.
The mechanism which gives rise to the cardiac symptoms of splanch-
noptosis (enteroptosis) has been investigated anatomically by Keith and
clinically by Wenckebach. The latter found, by means of the X-ray
(fluoroscope), that the most important effect of enteroptosis was to remove
the support of the liver and stomach from beneath the diaphragm. The
dome of the diaphragm was thus usually seen to be flattened
and to be situated a good deal lower than normal.
FIG. 327. — The low, normal and high hearts. (Semi-schematic.) I, first rib; X, tenth rib; VII,
VIII, spines of seventh and eighth thoracic vertebrae. The horizontal line represents the "xiphisternal
line" passing through the sterno-xiphisternal articulation. The small white arrow represents traction
upon the trachea. A, low heart; B, normal heart; C, high heart.
The normal summit of the dome in quiet- expiration is just above the level
of the fifth rib, and its horizontal shadow just obscures that of the tenth rib behind.
Keith finds that this is normally about 1 cm. above the ''xiphisternal line,'1
a horizontal line representing the level of the sternoxiphoid articulation. The upper border
of the fifth rib at the junction with the cartilage is just at this level. In enteroptosis Wencke-
bach is able to see the X-ray shadow of the origin of the tenth and often the eleventh rib
above the dome of the diaphragm, and the latter lies well below the xiphisternal line.
The writer finds that for ordinary purposes the most convenient landmarks are the
xiphisternal articulation and the tip of the spine of the eighth thoracic vertebra, which
is just above the upper border of the tenth rib. The xiphisternal articula-
tion, the dome of the diaphragm, and the tip of the eighth tho-
racic spine are normally on a level. In enteroptosis and low diaphragm
the ribs drop so that first two structures are below the eighth spine, while with a high
diaphragm the ribs are raised so that they are above it (Fig. 327).
Effect on Respiration. — The effect of this low position of the diaphragm
is exerted both upon the respiration and the heart. The abdominal respira-
tion, which is due to the descent of the liver, is much diminished. For
when the dome of the diaphragm is flattened, shortening of the diaphragm
does not push down the liver, but pulls upon the lower ribs in a hori-
zontal or even upward direction. The effect of this pull upon the lower
DISTURBANCES OF CARDIAC FUNCTION. 599
ribs (Fig. 327, A) is to narrow the cross section of the thorax (Duchenne)
at this level and to draw the epigastrium inward, and thus
by diminishing the air capacity in this portion of the lungs to decrease
greatly the effect of inspiration both in sucking air and in sucking blood
into the thorax. This is the so-called ''paradoxical type of
respiration.'' Naturally, its effect is to diminish the intake of air
and thus greatly to enhance the effect of any cardiac insufficiency.
Effect on Circulation. — On the other hand, the lessened up-and-down
movement of the diaphragm, coupled with the relaxation of the abdominal
walls, greatly diminishes the force-pump and suction-pump action by
which the blood in the abdominal veins is forced onward to the thorax.
There is, therefore, a tendency for
the blood to stagnate in the abdomi-
nal viscera. The venous pressure
becomes low. In consequence, as
Henderson and the writer have shown,
the filling of the heart is less complete
and the systolic output is diminished.
Leonard Hill has shown that if a
rabbit is supported in the erect posture
with feet down and head down, the
blood-pressure falls and cerebral anae-
mia sets in. If one presses on the
animal's abdomen, the blood-pressure
rises at once. Erlanger and Hooker pih3° , Zi
found that when normal men Were Schittenhelm.) The cardiac shadow i* separated
, , , • i A i from that of the diaphragm by a well-defined
supported and kept motionless in the space.
vertical posture, the blood-pressure
fell (e.g., maximum fell from 120 mm. to 103 mm., minimal from 92.5 mm.
to 86 mm., pulse-pressure from 26.7 mm. to 17 mm.1), and in one case there
was "pallor, yawning, a feeling of warmth, faintness, nausea," and
threatened syncope. These are the symptoms of arterial anaemia common
in patients with enteroptosis.
The low position of the diaphragm exerts another effect upon the heart.
The diaphragmatic platform on which it rests drops away like a trap-door
and leaves it suspended from the great vessels and vertebral column by
the aorta, trachea, mediastinum, and fasciae. The heart thus lies in the
longitudinal axis of the body; and, in systole, the apex can be seen to rise
and to pull down on the trachea instead of moving inward. As Osier and
Wenckebach have shown, atracheal tug may often be felt and this
may lead to a mistaken diagnosis of aneurism. However,
this error may be obviated when the enteroptosis is taken into considera-
tion, and especially when the tug diminishes upon pressing the liver upward
and inward.
Moreover, when the low diaphragm descends in inspiration it exerts
further traction upon the mediastinum and thus upon the aorta as well
as upon the great veins, thus bringing about an inspiratory diminution
1 The fall in pulse-pressure denotes diminished systolic output.
600 DISEASES OF THE HEART AND AORTA.
or dropping of the pulse-beats (pulsus paradoxus) , exactly
like that occurring in pericarditis, which the appearance of the patient
may suggest.
Physical Signs. — The upper border of cardiac dulness in these cases
does not usually extend above the third rib. The total area and the area
of the cardiac shadow are usually diminished and the area of flatness com-
pletely obliterated. The attachments of the heart have reverted to the
embryonic type, and that organ is suspended by the elongated pericardiac
ligament. The a p e x is usually inside the mammillary line. In extreme
cases the right ventricle is seen to beat in the epigastrium; but this often
signifies only a dilatation of that chamber. The sounds are usually clear,
but either sound may be reduplicated. There is usually a soft systolic
murmur of accidental type over the area of the right ventricle, or occa-
sionally at the apex.
The abdomen is often flat, and usually shows marked linese
albicantes. The disappearance of subcutaneous fat makes the walls flabby
and the viscera are easy to palpate. The liver can almost always be felt
when the patient is sitting or standing. The k i d n e y s are usually palpa-
ble and movable. When the patient stands, the viscera gravitate to the
hypogastrium, where a fulness is seen, giving the abdomen the profile of
an interrogation point turned upside down (^).
Pathogenesis. — Enteroptosis is far more common in women than in
men, owing to the stretching of the abdominal muscles and relaxation of
the perineal floor in pregnancy and labor. Hence it occurs more frequently
in women who have not remained in bed long enough during the puerperium.
Nevertheless, it is also common in single women and in men whose abdom-
inal muscles are atonic from lack of exercise, or in persons who from any
cause have rapidly lost weight. The rapid disappearance of the intra-
abdominal fat uncompensated by. contraction of the abdominal muscles
takes away the support from the liver and facilitates the occurrence of
enteroptosis. Indeed this latter factor is often more important than the
muscular element, and it is not uncommon to find most typical examples
of enteroptosis in thin persons whose abdominal walls are not abnormally
flaccid.
Tight lacing, as well as causing atony of the abdominal walls, causes
the viscera to tug at their ligamentous moorings and finally to stretch
them, and thus bring on an enteroptosis. However, while the corset is
being worn it pushes the liver and diaphragm up, the pelvic organs down.
The typical corset heart is the high heart and not the low heart (see
page 327, C). It is only when the corset is taken off that the heart and
abdominal organs drop.
Treatment. — The treatment follows from the mechanical conditions.
It is all-important to push up the liver. Fr. Glenard, who first described
enteroptosis, showed that symptoms were relieved by merely pressing up-
ward on the abdomen with the hand (just as in Leonard Hill's rabbit experi-
ment), and hence one of the oldest forms of treatment is the tightly fitting
abdominal binder. A specially made corset arranged so ay to bring an
upward pressure upon all the structures befow the costal margin gives
excellent results, especially when supplemented by pads over the kidneys.
DISTURBANCES OF CARDIAC FUNCTION. 601
Probably the best form is an adjustable air cushion resting upon an alumi-
num plate that is strapped to the abdomen (Wenckebach). For a time
the attention of physicians had been directed to the individual organ,
especially the kidneys, and these organs were sutured into place. But
experience has shown that this only remedies a small part of the trouble
and does not remove the real cause.
The only method of real physiological therapy is one which will at
once give support to the viscera within the abdomen and also restore the
tonic contraction of the abdominal wall. This can be accomplished by
accumulation of fat and by exercise. The former procedure
is the one to be attempted first. If the patient can be kept at absolute
rest in bed and overfed with a diet containing about
3500 or 4000 calories in twenty-four hours, a good deal of fat may
be accumulated in about six- weeks. The principal addition to the diet
should be olive oil (15 to 25 c.c. three times a day = about 500 calories
per day or about 60 Gm. (2 oz.) of adipose tissue). This can he taken
between meals, pure or flavored with a little lemon, sherry, brandy, etc.,
to suit the palate. It is most important that the patient's digestion should
not be disturbed by it. Salads with dressing, thick soups, and cereals
(especially with cream) should be given in as large quantities as the patient
will take, and she should be encouraged to drink milk instead of water.
Butter and cheese are also valuable additions to the diet when the patient
can be made to take them in liberal amounts. Cakes, sweets, and even
puddings fall into the same category, provided digestion is perfect. She
should receive milk or cocoa between meals and before going to sleep at
night. In short, every means should be adopted to overfeed the patient.
On the other hand, it must be remembered that if her digestion be spoiled
in the process, it will be impossible to secure a permanent gain in weight,
so that the process must be begun gradually and the patient's appetite
should be stimulated to keep pace with the diet.
In order that the fat should be deposited in the places where it will
give the most support (i.e., the re trope ri tone al tissue and gastrohepatic
omentum), the patient should be made to lie with a pillow under the small
of the back for as many hours as possible.
The result of the rest and overfeeding treatment, supplemented by
careful bandaging, is most gratifying. With the return of intra-abdom-
inal fat the patients usually improve in health and spirits, symptoms sub-
side, and the element of cardiac weakness may entirely disappear. The
patient's confidence in herself (or himself) returns and the neurasthenia
subsides.
CASE OF ENTEROPTOSIS.
The following case, under the writer's care in the Johns Hopkins Hospital Dispensary,
illustrates the course of the condition and the excellent results obtainable by treatment.
Mrs. Agnes L., aged 31, first seen Feb. 19, 1909. Complains of loss of strength,
weakness, and palpitation, especially on exertion. She is nervous
and readily exhausted. Has had no swelling of the feet.
Family history negative. Patient was always healthy, but has had diphtheria and
is subject to sore throat. Chlorosis at 16. Bowels constipated. Menstruation regular
but painful. She has had two children but no miscarriages. Drinks coffee and tea in
moderation.
602
DISEASES OF THE HEART AND AORTA.
Present trouble dates from birth of last child four years ago. She feels
tired all the time and is subject to weakness and palpitation after exertion. She sleeps
well, however. Her feet are never swollen. Two years ago she was treated by another
phvsician for the same trouble, which was then diagnosed neurasthenia. She was overfed
and made to lie down every day. Gained weight and improved somewhat, but has lost
weight since then.
Physical examination shows a fairly nourished woman, tall and sparely
built. Her eyes and cheeks are sunken, and expression is one of depression. Her color
is pale, but the haemoglobin is 90 per cent. Thyroid is not enlarged. No glandular enlarge-
ment. Thorax is long and flat and
held in the position of expiration. Costal angle
is very acute. There are a few rales at the
left apex (which were not present on subse-
quent examinations). The upper border of
cardiac dulness begins at the third rib and
extends in the fifth interspace to the left
mammillary line and in the fourth 30 cm. to
the right of the midline. Owing to the form
of the patient's chest, however, the fifth left
interspace is situated at a lower level (referred
to the spine) than is normal. The cervico-
xiphoid distance is long. Heart sounds are
clear and pulse is regular.
Abdomen . — The liver extends below
the costal margin. There is marked gastrop-
tosis, the stomach lying below the umbilicus.
Both kidneys palpable. Genitalia negative.
Extremities. — Sensation and re-
flexes normal.
Patient was given an abdominal
bandage and encouraged to full diet,
especially rich in butter, milk, eggs, and salad.
Besides this one tablespoonful of olive oil
three times a day. She was made to rest
and lie down several hours a day with a
pillow under the small of her
back to favor deposition of peri renal fat.
Within an hour after the abdominal binder wasfirst put on
her condition was markedly improved, her expression was brighter, and
she felt more active. The patient, however, still stood with stooping shoulders, which
caused the chest to continue in the position of expiration and allowed the heart to hang
low. This position was improved by the use of shoulder braces. The patient's condition
and strength steadily improved and her cardiac symptoms had entirely disappeared after the
abdominal bandage was put on. The gain in weight during three months was only 3£ pounds.
FIG. 329. — Photograph of a patient with eri-
teroptosis. The upper border of cardiac dul-
ness begins at the third rib (III); the heart is
small and lies vertically. The liver is low and
palpable.
CASE OF ENTEROPTOSIS SIMULATING ANEURISM OF THE DESCENDING AORTA.
P. R., a wool sorter, aged 42, came to the Johns Hopkins Hospital Dispensary on
March 5, 1909, complaining of a drawing pain in both sides and in the epi-
gastrium. The family history and personal history were negative. The patient denies
lues, but has had to lift heavy sacks in his work. His pain began about six weeks before
admission while he was at work and was accompanied by palpitation, and it has
continued since then.
The patient was a well-nourished man of good color. The left pupil was
larger than the right, but both reacted to light and accommodation. The thorax
was long and there was a slight funnel breast. The lungs were clear on percussion and
auscultation. The area of cardiac dulness was slightly smaller than normal; dulness
began above at the lower border of the third rib, extended 7.5 cm. to the left in the fifth
left interspace and 2.5 cm. to the right of the midline. The heart moved 6 cm. on
change of position. The apex is 3 cm. below the xiphisternal line. The left radial
'
DISTURBANCES OF CARDIAC FUNCTION. 603
pulse was slightly smaller than the right. There was well -marked pul-
sation in the epigastrium, and the liver was well seen and readily felt
below the costal margin. There was a well-marked tracheal tug
which diminished when the liver "was pushed upwards with
the hand.
The fluoroscopic examination by Dr. Baetjer showed that the aorta was clear. An
abdominal binder was applied. The abdominal pains and palpitation ceased and the
tracheal tug diminished markedly. The patient was able to continue work without dis-
comfort. His pains have been absent for over a year.
LOW HEART WITHOUT ENTEROPTOSIS (BATHYCARDIA).
There is another type of long, flat-chested individuals in whom, al-
though there is no enteroptosis, the diaphragm is low. The dome of the
diaphragm is not flat, but is well arched. The insertion of the diaphragm
may be somewhat lower, and the length of the thoracic cage, which is held
in the position of expiration, is considerably greater than normal (Fig.
327, A). As a result of this lengthening of the thorax, the distance from
the structures upon which the heart hangs (aorta, trachea, mediastinum)
to the diaphragm, which supports i.t, is lengthened, and just as in enterop-
tosis the heart hangs free above the diaphragm. It is therefore termed
the "hanging heart" or "dropping heart." It pulls upon the trachea in
systole and causes a tracheal tug. It pulls upon the aorta in inspiration
and causes a pulsus paradoxus. The interference with cardiac filling and
with the abdominal circulation gives rise to about the same symptoms
of cardiac weakness as are encountered in enteroptosis, though often to
a less marked degree.
The diagnosis is usually best made with the fluoroscope; for the pres-
ence of a mild brachial impulse and pulsus paradoxus may cause the con-
dition to be mistaken for either aneurism or mediastinitis. There may
even be a slight tugging on the low diaphragm (Broadbent's sign) at the
depths of respiration. It is extremely difficult to exclude mediastino-
pericarditis in many cases in which the palpitation, pallor, fatigue, short-
ness of breath, paradoxical pulse, etc., are intense. In some cases with
reduplicated first sound mitral stenosis may be thought of. Absence of
hypertrophy of the left ventricle (cardiac dulness inside mammillary line)
should exclude organic mitral insufficiency even in the presence of a sys-
tolic murmur. The diagnosis is made chiefly on fluoroscopic examination.
Treatment. — As the condition is due to the low diaphragm, just as in
actual enteroptosis, the chief indication is to raise the diaphragm. In
bringing this about with normal abdominal walls a bandage is of some avail,
but fattening is not successful.
On the other hand, the obliquity of the ribs is also at fault, and this
can be corrected by training the patient to take deep inspirations and to
stand with his shoulders and hips thrown back.
HIGH DIAPHRAGM.
The exact opposite condition, that in which the diaphragm is so high
that the heart is placed in a position in which it works at a disadvantage
(probably by interference with venous inflow), is found in fat persons, in
many dyspeptics with flatulence, in emphysema, and in women as a result
604 DISEASES OF THE HEART AND AORTA.
of tight lacing. In the first three conditions there is diminished respiratory
movement, especially the costal movements, since the ribs in most cases
are held in the position of expiration and the possible excursion thus dimin-
ished; while in persons who lace tightly abdominal respiration is impeded
and the respiration is mainly costal. In these cases the heart is raised by
the diaphragm, especially in inspiration, and thus comes to lie more trans-
versely to the axis of the body. In such persons the xiphisternal articula-
tion lies above the level of the eighth thoracic spine, the diaphragm shadow,
according to Wenckebach, obscuring the ninth and tenth ribs. The apex
lies in the fourth interspace outside the mammillary line, often leading
to the suspicion of valvular lesion or myocarditis.
This pushing up of the heart tends to impede the heart's action and
to produce fall of arterial pressure, as was first shown by v. Frey and Krehl
in 1890.
The clinical result of these conditions is to produce a syndrome not
unlike that of the exactly opposite conditions, "cardioptosis" and "drop-
ping heart," — i.e., a diminished cardiac filling, — and is undoubtedly in a
large ' measure responsible for many of the symptoms of the "heart of
obesity" and of indigestion.
Treatment must be directed to the cause, — regulation of diet for the
fat and dyspeptic, loosening of the corset for the woman who laces. How-
ever, the latter should be done gradually enough to give the abdominal
walls time to adjust themselves, lest a true splanchnoptosis replace it.
REFLEX CARDIAC DISTURBANCES.
GASTROINTESTINAL.
Patients with chronic gastro-intestinal disturbances often come to
consult the physician for the cardiac symptoms which these bring about,
— namely, palpitation, pain in the region of the heart, tachycardia, and
often irregularity of the pulse, — symptoms which are all more deeply
impressed on the patient's mind than are the heart-burn and belching from
the underlying indigestion.
As has been seen in connection with angina pectoris, gastric disturb-
ances may cause cardiac symptoms. .The motor disturbances (arrhythmia,
tachycardia, etc.) are in a large part due to the spread of stimuli from
the gastric branches of the vagus to the cardiac, while the sensory symp-
toms are due in part to false reference of impressions, in part to a
similar spreading of stimuli, and in part to an associated hypersestheria of
these branches of the vagus.
The chief irritants are butyric and lactic acids (acid fermentation),
excess of hydrochloric acid, and the gases of fermentation,— CO2 (40 per
cent, in the absence of HC1), H2, N2, O2, H2S, and often CH4 (inflammable)
in butyric acid fermentation (Hoppe-Seyler).
Air Swallowing. — One of the most important factors in pseudocardiac
dyspepsia is air swallowing. As Wyllie has shown, it is extremely
common for persons suffering from slight gastric discomfort to find them-
selves relieved by belching. As a result they seek further relief by forcing
DISTURBANCES OF CARDIAC FUNCTION. 605
themselves to belch. The forced belching gives only momentary relief,
but aggravates the discomfort, giving rise to a familiar sensation of an
object lying just behind the larynx. They belch again to remove it, and
the belching is thus continued indefinitely, always accompanied by a cer-
tain discomfort and often by a loud noise.
Mechanism of Acrophagia. — Wyllie and others have shown that the mechanism
of involuntary and voluntary belch ing is quite different. In the former
case an excess of the gases of fermentation is regurgitated from the stomach, and this
can occur only when there is an excess of gas. In the latter case the patient first swal-
lows or gulps the air by placing the tongue against the roof of the mouth (in the position of
pronouncing the consonant " T" and then exerting a deep inspiration. These movements
force the air into the oesophagus. It remains there an instant, and may then be either
swallowed or expelled by a forced expiration with the glottis closed, causing the loud
noise of belching as it forces apart the vocal cords and pushes up the epiglottis. Most
often part of the air is swallowed and part regurgitated, and a few bubbles of air remain
in the oesophagus most of the time, giving rise not only to the feeling of discomfort but
often to reflex cardiac disturbances. Wyllie calls attention to the fact that air gulping
occurs not only in man but also in horses and cattle, where the condition is known as
" wind colic " and " hoven," which often becomes so severe that it may cause the death
of the animal. The symptoms are " difficult breathing, bloodshot eyes, red mucous
membrane, loud tumultuous heart-beat, trembling of front legs, etc." This
can be brought about in dogs by inflating either stomach or intestines with air under
pressure, paralysis and heart-failure resulting. Wyllie believes that the condition is still
more common in infants and in children, and thinks that it is responsible not only for
wind colic but for certain cases of death with abdominal distention.
Palpitation when patients are quiet may be more striking than actual shortness of
breath on moderate exertion (unless anaemia is also present). But this is not an invariable
rule, for on account of the high diaphragm of flatulence, the intensity of the cardiac dis-
comfort, or, on the other hand, the habitual weakness of the patient's muscles, there may
be actual cardiac weakness as well.
The treatment of air gulping is of the greatest importance. Wyllie
states that this troublesome habit can be promptly overcome by keeping
the mouth open. For persons who swallow air in their sleep, a gag or cork
has to be tied in the mouth. This method is in general use among veterinary
surgeons and is uniformly successful. It is evident, therefore, that the
diagnosis of air swallowing must be carefully made. In many cases this
may be done by getting the patient to show you how she usually belches,
the voluntary procedure indicating the nature of the process. In doubtful
cases it may be necessary to analyze the gas by Hoppe-Seyler's method;
but, as Wyllie remarks, the diagnosis is best made ex juvantibus, by cessa-
tion of the condition when the mouth is kept open. The possibility of
unconscious quiet air swallowing in other cases of flatulence must also be
borne in mind.
Constipation. — An accumulation of fecal matter is also a very common
cause of cardiac symptoms. Extrasystoles are usually more common
when the patients are constipated. Kuthan has also seen patients in
whom attacks of angina pectoris occurred regularly during periods
of constipation and disappeared when the bowels were kept open. These
symptoms are produced partly by the lifting of the diaphragm and per-
haps also in part by the chemical action of indol, skatol (Russell,
Herter), and other fermentation products. These substances may act
directly upon the intestinal nerve endings or upon the heart muscle and
606 DISEASES OF THE HEART AND AORTA.
cardiac nerves after absorption into the general circulation (as assumed
by McCaskey). It must be admitted that the action of such products
is not very well known.
Apart from the general methods, treatment of the cardiac symptoms
is best accomplished by treating the gastric condition with appropriate
diet, lavage, galvanization (8 to 12 milliamperes), and faradization of the
stomach, etc. The bowels should be kept open. The various forms of
fermented milk containing lactic acid (buttermilk, kephyr, etc.) as well
as the preparations of lactic acid bacilli are often of benefit in the treat-
ment of intestinal fermentation.
Treatment of the constipation which is often present should consist
of free purgation with Epsom salts, followed by a course in cascara, hydro-
therapy, abdominal exercise, and a diet rich in fat, coarse foods, and in
liquids. The most important feature is forcing the patient to defecate at
regular hours and at no other times.
REFLEXES FROM THE SEXUAL ORGANS.
Practically all the disturbances of the sexual organs are accompanied
by the pseudocardiac syndrome. It occurs in both male and female after
sexual excesses and organic diseases.
MALE SEXUAL ORGANS.
In men gonorrhoea, prostatitis, and especially masturbation are among
the first conditions to be thought of when a patient presents himself with
these symptoms. Curschmann and Bachus have especially called attention
to the latter condition and have found that masturbation may even lead
tp cardiac hypertrophy. Bachus has made the very significant observa-
tion that in many of his masturbators the thyroid glands were
somewhat enlarged, so that he believed that the abnormal sexual
activity might have led to a secondary over-activity
of the thyroid. (Perhaps this may occur through the action of a
hormone in the testicles, seminal vesicles, or prostate.) At all events,
since this organ may be aftected reflexly, the secondary activity of the
thyroid is to be thought of in all cases of pseudocardiac disease of sexual
or of purely nervous origin. It is also possible that the prostate gland
may have an internal secretion of similar character.
The diagnosis must be made from the history, as well as from a careful
physical examination in which the mouth of the urethra is especially exam-
ined, and careful palpation of the prostate and prostatic secretion.
Treatment is directed mainly to the primary condition, but the bro-
mides should be used somewhat more freely in sexual disturbances than
in the other conditions.
FEMALE.
In women the pseudocardiac disturbances are not only more common
but more severe than is usual in men. Palpitation, with tachycardia and
weakness, is very common at the age of puberty and is practically universal
in chlorosis which is then so common.
DISTURBANCES OF CARDIAC FUNCTION. 607
In young and healthy married women Kisch has found that attacks
of palpitation with rapid pulse and dyspnoea may occur—
1. As the result of sexual excesses in women whose sexual desire is very keen.
2. After attempted coitus when vagiriismus is present (cured by operation upon the
vagina).
3. In women who have practised coitus interruptus for a long time without attaining
sexual satisfaction.
Kisch believes that in general coitus stimulates the cardiac nerves
in proportion to the intensity of the orgasm. Masturbation, on the other
hand, has a much less intense effect on women than on men (Kelly), and
is rarely responsible for cardiac disturbances.
Veit calls attention to the fact that asthmatic attacks from
cardiac insufficiency constitute an early symptom of
myoma. He believes that these arise in the early stages of brown
atrophy and cardiac obesity, as these lesions have been found by Lehmann
and Strassman and also by Fleck in 40 per cent, .of all cases of myoma.1
Kelly and Cullen, however, deny that myomata in
themselves are associated with any cardiac disturb-
ances except those due to the anaemia which is pres-
ent. In a very careful study of 1428 cases of myoma they found that
"In the majority of cases (with cardiac manifestations, 92) an apical sys-
tolic murmur was detected. This murmur was usually very soft in character.
In some it was limited to the apex, but in others it could be traced to the
axilla and in some patients to the base of the heart." In nearly all the
cases (92) in which cardiac lesions were present, the patient gave a history
of menorrhagia, often associated with intermenstrual bleeding. These
patients, as a rule, stood the anaesthetic well and in
a comparatively short time they had gained much in strength and their
cardiac murmurs had disappeared. Some authorities claim that the myoma*
in itself brings about cardiac changes. If such were the case, then the
larger the myoma the more pronounced should be the cardiac murmurs.
This has not been our experience. The largest tremors have not been
associated with any cardiac symptoms, but the heart complications have-
almost invariably been associated with copious bleeding from the uterus
(i.e., submucous myomata).
" Most of the murmurs noted in our cases were at the time considered
to be functional." (Cullen.) That there is little danger from functional
impairment of the heart is shown by the fact that Kelly and Cullen's mor-
tality in their last 240 cases of myoma was less than 1 per cent.
Lenhartz has found that cardiac symptoms are almost always more
frequent during the week preceding the menstrual flow. They
are also more frequent as the climacteric is approached, an angioneurosis
(flushing) with palpitation and more or less tachycardia being universal.
Strassman and Lehmann have called attention to the similarity between
these phenomena in ovarian secretion and those of the thyroid gland,
and, as has been stated, the thyroid varies in size with the changes in ova-
rian activity. Leo Loeb, Starling, and others have shown that this is due
1 In 34.6 i>er cent, of Fleck's cases there was no anaemia.
608 DISEASES OF THE HEART AND AORTA.
to the action of a hormone arising in the ovaries and especially in the corpus
luteum, which acts upon the uterus, mammary glands, and thyroid. No
doubt it also has some action upon the heart, but this is still obscure, and
it is difficult to determine how much of the effect is due to the ovarian
secretion itself and how much to the secondary hyperthyroidism.
Prognosis and Therapy. — The prognostic importance of cardiac dis-
turbances arising in the sexual organs varies with the primary lesion and
its chronicity. In the presence of gonorrhoea or pelvic abscesses the prob-
ability of a metastatic myo- or endocarditis must not be forgotten. In
the presence of anaemia the development of fatty degeneration and even
of insidious mitral stenosis must be borne in mind, while in the presence
of myoma myocardial changes which vary from primary hypertrophy to
a brown atrophy and cardiosclerosis (due chiefly to the anaemia) must be
thought of. In masturbating men there is a true cardiac hypertrophy with
the usual accompanying changes. These factors must, therefore, be ex-
cluded before the diagnosis of a true neurosis is made and an unqualified
favorable prognosis can be given.
In the simple cardioneurosis or pseudocardiac sexual disturbance
the cardiac outlook is favorable if the primary condition can be removed.
If not the prolonged reflex stimulation of the cardiac nerves leads first to
a "work hypertrophy" and then probably to cardiac overstrain and pre-
mature cardiosclerotic or atrophic changes.
The treatment is therefore in the field of the gynaecologist or genito-
urinary specialist and not in that of the internist. Even masturbation
and sexual excesses may have a basis in organic irritation and should not
be regarded as entirely psychogenic without examination. These may
be much helped by psychotherapy, cold baths in the morning and cold
packs at night, and exercise during the day. The psychic effect of the
treatment will be greatly enhanced if the impression is clinched at once
by the administration of potassium or sodium bromide (1 Gm. =gr. xv,
t.i.d. and before going to bed) disguised in elixir of calisaya or in com-
pound tincture of gentian or of cardamom; for the patient's confidence
in the outcome is gained by finding the abnormal desire to decrease at
once with the onset of treatment.
ADENOIDS AND RESPIRATORY OBSTRUCTION.
Adenoids. — The presence of adenoid growths in the nasopharynx is also
of importance, not only because they interfere with the respiratory intake of
air and thus bring about dyspnoea on exertion, which may simulate a true
cardiac weakness, but also because attacks of mild asphyxia may occur
during sleep and cause the patient to awaken suddenly with a severe palpi-
tation and other cardioneurotic symptoms. Besides this, during waking
hours the lesions may continue to produce reflex irritation of the cardiac
nerves and give rise to cardioneurotic symptoms in the same way as do
disturbances in other organs.
Arrhythmia of Nasal Origin. — A physiological basis for these clinical
findings has been furnished by Francois-Franck (1889), who found that
an arrhythmia of vagal origin could be produced by stimulating the nasal
DISTURBANCES OF CARDIAC FUNCTION. 609
mucosa. His studies have recently been confirmed by Koblanck and
Roeder, who found that in 8 cases with arrhythmia and nasal disease
there were alterations in the mucous membrane of the nasal septum in
a spot opposite the middle turbinate bone. There were often nose-bleeds
as well. Touching this s p o t with a blunt probe in man and animals
produced a similar arrhythmia. No other area of nasal mucosa
gave this reflex. The arrhythmia was characterized by series of beats with
increasing rapidity interrupted by long pauses, sometimes simulating
extrasystolic bigemini (Curves 1 (man) and 3 (rabbit), K. and R.), but it
could not be produced after either vagus was cut. Stimulation of other
mucous membranes in this manner did not give rise to such arrhythmia.
The authors showed that these stimuli are carried by the septal branch of
the trigeminus which lies in this vicinity, for they could not be produced
after cutting the trigemini, and believe that they are carried directly from
the trigeminus nucleus to that of the vagus through the fasciculus longi-
tudinalis medialis. With cure of the nasal condition the arrhythmia and
allied disturbances disappeared.
Cardiac Asthma from Disease of Nasal Septum. — Franc, ois-Franck also
showed by careful graphic methods that stimulation of the nasal reflex can
give rise to cough, laryngeal spasm, asthma, and even a reflex bronchitis,
reflexes which in themselves may add to the impression of a primary
cardiac disturbance. He found that these reflex conditions were more
pronounced in animals with aortic insufficiency than in normal animals.
The condition in man is similar, and in the presence of an organic cardiac
lesion these contributing factors may play a role which determines the
security of the cardiorespiratory symptoms, so that the cause of the
paroxysmal dyspnoea may in some cases have to be looked for in the nose.
TOXIC CARDIONEUROSES.
"TOBACCO HEART."
Persons who suffer from excessive use of tobacco may be divided into
three classes:
1. Non-smokers suffering from a single indulgence (acute tabagism or nicotinism).
2. Young habitual smokers, especially those who inhale cigarette smoke (subacute
nicotinism).
3. Old habitual smokers, especially of cigars and pipes, who suffer from the patho-
logical changes produced in the arteries (especially the coronary arteries) and
myocardium, and partly from the added effects of the nicotine.
PHYSIOLOGICAL EFFECTS.
The physiological effect of smoking has recently been studied by Lee,
as well as by Bruce, Miller, and Hooker.
Lee found that ordinary tobacco smoke obtained from 1000 Gm. tobacco contained
nicotine 1.165 Gm., pyridine bases (chiefly pyridine and collidine) 0.148 Gm., HCN 0.08
( JIM., NH3 0.36 Gm., CO 410 c.c. The chief toxic product is therefore nicotine. The
composition varied considerably with both the quality of the tobacco and the mode of
smoking. The greater part of the nicotine at the seat of combustion is destroyed, and that
39
610 DISEASES OF THE HEART AND AORTA.
which reaches the mouth is volatilized by the hot gases while passing over the unhurried
area. Accordingly a thick cigar has the worst effect, since it acts as a chimney leading
the gases to the mouth, while in a thin cigar, "stogie," or cigarette they escape into the
surrounding air. (In cigarette smoking inhaling the smoke more than compensates for
this difference in combustion.) In long-stemmed pipes much of the nicotine condenses
before reaching the mouth.
Lee found that in non-smokers the first effect of smoking a
cigar was to produce a rise of 10-20 mm. Hg in the maximal blood-pressure,
which was often associated with palpitation. Within five minutes after
this the maximal blood-pressure fell 50 mm. Hg, and this fall was accom-
panied by pallor, sweating, weakness, and colicky pains in the abdomen, as
well as by the appearance of muscae volitantes, irregularity and weakness
of the pulse, — or, in other words, the symptom complex of arterial anaemia.
In more habitual smokers, those of the second group, a single
cigar produced only the rise of blood-pressure and palpitation. The subacute
symptoms, therefore, come on only as the result of excessive indulgence.
In old habitual smokers these observers found either no
effect whatever or only a slight rise of pressure resulting from a strong
cigar, without any of the disagreeable symptoms.
Lee's observations have been repeated by Bruce, Miller, and Hooker,
who found that smoking increases the maximal, minimal, and
pulse-pressures in man, though later these return to normal. The
cardiac output, therefore, seems to be increased at first, as Lee had found
in cats. Bruce, Miller, and Hooker also found that the volume of
the hand always decreased during smoking (vasoconstriction) ,
whereas Lee found that the volume of the cat's intestine also decreased.
It is probable that a little later there occurs, in man, a dilatation of the
abdominal vessels, but it is not yet certain that it does so.
The chief sufferers from tobacco are the young cigarette smokers who
inhale the smoke and thus soon suffer immediately from the physiological
effects of the nicotine. They complain of weakness, giddiness,
intense palpitation and tachycardia (from continued stim-
ulation of the cervical ganglion cells), and often of irregularity of
the heart, which may be very distressing. It is most noticeable that the
intense sensory disturbances occur without any motor insufficiency of
the heart. Thus, a young man of 20 years, an habitual inhaler of cigarette
smoke, recently consulted the writer, complaining of fatigue, giddiness,
muses volitantes, intense palpitation, but, on further questioning, stated
that he was in the habit of running a quarter of a mile every evening for
exercise, and after this exercise he had neither palpitation nor shortness
of breath! Needless to say, he improved at once after stopping tobacco.
On the other hand, all sufferers from nicotine are not free from motor
symptoms nor do they recover so readily. In many cases the nicotinism
is supplemented by the use of alcohol, and secondary myocardial changes,
and in the older persons arteriosclerotic changes, have been superinduced.
In the middle-aged smokers the symptoms are chiefly those of angina
pectoris and precordial pain. Very commonly this is a true angina of cora-
nary sclerosis, but there is a certain number of cases in which the unpleasant
symptoms completely subside upon cessation of smoking.
DISTURBANCES OF CARDIAC FUNCTION. 611
It would be a very fascinating hypothesis to believe that in such cases the effect of
smoking is to produce a transitory constriction of the coronary arteries and this to cause
the symptoms, but, on the contrary, some recent experiments upon dogs, done under the
writer's direction by Dr. George Bond, have shown that the flow through the coronary
veins is actually increased by smoking.1 It is probable, therefore, that in early tobacco
poisoning at least, the sensory symptoms are due to stimulation of the cardiac nerves and
not to ischaemia of the myocardium. The commonness and insidiousness of coronary
sclerosis, however, render it difficult to decide in any individual case whether the effect
is entirely functional or has also a basis in arterial changes.
COFFEE AND TEA.
The palpitation, tachycardia, and tremor which result from over-
indulgence in coffee and tea are familiar to most persons from personal
experience. They often manifest themselves in chronic forms and cause
cardioneurotic symptoms. Precordial pain and tenderness are quite com-
mon. Foote and Simpson, under D. R. Hooker's direction, have found
that when a person accustomed to coffee takes a cup of it there is a transi-
tory rise in maximal and minimal blood-pressure and a
slight vasoconstriction of the hand. In persons unaccustomed to
coffee these changes are much more intense. Indeed this partial immunity
to coffee is very transitory, for the writer has found that after discontinuing
its use for several months a single cupful would give rise to palpitation,
tachycardia, and insomnia, while a few months before and a few months
later two cups could be taken at a time without producing symptoms.
Coffee, like tobacco, gives rise to sensory cardiac symptoms by
increasing the irritability of the nerves without causing any motor insuf-
ficiency, and consequently the patients, as a rule, do not show muscular
or cardiac fatigue on exertion in spite of the symptoms.
Tea. — Owing to its content of caffeine, tea causes the same symptoms
as coffee, but is less extensively used in large quantities. In England,
however, similar cases are occasionally reported.
ALCOHOL.
Palpitation and the other symptoms of "cardioneurotic" (pseudo-
cardiac) weakness also occur in persons who take alcohol in quantities
that are just in excess of their tolerance, and the possibility of this cause
must be borne in mind. In some individuals, as in Reissner's case, palpi-
tation and irregularity may follow the ingestion of a single glass of wine,
without any symptoms of intoxication setting in. That these conditions
may continue without the patient's recognizing the cause is a common
experience, and a considerable number of cardioneurotic cases result from
this unintentional over-indulgence in alcohol. Women and young persons
are more sensitive than men. The functional power and endurance of the
heart muscle is, moreover, weakened by alcohol; and acute dilatation may
set in from comparatively slight exertion. If the use of alcohol is long
continued, it may lead to fatty and fibrinous myocardial change, but this
in mild cases subsides when the cause is removed.
1 Bond registered the outflow from the coronary veins by the drop method.
612 DISEASES OF THE HEART AND AORTA.
SIMPLE EMOTIONAL CARDIONEUROSES.
As has been seen, by far the greatest number of so-called cardioneurotic
cases are of postural, reflex, or toxic origin. However, it still remains
beyond question that emotional disturbances alone, or in conjunction with
other conditions which in themselves are not sufficiently intense to pro-
duce symptoms, may give rise to cardioneurotic symptoms. Palpitation
and even precordial pain are almost universal after severe emotional
disturbances and shocks and during periods of worry.
The motor effects are usually shown by tachycardia, though occa-
sionally arrhythmias may occur. This the writer has observed upon him-
self on an occasion of intense emotion, .during which the pulse became
extremely rapid and seemed either to drop an occasional beat or to give
rise to an extrasystole. When the cause of the worry was removed, within
five minutes the pulse again became regular, so that the arrhythmia could
not be accurately studied nor has it recurred at any other time during the
four years that have' elapsed.
Similar cases are found in the literature (Reissner). In rare cases an
emotional shock may cause death, even when the heart is otherwise healthy
(Gibson), but the nervous mechanism by which this is brought about is
not clearly understood. It is probably a condition of exaggerated vaso-
motor shock arising in response to a cortical stimulus, just as it may
result from over-stimulation of a peripheral nerve. In most cases of
the sort, however, the heart and especially the coronary arteries are
already diseased (see page 281).
BIBLIOGRAPHY.
CARDIAC NEUROSES.
Hoffmann, Aug.: Pathologie und Therapie der Herzneurosen, Wiesbaden, 1901.
Mackenzie, James: The Study of the Pulse and Movements of the Heart, Edinb. and Lond.,
1903. Diseases of the Heart, Lond., 1908.
Reissner, O.: Ueber unregelmassige Herztatigkeit auf psychischer Grundlage, Ztschr. f.
klin. Med., Berl., 1904, liii 234.
Einthoven, W., Flohil, A., and Battaerd, P. J. T. A.: On Vagus Currents examined with
the String Galvanometer, Quart. J. Exper. Physiol., Lond., 1908, i, 243.
Stadler, E., and Hirsch, C.: Meteorismus und Kreislauf (eine experimentelle Unter-
suchung), Mitth. a. d. Grenzgeb. d. Med. u. Chir., Jena, 1906, xv, 449.
McCaskey, G. W.: Diseases of the Digestive Organs in the Pathogenesis of Arterial Hyper-
tension, N. Y. M. J., 1906, Ixxxiv, 76.
Russell, W.: Arterial Hypertonus, Sclerosis, and Arterial Pressure, Phila. and Edinb., 1908.
Hering, H. E.: Zur experimentellen Analyse des unregelmassigen Pulses, Arch. f. d. ges.
Physiol., Bonn, 1900, Ixxxii, 1.
Miiller, F.: The Nervous Affections of the Heart, Arch. Intern. Med., Chicago, 1903, i, 1.
For an excellent general discussion see —
Wenckebach, K. F.: Ueber Pathologische Beziehungen zwischen Atmung und Kreislauf,
Samml. klin. Vortr., Leipz., 1907, Nos. 465 and 466.
Kraus, F.: Ueber konstitutionelle Herzschwache (discussion), Deutsch. med. Wchnschr.,
Leipz., 1905, xxxi, 1986, 2081.
Herz, M.: Herzmuskelinsufncienz durch relative Enge des Thorax (oppressio cordis),
Verhandl. d. Kong. f. innere Med., Wiesb., 1908, xxv, 292.
Einhorn, M.: Cardioptosis and its Association with Floating Liver (Proc. N. Y. Acad.
Med., Jan. 15, 1903), Med. Record, N. Y., 1903, Ixiii, 647 (with excellent bibliography).
DISTURBANCES OF CARDIAC FUNCTION. 613
Mosse: Demonstration eines Falles von icliopathischer Bathycardie, Deutsch. med. Wchn-
schr., Leipz., 1900, Ver. Beil. 266.
Janeway, E. G.: Bathycardia, Trans. Asso. Am. Physicians, Phila., 1903, xviii, 5 (also
discussion by Osier).
Keith, A.: The Nature and Anatomy of Visceroptosis, Lancet, Lond., 1904, i, 551, 631,
709, 818. A Method of Indicating the Position of the Diaphragm and Estimating the
Degree of Visceroptosis, J. Anat. and Physiol., Lond., 1908, xlii, 26.
Hill, L.: The Mechanism of the Circulation, Schafer's Text-book of Phsyiol., Edinb. and
Lond., 1900, ii, 46.
Erlanger, J., and Hooker, D. R.: An Experimental Study of Blood-pressure and of Pulse-
pressure in Man, Johns Hopkins Hosp. Rep., Baltimore, 1904, xii, 147.
V. Frey, M., and Krehl, L.: Untersuchungen iiber den Puls, Arch. f. Physiol., Leipz.,
1890, 31.
Hoppe-Seyler, G.: Zur Kenntniss der Magengahrung mit besonderer Berucksichtigung
der Magengase, Deutsch. Arch. f. klin. Med., Leipz., 1892, 1, 82.
Wyllie, J.: On Gastric Flatulence, Edinb.' Hosp. Rep., 1895, iii, 21.
Special Report on Diseases of Cattle, U. S. Dept. of Agriculture, Washington, 1904.
Special Report on Diseases of the Horse, ibid., 1903.
Kuthan, F.: Die Obstipation und ihre Einfluss auf die Herztatigkeit, Zentralbl. f. innere
Med., 1906, xxvi, 1076.
Veit: Aetiologie und Symptomatologie de Myome, Handb. d. Gynakol., 1898, ii.
Strassmann and Lehmann. Quoted from Fleck.
Fleck, G.: Myom und Herzerkrankungen in ihren genetischen Beziehungen, Arch. f. Gyna-
kol., 1904, Ixxi, 258.
Kelly, H. A., and Cullen, T. S.: Myomata of the Uterus, Phila., 1909.
V. Rosthorn, Lenhartz, Link, Schott, Krehl, Klemperer, Groedel, Janowski, Fellner:
Discussion of " Die Beziehungen der weiblichen Geschlechtsorgane zu inneren Erkran-
kungen, Verhandl. d. Kong. f. innere Med., Wiesbaden, 1908, xxv, 29.
Lazarus: Die adenoide Vegetationen und ihre Beziehungen zur dilatativen Herzschwache,
Festschr. f. Leyden, 1902.
Franc, ois-Franck, Ch. A.: Contribution a l'e"tude cxperimentale des nevroses reflexes
d'origine nasale, Arch, de physiol. de 1'homme et des anim., Par., 1889, 5e Se>. i, 538.
Koblank and Roeder H.: Experimental^ Untersuchungen zur reflektorischen Herzarhyth-
mie, Arch. f. d. ges. Physiol., Bonn, 1908, cxxv, 377.
Lee, W. E.: The Action of Tobacco Smoke, with Special Reference to Arterial Pressure and
Degeneration, Quart. J. Exper. Physiol., Lond., 1908. i, 335.
Bruce, Miller, and Hooker: The Effect of Smoking on the Blood-pressures and the Volume
of the Hand, Am. J. Physiol., Bost., 1909.
Foote and Simpson: Unpublished experiments, communicated by Dr. D. R. Hooker.
Gibson, G. A.: The Nervous Affections of the Heart, Edinb. and Lond., 1905.
Muller, L. R.: Klinische Beitrage zur Physiologic des sympathischen Nervensystems,
Deutsch. Arch. f. klin. Med., Leipz., 1907, Ixxxix, 432.
INDEX
Abdominal aorta, aneurism of, 550
Abdominal pain from distended liver, 159
in tricuspid insufficiency, 400
Abscess of heart-muscle, 226
Absolute arrhythmia, effect of digitalis in, 78
(see also Arrhythmia)
Acapnia, Cheyne-Stokes breathing from, 152
in shock and fevers, 31
Accelerations, reflex, 62
Accessory heart-sounds, 104
Accidental murmurs in splanchnoptosis, 600
Acetonitrile test for hyperthyroidism, 578
Aconite, 185
pharmacological action of, 185
therapeutic use of, 185
with digitalis, 186
Aconitin, 185
Acrocyanosis, 274
Acroparsesthesia, 274
Adams-Stokes disease (see also Adams-
Stokes syndrome; Heart-
block), 460
auricular heart sounds in, 461,
474
blood-pressure in, 30
differential diagnosis of, 474
effect of atropine in, 472
effect of iodides in, 476
effect of posture on, 476
etiological factors, 472
experimental, 465
lesions of auriculoventricular
bundle in, 470
occasional confusion with
paroxysmal tachycardia,
475
cesophageal tracings in, 474
prognosis in, 475
relation of heart-block to, 467
stoppage of ventricles in, 468
stoppage of ventricles in tor-
toise, 462
syncopal bradycardia, 460
treatment of, 476
X-ray examination in, 474
Adams-Stokes syndrome (A'dams-Stokes
disease), 460
from extrasy stoles alone, 471
without lesion of auriculoven-
tricular bundle, 471
Adenoids as cause of Basedow's disease, 585
asthma due to, 608
cardiac disturbances due to, 608
Adherent pericardium, 500
absence of symptoms from intra-
pericardial adhesions, 500
anginal attacks in, 291
ascites and hydrothorax in, 503
ascites in, 503
Broadbent's sign (retraction of
ribs) in, 504
cardiac dulness in, 504
cardiolysis for, 510
diastolic shock in, 505
effect on circulation, 501
fixation of lung borders in, 505
hallucinations in, 503
hydrothorax in, 503
indications for cardiolysis, 510
paradoxical respiratory ratio in,
504
physical signs of, 504
polyserositis in, 509
pseudocirrhosis of liver in, 509
pulse in, 504
pulsus paradoxus in, 504, 506
reduplication of first heart sound
in, 506
Riegel's pulse in, 506
sites of adhesions, 501
sounds over stomach in, 506
third heart sound and shock in,
505
treatment of, 509
X-ray shadows in, 507
Adhesions, pleural, simulating adherent
pericardium, 505
Adrenalin, 186
production of aneurism with, 525
test for hyperthyroidism, 578
Adrenals, hypersecretion in arteriosclerosis,
258
Air in pericardial cavity (pneumopericar-
dium), 494
Air-swallowing, 604
in angina pectoris, 296
treatment of, 605
Albuminous expectoration, test for, 150
Albuminuria, 156
Alcohol as cause of arteriosclerosis, 255
615
616
INDEX.
Alcohol, cardiac weakness from, 611
in cardiac disease, 168
Allorrhythmias, 61
classification of, 62
neurogenic, 62
reflex, 63
from nose, 63
from stimulation of gastric walls,
63
Amyl nitrite, action of, in man, 187
Anacrotic pulse, 47
Anaemia in cardiac overstrain, 124
in endocarditis, 317
Anatomical terms, synonymous, xxiii
Aneurism, 521
age of occurrence, 523
angina pectoris in, 291
blood-pressure in, 534
brassy cough in, 530
characteristics at various sites, 537
classification of, 521
delay of pulse wave in, 534
development of, 527
diagnosis of, 546
differentiation from tortuous arteries,
546
dilatation of pupils in, 533
dissecting, 547
pathology and pathogenesis, 547
symptoms and signs, 548
dulness over, 532
dysphagia in, 531
electrolysis in (Moorc-Corradi method),
552
embolic, 526
erosion from, 527
etiology, 522, 526
experimental, 525
frequency of, in women, 523
inequality of pulse in, 534
ligature of, method of Antyllus, 554
method of Brasdor, 555
method of Hunter, 554
low diet (Tufnell's) in, 551
mesarteritis in, 525
multiple, 523
murmur in, 531
mycotic, 526
of abdominal aorta, 550
pain in, 550
paralysis in, 551
rupture of, 551
tumor in, 550
of the heart, 234
of the pulmonary artery, 549
signs of, 549
pain in, 531
pulsations in, 532, 533
role of syphilis in, 522
rupture of, 527, 529
Aneurism, shock in, 531
sites of, 522
spontaneous clotting in, 529
suffocation in, 530, 531
symptoms of, 530
tracheal percussion shock in, 533
tracheal tug in, 533
treatment by compression, 554
by obliteration of sac (Matas), 556
by occlusion with metal bands, 555
use of calcium chloride in, 552
use of gelatin in, 552
use of potassium iodide for, 552
venesection in, 551
wiring of (Moore's), 552
X-ray examination in, 536
Angeioneuroses, 274
treatment of, 278
Angina pectoris, 284
and palpitation, 286
diagnosis of, 294
due to coronary sclerosis, 288
from tobacco, 293, 610
Heberden's description of, 284
hysterical, 292
importance of diet in, 296
in acute dilatation, 290
in aneurism, 291, 531
in children, 291
in hyperthyroidism, 293
in valvular diseases, 290
referred pains in, 287
sudden death in, 288
symptoms of, 284
theobromine in treatment of, 185
treatment of, 185, 295
varieties of, 288, 292
vasomotor, 291
Anginal pain, theories as to causation of, 289
Antagonistic muscles, contraction of, 142,
194
Aorta, dextroversion (Rechtslage) of, 433
hypoplasia of, 455
stenosis of isthmus, 453
adult type, 454
signs of, 455
treatment of, 455
type of new-born, 453
I Aortse, primitive, 422
| Aortic area, 102
Aortic disease in pregnancy, 419
Aortic facies, 367
Aortic insufficiency, 360
amount of blood regurgitating, 363
and mitral stenosis, differentiation
between, 353
asthma from lesion of nasal septum
in, 609
blood-pressure in, 29, 365, 372
cardiac outline in, 368
INDEX.
617
Aortic insufficiency, Cheyne-Stokes respi-
ration in, 366
diagnosis of, 376
diastolic murmur in, 369
double murmur (Duroziez's) over
the arteries in, 370
Flint's presystolic rumble, 371
functional, 360, 362
hallucinations in, 366
historical, 360
mitral insufficiency in, 377
organic, 360
pathological physiology of, 362
precordial pain in, 366
presystolic thrill in, 367
prognosis, 376
propagation of murmurs in, 370
pulmonary circulation in, 365
pulse-rate in, 365, 374
relation of collapsing pulse to
blood-pressure, regurgitation,
and resistance, 373
rupture of valves, 361
sclerosis of aortic valves, 361
treatment, 376
of anginal attacks in, 379
use of digitalis and strophanthus,
377
venesection in, 378
X-ray shadow in, 368
Aortic sclerosis, 263
Aortic stenosis, 381
anacrotic pulse in, 386
arrhythmia in, 383
atheromatous, 381
blood-pressure in, 387
cardiac outline in, 384
congenital, 452
endocarditic, 381
etiology of, 382
extrasystoles in, 387
failing compensation in, 383
intraventricular pressure in, 383
occurrence of, 382
pathological anatomy, 381
pulsus tardus in, 382, 385
symptoms of, 383
thrill and murmur in, 384
treatment of, 388
with aortic insufficiency, 382
Aortitis, 2r>:{
acute, 254
Apex beat, mechanics of, S!t
method of recording, 89
" mixed type," 91
time of, 89
Apex in mitral insufficiency, : '>-'•'
Apnoea, derivation of, in cardiac and pul-
monary diseases, 150
Apoplexy, blood-pressure in, 29
Arches, visceral (branchial), 423
Arrhythmia, 61
absolute, 75
effect of, on circulation, 77
from emotional excitement, 612
from lesions of nasal septum, 608
in increased intracranial tension, 64
in myocarditis, 238
in tricuspid insufficiency, 402
of psychic origin, 64
permanent, electrocardiogram in, 77
respiratory, 64
vicious circle of, 78
youthful type, 64
Arterial tension, 18
Arteries, changes in, in congenital heart
disease, 434
normal changes in, 249
sounds in, 117
strength of walls of, 523
tortuous, resembling aneurism, 546
Arterionecrosis, experimental, from adrena-
lin, 257
from tobacco, 256
from toxins, 256
in animals, 256
Arteriosclerosis, 249
blood-pressure in, 28, 261
diet in, 264, 265
etiology of, 254
following infectious diseases, 255
in children, 258
in hypothyrpidism, 575
intermittent claudication from, 259
nervous symptoms from, 259
nitrites in, 266
of abdominal aorta, 260
of abdominal vessels, 258
of retinal vessels, 260
potassium iodide in, 266
pulse in, 261
role of salt in, 258
second heart sound in, 263
theories of, 249, 257
unity of, 254
use of warm water in, 265
venesection in, 266
X-ray examination, 260
Arteriosclerotic changes in vasa vasoruni. •_'.">()
lesions, classification of, 251
distribution of. '2:*
Ascites, 155
in adherent pericardium, 503
Asphyxia, effects of. '27
Aspiration of hydrothorax, dangers in. l.'.f,
technic of, 156 (see also Para-
erntesis)
Astasia abasia iii Basedow's disease
Asthma, cardiac, 148
Asthma from lesions of nasal soptun
618
INDEX.
Atrioventricular bundle (see Auriculoven-
tricular bundle)
Atrophy of the heart, 211
Atropine, effect of, in heart-block, 466
effect of, on changes in tonus, 13
effect of, on extrasystoles, 73
test in heart-block, 472
use of, in pulmonary oedema, 151
Auricles, mitral stenosis in paralysis of, 345
Auricular paralysis, arrhythmia in, 140
cardiac overstrain in, 140
venous pulse in, 57
Auriculoventricular bundle, anatomy of, 463
clamping of, 464
lesions of, in Adams-Stokes disease,
470
physiology of, 464
Auscultation, 98
in suprasternal notch, 102
through the stomach tube, 104
Azygos vein, role in hydrothorax, 155
Bacterial vaccines in treatment of endo-
carditis, 311
Basedow's disease, 574, 576
acute, 587
anginal attacks in, 586
arrhythmia in, 583
astasia abasia in, 584
blood count in, 581
blood-pressure in, 30, 583
calcium salts in, 588
diagnosis of, 585
in " formes frustes," 586
etiological factors, 579
eye signs, 583
Dalrymple, 583
Mobius, 583
v. Graefe, 583
v. Stellwag, 583
force of heart in, 582
galvanization of cervical sympa-
thetic, 588
Jeffrey's sign of, 581
loss of weight in, 584
metabolism, 581
mortality in, 587
psychic symptoms, 582
psychotherapy in, 588
relation to hysteria, 579
secondary to adenoids, 585
specific sera in, 588
spontaneous recovery in, 587
sympathectomy for (Jonnesco),
590
symptoms and signs of, 581
tachycardia in, 582
thyroidectomy for, 589
indications for, 589
Basedow's disease, thyroidectomy for, re-
sults of, 589
treatment of, 587
tremor in, 584
triad and tetrad of symptoms, 580
wet packs in, 588
X-ray treatment of, 588
Baths, Nauheim, artificial, 201
Nauheim, natural, 201
physiological action of, 200
precautions of, 200, 201
Bathycardia, 603
Beer in cardiac disease, 168
Belts, effect of, in producing cardiac over-
strain, 134
Bicycle riding, effect of, on heart, 133
Bigeminal pulse, 72
causes of, 74
Bigeminus, 69
full, 69
shortened, 69
Bleedings in congenital heart disease, 437
Blood count in congenital heart disease, 441
Blood flow through muscles during exercise,
129
Blood, viscosity of, 38
Blood-pressure, 18, 141
apparatus, Erlanger's with Hirsch-
felder's polygraph attachment, 52
apparatus, forms of, 23
changes in exercises of speed, 130
determination of, auscultatory
method for, 23
of maximal, 19
of minimal, 20
Erlanger, 21
Janeway, 20
Masing, 20
Mosso, 20
Sahli, 20
Strasburger, 20
effect of digitalis on, 175
effect of exercises of strain on, 132
end pressure, 18
in aortic insufficiency, 365
in Basedow's disease, 583
in different parts of the vascular
system, 23
in normal individuals, 23
in paroxysmal tachycardia, 566
in various diseases, 28
lateral pressure, 18
maximal, 19
minimal, 19
physiological factors influencing,
25
variations in, under physiological
conditions, 26
Blowing diastolic murmur in mitral stenosis,
351
INDEX.
619
Blue babies, 437
Bradycardia, 48
in Adams-Stokes disease, 460
Brain tumors, blood-pressure in, 29
Brandy in cardiac disease, 168
Brauer chamber in operations on heart, 517
Breath-holding test, 150
Breathing, Cheyne-Stokes, 152
Broken compensation as indication for in-
ducing labor, 417
blood-pressure in, 30
functional valvular insufficiencies
in, 139
pseudo-elephantiasis in, 154
pulmonary, 139
systemic, 138
venous pressure in, 141
Broken pulmonary compensation in mitral
insufficiency, 327
Bronchitis in mitral insufficiency, 334, 337
Cachexia, blood-pressure in, 32
Caffeine, 184
in cup of coffee, 169
Calcification in arteriosclerosis, 252
pathogenesis of, 252
Calcium chloride for aneurism, 552
Calcium salts as cardiac tonics, 184
effect of, on cardiac contraction, 2
in Basedow's disease, 588
Calomel, 170
Camphor, 183
Canalis auricularis, 423
Capillaries, changes in, in congenital heart
disease, 434
determination of the pressure in, 33
malformation of, in congenital heart
disease, 435
Capillary pulse in aortic insufficiency, 367
Carbon dioxide, effects of, 27
Cardiac and adrenal hypertrophy, 208
Cardiac area, diameter of, 95
Cardiac asthma, 148
from coronary sclerosis, 283
from nasal disease, 149
Cardiac cicatrices, 234
Cardiac dilatation, mountain sickness as
cause of, 127
recovery from, 127
transitory, 127
fright as cause of, 127
Cardiac disease, symptoms of, 147
Cardiac diseases, acute, blood-pressure in, 32
Cardiac disturbances due to myoma, 607
due to sexual disorders, 606
in females, 606
in males, 606
from lesions of nasal septum, 608
from masturbation, 606
Cardiac disturbances, reflex, 604
air-swallowing in, 604
associated symptoms, 604
gastro-intestinal, 604
relation to menstrual flow, 607
sexual, treatment of, 608
Cardiac dulness area in children, 96
relative, 93
Cardiac dyspnoea, morphine and strychnine
in, 149
Cardiac efficiency, functional tests of, 141
Cardiac facies, 159
Cardiac failure with a small heart, 141
Cardiac flatness, 96
absence of, 96
fixation of area of, in adherent
pericardium, 505
pear-shaped, in pericarditis with
effusion, 490
variations in, 96
Cardiac impulse, 89
course of, 4
mechanics of, 89
movements in, 90
origin of, 4
protodiastolic wavelet on, 90
Cardiac muscle, tonicity of, 11
Cardiac nerves, action of, 13
effect of exercise on, 14
excision of, 14
tonic action of, 13
Cardiac neurasthenia, 593
Cardiac neuroses, 593
arrhythmia in, 593
classification of, 595
sexual, 606
symptoms of, 593
venous pressure, 593
Cardiac overstrain, anaemia in, 124
as cause of Adams-Stokes disease,
473
auricular paralysis and arrhythmia
in, 140
cases of, 121
chlorosis in, 124
diagnosis of, 128
dilatation of heart in, 125
extrasystoles in, 126
mountain climbing as cause of, 124
precordial pain in, 125
primary, 121
etiology of, 124
sexual excess as cause of, 124
tight belts as cause of, 124
Cardiac shadow as an index of cardiac vol-
ume, 13
Cardiac tonicity, effect of, on regurgitation,
363
Cardiac tonus in functional insufficiency,
324
620
INDEX.
Cardiac volume, cardiac shadow as an index
of, 13
Cardiohepatic angle (Ebstein's) in pericar-
dial effusion, 489
Cardiolysis for relief of adherent pericar-
dium, 510
Cardiometer, 9
Cardiopathia thyreopriva (hypothyroidism),
575
Cardioptosis, 596
Cardiosclerosis, 235
Cardiosphygmograph, 52
Cerebral thrombosis, blood-pressure in, 29
Chest, flat, in congenital heart disease, 440
Cheyne-Stokes breathing, 152
from acapnia, 152
treatment of, 153
types of, 152
Chlorosis in cardiac overstrain, 124
Choc en dome, 367
Cholera, blood-pressure in, 32
Chronic hypertrophy of the heart, blood-
pressure in, 29
Circulation in foetus, mechanics of, 427
Claudication, intermittent, 273
Clubbed fingers in congenital heart disease,
439
Coffee, effect of, 611
prohibition of, 169
Coitus, avoidance of, in cardiac disease, 419
Cold applications over the heart, 164
Collapse, blood-pressure in, 32
hypotension in, 32
Collapsing pulse, 47
Compensation, broken, hydraemia in, 39
broken pulmonic, 138
broken systemic, 138
symptoms of broken, 138
Concato's arch in pericarditis with effusion,
490
Concretio pericardii cum corde, 500
Connective-tissue proliferation, interfas-
cicular, 235
Constipation, effect on heart, 605
Constricting the femoral arteries, rise of
blood-pressure on, 142
Constriction, effect of, in producing cardiac
overstrain, 134
Contractility, diminished, in pulsus alter-
nans, 67
Contractions of heart, maximal, 4
Conus arteriosus, dilated, in mitral stenosis,
347
Convulsions in congenital heart disease, 437
Coordination of the cardiac chambers, 7
Cor biatriatum triloculare, 434
Coronary arteries, distribution of, 280
ligation of, 280
sclerosis of, 281
vasomotor nerves in, 281
Coronary circulation, physiology of, 280
Coronary sclerosis in patients with paroxys-
mal tachycardia, 283, 562
symptoms of, 283
Corrigan's pulse, 47
"Corset heart," 600
Corsets, effect of, in producing cardiac over-
strain, 134
Cough, 153
(brassy, stenotic, paretic) in aneurism,
530
Cyanosis, blood-pressure in, 30
in congenital heart disease, theories of,
438
in pulmonary stenosis, 437
in tricuspid stenosis, 408
Dalrymple's sign in Basedow's disease, 583
Death from labor, cause and frequency of,
414
Degeneration, calcareous, 224
hyaline, 224
parenchymatous, 224
waxy, 224
Delusions, 160
from digitalis poisoning, 160
typical, 161
Determination of the blood-pressures, aus-
cultatory method for, 23
Dextrocardia (dexiocardia), relation to
transpositions in embryo, 456
Diaphragm, high, 603
high, in fat persons, 603
Diarrhoea, blood-pressure in, 32
Diastasis and diastole, 9
Diastole and diastasis, 9
position of the valves in, 10
Diastolic closure of auriculoventricular
valves, 10, 56
Dicrotic notch, time of, in cardiac cycle, 55
pulse, 47
wave, 45
of pulse, 45
Diet, 167
Carell's, 168
effect of, on viscosity, 39
in cardiac disease, 167
lacto-vegetarian, 167
limited milk, 168
restricted liquids (Carell), 168
restriction of salts, 168
Digalen, 176
Digestive disturbances, 159
Digitalis, 172, 176
action of, 174
on coronary arteries, 175
stage of incoordination, 174
stage of irregularity, 174
therapeutic stage, 174
INDEX.
621
Digitalis, administration in fresh mitral
endocarditis, 337
and nitrites, 179
and strophanthus in aortic insuffi-
ciency, 377
arrhythmia and heart-block caused by,
179
drugs of series, 172, 173
effect of, on normal heart, 174
effect of, on the blood-pressure, 175
effect of, on tonicity, 176
flavoring of, 178
hallucinations from, 180
in second stage of mitral insufficiency,
338
in weakened hearts, 179
methods of administration, 178
period of administration, 178
poisoning, delusions from, 160
preparations of, 173
choice of, 176
rectal administration of, 178
standardization of, 173
Digitoxin, 176
Dilatation of the heart, acute, angina pec-
toris in, 290
acute, pain due to, 289
from constriction, 134
in cardiac overstrain, 125
in myocarditis, 227
physiological factors bringing
about, 135
transitory, 127
Diphtheria as cause of endocarditis, 303
blood-pressure in, 31
Diplococcus rheumaticus, 301
Displacement of the heart, 595
Drugs, mode of action on circulation, 172
Duct of Cuvier, 422
Ductus arteriosus (Botalli), closure of, 449
factors causing persistence of,
449
open, 434
patent, 448
diagnosis of, 452
murmur in, 450
pathogenesis of, 448
pulsus paradoxus in, 451
respiratory interchange
in, 452
signs of, 450
symptoms of, 450
treatment of, 452
X-ray shadow in, 450
role in foetus, 428
Ductus venosus, atrophy of, 429
Duroziez's double murmur over the arteries
in aortic insufficiency, 370
Dysentery, blood-pressure in, 32
Dyspnoea, 147»
Dyspnoea in congenital heart disease, 437
mechanical changes in circulation, 147
Ebstein's cardiohepatic angle in pericardial
effusion, 489
Ectopia cordis, 429
Effusion in pericarditis, 487
Electricity in treatment of angina pectoris,
297
Electrocardiogram, 60
in extrasy stoles, 70
in hypertrophy of left ventricle, 60
in hypertrophy of right ventricle, 60
Embolism in mitral stenosis, 356
pulmonary, 151
Embryocardia, 104
in paroxysmal tachycardia, 568
Emotion, arrhythmia from, 612
effect of, on the heart, 612
Emptying of the heart, 8
Endarteritis, 251, 253
Endocarditic vegetations, bacterial origin,
299
development of, 299
Endocarditis, 299
anaemia in, 317
cerebral embolism in, 308
cerebral type, 308
choked disk in, 308
chronic, 300, 306
chronic infective, 309
complications of, 315
differential diagnosis of, 309
digitalis in, 316
due to pyogenic cocci, 302
effect on circulation, 304
from miscellaneous infections, 303
gonorrhoeal, 303
involvement of valves, 312
jaundice in, 307
malignant, 305, 306
complications, 306
brain symptoms, 306
embolic aneurisms, 306
enlarged spleen, 306
haematuria, 306
heart failure, 306
petechiac, 306
retinal hemorrhages, 306
frequency of, 306
valves involved in, 306
microbes producing, 301
mural, 300
palliative treatment of tonsils in, 318
pathological physiology of, 304
pathology of, 300
pneumococcic, 303
prophylaxis, 317
reinfection, 315
622
INDEX.
Endocarditis, retinal hemorrhages, 308
rheumatic, 301, 311
septicaemic, 307
simple acute, 305, 311
compensation in, 315
course of, 314
pathology of, 313
signs, 314
symptoms of, 313
statistics of, 311
treatment of, 317
typhoidal type, 308
ulcerative, 300
Endocardium, atheroma of, 304
pockets of, in aortic insufficiency, 433
Endothelial cells in sputum, 153
Endurance, exercises of, 131
Energy, waste of, in fatigue, 131
Enteroptosis (see Splanchnoptosis)
Epilepsy, blood-pressure in, 29
Ergotism, resemblance to Raynaud's dis-
ease, 275
Erosion of bone by aneurism, 527
Erythromelalgia, 274
Erythromelia, 277
Exercise, choice of, 198
effect of, on blood-pressure, 26
systems of, in therapeutics, 193
test of cardiac function, 142
Exercises, effect of, on size of heart, 133
of endurance, 131
circulation in, 131
mechanics of, 129
of speed, mechanics of, 129
of strain, 132
effect on blood-pressure, 132
mechanics of, 129
Exophthalmic goitre (see Basedow's disease)
Exophthalmos from stimulation of sympa-
thetic, 583
Extrasystoles, 68
auricular, 69
auriculo(atrio)ventricular, 73
auriculoventricular, lesions in, 74
diagnosis of, 71
effect of atropine on, 73
electrocardiogram in, 70
experimental production of, 71
heart sounds in, 72
in cardiac overstrain, 126
in myocarditis, 238
ineffectual, 72
palpitation with, 71
stimuli causing, 70
venous pulse in, 70
ventricular, 69
Face, oedema of, 154
Fades, aortic, 88
Facies, cardiac, 88, 159
mitral, 88
Fatigue, effect of, on energy used up, 131
Fats, diminished absorption of, 159
Fatty degeneration of the heart, 219
etiology, 221
nature of, 220
pathological anatomy of, 219
rupture of the heart in, 223
strength of heart with, 221
symptoms and signs of, 222
Fatty infiltration of the heart, 214, 215
nature of the fatty deposit,
215
physical signs of, 217
treatment of, 217
Fetal heart sounds, graphic record of, 104
Fevers, acapnia in, 31
Filling of the heart, 8
of the ventricles, 9
First sound at aorta, 100
cause of, 99
character of, 99
duration of, 100
in suprasternal notch, 100
reduplicated, 104, 105
Fluoroscope, 82
diagnosis by, 85
Foetus, circulation in, 427
Football playing, effect of, on heart, 133
Foramen ovale, development of, 425
effect of patency on circulation, 447
open, 434
patent, 446
crossed embolism in, 448
occurrence and pathogenesis,
446
paroxysmal cyanosis in, 448
signs of patency, 448
symptoms of patency, 447
treatment of, 448
vicious circle in, 436
Formative stimulus in arteriosclerosis, 253
Fragmentation of muscle fibres, 225
Friction in pericarditis, 484
pleuropericardial, 484
Functional mitral insufficiency, 322
Functional tests of cardiac efficiency, 141
of cardiac insufficiency, valueof , 143
relation of, to mode of life, 143
Gallop rhythm, presystolic, 105, 106
protodiastolic, 105, 107
Gastric ferment action, 604
Gonococcus as cause of endocarditis, 303
Graefe's sign in Basedow's disease, 583
Graves's disease (see Basedow's disease)
Gymnastics, 193
fundamental principles of, 193
INDEX.
623
Hsemopericardium, 493
from cardiac tumors, 246
Haemoptysis from pulmonary stasis, 151
in pulmonary insufficiency, 392
Hsemosiderin in Herzfehlerzellen, 153
Hallucinations, 160
in adherent pericardium, 503
Headaches in congenital heart disease, 437
Heart, changes in position of, 97
changes in size of, 97
development of, early stages, 421
dilatation of, from constriction, 134
diminution in size of, in exercise, 133
disease and matrimony, 419
congenital, 421
blood count in, 441
etiological groupings, 430
flat chest in, 440
groups of lesions in, 429
syndrome of, 430
displacement of, 595
effect on circulation, 596
cndothelial tube in embryo, 422
high, 604
effect on circulation, 604
treatment of, 604
xiphisternal line with, 604
insensibility of, 286, 515
lesions, congenital, classification of, 429
low, 596, 603
signs of, 603
mobility of, in cardioptosis, 596
muscle, properites of, 1
structure of, 1
muscular tube in embryo, 422
non-perforating injuries of, 518
normal mobility, 596
nourishment of, 281
small, in cardiac failure, 141
sound, first, reduplication of, in adhe-
rent pericardium, 506
second aortic, in arteriosclerosis,
263
second, in mitral insufficiency, 333
third, in adherent pericardium, 505
sounds, accessory, 104
causes of, 99
clinical diagram for, 99
digital imitation of, 115
graphic record of, 98
reduplicated, 104, 105
split, 105
three-chambered, 434
tumors of, 245
work of, 26
wounds of, 513
cause "f ,!,.;, th from, 514
experimental Mirjrory of, 513
hemorrhage in. ~>17
murmurs in, 515
Heart, wounds of, operative treatment of, 515
spontaneous recovery in, 513
suture of, 516
symptoms of, 515
X-ray examination of, 515
Heart-beat, origin of, 2
Heart-block (see also Adams-Stokes dis-
ease), 65, 460, 462
auriculoventricular, 66
complete, 66, 466
effect of atropine on, 466
effect of vagus on, 466
from cutting interauricular sep-
tum, 461
functional, 66
in infectious diseases, 472
in tortoise, 462
organic, 66
partial, 66, 466
effect of heart rate in, 466
from digitalis, 473
relation to Adams-Stokes syn-
drome, 467
rdle of vagus in, 461
sino-auricular, 67
Hemorrhage, blood-pressure in, 32
fall of blood-pressure in, 32
from the lungs, 151
in wounds of heart, 517
intracranial, blood-pressure in, 29
Heredity in arteriosclerosis, 256
Herzfehlerzellen, 153
Hiccough in pericarditis, 483
High diaphragm, 603
heart, 604
Hippocratic fingers, 439
His bundle, anatomy of, 463
Hoarseness in pericarditis, 483
Hormone action in cardiac symptoms, 608
Hydropericardium, 493
Hydrotherapy, 200
in arteriosclerosis, 265
Hydrothorax, 155
in adherent pericardium, 503
production of, 155
Hyperdicrotic pulse, 47
Hypertension as factor in production of
arteriosclerosis, 257
diseases with, 28
Hyperthyroidism, 576
acetonitrile test for, 578
adrenalin test for, 578
angina pectoris in, 293
effect on heart muscle, 578
effect on nervous system, 578
vicious circle of, 579
Hypertrophied heart, reserve force of, 210
Hypertrophy, 203
adrenal, 208
and abdominal arteriosclerosis, 208
624
INDEX.
Hypertrophy and arteriosclerosis, 207
cardiac, 208
concentric, 205
excentric, 205
from overdrinking, 207
from work, 205
in chronic nephritis, 207
of the auricles, 210
of the heart in Basedow's disease, 583
of the left ventricle, 209
of the right ventricle, 209
pathological anatomy of, 203
sites of, 205
Hypotension, failure of vasomotor centre
in, 30
Hypothyroidism, effect on circulation, 575
Hysterical angina, 292
Ice-bag over heart, 165
contraindications to, 165
effect on pulse rate, 165
Increased intracranial pressure, blood-pres-
sure in, 29
Infectious diseases as causes of arteriosclero-
sis, 255
as causes of Basedow's disease, 579
hypotension in, 31
Influenza as cause of Basedow's disease, 580
as cause of endocarditis, 303
Injuries of heart, 518
Insufficiency, mitral, 321
of valves in broken compensation, 139
Intermittent claudication, 273
Interstitial pneumonia, 153
Intervenous area, physiology of, 7
Interventricular septum, defects in, 442
patent, 442
with pulmonary stenosis, 433,
437
Intravenous injections in treatment of endo-
carditis, 311
Intraventricular pressure, 18
lodothyrin, 576
Irregularity, permanent, 76
Irritability in cardiac disease, 160
Jaundice, catarrhal, in broken compensa-
tion, 159
in endocarditis, 307
Jellinik's sign of Basedow's disease, 579
Jeffrey's sign of Basedow's disease, 581
Labor (see Pregnancy)
and pregnancy in persons with heart
disease, prognosis, 415
cardiac overstrain during, 414
Langendorff's perfusion apparatus, 3
Laryngeal paralysis in aneurism, 530
Lead poisoning, blood-pressure in, 29
Left auricle, pressure in fetal life, 429
Liquids, restriction of, in arteriosclerosis,
265
Liver, abdominal pain from distended, 159
presystolic pulsation in tricuspid steno-
sis, 408
pulsation of, in tricuspid insufficiency,
402
signs simulating cirrhosis of, in adhe-
rent pericardium, 509
Low heart, 603
Lungs, hemorrhage from, 151
Magnesium sulphate, 170
Marching, effect of, on heart, 133
Masturbation, effect of, on heart, 606
Matrimony and heart disease, 419
Meals, effect of, on blood-pressure, 26
Measles, blood-pressure in, 31
Mechanical factors in the production of mur-
murs, 109
Mechanogymnastics, 197
Medial changes in aneurism, 525
Mediastinopericarditis, 500
Meningitis, blood -pressure in, 29
Menstruation, relation of, to cardiac symp-
toms, 607
Mental distraction, 163
exertion, effect of, on blood-pressure, 27
Mesarteritis, 251, 252
Metabolism, increase from thyroid secretion,
577
Micrococcus rheumaticus, 301
Mid-diastolic rumble stenosis, 350
Mill-wheel murmur in pneumopericardium,
494
Mitral area, 102
Mitral disease, pulmonary complications of,
327
Mitral facies in mitral insufficiency, 329
Mitral insufficiency, 321
and tuberculosis, 336
arrhythmia in, 334
blood-pressure in, 333
broken compensation in, 339
broken pulmonary compensation
in, 327
broken systemic compensation in,
328
cardiac area in, 330
digitalis in, 338
early administration of digitalis in,
337
functional, 322, 323, 324
mechanics of, circulation, 324
murmur and sounds in, 331
oesophageal tracing in, 58
INDEX.
625
Mitral insufficiency, organic, 321
outward displacement of apex in,
329
papillary, 322
pathology of, 321
prognosis in, 339
propagation of murmur, 332
pulmonary stasis in, 325, 336
purgation in, 338
re-education of heart muscle in,
337
relative, 322
second heart sound in, 333
second stage of, 327
stages of, 326
stasis in left auricle, 324
statistics of, 321
systolic murmur in, 331 *
third stage of, 328
tonicity of the heart in, 328
treatment of second stage of, 338
with mitral stenosis, 349
without symptoms, 326
X-ray shadow in, 330
Mitral stenosis, 341
anaemia in, 357
and aortic insufficiency, differen-
tiation between, 353
and tricuspid stenosis, 355
blood-pressure in, 32
blowing diastolic murmur in, 351
cardiac outline in, 347
complications, 355
congenital form, 342
diagnosis, 352
digital and phonetic imitation of
the heart sounds in, 349
dilated conus arteriosus in, 347
disappearance and reappearance
of presystolic rumble in, 345
effect of auricular contraction on
filling of ventricles, 344
embolism in, 356
endocarditic form, 342
etiology, 342
historical, 341
laryngeal paresis in, 345
mid-diastolic rumble in, 3"0
operations on mitral valve, 357
paralysis of auricles in, 345
pathological physiology of, 343
pathology of, 341
presystolic rumble in, 317
thrill and systolic tap in, 346
prognosis, 357
pulmonary cedema in, :'..~>ii
pulse in, 352
«|ii:ility ;m<l production of tho
sounds, 348
role of oedfiiKi and anaemia in, 342
40
Mitral stenosis, sclerotic form, 342
snapping first sound in, 348
stages of, 351
symptoms and signs, 345
third heart sound in, 350
thrombosis in left auricle in, 356
treatment of, 356, 357
tuberculosis in, 342
volume of ventricles in, 343
with mitral insufficiency, 342, 349
X-ray shadow in, 348
Mitral valve, atheroma of, 323
hemorrhage in, 323
malformation of, 458
tests for sufficiency, 322
demonstration of action of, 10
Mitralized pulse, 334
Mobility of heart, 98
Mobius' sign in Basedow's disease, 583
Monckeberg's arteriosclerosis, 251
Moore-Corradi method, reasons for failure
of, 553 .
Morbus coeruleus, 436
Morphine, dangers from, in myocarditis,
243
in cardiac dyspnoea, 149
Movements, resisted, 194
Schott, 194
Murmur at back in patent ductus Botalli,
440
diastolic, in pulmonary insufficiency,
393
mitral, differentiation from accidental
and tricuspid, 332
digital imitation of, 331
phonographic tracing of, 331
propagation of, 332
Roger's systolic in open septum ventric-
ulorum, 444
systolic, in aortic stenosis, 384
in mitral insufficiency, 331
in tricuspid insufficiency, 400
Murmurs, 109
accidental, 111
causation of, 113
differential diagnosis of, 112
nature of, 113
time of, 112
cardiopulmonary, 111, 114
character of, 110
differentiation between cardiopulmo-
nary and other accidental murmurs,
115
functional, 111
haemic, 111, 113
mechanical factors in the production
of, 109
phonetics of, 109
tabulation of, 116
Myocardial changes, distribution of, 225
626
INDEX.
Myocarditis, 224
acute, arrhythmia in, 228
alcoholic, 231
and nephritis, 240
arrhythmia in, 237, 238
bronchitis in, 238
catalase in, 240
chronic, 234
blood-pressure in, 237
diagnosis of, 232
differential diagnosis in, 241
dilatation in, 227
diphtheric, 230
extrasystoles in, 238
hypersensibility to digitalis, 233
influenzal, 230
murmurs in, 238
pathological physiology of, 236
rheumatic, 229
signs and symptoms of, 229
strychnine in, 234
symptoms and signs of, 238
treatment of, 232, 242
weakness of heart in, 228
Myocardium, affections of, 224
syphilis of, 244
Myoma as cause of cardiac weakness, 607
Nasal disease, cardiac asthma from, 149
Nasal septum, arrhythmia from lesion of,
608
asthma from lesion of, 609
Nauheim treatment, 164
Nephritis and myocarditis, 240
blood-pressure in, 28
Nerve-fibres producing changes in tonus, 13
Neurasthenia, cardiac, 593
Nitrites, 186
action of, 187
and digitalis, 179
effect of, in hypertension of intracranial
origin, 30
use of, in angina pectoris, 295
in aortic insufficiency, 377
in arteriosclerosis, 266
Nitroglycerin, 186, 188
mode of administration, 188
tolerance to, 188
Oarsmen, longevity of, 137
Obesity, diet in, 218
high diaphragm in, 216, 603
of the heart, 214
physical signs of, 217
treatment of, 217
with cardiac atrophy and cardiosclero-
sis, 216
with coronary sclerosis, 216
(Edema, 153
effect of drugs and diet on, 154
fluid, salt content of, 154
lymphagogue substance in the blood in,
153
of face, 154
of heart muscle, 138
pulmonary, 150
treatment by drainage, 155
types of, 153
Oertel's mountain climbing, 198
(Esophageal auscultation, 104
of mitral murmur, 332
tracings, 58
in mitral insufficiency, 58
Orthodiagraph, 85
Orthopercussion, 93
Orthoplessimeter, 94
Orthopncea, 148
mechanical changes in circulation, 148
Outflow during systole, 9
Pain down the arms, 158
on swallowing in pericarditis, 483
precordial, 158
referred from cervical ganglia, 158
sensations, paths traversed by, 286
Palpation of heart, 92
Palpitation, 157
and angina, 286
cardiac sensations in, 157
with extrasystoles, 71
Papillary insufficiency, 323
muscles, fatiguing of, 55
in propagation of mitral murmur,
332
Paracentesis abdominis, 155
Paradoxical respiration in enteroptosis, 599
Pararrhythmias, 62, 75
Paroxysmal tachycardia, 78, 560
associated lesions, 562
auricular fibrillation in, 564
belching in, 572
cardiac dulness during attacks, 568
cerebral anemia in, 568
coronary sclerosis in, 562
diagnosis of, 570
differentiation from simple tachy-
cardia, 570
doubling of rate in, 560
drugs in, 571
dyspnoea in, 567
effect on circulation, 566
embryocardia in, 568
fall of blood-pressure in, 566
from ligature of coronary arteries,
565
fulness of neck in, 567
in coronary sclerosis, 283
INDEX.
627
Paroxysmal tachycardia, inactivity of car-
diac nerves in, 565
inception of rhythm by auriculo-
ventricular bundle, 564
interpolated extrasystoles, 563
lesions in auriculoventricular bun-
dle in, 563
lesions in vagus nucleus, 563
occasional confusion with Adams-
Stokes disease, 475
precordial pain in, 567
rise of venous pressure in, 566
sino-auricular block, 464
stimulation of vagi in, 571
sudden exercise in, 571
swallowing in, 572
symptoms of, 567
theories as to origin, 563
treatment of, 571
tricuspid insufficiency in, 568
types of, 561
venous pulse in, 561
vomiting in, 572
Parry's disease (see Basedow's disease)
Passive movements, 194
Patent foramen ovale, 466
pathogenesis of, 466
Percussion, 92
errors in, 94
methods of, 93
Perfusion of excised mammalian heart, 3
Periarteritis, diffuse, 252
Periarteritis nodosa, 251
Pericarditis, 480
adhesfve (see Adherent pericardium),
500, 504
blood-pressure in, 32, 485
etiology of, 480
friction at back in, 485
friction sound in, 484
hiccough in, 483
hoarseness in, 483
pain on swallowing in, 483
precordial pain in, 483
purulent, 493
simple fibrinous, 483
diagnosis of, 485
prognosis in, 487
treatment of, 486
signs of, 483
symptoms of, 483
tuberculous, 494
fluid in, 494
with effusion, 487
amount of fluid, 487
blood-pressure in, 491
drainage in, 497
Ebstein's cardiohepatic angle
in, 489
effect on circulation, 487
Pericarditis with effusion, enlargement of
liver from, 490
fulness of interspaces in, 489
irrigation of pericardium in,
498
paracentesis of, 495
pericardiotomy in, 497
position of heart in, 490
Rotch's sign in, 489
signs at back in, 490
signs of, 489
symptoms of, 488
treatment of, 495
X-ray examination of, 491
Pericardium, adherent, 291, 500
development of, 426
Peripheral resistance, 44
Peritonitis, blood-pressure in, 31
Petechiae in endocarditis, 307
Phosphorus poisoning, effect of, on heart in
fatigue, 134
Phthisis, blood-pressure in, 31
Physiological conditions, variations in blood-
pressure under, 26
Pigmentation in hyperthyroidism (Jellinik's
sign), 579
Placenta, vessels to, 422
Pleurisy, blood-pressure in, 32
Pleuropericardial friction, 484
Pneumococci as causes of endocarditis, 303
Pneumonia as cause of pericarditis, 480
blood-pressure in, 31
interstitial, 153
Pneumopericardium, 494
Polycythsemia, blood-pressure in, 30
Polygraph, Mackenzie, 52
Marey, 52
Uskoff, 53
Position, changes in, 97
effect of change of, on blood-pressure, 26
Posture, effect of, on pulse-rate, 142
Potassium iodide, 189
effect of, on viscosity of blood, 39
for aneurisms, 552
in angina pectoris, 295
in arteriosclerosis, 266
mode of administration, 189
supposed effect on viscosity of
blood, 189
salts, effect of, on cardiac contraction, 2
thiocyanate, 190
therapeutic use of, 190
Precordial pain, 158
in cardiac overstrain, 125
in pericarditis, 483
Pregnancy and labor, pulmonary cedema in,
414
aortic disease in, 419
as cause of Basedow's disease, 579
blood-pressure in, 30
628
INDEX.
Pregnancy, broken compensation in, 416
effect on pulse and blood pressure, 413
hypertrophy during, 413
termination of, 418
in broken compensation, 417
treatment of heart lesions during, 416
Presphygmic period, 8
Presystolic gallop rhythm, resemblance to
mitral stenosis, 353
rumble, disappearance and reappear-
ance of, in mitral stenosis, 345
(Flint's) in aortic insufficiency, 371
in mitral stenosis, 347
in tricuspid stenosis, 409
Pseudo-anginal pain, 289
Pseudo-aortic insufficiency, 367
Pseudocardiac disturbances, 595
Psychic disturbances, 159
Psychotherapy in Basedow's disease, 588
Puerperal infection as cause of Basedow's
disease, 580
Pulmonary area, 102
Pulmonary artery, aneurism of, 549
blood-pressure in, before birth, 33
development and maldevelopment
of, 432
sclerosis of, 264
vasomotor nerves in, 34
Pulmonary circulation, 33
action of drugs on, 34
Pulmonary embolism, 151
Pulmonary hemorrhage, 151
Pulmonary insufficiency, diagnosis of, 394
diastolic murmur in, 393
etiological factors, 391
forms of, 390
functional, 390
haemoptysis in, 392
pathological physiology, 391
prognosis in, 394
pulse in, 393
signs of, 392
symptoms of, 392
treatment of, 394
with pulmonary stenosis, 440
Pulmonary oedema, 150
artificial respiration in, 150
in mitral stenosis, 356
in pregnancy and labor, 414
signs of, 150
treatment of, 151
Pulmonary pressure, 34
conditions affecting, 34
Pulmonary stenosis and atresia, causes of,
430
due to endocarditis, 430
due to maldevelopment of
branchial arches, 431
duration of life in, 441
statistics of, 430, 441
Pulmonary stenosis in open interventric-
ular septum, 439
pathological physiology of, 435
with patent interventricular sep-
tum, 433, 437
Pulsations, inspection of, 532
over chest, 92
Pulse, anacrotic, in aortic stenosis, 386
arterial, 41
curve, significance of, 44
dicrotic, 41
discrepancies in examining, 43
examination of the, 41
form, 44
in aortic insufficiency (Corrigan, water-
hammer, collapsing), 372
qualities- of the, 41
rate, 46
effect of ice-bag on, 165
effect of posture on, 142
relation to temperature, 46
types of, 47
anacrotic, 47
bisferiens, 47
collapsing, 47
dicrotic, 47
hyperdicrotic, 47
normal, 47
tardus, 47
venous, 49
wave, inequality and delay of, in aneu-
risms, 534
Pulse-pressure, 19
Pulsus alternans, contractility diminished
in, 67
Pulsus tardus in aortic stenosis, 382, 385
Pupils, inequality of, in aneurism, 533
Purgation, 169
in broken compensation, 169
rise of venous pressure during, 170
Purgatives, 170
Quiet in treatment, 163
Radiographs, technique of, 86
Raynaud's disease, 274
pathology of, 275
Rectal administration of digitalis, 178
Reduplicated heart sounds, 104
Re-education of heart muscle in mitral in-
sufficiency, 337
Referred pains in angina pectoris, 287
Reflex cardiac disturbances, 604
air-swallowing in, 604
associated symptoms, 604
gastro-intestinal, 604
Relative insufficiency, 323
Renal complications of cardiac diseases, 156
INDEX.
629
Residual blood, 12
Respiration, method of recording, 52
paradoxical type, 599
Respiratory ratio, 150
in adherent pericardium, 504
Rest in bed, 164
Retina, arteriosclerosis of, 260
dilatation of veins of, in tricuspid insuf-
ficiency, 400
Retinal changes in congenital heart disease,
438
Rheumatic fever as cause of pericarditis, 480
foci of myocarditis in, 226
Rheumatism, blood-pressure in, 31
cocci causing, 301
Riess' sign of adherent pericardium, 506
Right ventricle, tonicity of, 34
work of the, 33
Rise of blood-pressure on constricting the
femoral arteries, 142
Rotch's sign of pericardial effusion, 489
Rupture of aneurism, 527
" Safety-valve " action of tricuspid valve,
397
Salt, restriction of, 168
Salts, role of, in origin of heart beat, 2
Sauerbruch chamber in operations on heart,
517
Scarlatina as cause of endocarditis, 303
blood-pressure in, 31
pericarditis from, 481
Schott movements, 194
effect of, in reducing cardiac dila-
tation, 197
precautions in, 195
Second sound, 100
Second wind, 130
Sensory stimulation, effect of, on blood-
pressure, 27
Septum auriculorum, 424
Septum interpositum, 425
Septum ventriculorum, 424, 442
patent, effect on circulation, 443
prognosis in, 445
signs of, 443
symptoms of, 443
systolic murmur in, 444
trauma as cause of, 442
treatment of, 445
tuberculosis in, 442
Sexual cardiac disorders, 606, 608
Sexual excess as cause of Basedow's disease,
580
Shock, acapnia in, 31
l)lo(xl-pressure in, 31
diastolic, over aneurism, 546
Sino-auricular block from cooling sinus, 5
in in;mmi:ils, 7
Sino-auricular block in paroxysmal tachy-
cardia, 564
Sinus as "pace-maker" of the heart, 4
Sinus region in mammals, anatomy of, 5
Sinus reuniens, 424
Sinus, role of , in mammals, 6
Sinus wave on venous pulse, 56
Situs transversus, 456
Skull, fracture of the, blood-pressure in, 29
Sleep, effect of, on blood-pressure, 27
importance of, 163
Smallpox as cause of endocarditis, 303
Smoke, tobacco, composition of, 609
Smoking, effect of, on circulation, 610
precordial pain from, 6l6
Snapping first sound in aortic insufficiency.
371
in mitral stenosis, 348
Sounds, alteration of, by pressure, 101
in arteries, 117
over veins, 118
Southey's tubes, 155
Spa treatment, 164
Sphygmobolometer, Sahli, 23
Sphygmogram, the absolute, 43
Sphygmograph, clinical, 41
Dudgeon, 42
v. Jaquet, 42
Marey, 42
Roy and Adami, 42
Sphygmogfaphy, errors in, 42
Sphygmomanometer, v. Basch, 19
Erlanger, 21
Gibson, 23
Hill and Barnard, 20
Marey, 19
Potain, 20
v. Recklinghausen, 19
Riva-Rocci, 20
Sphygmoscope, Pal, 22
Sphygmotonometer, v. Recklinghausen, 22
Splanchnoptosis, 598
abdominal binder in, 600
air-cushion for, 601
blood-pressure in, 599
corset in producing, 600
effect on circulation, 599
effect of, on respiration, 598
level of diaphragm, 598
overfeeding in, 601
pulsus paradoxus in, 600
syncope from, 599
tracheal tug in, 599
treatment of, 600
Sputum, prune-juice, 151
Stair climbing, beneficial effects of graded
pauses, 198
Stasis, effect of, on producing cardiac
redema, 138
Stellwag's sign in Basedow's disease, 583
630
INDEX.
Stenosis of isthmus of aorta, 453
Sterilization of patients with broken com-
pensation, 419
Stethoscope, binaural, essentials of, 101
monaural, 100
Stohiach, sounds over, in adherent pericar-
dium (Riess), 506
Stoppage ot ventricles, 465
in Adams-Stokes disease, 468
Strain, effect of, on the heart, 136
exercises of, 132
Strophanthus, 173
Strychnine, 181
and digitalis, 316
clinical effects, 181
effect on blood-pressure, 182
effect on cardiac tonicity, 181
in cardiac dyspnoea, 149
indications for, 183
pharmacological action of, 181
preparations of, 181
Sudden death in angina pectoris, 288
Suture of wounds in heart, 516
Swimming, effect of, on heart, 133
Sympathectomy in Basedow's disease, 590
Sympathetic nerves, relation to exophthal-
mos, 583
stimulation by thyroid secretion,
577
Symptoms of adherent pericardium, 503
of cardiac disease, 147
Syncope in paroxysmal tachycardia, 568
Synechiae pericardii, 500
Syphilis as cause of arteriosclerosis, 155
as cause of endocarditis, 304
in etiology of aneurism, 522, 526
of the myocardium, 244
with precordial pain, 244
Systolic murmur in mitral insufficiency,
331
retraction along left cardiac border,
329
retractions over heart, 91
Tabagism, 610
Tachycardia, paroxysmal, 560
Tea, effect of, 611
prohibition of, 169
Tests, functional, of cardiac efficiency, 141
Theobromine, 185
in angina pectoris, 185, 296
Theocin, 185
Theophylline in angina pectoris, 296
Theories of heart-beat, 3
myogenic, 3
neurogenic, 3
Third heart sound, frequency of, in normal
individuals, 109
in aortic insufficiency, 371
Third heart sound in mitral stenosis, 350
mechanism producing, 107
Thread galvanometer, 60
Threshold percussion, 93
Thrill, systolic, in aortic stenosis, 384
in congenital heart disease, 439
in mitral insufficiency, 330
Thrills, mechanics of, 92
Thrombi in cardiac chambers, 243
in mitral stenosis, 243
Thromboangitis obliterans, 276
differentiation from angeioneuro-
ses, 276
Thyreoglobulin, 576
Thyroid gland changes in Basedow's disease,
585
size of normal, 585
Thyroid heart, 574
(hypothyroidism), 575
formes frustes, 574
from pressure, 574
in simple goitre, 574
Thyroid secretion (see Hyperthyroidism),
578
of thyreoglobulin and iodothyrin,
576
physiological effects of, 577
relation to histological structure,
576
Thyroidectin, 588
Thyroidectomy, 589
Tobacco angina, 293
Tobacco, effect of, on circulation, 610
on coronary circulation, 611
"Tobacco heart," 609
Tobacco, precordial pain from, 610
prohibition of, 169
Tobacco smoke, composition of, 609
Tonicity, effect of digitalis on, 176
effect of, on cardiac overstrain, 135
effect of, on residual blood, 135
factors producing changes in, 13
of the cardiac muscle, 11
of the heart in mitral insufficiency,
328
of the right ventricle, 34
Tonograph, 22
Tonsillectomy in endocarditis, 317
in mitral insufficiency, 337
Tonsillitis as cause of Basedow's disease,
580
Tonus (see Tonicity)
Tortuous arteries, 260
Tracheal percussion shock in aneurism,
533
tug in aneurism, 533
Training at end of treatment, 199
effect of, 130
Trauma as cause of thoracic aneurism, 526
cardiac, 513
INDEX.
631
Trauma, lesions due to, 519
of heart, 518
Treatment of heart failure, general princi-
ples, 163
relation of, to occupation, 199
Tricuspid area, 102
Tricuspid insufficiency, arrhythmia in
cases of, 402
diagnosis of, 404
effect on circulation, 397
functional, 396
in paroxysmal tachycardia, 568
organic, 396
pathological physiology, 397
symptoms of, 399
systolic murmur in, 400
treatment of, 404
variations in murmur, 401
venous pulse in, 398
Tricuspid stenosis, 406
cyanosis in, 408
effect on the circulation, 407
etiology of, 406
occurrence of, 406
pathology of, 407
presystolic rumble in, 409
pulmonary infarction in, 409
treatment of, 411
Tricuspid valve, demonstration of action of,
10
malformation of, 458
opening of, 55
Trigeminal pulse, 72
Truncus arteriosus, 422
division of, 425
Tuberculosis as cause of endocarditis, 303
in persons with mitral stenosis, 342
in pulmonary stenosis, 440
of the heart, 244
Tumors of the heart, 245
hsemopericardium from, 246
Typhoid fever as cause of Basedow's disease,
580
blood-pressure in, 31
Uraemia, blood-pressure in, 28, 29
Urine, albumin and casts in, 156
amount of in cardiac disease, 156
chloride metabolism in, 156
Vagus currents, with heart-beat, 157
with respiration, 157
Vagus effect in producing heart-block, 461
Valve, Eustachian (of the inferior vena
cava), 424
Valves, auriculoventricular, diastolic closure
of, 56
in veins, closure of, 50
Valves, movements of, 8
position of, in diastole, 10
Valvular areas in auscultation, 102
Vasa vasorum, changes in, in arteriosclero-
sis, 250
Vascular crises, blood-pressure in, 30
Vasomotor angina, 291
Vasomotor crises, 270
hypotensive, 274
use of nitrites in, 270
Veins, cardinal, 422
sounds over, 118
umbilical (omphalomesaraic), 422
visible pulsations in, 49
vitelline, 422
Venesection, 165
contraindications to, 166
effect of, in hypertension of intracranial
origin, 30
effect of, on the circulation, 166
in arteriosclerosis, 266
technique of, 165
Veno-auricular junction, anatomy of, 5
Venous pressure, 141
determination of, 32
effect of, on filling of the heart, 11
in broken compensation, 141
in neurasthenics, 593
in paroxysmal tachycardia, 566
Venous pulse, 49
diastolic, 56
double, 49
in auricular paralysis, 57
in paroxysmal tachycardia, 561
information furnished by, 58
negative, 49
physiological, 49
positive, 57
presystolic, 56
relation to atmospheric pressure,
50
technique of tracings, 50
visual examination of, 56
Venous tracing, interpretation of, 53
Ventricle, left, pressure within, 18
Ventricle, third, 432
Ventricles, filling of, 9
Ventricular muscle, anatomy of, 8
Viscosity of the blood, 38
apparatus for clinical determina-
tion of, 38
factors influencing, 38, 39
diet, 39
hydrsemia, 39
number of red blood-cells,
39
Volume curve, method of recording, 9
Vomiting, blood-pressure in, 32
Von Graefe's sign in Basedow's disease,
583
632
INDEX.
Walking in treatment of heart lesions, 197
regulation of speed and respiration, 198
Water-hammer pulse, 47
Weather, effect of, on cardiac symptoms, 147
Whiskey in cardiac disease, 168
Wiring treatment of aneurism, 552
Work of the heart, 26
Worry, effect of, on circulation, 612
Wounds of the heart, 513
control of hemorrhage from,
517
results of operation, 518
suture of, 516
Wrestling, effect of, on the heart, 133
Xiphisternal line as sign of level of dia-
phragm, 598
X-ray, cardiac shadow, 83
examination in oblique axes, 84
of adherent pericardium, 507
of sclerotic arteries, 260
magnification of shadow, 82
methods of examination, 82
oblique illuminations, 83
pulmonary shadows, 83
shadow in aneurism, 536
Zander exercises, 197
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