TOLUMBIA LIBRARIES OFFSITE HFWiHsaiNf;is;-ji, | ANrJA | < 1 J ... HX641 29098 RC683 .H25 1917 The diagnosis and tr :■{; !;: 52. Electrocardiogram: Bigeminus 81 53. Electrocardiogram: Ihgeniinus Si 54. Electrocardiogram: Auricular and Ventricular extra- systoles 81 55. Electrocardiogram: Ventricular extrasystoles (two types) 81 56. Polygram: Accelerated heart 87 57. Polygram: Accelerated heart (Graves' disease) ... 87 58. Electrocardiogram: Accelerated heart 89 59. Electrocardiogram: Accelerated heart 89 60. Diagram : Auricular tachycardia 93 61. Diagram: Ventricular tachycardia . . .... 93 62. Polygram: Auricular tachycardia (between attacks) . 99 63. Polygram: Auricular tachycardia 99 64. Polygram: Auricular extrasystole 101 65. Polygram: Auricular tachycardia 101 66. Polygram: Auricular tachycardia 103 67. Polygram: Ventricular tachycardia 103 68. Electrocardiogram: Auricular tachycardia (between attacks) ... 105 69. Electrocardiogram: Auricular tachycardia .... 105 70. Electrocardiogram : Auricular tachycardia (between attacks) 107 71. Electrocardiogram: Auricular tachycardia .... 107 72. Electrocardiogram: .Auricular tachycardia (between attacks) 109 y^- Electrocardiogram: Auricular tachycardia .... 109 74. Electrocardiogram : Ventricular extrasystole . . .111 75. Electrocardiogram: Nodal tachycardia 11 1 76. Electrocardiogram: Paroxysmal tachycardia (transition) 113 77. Electrocardiogram: Paroxysmal tachycardia ( transition 1 113 78. Electrocardiogram: Paroxysmal tachycardia (transition) 113 7'i. Electrocardiogram: Auricular tachycardia (transition) 115 80. Electrocardiogram: Ventricular tachycardia (transition) 115 81. Diagram: Auricular flutter 119 Illustrations xiii FIGURE PAGE 82. Diagram: Auricular flutter [19 83. Polygram: Auricular flutter ui 84. Polygram: Auricular flutter \2\ 85. Electrocardiogram: Auricular flutter 123 86. Electrocardiogram: Auricular flutter 123 87. Electrocardiogram: Auricular flutter 123 88. Electrocardiogram: Auricular flutter 125 89. Electrocardiogram: Auricular flutter 125 90. Electrocardiogram: Auricular flutter 125 91. Electrocardiogram: Auricular flutter 127 92. Electrocardiogram: Auricular flutter 127 93. Electrocardiogram: Auricular fibrillation . . . .127 94. Electrocardiogram: Auricular flutter 129 95. Electrocardiogram: Ventricular extrasystole . . . .129 96. Electrocardiogram: Auricular flutter 131 97. Electrocardiogram : Sequential rhythm 13] 98. Electrocardiogram: Auricular fibrillation 131 99. Diagram: Auricular fibrillation 137 100. Diagram: Age incidence of Auricular fibrillation . . 139 101. Sphygmogram : Auricular fibrillation 143 102. Sphygmogram: Auricular fibrillation 143 103. Sphygmogram: Auricular fibrillation 143 104. Sphygmogram: Auricular fibrillation 143 105. Sphygmogram: Auricular fibrillation 143 106. Polygram: Auricular fibrillation 145 107. Polygram: Auricular fibrillation . 145 108. Polygram : Auricular fibrillation 147 109. Polygram : Auricular fibrillation 147 no. Polygram: Auricular fibrillation 149 in. Electrocardiogram: Auricular fibrillation 151 112. Electrocardiogram: Auricular fibrillation 151 113. Electrocardiogram: Auricular fibrillation 153 114. Electrocardiogram: Auricular fibrillation 153 115. Electrocardiogram: Auricular fibrillation 155 116. Electrocardiogram: Sinus rhythm 157 117. Electrocardiogram: Auricular flutter 157 118. Electrocardiogram: Sinus rhythm 157 119. Electrocardiogram: Paroxysm of Auricular fibrillation 159 120. Electrocardiogram: Extrasystoles 159 121. Electrocardiogram: Auricular extrasystole .... 161 122. Electrocardiogram : Auricular fibrillation 161 123. Electrocardiogram : Auricular fibrillation 161 124. Diagram: Pulse deficit 163 125. Electrocardiogram : Auricular fibrillation 163 XIV Illustrations figure PAGE [26. -7- [28. [29. [30. 31. >3-'- [33- [34. 135- 36. ^7- 138. 139- [40. [41. [42. 143- 144. '45- [46. [47. [48. [49. SO- 5 1 - : 5 2 - 53- 54- 55- 56. 57- 58. 59- [60. 161. [62. [63. 164. 165. if. 6. (67. [68. [69. Electrocardiogram : Electrocardiogram ; Electrocardiogram : Electrocardiogram : Electrocardiogram : Electrocardiogram : Electrocardiogram : Electrocardiogram : Diagram : Pulse deficit and blood pressure Electrocardiogram: Auricular fibrillation . Auricular fibrillation . Auricular fibrillation . Auricular fibrillation . Auricular fibrillation . Auricular fibrillation . Auricular fibrillation . Auricular Butter and fibrillati Auricular tachycardia Electrocardiogram: Auricular flutter . Polygram: Auricular Mutter and tachycardia . Polygram: Alternation Electrocardiogram : Alternation .... Polygram: Alternation in tachycardia . Sphygmogram: Alternation Sphygmogram: Alternation Polygram: Alternation (apex and radial) Polygram: Alternation Polygram: Alternation Electrocardiogram : Alternation .... Electrocardiogram : Pseudo-alternation Electrocardiogram : Alternation .... Electrocardiogram : Alternation .... Electrocardiogram : Tachycardia and alternation Electrocardiogram: Tachycardia and alternation Diagram: Distribution of cardiac nerves . Electrocardiogram : Pressure on right vagus nerve Electrocardiogram: Pressure on left vagus nerve Electrocardiogram : Right ocular pressure Electrocardiogram : Right ocular pressure Polygram : Respiratory sinus arrhythmia . Polygram: Respiratory sinus arrhythmia . Electrocardiogram : Respiratory sinus arrhythmia Electrocardiogram : Respiratory sinus arrhythmia Electrocardiogram: Respiratory sinus arrhythmia Polygram : Respiratory sinus arrhythmia . Polygram: Cribber, Complete irregularity Electrocardiogram : Dropped beat .... Electrocardiogram : Sino-auricular block . Combined record: Sinus complete irregularity Electrocardiogram: Sinus arrhythmia, phasic Electrocardiogram: Sinus arrhythmia, phasic Polygram: Sinus arrhythmia, complete irregularity <>5 [69 [69 73 73 7? 75 75 7 77 77 79 [83 [83 '85 [87 .87 [89 [91 [91 '93 '93 [95 [ 95 197 197 201 203 203 205 205 207 207 209 209 21 1 213 2 1 3 215 215 21 217 217 219 Illustrations XV FIGURE 170. 171. 172. 173- 174. 175- 176. 177. 178. 179. 180. l8l. 182. 183. 184. 185. 186. 187. 188. 189. 190. 191. 192. 193- 194. 195- 196. 197. 198. 199. 200. 201. 202. 203. 204. 205. 206. 207. 208. 209. irregu Electrocardiogram: .Sinus arrhythmia, phasic Electrocardiogram: Sinus arrhythmia, complete larity Electrocardiogram: Sinus arrhythmia and condu* defect Electrocardiogram: Sinus arrhythmia and condu< defect Electrocardiogram: Sinus arrhythmia variation in ricular complexes Electrocardiogram: Fibrillation and extrasystoles Electrocardiogram : Fibrillation, block and extrasystoles 225 Polygram : Fibrillation, bloek and extrasystoles Electrocardiogram : Auricular fibrillation and block Polygram: Block and extrasystoles .... Electrocardiograms : Block and extrasystoles . Electrocardiogram : Lesion of branch of His' bundle Polygram : A-V bundle lesion Diagram : Action currents of heart .... Diagram : Action currents of heart .... Electrocardiogram: Dextrocardia (lead I) Electrocardiogram: Dextrocardia (lead II) Electrocardiogram: Dextrocardia (lead III) Electrocardiogram: Dextrocardia (lead IV) Dextrocardia (lead V) Dextrocardia (lead VI) Hypertrophy of left ventricle Hypertrophy of left ventricle Hypertrophy of left ventricle Electrocardiogram : Hypertrophy of right ventricle Electrocardiogram : Hypertrophy of right ventricle Electrocardiogram : Hypertrophy of right ventricle Electrocardiogram : Hypertrophy of left ventricle Electrocardiogram : Hypertrophy of left ventricle Electrocardiogram : Hypertrophy of left ventricle Electrocardiogram : Hypertrophy of right ventricle Electrocardiogram: Hypertrophy of right ventricle Electrocardiogram: Hypertrophy of right ventricle Polygram : Digitalis effect, delayed conduction . Polygram : Digitalis effect, block Polygram : Digitalis effect, coupled rhythm . Electrocardiogram : Before digitalis .... Electrocardiogram: Digitalis effect, sinus slowing Electrocardiogram : Digitalis effect, block Electrocardiogram : Digitalis effect, coupled rhythm Electrocardiogram Electrocardiogram Electrocardiogram Electrocardiogram Electrocardiogram tioi PAGE 22] 221 223 223 223 22^ 227 22"] 23I 23I 2 33 235 235 237 237 237 237 237 237 239 239 239 239 239 239 241 241 241 241 241 241 265 265 265 267 26- 267 267 xvi Illustrations FIGURE PAGE 210. Electrocardiogram: Digitalis effect, coupled rhythm . 269 211. Electrocardiogram: Digitalis effect, coupled rhythm . 269 212. Electrocardiogram: Before digitalis (lead 1) . . . 271 213. Electrocardiogram: Before digitalis (lead II) . . . -71 214. Electrocardiogram: Before digitalis (lead 111) . . 271 215. Electrocardiogram: After digitalis, change in T wave (lead I ) . . . 271 216. Electrocardiogram: After digitalis, change in T wave ( lead II ) 271 217. Electrocardiogram: After digitalis, change in T wave (lead II h . . . .' . . 271 218. Electrocardiogram: Block complete 279 219. Electrocardiogram: After atropine 279 220. Electrocardiogram : After atropine 279 221. Electrocardiogram: After atropine 279 222. Electrocardiogram: Block complete 28] 223. Electrocardiogram: After atropine 281 224. Electrocardiogram: After atropine 281 225. Electrocardiogram: After atropine 281 226. Electrocardiogram: Auricular flutter, right vagus pres- sure 289 227 . Electrocardiogram: Auricular flutter, left vagus pres- sure 289 228. Electrocardiogram: Auricular flutter 29] 22i). Electrocardiogram: Auricular flutter, digitalis effect . 29] 27,o. Electrocardiogram: Auricular flutter, digitalis effect ■ 29] 231. Electrocardiogram: Sinus rhythm 291 232. Sphygmogram: Auricular fibrillation 295 -'33. Sphygmogram: Digitalis effect 295 234. Sphygmogram : Digitalis effect 295 235. Sphygmogram: Digitalis effect 2<>^ 236. Sphygmogram: Digitalis effect 295 2 37- Sphygmogram: Digitalis effect 295 238. Polygram: Auricular fibrillation 297 239. Polygram: Digitalis effect 2<)J 240. Polygram: Digitalis effect 297 241. Electrocardiogram: Auricular fibrillation 299 242. Electrocardiogram: Coupled rhythm 299 243. Electrocardiogram: Auricular fibrillation 301 244. Electrocardiogram: Digitalis effect 301 245. Electrocardiogram: Digitalis effect 301 246. Electrocardiogram: Digitalis effect 3 01 247. Diagram: Pulse deficit and blood pressure .... 303 248. Diagram: Pulse deficit and blood pressure .... 303 CHAPTER I Introduction The diagnosis of cardiac abnormalities requires a knowledg three elements: (i) Etiological, (2) Anatomical and (3) Func- tional. In the past while all these features have been considered, the greater stress has been laid on the anatomical diagnosis, etiology has taken a somewhat less conspicuous place and function has per- haps received the least attention. Again until recent years atten- tion has been most closely directed to the anatomical abnormalities of the valves, the endocardium and the pericardium, while the myo- cardium has received relatively little clinical study. The explanation of such a development is perfectly simple; our methods of examining the heart mainly by the employment of physi- cal signs were such as to lend themselves particularly to the elucida- tion of the conditions of the endocardium and the pericardium. Reasoning from our physical signs we were fairly sure to correctly interpret the kind and extent of the damage to the valves and the pericardium ; beyond determining the presence or absence of hyper- trophy and dilatation our anatomical diagnosis of the condition of the myocardium was little more than a shrewd guess. The methods of cardiac examination which have been so rapidly developed in the past decade have afforded us the means of studying the heart from an entirely new standpoint. The polygraph and the electrocardiograph have put us in the way of studying many cardiac conditions which had hitherto been un- recognized. These instruments afford us records of the functional activities of the heart; in the main they are records of myocardial function. Such studies often permit us to draw inferences in regard to the anatomical condition of the heart muscle. They have already helped us materially in formulating our prognosis, and our accuracy in this regard should be greatly improved as time passes and we are able to correlate our findings with the events which follow as the years in which such observations are made increase in numbers. They have furnished information which has greatly modified our methods of treatment ; they should be very useful in the 1 Introduction study of the effect of drugs on myocardial function. Such records are extremely valuable in that they register graphically the func- tional condition and can he preserved for future reference and com- parison with later observations, unclouded by the haze with which time is so apt to obscure the evidence obtained by the eye, ear and finger, even though these are reinforced by carefully written notes. Perhaps the most important contribution which these later methods have made to the average clinician is that they have made his powers of observation more acute; they have given new mean- ing to the old physical signs and, with a knowledge of what the polygram and the electrocardiogram have disclosed, he is able to detect and interpret physical signs which hitherto went unrecog- nized or were without meaning. Every patient with abnormal cardiac function cannot be brought within the sphere of the electrical attachments of an electrocardio- graph. The electrocardiograph is an expensive laboratory instru- ment suited to the facilities of the large hospitals or the office of the consultant and cannot be included in the armentarium of the aver- age general practitioner. Even the polygraph, although portable and not particularly expensive either in its first cost or upkeep, is an instrument which requires a certain amount of training and a very large expenditure of time for its successful operation. It is therefore comforting to know that if one sufficiently fa- miliarizes himself with the kind of evidence which these instruments afford, and the nature of the cardiac abnormalities upon which they throw light, he should by carefully cultivating his powers of ob- servation be able to detect on physical examination the signs which in 90 per cent, of all cases will allow him to make as correct a diag- nosis and apply as well a directed course of treatment as he could if his observations were reinforced by the most elaborate records. CHAPTER II Anatomy In order to elucidate our conception of the functional activities of the myocardium it will be well for us to briefly review a few ana- tomical facts. The embryonic heart of the vertebrates first appears as a tube, at the posterior portion of which the veins coalesce to form a cavity which is known as the sinus venosus. In the course of development the tube is bent upon itself and from its wall a series of chambers are formed which ultimately become the auricles and ventricles. These features are more clearly seen in some of the lower verte- brates. In the higher vertebrates the separation of these chambers becomes less distinct ; the sinus venosus disappears as a distinct structure and is fused with the tissues of the superior and inferior cavse and that portion of the right auricle which lies between the termination of these veins. Recent histological studies have afforded facts of peculiar interest and lend support to the theory of myocardial function, which is to- day pretty generally accepted. The study of serial sections of the mammalian heart has served to demonstrate certain structures which up to this time had been unrecognized. Keith and Flack have de- scribed a collection of muscle cells of such structure as to distin- guish them from the surrounding tissue lying near the junction of the superior cava with the right auricle and extending along the sulcus terminalis for a distance of about 2 cm. (in man). These cells are fusiform, striated, have elongated nuclei and are embedded in dense connective tissue ; they have a special arterial supply and intermingled with them are some nerve cells and nerve fibers which connect with the vagal and sympathetic nerve trunks. This special- ized tissue is known as the sino-auricular node and is believed by Keith and Flack to be a remnant of the original sinus tissue. Simi- lar isolated masses, which are believed to be remnants of the primi- tive canal as it passed through the auricle, have been found near the coronary sinus, in the auricular septum, in the valve of Eu- stachius and at the mouths of the pulmonary veins. 3 4 Anatomy A differentiated mass of tissue similar in structure to the sino- auricular noile and known as the auriculo-ventricular node, was first described by Tawara. It is situated low down in the auricular tissue at the right posterior edge of the septum; at the anterior end of the auriculo-ventricular node these specialized muscle cells become more parallel in arrangement and form a narrow band ensheathed in a fibrous canal. This structure is known as the bundle of His. It runs forward and to the left in the central fibrous portion of the heart to the membranous septum of the ventricles; at a point a little in front of the anterior end of the attachment of the median seg- ment of the tricuspid valve the bundle divides into two branches; the left branch immediately passes through the membranous sep- tum and is continued downward along the septum beneath the endo- cardium of the left ventricle ; branches are given off all through its course in the septum; the principal branches going to the papil- lary muscles of the mitral valve; the right branch of the bundle is directed downward beneath the endocardium of the right ventricle to the papillary muscles where subdivisions begin to be given off from the main trunk. The subdivisions of the conducting system are continued into that complex network lying beneath the endocardium of both ventricles known as Purkinje's fibers and these in turn make direct connection with the muscle fibers of the ventricles. Anatomy Figure i Diagram of the specialized conducting system of the heart. CH AFTER III Physiology As an introduction to the study of certain types of cardiac func- tion, it will be well for us to consider briefly the theories which are at present in vogue as to the mechanism of cardiac activity, THE NEUROGENIC THEORY Up to a few years ago it was generally held that the origin and regulation of the heart beat must be located in some part of the nervous system. The discovery that the contraction of the volun- tary muscles had its origin in the central nervous system made it seem probable that the contraction of the heart was the result of a stimulus arising in a nerve center which was conveyed to the heart by nerve fibers, thus a musculo-motor nerve center was as- sumed to exist and efforts were made to locate it. When it was discovered that the excised heart of many animals, under suitable conditions, was able to continue its rhythmical action for a con- siderable period, it seemed necessary to assume that this motor center was located in the nervous substance embedded in the cardiac tissue. Further, since it was recognized that the heart muscle did not contract as a whole, but that the activity was first seen at the sinus and thence spread successively over the auricles and ven- tricles, it was supposed that the nerve center originating this stim- ulus was located in the wall of the sinus and that from this point the impulses were carried by the intrinsic nerves of the heart to muscle fibers of its successive chambers. The influence of the vagus and accelerator nerves was recognized and their activity was be- lieved to heighten and depress the automatic nerve center which originated the rhythmic contraction of the heart. Briefly, the "neurogenic theory" is as follows: The initiation of the rhythmic activity of the heart resides in an intra-cardial nerve center, the muscle fibers respond to stimuli originating in this center, the activities of this nerve center are modified by positive and nega- tive influences conveyed to it by the vagus and sympathetic nerves, thus permitting an adjustment of the activity of the heart in ac- 6 Physiology 7 cordance with the needs of the body at any particular moment by a reflex mechanism. The important point in which this theory differs from the one at present generally accepted is that it ascribes to the muscle cells an entirely passive role, making their activity directly dependent on the activity of the intra-cardial nervous tissue. THE MYOGENIC THEORY As a result of physiological investigations of the last two decades the theory of the neurogenic origin of the heart action has been opposed by the view that the source of the rhythmical movement is to be found in the heart muscle itself. This is known as the "myogenic theory." This theory has been formulated to explain and harmonize the facts discovered by the older investigators, such as Bowditch, Traube and Ludwig, and the newer facts brought to light especially by the researches of Gaskell and Engelmann. According to this theory, the stimulus arises not in a nervous center, but in the muscle cells of the heart and is conveyed to the successive portions of the heart not by the nerve fibriles, but by the cells of the contractile tissue itself. The "myogenic theory" is of the highest importance in analyzing and explaining the mechanism of the activity of the heart, and affords us a practical working hypothesis of great value in the study and treatment of pathological conditions of the myocardium. It will be impossible for us to present here the detailed evidence upon which this theory is based. This can be obtained from the critical reviews, such as have been written by Biederman and Langendorff (Ergebnisse der Physiologie), and from the original papers, especially those of Engelmann. For our purpose it will be sufficient to review briefly a few of the main facts upon which this theory rests. The muscle cells of the wall of the heart have been found to possess five properties, which, while interdependent to a certain extent, are sufficiently distinct to permit of separate study and description. These five properties are : 1. Stimulus production. 2. Stimulus conduction. 8 Physiology 3. Excitability. 4. Contractility, 5. Tonicity. The cooperation of the first four of these properties are the means through which the rhythmical movements of the heart are initiated and maintained, and are efficient even when the heart is removed from the body. In the intact animal its needs at any particular moment are met by a reflex regulation through the nerves. The influences thus brought to the heart may affect any one of these five properties, and these nerve influences may have a positive or negative effect, heightening or depressing- one or more of these five properties of cardiac tissue. STIM ULUS PRODUCTION The nature of the stimulus which is automatically found in the cardiac muscle cells is not as yet definitely settled. There is, how- ever, considerable evidence which indicates that it consists of a stimulus-material, a chemical compound the constituents of which are not as yet determined, but which has definite affinities and is governed by physico-chemical laws the nature of which we are just beginning to unravel. It seems that this stimulus-material is being continuously manufactured and consists of molecules which increase in size and complexity until a point is reached where its mere complexity renders it an unstable compound, and it is, there- fore, suddenly decomposed into its constituent ions. All the stim- ulus-material in existence at this particular moment is destroyed by this sudden dissociation, but immediately its manufacture is recommenced. This continuous formation of stimulus-material, with its automatic periods of dissociation, constitutes the basis of the rhythmic stimulation of the heart. This property, the manufacture of stimulus-material, is a func- tion of the muscle cells of all parts of the heart, but is most highly developed in the region of the junction of the superior cava of the right auricle (the homologue of the sinus venosus of the lower animals), hence the stimulus arising here sets the pace, under nor- mal conditions, for the rhythmic activity of the heart, the stimulus passes from the pacemaker to the successive portions of the heart, and as each muscle cell is stimulated all the stimulus-material pres- Physiology g cut in the cell at that particular moment is dissociated into its con- stituent ions. Under certain pathological conditions parts of the heart than the area at the roots of the great veins may have this prop- erty (the construction of stimulus-material) heightened, and these parts may, through this process, become the pacemaker for the whole heart. The property of the formation of stimulus-material may be height- ened or depressed by the influences brought to the muscle cells by nerve influences and probably also by variations in the chemical constitution of the blood supply. Those influences which accelerate this process are known as positive chronotropic, those which de- press are known as negative chronotropic. EXCITABILITY is that property 01 the cardiac muscle by virtue of which it responds to stimuli. It is probably, as Engelmann's experiments show, quite distinct from the properties of stimulus produc- tion, conduction and contractility, and is dependent upon mole- cules entirely different from those upon which these other depend. Excitability may be heightened or depressed quite aside from the positive or negative changes which may occur in the other fundamental properties. Excitability is measured, not by the amount of the reaction resulting from a stimulus, but by the strength of the smallest stimulus that is sufficient to produce a contraction. Thus when a very small stimulus is effective in pro- ducing a contraction the degree of excitability is high, when a con- traction can be produced only by a relatively large stimulus the degree of excitability is low. Each contraction of the heart tem- porarily destroys the irritability of its muscle cells. During systole and for a short time after it the heart cannot be excited even by the strongest stimuli. After the systole the property of ex- citability gradually increases, and smaller and smaller stimuli are effective in producing a contraction. "When excitability is height- ened, it is assumed that this is due to a more rapid formation of irritable-material ; when it is lowered, it is probable that the irritable-material is formed less rapidly. Nervous and nutritional influences which increase and diminish io Physiology irritability have been named by Engelmann positive and negative bathmotropic. Increase in excitability tends to shorten the cardiac cycle, thus increasing the rate and making the heart susceptible to smaller stimuli. Whether they he intrinsic or extrinsic, such a change is probably an important predisposing element in the production of extras\ stoles. A decrease in excitability will tend to lengthen the cardiac cycle and, hence, will slow the heart. CONDUCTIVITY Formerly it was believed that the conduction of stimuli to successive portions of the heart was a function which helonged exclusively to the intrinsic nerves of the heart wall. To-day the evidence is very strong that the function of conducting stimuli is a property of the muscle cells of the heart wall. Without attempting to give all the evidence upon which the latter assump- tion rests, we may mention the following facts: Morphological and embryological evidence lend probability to the theory that the heart muscle cells are capable of transmitting stimuli from muscle cell to muscle cell. Experimentally the wave of conduction can be made to start from any point in the wall of the heart and pass in a direction opposite to that which it normally takes. This would be exceedingly difficult to explain on the assumption that conduction is dependent on a reflex nervous mechanism, while the hypothesis which assigns this to the muscle cell renders this phenomenon quite intelligible. The rate of conduction in the heart is relatively slow. In the frog's heart (according to Engelmann) it is three hundred times slower than in motor nerves, and the rate of conduction from auricle to ventricle, where connection is made by a very narrow strip of muscle, the conduction is even slower. Conductivity is temporarily destroyed during the systole of the heart, but returns gradually after each contraction; hence, this property is believed to be dependent upon molecules wdiich on stimulation are broken down into their constituent ions, whence they are gradually rebuilt, becoming less stable as the molecule increases in size. Physiology ii Conductivity can be heightened and depressed by nervous influ- ences by the application of heat and cold and the employment of chemicals which modify the normal metabolism. It is slowed or abolished by mechanically narrowing the muscle mass. Such influences are termed positive and negative dromotropic effects. CONTRACTILITY is that property by virtue of which the muscle cells become short- ened, thus narrowing the chambers of the heart and emptying them of their contents. Since, in accordance with the law established by Bowditch, the contractions of the heart are always maximal, i.e., if it contracts at all, it contracts with all the power of which it is capable at the particular moment. The size of the contraction is a measure of its contractility. The property of contractility, as is the case with the other funda- mental properties, is destroyed for the time being by the contrac- tion of the muscle cell, and, as is the case with the others, this function is gradually restored during systole. The contractile power, therefore, varies with the length of the diastole ; that is to say, the longer the period allowed for recuperation, the greater will be the power of the succeeding contraction. Nervous and nutritional influences which heighten or depress con- tractility are termed positive and negative inotropic effects, re- spectively. While the functions of stimulus production, excitability, con- ductivity and contractility can be shown to be distinct properties of cardiac muscle, their interdependence is well illustrated by the effect which a modification of one or more of these may have upon contractility. For example, any considerable increase in the properties of stimulus formation and excitability have a negative inotropic effect and contractions are less powerful, while a de- pression of stimulus production and excitability have a positive inotropic effect and contractility is increased. TONICITY Every muscle normally possesses a certain tone ; that is to say, even when it is not contracting it maintains a position which is [2 Physiology somewhat short of complete relaxation. The muscle of the heart is no exception in this general rule. Tonus, while related to the other fundamental properties of heart muscle, is probably quite distinct from them; for example, Porter* has shown that, unlike the other fundamental properties, "tonus contractions" are proportional to the strength of the stim- ulus employed and have no refractory period. In the frog, Ilolf- mannt was able to demonstrate that stimulation of certain vagus fibers increase the size and force of the contractions of the heart and increase its tonicity without modifying the cardiac rate. Tonus allows the heart wall to resist stretching during diastole. The force which stretches the heart during diastole is the pressure of the blood flowing from the great veins. This flow will continue until an equilibrium is established between venous pressure and the tonicity of the heart. A normal tone aids in maintaining the efficiency of the heart (i) by resisting over-filling, and (2) by promoting an initial ten- sion which is favorable to an effective contraction. Changes in tone are essential in order that the ventricles may be capable of receiving varying quantities of blood, but an excessive tone may lead to a ventricular capacity which is too small and a diminished tone may admit too large a volume of blood and, therefore, lead to dilatation and an inefficient emptying of the ventricles. The relation of tonus to dilatation and cardiac insufficiency in the individual case is obscure and is a subject which requires further careful investigation. In order to intelligently interpret the myocardial activities sev- eral other features should be held prominently in mind. The law of "All or None" or of "Maximal Contractions" was discovered by Bowditch in 1871. lie showed that if a stimulus was strong enough to induce a contraction, the cardiac muscle responded to that stimu- lus with all the contractile power of which it was capable at that particular moment ; also that the size of the contraction was inde- pendent of the strength of the exciting stimulus; a small stimulus, if effective, produced a contraction just as large as a stronger stimu- *Amer. Jour. Physiol., 1906, xv, I. "rArch. f. d. ges. Physiol., 1895, lx, 139. Physiology 13 lus. When the heart muscle was stimulated it responded with a maximal contraction or none at all. That the cardiac muscle cells possess a "Refractory Period" was discovered by Marey in 1875. lie was able to show that there was a period beginning just before systole and continuing a short time after it during which the heart will not respond to stimuli even if these are of great strength. The studies of Engelmann have demon- strated that during the refractory period the properties of excita- bility, conduction and contractility arc all abolished. After systole excitability is gradually restored so that, whereas immediately after the refractory period the heart will respond only to stimuli of great strength, as diastole advances the minimal stimulus necessary to pro- duce a contraction becomes progressively smaller. Engelmann showed in like manner that the conductivity and contractility grad- ually increased with the lengthening of the time between the end of the refractory period and the time when the stimulus was applied. When we come to study the functions of the primitive cardiac tube in the lower vertebrates (as for example the frog, in which portions of the primitive tube still exist, as the sinus venosus, au- ricular canal and the aortic bulb), we find that all of its parts pos- sess in a high degree the power of originating stimuli, but the pos- terior portion of the tube as represented by the sinus venosus is even more excitable than the other parts of the tube, hence normally the cardiac contractions start from the sinus. The capability of parts of the frog's heart, ether than the sinus, to originate stimuli resulting in contraction, is demonstrated by the Stannius experiment. When a ligature is so applied as to separate the sinus venosus from the auricle, the sinus will continue to con- tract rhythmically, but the rest of the heart ceases to move ; after a time, however, the auricle and ventricle again begin to beat, but at a rate slower than that of the sinus and quite independent of the sinus rhythm. If now a second ligature be applied between the auricle and the ventricle, the auricle will continue to beat and after a short pause the ventricle will begin to contract rhythmically at a rate slower than that of the auricle and independent both of the sinus and of the auricle. There are several phenomena presented in this experiment which particularly attract our attention. 14 Physiology i. The capacity of each chamber to initiate rhythmic contractions independent of the other parts of the heart. 2. The rate of the spontaneous rhythmic contractions is fastest for the sinus, intermediate fur the auricle, slowest for the ventricle. }. In the intact heart, before such ligatures arc applied, the rate of the rhythmic contractions of the whole organ is determined by the rate of the sinus, i.e., by the portion which has the fastest rate, or, in other words, that which has the greatest excitability. In a similar manner, when the sinus is cut oli", the auricle sets the pace for the ventricle. As was pointed out in the preceding section on the histology of the mammalian heart certain special structures have been found in different portions of the heart which have many features in com- mon. These are the "Sinus Node," the "Auriculo-voitricular Node" and the "Bundle of His." A study of the functions of these structures leads us to believe that they are remnants of the primi- tive cardiac tube and retain the qualities of the original tube in a higher degree than other portions of the cardiac musculature. Anatomical, morphological and developmental evidence indicate that the "Sinus Node" is the normal pacemaker of the mammalian heart. This evidence has been reinforced by considerable experi- mental work, a brief digest of which may be found in Thomas Lewis' valuable work, "The Mechanism of the Heart Beat," Chap- ter IV. There is certain evidence that under pathological conditions the "Auriculo-ventricular Node" may become the pacemaker of the heart, giving rise to a form of heart activity that is known as "Nodal Rhythm." In other pathological conditions when the conducting path from the auricle to the ventricle is severed (termed auriculo-ventricular block), the evidence is in favor of the assumption that the main trunk or one of the branches of the "Bundle of His" originates the stimuli which set the pace for the ideo-ventricular rhythm which is then established. CHAPTER IV Graphic Aids to Diagnosis Two of the aids which have of late been extensively utilized to interpret myocardial function arc the polygram and the electro- cardiogram. The polygram is a graphic, synchronous record of two or more parts of the circulatory system, usually of the radial and jugular pulses. The main facts of clinical importance which have been obtained from polygraphic studies of the circulation have been derived from a comparison of the relations of the auricular and ventricular activities. The value of records of the apex beat, carotid, brachial and radial arteries, depends on the fact that they represent more or less accurately the activities of the left ventricle, while the movements of the jugular veins or pulsating liver give us a certain insight into the activities of the right auricle. In clinical work we usually make use of synchronous records of the radial and jugular tracings (Figure 2). The principal waves of the jugular tracings are, the wave of auricular systole (a) ; the wave synchronous with, and probably due to carotid pulsation (c) ; the (v) wave, due to rising auricular pressure during the ventricu- lar systole ; the depression (x) is mainly due to the relaxation of the auricle after its systole; the depression (y) is due to emptying of the auricle after the opening of the tricuspid valve ; the closure of the semi-lunar valve is frequently marked by a notch in the ascend- ing limb of the (v) wave, and the two portions of the wave have been designated (z^ s ) and (z ,d ) (Rihl), to indicate their relations to systole and diastole. The opening of the tricuspid valve is indicated by the termination of the (v) wave. A fourth wave, which sometimes appears in diastole and called the (h) wave (Gibson), is believed to mark the closure of the auriculo-ventricular valves. The first step necessary in analyzing the jugular tracing is to locate the (c) wave. To accomplish this one measures accurately with dividers the distance of the foot point of any given radial wave from the line marking the beginning of the radial tracing. One then measures oft" the corresponding distance from the start- a 16 Graphic Aids to Diagnosis ing place oi the jugular tracing; at the distance equivalent to o.i md preceding this point will be found the (c) wave, since the pulse wave requires o.i second to travel from the carotid to the radial at the wrist. In the normal tracing the (a) wave will he found preceding the (c) wave by 0.2 second. 'The {■:■) wave fol- lows the (c) wave, separated from it hy the depression (.r). The depression (y) follows the (y) wave. In various arrhythmic conditions of the heart there will he found variations in the relations of these waves of the jugular pulse. These variations afford us the means of determining the time re- lations of the auricular and ventricular activities, and from these can be deduced certain abnormalities in the fundamental properties of the cardiac tissues. Much time and annoyance in taking polygrams may be saved if one systematically pays attention to the following apparently in- significant details. One should always first examine his instrument to see if all parts, particularly the tambours, are in good working order; the clockwork (usually two sets) should be wound. If smoked paper is to be used, an ample supply should be prepared, so that one need not interrupt his work for this purpose during the record-taking period. For smoking the paper a large candle, a kerosene lamp, burning camphor or a gas burner fitted with a fantail may he employed. Personally I prefer the gas burner when practical, as by this means the smoke is laid on the paper more evenly and less heavily than by the other methods. If the ink polygraph is used, the pens should be carefully cleaned and filled with the writing fluid. The patient should be placed on a couch or bed with clothing loosened, to allow access to the parts which it is wished to in- vestigate. He should be in a comfortable position, so that he may relax and lie quietly. In taking a record of the jugular pulse, the shoulders should be slightly raised, the head somewhat flexed for- ward and rotated to the right and supported by pillows so that the sternocleidomastoid muscles may be perfectly relaxed. When a radial tracing is taken, the position of the radial artery should be marked with a skin pencil ; this will be found to facilitate greatly the correct adjustment of the spring of the instrument over the radial artery. The spring of the instrument should rest immedi- Graphic Aids to Diagnosis U Figure 2. Normal Polygram 1, beginning of auricular contraction; 2, beginning of apex beat; 3, beginning of carotid wave; 4, beginning of radial wave; 5, closure of semi-lunar valves; 6, opening of tricuspid valve; E = 3 - 5 = ventricular systolic period. i8 Graphic Aids to Diagnosis atcly over the artery to avoid distortion of the form of the pulse tracing, which a lateral displacement may cause. If the pressure of the spring on the arterial wall is equivalent to the diastolic pres- sure of the patient, the movements of the spring will he maximal; if this gives a movement to the writing lever greater than is de- sired, the excursions may he reduced by slightly increasing or dimin- ishing the pressure of the spring. ( In polygraph work the time rela- tions of the various tracings are usually of greater importance than the size of the various waves. ) In adjusting the brachial cuff of the Uskoff or Erlanger apparatus, the pressure is usually raised to a point equivalent to the patient's diastolic pressure. ( In using this instrument one sometimes meets with difficulty in securing a sharp "footpoint" for the waves of the brachial record.) The re- ceiving apparatus for an apex tracing may he a small Mackenzie cup or one of the more elahorate forms of the so-called "cardio- graphs," which may he strapped to the chest wall or held by an assistant. The position of the apex thrust should he marked with a skin pencil and care should be taken to adjust the receiver to this point. (A receiver placed inside the apex beat will often record the systolic retraction of the tissues near the apex, giving the so- called "inverted cardiogram.") The jugular tracings are best taken with a Mackenzie cup about one and one-half inches in diameter and slightly flattened on one edge. The cup is placed over the jugular bulb, just above and about one-half inch to the right of the right sternoclavicular junction. The flattened edge of the cup should be parallel to the upper border of the clavicle and should be held gently in position by the operator's hand, which is steadied by resting lightly on the chest wall ; the cup is provided with a pin-hole vent, which may be covered by the operator's finger, who can thus adjust the internal air pressure without removing the cup. Any considerable pressure of the cup over the veins must be avoided. The receiving cup may be shifted about to obtain the point of maximum venous pulsation ; at times the best tracings are obtained at a point higher up on the neck. In taking tracings of the movements of the liver, a larger cup with a flattened edge should be employed ; the abdomen should be relaxed and the cup brought in contact with the under surface of the liver. Graphic Aids to Diagnosis J t T ■" ■■» 11 nrA |> ^ . (1 ,^h ll -«. li j^ BftB^^Mllilljil^iwiiilW^Bn ~ ^ ■$ -t- : --t---iL- _'w. nJtanA Figure 3 Lead I (right arm — left arm) Figure 4 Lead II (right arm — left leg) Figure 5 Lead III (left arm— left leg) J4 Graphic Aids to Diagnosis lead I Current from right arm and left arm. LEAD II Current from right arm and left leg. LEAD III Current from left arm and left leg. Electrocardiograms obtained from a normal individual by the three leads as described present different features. The wave i/'i is positive in all leads. (P) to (R) interval varies slightly in the three leads. All the waves of lead n are greater than those of leads i and [II. The wave ( 1\ ) is positive in all leads. (T) is usually positive in all leads, but is occasionally negative in lead III. Even in normal individuals there is a considerable range of variation in the electrocardiogram which lies within the limits of the normal. Among these physiological variations may be mentioned a shorten- ing of the diastolic period in increased frequency of the heart, and variation in the aptitude of the (R) wave synchronous with respira- tion ; the increase in the size of the (T) wave with increased exer- tion; the changes in (Q) and (S) coincident with the changes of the position of the heart in the thoracic cavity. In comparing the value of the polygram and the electrocardio- gram as means of interpreting the changes in anatomical and func- tional conditions of the heart we should observe first of all that these two methods record different sets of phenomena. The poly- gram is a graphic time pressure curve. The electrocardiogram is a graphic portrayal of the variation of electrical potential during muscular activity. By both of these methods we can study the functions of stimulus production, irritability, conductivity and con- tractility, but each method has certain advantages and is successful in points where the other is inadequate. They do not portray the same phenomena and are therefore supplemental and corroborative rather than identical. For this reason we have adopted a scheme for taking combined records, i.e., we often record on the same film figures of the electrocardiographic and time pressure curves of the arterial and venous pulses. Conclusions drawn from both types of records are remarkably in accord, thus strengthening the evidence obtained. Graphic Aids to Diagnosis 25 Figure 6 Diagram of the pressure changes in the cardiac chambers and their time relations to the aortic, carotid, iugular and electrocardiographic curves and heart sounds. (After Lewis.) CHAPTER V Classification of Disturbances of Myocardial Function The ideal analysis of myocardial functions is based on an ex- amination of the fundamental properties of the muscle cells. Such an examination would show that — Stimulus production is normal, increased or diminished. Excitability " " " " Conductivity " Contractility " Tonicity If there is a departure from the normal (i.e., a depression or an increase in one of these properties) the abnormality may involve the entire musculature or a limited portion of it. Such a classi- fication should therefore indicate the location or site of the ab- normality. That is to say, it should indicate the particular part in- volved, as, for example, the sinus node, the auricular tissue, the auriculoventricular node, the bundle of His or one of its branches, the ventricular muscle, etc., etc. To complete such a classification the etiological condition should he investigated and we should assign the change in function to some underlying condition, anatomical, nutritional, reflex, etc. While at present the state of our knowledge and our means of ob- taining evidence in regard to all these factors are too incomplete to permit us to make a final analysis in every instance and to assign the existing abnormality to a definite change in one or more of the fundamental properties of cardiac muscle, with an exact site and an accurate causal factor, we are able to accomplish this to a limited extent, but the advances of the past decade, the result of careful clinical observations and well-conceived experiments on animals give us promise of a more extensive knowledge in the near future. It is important that the study of remedies should be based upon a similar analysis so that we may know, for example, whether a particular drug or hydrotherapeutic procedure will heighten or depress excitability in a particular portion of the heart and thus lead 26 Disturbances of Myocardial Function 27 us to its logical utilization in correcting an abnormal state of this property. As an example of the present possibilities of the use of such a classification, we may cite a case in which we have evidence that all the fundamental properties arc normal except that of conduction. We may also have evidence that the conduction is depressed and that the abnormality is localized in the cells of the bundle of 1 lis, if the patient has been taking large doses of digitalis (we know that digitalis depresses conductivity), we may find that the withdrawal of this drug allows the cells to recover their property of conduc- tion to the normal degree. CLINICAL CONSIDERATIONS For the clinician one of the most common and often an early feature of change in myocardial function is an alteration in the rate and rhythm of the heart action. Since we are to consider these myocardial changes from the standpoint of the everyday practitioner it will be well for us to take our start from this point, and to subdivide our cases into classes, grouped on the basis of easily elicited physical signs, viz. varieties of rate and rhythm. By the employment of graphic methods and other means at our disposal we will endeavor to further analyze each group and to point out as far as we are able the fundamental properties which are disordered, the site of the abnormality and its cause. We will therefore con- sider our cases in the following groups : A Regular. B Irregular. 1. Bradycardia. 2. Tachycardia. 3. Sinus arrhythmias. 4. Extrasystoles. 5. Alternation. 6. Complete irregularity. THE REGULAR HEART By the term regular heart we understand one which conforms to the rule (regula) of the normal heart. As opposed to the term 28 Disturbances of Myocardial Function regular, the term irregular heart includes nil changes in rate, rhythm and character of cardiac contractions which do not conform to the rule of the normal heart. What then are the rules of the normal heart heat? i. The rate of the normal heart is not fixed at any definite figure ; it is dependent on the needs of the body at any particular moment. The heart is a pump which has its greatest efficiency when it is maintaining the needs of the individual organism with the least expenditure of cardiac energy. Any very considerable varia- tion in rate will either fail to meet the needs of the body, or will meet these needs with lack of economy in the expenditure of energy. Hence, the rate, whether too fast or too slow, which per se falls short in maintaining an adequate circulation or which does this with an undue expenditure of energy, is inefficient and, therefore, not according to the rule of the normal heart. Within such limits the rate may vary and yet be normal, but such variations must be gradual. Change in rate in the normal heart is accomplished by a change in the length of the diastolic period, but to conform to the rule the difference in length of suc- cessive diastolic periods must be infinitesimal. A regular heart always has a rate within the normal limits, but a heart with a normal rate may be irregular since in some other features it does not conform to the rule of the normal heart, 2. The rhythm; the rule of the normal heart is that it must not only beat rhythmically, but also that the rhythm must have a special well-defined character ; the individual cycles which compose the rhythm must all be of the same kind and size, and the diastolic portions of successive cycles must be of equal length. A regular heart is always rhythmic, but a rhythmic heart is not necessarily regular. The pulsus altcrnans is an example of heart activity which is perfectly rhythmic and yet, according to our definition, is irregular; it is composed of alternating large and small beats which succeed each other at equal intervals and is therefore absolutely rhythmic, yet since the kind of rhythm does not conform to the rule, since successive beats are unequal in size, it falls into the class of irregularities. 3. The pacemaker of the regular heart is the sinus node; Disturbances of Myocardial Function 29 when any other portion of the heart cither customarily or occasion- ally initiates the stimulus which results in a contraction, this heart must be included in the class of irregular hearts. 4. In the regular heart the wave of contraction must sweep over its chambers in an orderly sequence and the stimulus must follow the path which zve have learned to recognize as normal. Any devia- tion in the path which the stimuli follows or any abnormality in the sequence of contraction of the chambers brings it into the group of irregular hearts. 5. In the regular heart not only must the stimulus sweep over the heart by the normal paths and in the normal direction, but it must travel at a speed which is normal. Any delay in transmitting stimuli places a heart among those classified as irregular. 6. Among other features to which the heart must conform to be considered regular are uniformity in the size and duration of suc- cessive systoles, and a condition of the muscle mass which is some- what short of complete relaxation during diastole. The departure from the normal in (1) rate and (2) rhythm are easily detected by the ordinary methods of inspection, palpation and auscultation. An abnormal (3) pacemaker; an unusual (4) path or direction taken by the stimulus; (5) a delay in the speed of the passage of the stimulus and the finer variations (6) in the character of the contractions of the ventricles are often best de- tected by the employment of graphic methods, but when one has once become familiar with the evidence obtained by such means, physical signs are quite sufficient in the majority of instances to afford us data upon which to base a correct interpretation of the abnormalities which are present. THE IRREGULAR HEART In the preceding section it was stated that the group of irregular hearts includes all those which show a departure from the normal in rate, rhythm and character of contractions. In the succeeding paragraphs an attempt was made to define the "rules" of normal cardiac activity. We will next consider the various types of irregular hearts which are distinguished by well-defined changes in rate and rhythm. 30 Disturbances of Myocardial Function ABNORMAL CHANGES IN RATE Under irregularities of the heart are included all those changes of rate which exist at the expense of the functional efficiency of the heart. The normal heart is a machine which provides the individual at any particular moment with a sufficient hlood supply, and at the same time is working with an economical expenditure of energy; it is working at an optimum. The adaptation of the rate of the heart to the needs of the body is controlled very largely through the extracardial nerves. Anatomical and functional evidences show that for the most part the fibers of the right vagus and the right accele- rator (sympathetic) nerves terminate in the tissues in the region of the sinus node while the left vagus and left accelerator are more particularly distributed to the auriculo-ventricular node and the tis- sues junctional between the auricle and ventricle. By reflex activity through these paths the rapidity of stimulus production is modified. There is considerable physiological and clinical evidence that both these nerves possess what is known as "tone," that their activity is continuously modifying the stimulus production of the cells of the heart ; the vagus tends to hold this property in check, the accelerator tends to heighten its activity ; it is through a correct balance of these forces that the heart activity is varied with the momentary demands of the organism. Hypertonus of either of these nerves results in a heart rate ab- normally rapid or abnormally slow. Among the factors which modify the rate of the heart are indi- vidual differences in the age, size of body, build, work, temperature, nervous constitution, arterial pressure, etc., etc. CHAPTER VI Bradycardia. Heart Block It is well to recall first of all that a slow pulse is not necessarily synonymous with a slow heart. The heart contractions may be of such unequal strength that only a portion of them are detected in the radial artery; some of the systoles may be so lacking in force that the resulting arterial wave may be insufficient to affect the pressure in the radial artery, or again they may even fail to open the aortic valves (pulsus frustrans). We should therefore always check up our finding of a slow pulse by counting the apex beat by ausculta- tion. Hence a radial count alone is not sufficient to establish the existence of a bradycardia. All really slow hearts are comprised in two classes : 1. True Bradycardia. 2. Heart Block. i. In true bradycardia all the chambers of the heart contract at a slow rate and in the normal sequence and relationship. It might be fairly questioned whether such hearts should be in- cluded in the class of irregular hearts, since although slow, their ac- tivity is usually efficient in maintaining an adequate circulation, economical in the expenditure of energy, and in other respects con ~ forming to the rules of the normal heart. However, some of these hearts are too slow to properly supply all parts of the organism with sufficient blood, and therefore this group of bradycardias may fairly be included among the irregular hearts. A slow heart is not a very rare occurrence, a rate between 50 and 60 is common in tall persons, in those with increased arterial pres- sure, aortic stenosis, pregnancy, convalescence from acute fevers, in typhoid fever, meningitis, chronic nephritis, cerebral hemorrhage and tumors; it is often associated with jaundice and some digestive reflexes, such as vomiting, etc. When we attempt to classify these heterogeneous clinical manifestations it seems reasonable to divide them into two groups : 3i 3-j Bradycardia. Heart Block i a I Toxic agents, which probably have a direct depressing ef- fect on the sinus node (typhoid fever, jaundice). ( /> ) Heightened vagus tone, cither from direct irritation of the pneumogastric center (meningitis, cerebral hemorrhage), or a reflex activity (vomiting, pregnancy, increased arterial tension, etc.). It is to be noted that a true bradycardia is due to a depression of activity of the sinus node, either through the chemical constitution of its blood supply, or through the nervous influences brought to it through the extracardial nerves, particularly the right vagus. The change which takes place in the node is a depression of the property of the formation of stimulus material or of its excitability, or both; at present we have no clinical method of determining which one of these properties is the one affected in any particular case. At a later time the effects of vagus activity will be more fully discussed ; in passing it will be sufficient to note that by the adminis- tration of atropin, vagus impulses may be cut off and thus a clinical estimate may be made of the influence which it has hitherto been exerting. A true bradycardia is never encountered with a rate under 40. Probably every heart with a rate less than this belongs to the second group of slow hearts, viz. : HEART DLOCK 2. Which is the result of interference in the conduction of stimuli from one part of the heart to another. Theoretically such an abnormal condition may occur in any part of the mus- culature of the heart; practically it is rarely recognized, except when it involves the bundle of His or one of its branches. Here the cells of the conducting system are grouped in a narrow band so that a very limited lesion or functional derangement of moderate extent is sufficient to produce marked clinical phenomena. In accordance with the degree of functional disorder we may recognize : (a) Total Heart Block, complete dissociation. (b) Partial Heart Block, partial dissociation. (c) Delayed Conduction, without dissociation. Bradycardia. Heart Block 33 ytt) TOTAL HEART BLO< K ; COMPLETE DISSOCIATION It will be recalled, as was pointed out in the paragraphs on the anatomy and function of the heart tissue, that stimuli normally originate in the sinus node, thence spread over the auricle to the auriculo-ventricular node of Tawara, where connection is made with the bundle of His; through this the impulses pass to be distributed first by the two branches of the bundle, and later by its subdivisions and their connections with the Furkinjc's fibers to all parts of the ventricular muscle. It will also be recalled that in the Stannius ex- periment on the frog's heart, when the second cut or ligature is applied so as to separate the auricle and the ventricle, the auricle continues to contract rhythmically in the normal manner and after a considerable pause the ventricle begins to contract at a slow rhythm entirely independent of the auricular contractions. This is precisely what happens in man when the property of conduction of the bundle of His is destroyed. The auricles continue to contract in a normal manner in response to the rhythmic stimuli arising in the sinus node ; these impulses are unable, however, to pass the obstruc- tion in the bundle of His and hence are unable to influence the ac- tivity of the ventricle. Since, however, the uninjured portions of the bundle still possess the fundamental properties of the production of stimulus material and excitability, stimuli will be set free at this point and the ventricle will respond by slow rhythmic contractions entirely independent of the contractions of the auricle and of the stimuli originating in the normal pacemaker. This condition is known as complete dissociation and the activity of the ventricle as the ideo-ventricular rhythm. (b) PARTIAL HEART BLOCK J PARTIAL DISSOCIATION If the bundle of His is not completely functionally severed but is merely injured so that the property of conduction is depressed (that is to say if the formation of the molecules upon which the con- duction of impulses is dependent is abnormally slow) the ventricle may not respond to every impulse from the auricle. This condition is known as partial dissociation. If the ventricle ordinarily responds to the stimuli from the normal pacemaker, and only occasionally fails to contract in this manner, the condition is known as the 34 Bradycardia. Heart Block dropped beat. If the ventricle responds to every second or third auricular contraction it is called a 2 to i or a 3 to 1 rhythm. Or, if for every 5 beats of the auricle we have 3 contractions of the ventricle the condition is known as partial dissociation with a ? to 5 rhythm. At times the periods of ventricular response may he so long that an occasional stimulus may be initiated in the bundle and we then have a partial dissociation with interspersed ideo-voitricular contractions {"escape of the ventricle"). (C) DELAYED CONDUCTION WITHOUT DISSOCIATION The conducting tissues may be so affected that the rate of con- duction may be much less than the normal so that the passage of the stimulus from the auricle to the ventricle consumes a period of time appreciably in excess of what is usual; if, however, the ven- tricle responds to each stimulus originating at the pacemaker there is no dissociation. This form of impaired function may easily pass over to a partial heart block, or even a complete block and a single case may exhibit grades of conduction changes comprising delayed conduction, partial and complete block on successive observations. TATIIOLOGY Heart block of all degrees has been produced experimentally by various procedures which have had for their object the destruction or injury of the bundle of His. Ligature of the bundle in the perfused heart (Humblet) and the dog's heart in situ (Erlanger), crushing by means of an auriculo-ventricular clamp (Erlanger), section of the bundle in the perfused heart (Cohn and Trendelenburg) have uniformly produced some degree of block whenever subsequent histological examination demonstrated injury to the bundle. Heart block has been produced by stimulation of the vagus (Chauveau) and as a direct result of asphyxia (Lewis, Sher- rington). Various degrees of temporary or permanent block have been produced by the injection of various cardiac poisons such as digitalis (Cushny, Tabora), adrenalin (Kahn), aconite (Cushny), muscarine and physostigmine (Rothberger and W'interberg). Cases which have exhibited the evidence of heart block have almost invariably shown some histological alteration in the bundle Bradycardia. EJeart Block of His when such an examination has been made. As a gen- eral rule the degree of heart block corresponds with the extent of the histological change which is found in the bundle; a complete heart block usually corresponds to a complete destruction of the bundle, while delayed conduction is more apt to be associated with a moderate degree of infiltration,* in the exceptional case a complete block may occur with but very little apparent histological changef and a case of partial block may exhibit an extreme degree of bundle destruction. These exceptional cases merely emphasize the fact that histological observations cannot always be relied on to measure the degree of functional impairment. Bachmann$ has collected from the literature sixty-three cases of heart block reported since 1899. Complete clinical and histolog- ical data w r erc obtained in twenty-four or these ; in the others the information obtained was interesting, but incomplete in all details. In all cases where a complete transverse lesion was found, there had been a complete heart block. In a group of cases showing varia- tions from partial to complete block, the extent of the histological examination did not show changes which could be regarded as pro- portional to the degree of functional disturbance. In five cases, including those showing both partial and complete block, no histo- logical alterations in the bundle of His were found. Bachmann calls attention to the fact that other parts of the conducting system were not minutely studied, hence the evidence of absence of all histological change is not absolutely conclusive in these cases. Probably the lesion of the bundle of His wdiich has been most frequently found is the result of a syphilitic infection, either a gumma or an old syphilitic scar. Calcareous nodules, chronic inflam- matory changes, fibrosis, calcareous degeneration and necrosis in- volving the bundle, have been found ; more rarely an ulcer penetrating the septum ; atheromatous changes in the central fibrous body ; fibroid and epithelial tumors have been described. Acute inflammatory conditions may be present with leukocyte infiltration and degeneration of the cells of the bundle. *Pardee: Arch. Int. Med., 1913, xi, 641. fKrumbhaar : Arch. Int. Med., 1910, v, 583. ^Bachmann : Jour. Exp. Med., 1912, xvi, 25. 36 Bradycardia, Heart Block etiology In addition to the cases of distinct syphilitic origin, others Seem to hear a direct relationship to the more acute infections. More or less severe cases of heart block have followed diph- theria, typhoid fever, influenza, septic poisoning, puerperal fever and pneumonia ; these diseases naturally supply the etiological factor in heart block as found in youth and young adults. In elderly people the lesion, when not syphilitic, is often merely a phase of one of the common general chronic inflammatory or degenerative processes, whose etiology is still for the most part shrouded in so much obscurity. The degenerative changes accompanying arterio- sclerosis of the coronary arteries are sometimes associated with various degrees of heart block. There is a group of cases, the majority of which show only mild grades of interference with conduction, which are undoubtedly of rheumatic origin. Mackenzie was the first to draw attention to this group. Many of them have had pericarditis or endocarditis particularly with involvement of the mitral valve. There seems to be little question that the acute and subacute rheumatic inflam- matory processes have a tendency to implicate not only the peri- cardium and the endocardium, but the myocardium as well. Keith's examination of hearts which had been observed clinically by Mac- kenzie* showed that the inflammatory process had a tendency ''to extend from the base of the valve into the central fibrous body, and to involve the bundle." It has been pointed out that experimentally toxic doses of digi- talis may produce block in the normal heart ; the administration of such doses is, of course, impossible in many, but the effect of moderate doses of digitalis and other drugs of the same group on hearts with impaired conduction may often be observed in the clinic. Given in such cases digitalis usually lengthens the con- duction time and may even induce a partial or a complete block. The question is still unsettled as to whether digitalis acts in these cases directly on the heart tissues or through the vagus nerve. Heart block has been produced experimentally by stimulation of the vagus nerve. It is a question whether a clinical heart block ♦Mackenzie: Diseases of the Heart, p. 179. Bradycardia. 1 1 eari Blo< k 37 As A-V V. Figure 7 delayed conduction producing partial block Aj A-V V5 1 1 1 1 1 \ \ \ \- Figure 8 partial block A-V Vs Figure 9 complete block Diagrams showing the mechanism of various degrees of heart hlock. As = auric- ular contraction. A-V = conduction from auricle to ventricle (note the variation in the length of this period). Vs =: ventricular contractions. 38 Bradycardia. Heart Block can be initiated by vagal changes, but in damaged hearts the con- duction abnormalities may be accentuated by vagal reflexes. A very beautiful illustration of this influence is a case reported by Mackenzie*; the conduction time was usually slow and the reflex obtained by swallowing repeatedly produced a partial block when the patient was under the influence of digitalis. Conduction dis- turbances following vagus stimulation have been studied by Robin- son and Draper, f who have published some very beautiful electro- cardiograms showing changes in conduction of various degrees. They reached the conclusion that the left vagus has as a rule a greater influence on the property of conduction than the right vagus. IDENTIFICATION Clinical: When the pulse rate is under 60 one may sus- pect some degree of interference with the property of conduc- tion ; in such a case, however, one should always compare the rate of cardiac contractions as determined by auscultation with the pulse rate, since not infrequently one finds a large number of ventricular systoles which are so inefficient as to make no im- pression on the radial pulse (when at a later time wc take up the discussion of extrasystoles and auricular fibrillation it will be pointed out that in these conditions many ventricular contractions may be detected on auscultation over the precordium which afford in the radial artery no evidence of their presence). If the heart is perfectly rhythmic and has a rate in the neigh- borhood of 30 it is practically certain that a complete block is present. A faster ventricular rate does not, however, rule out the possibility of a complete block, 8 out of 34 cases of complete block which I have studied by graphic methods had a ventricular rate of over 45. In a partial block the ventricle may contract rhythmically or at times may be quite arrhythmic, the rate, while usually a slow one, is as a rule faster than in complete block. A partial block is to be suspected when the ventricular rate suddenly changes to one half its former rate. A single dropped beat is usually due *Ibid., p. 340, also Plate IV, Figs. 258 and 259. tjour. of Exper. Med., xv, No. I, 1912. Bradycardia. Heart Block 3'J ;■ .''..' Brachial 0.2 second Figure io Delayed conduction. No dissociation, a-c interval = 0.3 second. Auricular rate = 73- Ventricular rate = 73. Jugular Erachial 0.2 second Figure ii Partial block. For the most part this is a 2 to 1 block, but occasionally an extra auricular impulse passes the block. Auricular rate = 92. Ventricular rate — 42. Jugular Brachial 0.2 second Figure 12 Complete block. Auricular rate = 9S. Ideo-ventricular rate = 31. 40 Bradycardia. Heart Block to a partial block, but this can only surely be determined by the evidence of graphic records. When the pulsations of the jugular vein are visible they are of considerable aid in making a diagnosis of the character of the irregularity. In complete block the jugular pulsations are usually rhythmic, but occur at much more frequent intervals than and quite independent of the ventricular impulses. Occasionally there may be seen a large jugular pulsation in place of one of the usual smaller ones, and if this phenomenon is closely observed it will be apparent that it occurs at a time when the ventricle con- tracts synchronously with the jugular pulsation, that is when the auricles and ventricles contract simultaneously. In incomplete block the jugular pulsations usually bear a definite numerical ratio to the ventricular contractions, for example, we may see in a 2 to I block, two jugular pulsations to one apex beat, or three jugular to two ventricular in a 3 to 2 block, etc. In delayed conduction it is sometimes possible to detect a longer than the normal interval between the first venous wave and the carotid pulsation, or this prolonged interval may become evident when we note the time by which the first wave of the jugular pulse precedes the apex beat. In a few cases of block a low muffled sound may be heard during ventricular diastole; this is the auscultatory evidence of the auricular contraction which is sometimes heard ; when this occurs soon after the second sound or a distinct interval before the first sound it sometimes gives the impression of a reduplication of the second or of the first sound, as the case may be. In certain cases of mitral stenosis associated with heart block there have been described (Mackenzie) short, harsh murmurs which occurred synchronously with the pulsations of the jugular vein and quite independent of the ventricular contractions. These were as- cribed to the acceleration of the flow of blood from auricle to ventricle at the time of the independent auricular systole. When present this sign should be of assistance in recognizing the inde- pendent activities of the auricles and ventricles ; personally it has been my fortune to see only one case of this kind. The Adams-Stokes syndrome, attacks of unconsciousness asso- ciated with a slow pulse, should always suggest the possibility of BR^DVCAKDIA. llhART liLOCK 4' Tuff u la r Brachial Figure 13 Delayed conduction a-c interval = 0.35 second. A] • Brachial Figure 14 Delayed conduction. Apex and radial tracings. The auricular wave is seen in the apex curve and precedes the ventricular wave by 0.35 second. 4- j Bradycardia. Heart Block heart block. It should be remembered, however, that heart block and the Adams-Stokes syndrome are not interchangeable terms. A fluroscopic examination often will demonstrate the independ- ent activities of the chambers. Polygraphic tracings | Kigures 10, n and u) will usually give conclusive evidence of conduction defects when these air present. If this property is only moderately depressed, the ventricle (as shown by the apex or arterial tracing) will have a normal or slow rate and the intersystolic periods will be uniform in length (Figure io), the jugular tracing, representing the activity of the right auricle, will show an a wave preceding each c wave at a uniform interval, but this a-c interval will exceed 0.2 second, the time occu- pied by the normal a-c interval. If conduction is a degree more defective the arterial pulse may show a rhythmic activity indicated in the diagram (Figure 7), the diastolic periods gradually increase in length until the longest pause is reached at the time of a "dropped beat," then suddenly this period is shortened only to be again gradually lengthened until another beat is dropped. When we examine the auricular diagram wc see that the auricular (a) waves recur at regular intervals; the a-c interval following the "dropped beat" may be normal, 0.2 second, in length ( it usually exceeds this), but each successive a-c interval is longer, since the property of conduction is becoming more and more exhausted, and each ventricular response is thus delayed until one of the auricular impulses reaches the junctional tissues while they are still in the refractory state, hence no im- pulse is conveyed to the ventricle and a "dropped beat" results. At the time of the next auricular impulse the long preceding rest has considerably restored the functional condition of the auriculo- ventricular bundle, consequently the a-c interval is much shorter and the ventricular response is prompt. This rhythmic lengthening of the ventricular cycle superficially resembles the respiratory sinus arrhythmia, it can be differentiated from this condition by observ- ing that in conduction defects (1) the rhythmic change in the length of the ventricular cycles is not synchronous with the phases of respiration ; (2) the a waves of the jugular tracing are separated by equal intervals; (3) the a-c intervals exceed 0.2 second. When the conduction is even more abnormal the arterial pulse Bradycardia. Heart Block 43 V m A A. X? 1 1 V M_MJH '* - 5^ MJ-U4 i-fyyfi. 1 / A-CAJL Jugular Brachial 0.2 seconfl Figure is 2 to i block. Auricular rate 70. Ventricular rate 35. Jugular Brachial Figure 16 Complete block 44 Bradycardia, Heart Block will be slow (usually 40 to 50 per minute). In the jugular record rhythmically recurring a waves will be found | Figures S and 11 1. but the ventricle responds only to every other or every third impulse from the normal pacemaker. The a-c interval when present may be of normal duration; it is usually prolonged. In complete block | Figures <> and u | the arterial pulse is slow, usually 30-35 per minute and perfectly rhythmic, in the jugular tracing are found the equally spaced a waves which hear no fixed relation to the ventricular waves. The a waves are equi- distant from one another as are also the c waves but the two rhythms are entirely independent of one another. The Electrocardiogram furnishes evidence of conduction defects which is even more clear than the polygram. As has been pointed out, the P wave represents auricular activity, R S T ventricular activity. Normally the P-R interval, measured from the beginning of the P wave to the beginning of the R wave, is between 0.14 and 0.1S second; a P-R interval occupying more than 0.18 second indicates a delay in the passage of the stimulus from the auricle to the ventricle and is due to a defect in t he property of conduction. The simplest form of this irregularity is shown in Figures 17, -'i and 22, the pulse is beating slowly and rhythmically at a rate of 60. Each ventricular complex is of the normal type and is pre- ceded by a P wave; the P-R interval is always of the same length, but is excessively long, measuring 0.37 second (Figure 17). Such a heart, on physical examination, might show little deviation from the normal, but the electrocardiogram makes very evident the under- lying defect. The records of cases of partial block resulting in the "dropped beat" is shown in Figures 18 and 23. The P waves are picked out from such a record with little difficulty. The ventricular complexes (Q R S T) are quite normal in form except when they are dis- torted by a superimposed P wave. The P waves of the first two cycles shown in the record (Figure 18) are easily recognized, if one measures the time between these P waves (approximately 0.6 sec- ond ) and, beginning with one of these easily identified P waves, lays off on the remainder of the record intervals similar in length, one will find at each one of these points a wave either clearly de- Figure 17 Delayed conduction. Every ventricular complex (QRST) is preceded by an auricular complex (P)-. The PR interval is excessively long, 0.37 second. The notch in the P wave is a slight abnormality not infrequently seen in cases of mitral stenosis. Auricular rate — 60. Ventricular rate = 60. Figure 18 Partial block. Auricular rate = 102. Ventricular rate = 89. P-R = 0.18 to 0.43 second. Note grad- ual lengthening of the P-R interval resulting in the "escape of the ventricle at x, also the rhythmic lengthen- ing and shortening of the ventricular cycles. P recurs at equal intervals of time, but its relation to the ventricular waves varies, note how the P wave distorts Q.R.S. and T at various points. * 1 s Us t- 5j X s 55 O.l '5tean3T" Figure 19 Partial (2 to 1) block. Auricular rate = 86. Ventricular rate = 43- Every other auricular impulse is blocked. P-R interval =0.15 second. _Note alternate short and long auricular cycles (sinus arrhythmia) and slow regular contractions of the ventricle. Figure 20 Complete block. Auricular rate 60. Ventricular rate 37- The auricular and ventricular activities are entirely independent of each other. Note P is slightly notched. The ventricular complex (RbT) is normal in type except when distorted by a superimposed P wave. 4<> Bradycardia. Heart Block fined or appearing as a notch changing the normal form of the ventricular complex; these are the P waves representing the auricular activity which recur rhythmically at equal time intervals. The P-R intervals vary in length from 0.18 second to 0.43 second; this gradually lengthening indicates a progressive exhaustion of conductivity, at last (at x) the period becomes so long that the ventricle contracts spontaneously (known as the "escape of the ventricle") without waiting for an impulse to reach it from the normal pacemaker; the auricular impulse (indicated by the P which merely notches the ascending limb of the R wave at x) reaches the ventricle while it is in the refractory period, hence there is no ventricular response to this impulse. After the rest thus afforded to the junctional tissues the ventricle responds promptly to the next auricular impulse and the P-R interval measures only 0.18 second only again to be gradually lengthened. The record shows an auricular rate of 102, a ventricular rate of 89. The mechanism which underlies the gradual lengthening and the sud- den shortening of the ventricular cycles is quite evident. Another type of partial block is shown in Figures 8 and 19. In this case the ventricle responds to every other auricular impulse. The P-R interval conforms to the normal length (0.15 second) but the exhaustion of the A-V bundle is shown in its inability to transmit the next succeeding impulse coming down from the sinus, so that ventricular responses and "dropped beats" alternate, showing a 2 to 1 block. The existence of a sinus arrhythmia evidenced by the alternating short and long periods between the auricular contractions, may be, in this case, an additional element in favor- ing a partial block. If the auricular responses were equidistant it is quite possible that the junctional tissues would have re- covered sufficiently to convey the impulse to the ventricle, but the shortened auricular diastole which regularly follows a ven- tricular response does not allow enough time for the recovery of the functionally defective conduction. A comparison of these two cases of partial block represented in Figures 18 and 19 is interesting. In the first case (Figure 18) the auricle contracts regularly, the ventricle irregularly. In the second case (Figure 19) the auricle contracts irregularity, the ventricle regularly and at a much slower rate than in the preceding case. The Bradycardia. Heart Block 47 Figure 21 Delayed conduction. P-R interval = 0.2 second. Figure 22 Delayed conduction. P-R interval = 0.6 second. From the same case as Figure z\ after a considerable amount of digitalis had been given. 48 Bradycardia. Heart Block irregularity in each case is a rhythmic one. In the first case a regular auricle associated with a defect in conduction produces a rhythmic irregularity of the ventricle. In the second case the rhythmic irregularity of the auricle associated with a defect in con- duction produces a regular activity of the ventricle. The electrocardiogram of a case of complete block is shown in Figure 20. Here it is to he noted that the ventricular complexes (R S T) are normal in form except when they are distorted by superimposed P waves which recur at regular intervals hut with no fixed relation to successive ventricular complexes. The P waves are equidistant from one another but fall in any portion of the ventricular cycle (both systole and diastole). The ventricle is contracting at the rate of 27 an d is perfectly regular, the auricle with a slight arrythmia contracts at a rate of 60. The activities of the upper and lower chambers are quite independent. This complete dissociation of auricles and ventricles is entirely charac- teristic of complete block. No impulses can pass from the auricle to the ventricle and each has its independent rhythm. The pace of the auricle is set by the normal pacemaker, the sinus node. The ideo-ventricular pacemaker is in this case located in the bundle of His above its bifurcation (if the impulses which initiate the contractions of the lower chamber were in some other portion of the ventricular musculature, as is sometimes the case, the ven- tricular complexes would be of an entirely different type). Only those cases have been described which represent distinct types of block; it should be said, however, in passing that a single case may present various degrees of block at different times, delayed conduction, partial and complete block may present them- selves in a single case at successive periods and more rarely one may follow a case passing through the stages of complete and partial block back to a condition of normal activity. A number of the simpler and more common types of partial and complete auriculo-ventricular block have been discussed ; this list, however, by no means exhausts the varieties of heart block which are seen in the clinic. Block associated with sinus irregu- larities, extrasystoles and auricular fibrillation are some of the types which will be taken up in subsequent chapters. The differentiation of a block produced by an organic lesion 5o Bradycardia. Heart Block from that resulting from a hypertonic condition of the vagus may often be made by noting the effect of the administration of atropin. In cases of Vagus block, the paralyzing of the terminal nerve endings with atropin abolishes the block. CLINICAL FEATURES AND SIGNIFICANCE The milder grades of interferences with the property of con- duction are often associated only with those signs which we have described in pointing out the means for their clinical recognition. The patient may be entirely unconscious of any abnormality and his attention may first be called to the condition by the physician who discovers the arrhythmia. While a moderate degree of de- layed conduction may be accompanied by no other symptoms, its recognition and true evaluation is important, for it means, as a rule, intrinsic myocardial defect. This may be either an organic or a chemical change in the muscle cells. It may be permanent or temporary, but it nearly always means some sort of damage to the slender bundle of muscle connecting auricles and ventricles. In taking this stand, I am quite aware that a considerable degree of impaired conduction may be produced both experimentally and clin- ically by stimulation of the left vagus nerve, and yet I believe that clinically these vagus effects are usually only in evidence when the tissues under their control are functionally damaged. The recognition of this defect is also important, because it usually indicates extensive myocardial change. It is the most evident feature because the integrity of the A-V bundle is essential to the sequential co-ordination of auricles and ventricles, and yet it is rare to find a lesion of the bundle without other widespread dam- age in the walls of both the upper and lower chambers. Indeed, it is the rule, rather than the exception, that the injury to the A-V bundle is merely a part of the pathological process involving a large portion of the heart muscle. The identification of this defect is of considerable practical value, since these hearts are particularly susceptible not only to vagus influences, but also to drugs of the digitalis group. Some degree of block may often be initiated in a normal heart by the adminis- tration of toxic doses of digitalis. In those showing an abnormal conduction, digitalis is frequently a potent influence in accentuat- Bradycardia. Heart Block 51 ing the defect. It does not follow from this that digitalis is always eontraindicated in conduction abnormalities. Some of these pa- tients seem to improve when the block is increased, but in such cases it should be given with caution and with a knowledge of the effect which may be expected. A complete functional destruction of the bundle of His i not necessarily followed by cardiac insufficiency. I have had under my observation for the past three years a young woman referred to me by Professor Janeway, in whom a complete heart block was discovered during a routine examination. She has at no time given any evidence of cardiac insufficiency and during this period has completed a course of training as nurse in the Presbyterian Hos- pital, involving no small amount of physical exertion. Cardiac insufficiency in cases of dissociation is more often due to the inability of a damaged ventricle to maintain its part, rather than the result of the cutting off of the normal auricular impulses. During the course of acute rheumatic fever, diphtheria, pneu- monia and other infectious diseases, one should be on the outlook for conduction disturbances. These are met with not only during the height of the active process, but also during convalescence. I have seen its development on several occasions, some days after the defervescence of an acute lobar pneumonia, in diphtheria long after the subsidence of the acute symptoms, and in rheumatism when the patient was beginning to move about. Under these con- ditions the block is frequently only a temporary affair and even- tually disappears with the removal of the toxins and the restitution of the cells of the myocardium. The indiscriminate use of digitalis in the acute infections is to be deprecated. It may be of great service when properly used, but may also do distinct injury unless carefully adapted to the needs of the individual patient. In complete block the rate of the ventricle is quite independent of reflex influences ; excitement may increase the auricular rate in its accustomed manner, but the ventricular rate is undisturbed. The same has been noted in regard to the effects of the administration of alcohol and chloroform (Mackenzie). We have discussed the cases of heart block in which the arrhythmia is the only symptom and in which there is no altera- 52 Bradycardia. Heart Block tion in the general blood distribution, also a group of cases in which the arrhythmia may or may not be the only evidence of a myo- cardial lesion, but in which the heart is unable to maintain an adequate circulation, with a result that the ordinary symptoms of cardiac insufficiency ensue. In the latter we conclude that there is always a defective ventricular muscle in addition to the abnormal condition of the A-V bundle. There remains for our consideration a group of cases which is characterized by symptoms which are directly dependent upon the arrhythmia for their development. This is the group that has long been recognized as the Adams-Stokes syndrome. Its distinctive features are attacks of unconsciousness, with or without convulsive movements, associated with a sudden slowing of the usual pulse rate. The seizures are probably the result of a sudden cerebral anaemia attending the abrupt slowing of the left ventricle. The attacks may be very infrequent and occur at intervals of months or may follow one another with great rapidity, so that "twenty to thirty" may be counted in twenty-four hours. They differ greatly in their duration and in their severity. Sometimes the loss of con- sciousness is merely momentary or it may be prolonged for sev- eral minutes. The breathing may be at first stertorous and be fol- lowed later by apnoea, or the respiration may be normal through- out the attack. If the attack is momentary there is usually a pallor of the face; in a prolonged attack there is venous congestion with extreme cyanosis. The convulsion may consist of slight twitching of the face or of one arm or in the more severe parox- ysms it may become general. The attack is usually ushered in with a sudden decrease in the ventricular rate and with pauses between the beats of varying duration. The change may consist in a fall of rate from the normal to the neighborhood of 30, or, in cases with a block of considerable duration and an established rate of 30, the rate may suddenly fall to 7 or 8 per minute. Dur- ing the attack the veins of the neck may be prominent and are seen pulsating rhythmically at the rate of 60 or over per minute. After the attack the heart will usually be found to be beating rhythmically at about 30 per minute. This sudden change in an established ideo-ventricular rhythm, with its associated loss of con- sciousness, is additionally suggestive of serious damage to the veil- Bradycardia Heart I '.lock 53 tricular muscle, for a normal ventricle should maintain its ideo- ventricular rhythm unimpaired. The exciting cause of this syndrome is often found in a little unusually physical exertion. In extreme cases, walking a short distance has been found sufficient to induce an attack, while in others a moderate amount of exertion is endured with impunity. Since the ordinary path by which the ventricles are influenced is severed, we do not know the mechanism through which exercise may affect them. It may be by a direct effect on the myocardium of an altered blood supply, or possibly by reflex influences through those few fibers of the extracardial nerves which are known to terminate in the ventricular muscle. It should always be remembered that the terms heart block and Adams-Stokes syndrome are not synonymous. The former desig- nates a dissociated activity of the auricles and ventricles, and may continue indefinitely without the attacks of cerebral anjemia and unconsciousness, which are characteristic of the Adams-Stokes complex. COURSE AND PROGNOSIS Every case of heart block, even those of the mild degree show- ing only a prolonged auricu'lo-ventricular interval or occasional dropped beats, demand close observation over a long period of time. This is not because the defect in the A-V bundle is in itself a serious matter, but because it is usually indicative of more ob- scure and more extensive lesions of the other parts of the myo- cardium, and because it often affords the earliest evidence of a functional impairment which is progressive. It is rarely the only evidence of heart damage; usually one finds, in addition, a valvular defect, signs of a pericarditis, dilatation, hypertrophy, or other direct evidences of more extensive myocardial damage. A mild degree of the depression of conduction in itself rarely induces cardiac insufficiency, but aside from the concomitant lesions which may be present and which have been referred to above, such hearts have a "margin of safety" under the normal. In my experience a very large proportion of hearts which show this abnormality during the course, or subsequent to the acute mani- festations of influenza, pneumonia or typhoid fever, entirely recover 34 Bradycardia. Heart Block their normal function. When the defect follows diphtheria, rheuma- tism or a syphilitic infection, it is more apt to he permanent. The prognosis in these mild types depends primarily on the func- tional condition of the heart, aside from the arrhythmia due to the injury to the bundle. If the lesion of the bundle is stationary, and if it is the only evidence of cardiac damage, it may he re- garded with little apprehension. Patients do not die of mild degrees of heart block, nor is the reserve force of the heart greatly re- duced thereby. Unfortunately, in a considerable number of instances, a per- sistent heart hlock shows itself to be part of a progressive lesion. Symptoms of ventricular damage gradually develop or the evidences of bundle defect gradually or abruptly indicate a transition to a more severe type of abnormal function. It is at the time of the sudden change from a mild degree of block to the more severe grades that the attacks of unconscious- ness and convulsions, which are characteristic of the Adams-Stokes syndrome, are wont first to appear. The cerebral anaemia seems to be induced by the sudden transition from the faster to the slow rate. 'When the block becomes complete and the lower chamber takes on its slow rhythmic ideo-ventricular rhythm, there is less liability to these seizures. Later there may be other abrupt falls in rate (manifestly due to defects of the ventricular myocardium) and once more the attacks of unconsciousness appear with renewed severity and frequency. A severe grade of heart block is a serious condition. It is usually associated with widespread myocardial damage and consequent cardiac insufficiency. The latter is most commonly the cause of the gradual incapacitating of the patient and ultimately of his death. That these associated conditions are usually the factors of moment is evidenced by the fact that one sees cases of complete block who for years follow their accustomed activities unconscious of any abnormal circulatory condition and are incommoded only when other evidences of myocardial change appear. The development of fits, which, however, occurs in only a small percentage of those afflicted with heart block, is a grave sign. The first attack may be fatal and the only prodrome recognized may have been a slow or irregular heart action. More commonly the Bradycardia. Heart Block 55 patient has a number of attacks often with very little apparent harm. The attacks once established are prone to recur at shorter intervals and with increasing severity. One cannot predict when a seizure is likely to prove fatal. Even the majority of those who develop the Adams-Stokes syndrome, however, do not die in one of the attacks. They are far more apt to succumb to a gradually increasing cardiac insufficiency terminating in heart failure with- out cerebral symptoms. Prognosis, on the whole, should rest on a study of the extent and progress of the myocardial defect and an estimate of the ven- tricular efficiency. Few patients survive the inception of attacks of cerebral anaemia more than two or three years. The end may come at any time. Exceptionally the duration of life is longer. Several of Edes' cases lived seven or eight years after the onset of the Adams-Stokes syndrome. A case reported by Osier lived thirty years after the discovery of brachycardia and seven years after the first syncopal attack. Gerhardt has reported three cases in which syncopal attacks and heart block completely disappeared. CHAPTER VII The Extxasystole In the routine examination of the pulse our attention is frequent- ly attracted by a form of irregularity which has the following char- acters : the rhythm is for longer or shorter periods that of a normal pulse, but at intervals this rhythm is interrupted by a pause during which one may get the impression that one pulse beat has failed in its normal sequence; it appears as if one pulse beat had been omitted and the impression is often described as "a dropped beat" or as "an intermittent pulse." When we come to verify our impressions by more careful observation we may find that, during this pause in which we at first thought a beat had been missed, v%'e are able to detect on delicate palpation, a small pulse wave which had at first escaped our attention ; this wave is usually much smaller than the waves of the normal rhythm ; it occurs at a time which is a little too early for the occurrence of a beat of the normal rhythm and is followed by a pause which is somewhat greater than the inter- val between the beats of the normal rhythm ; this pause is usu- ally followed by a pulse wave which is a little larger and more forcible than the waves of the normal. This irregularity is known as an cxtrasystole. It is evidently the result of a ventricular con- traction which has occurred too early and which is less forcible than the normal rhythmic contractions of the heart; it is therefore also known as premature contraction. On auscultating such a heart we will detect a rhythmic series of normal sounds interrupted at inter- vals by a group of sounds which are weaker and occur earlier than those of the normal cycles; this first and second sounds of the weak group are followed by a silence which is considerably longer than the normal diastolic period. In some of the hearts of this group the extrasystolic contraction will be represented by a single sound only, and no corresponding wave even of an abortive character can be detected in the peripheral arteries. These signs indicate that the premature beat was wanting in force sufficient to open the aortic valve. The question of the 56 The Extrasystole 57 opening of the aortic valve depends on three factors : (a) the energy of the premature ventricular contraction; (b) the volume of the blood in the ventricle at the moment; and (c) the blood pressure in the aorta. These factors depend in turn upon the time of the occurrence of the extrasystole. If this comes early in diastole the contractile power of the ventricle will have recovered to only a moderate degree; the volume of blood in the ventricle will then be small and the aortic pressure will be near its highest point ; hence it is hardly probable that the aortic valves will be opened and such a premature contraction will be accompanied by the first heart sound only; the second sound, due to the closure of the aortic valve, will be absent and there will be no corresponding pulse wave. If. how- ever, the extrasystole comes later in the diastolic period, contrac- tility will have more completely recovered ; the volume of blood which has passed into the ventricle will be greater and the aortic pressure to be overcome much less ; hence the aortic valve will be opened; the second heart sound will be heard and the small extra- systolic wave may be felt at the wrist. PATHOLOGY AND ETIOLOGY In the sections on the physiology of the heart it was pointed out that all portions of the musculature of the heart have the property of excitability, that is that any muscle cell can respond to stimuli at any time except during the "refractory period" which lasts for a short time after the cell has been stimulated. Also that normally stimuli are rhythmically originated at the "sinus node" and sweep over the tissues of the heart in an orderly manner, exciting to activity its chambers in a definite sequence. If electrical stimuli of the proper strength be applied by means of suitable electrodes to the wall of the heart of the experimental animal (frog, turtle rabbit, dog, etc.), it will respond by a contrac- tion, no matter what portion of the musculature is excited ; the ac- tivity thus produced will spread downward in the direction taken by physiological stimuli and also from the point of stimulation up- ward toward the sinus node, i.e., in a direction the reserve of that of physiological stimuli, and the chambers of the heart will contract in the order in which the stimuli reach them. Contractions thus excited from an abnormal focus are known as extrasystoles, and, 58 TlIF. E.XTR ASYSTOLE according to their point of origin, are known as auricular, ventric- ular, etc. If, in this manner, the heart is systematically studied by applying stimuli in the various phases of the cardiac cycle while the heart is beating rhythmically, it will be found that for a period beginning just before and extending a short time after systole, the heart is not excitable even by very powerful stimuli, i.e., the heart is in the "re- fractory phase" because the molecules upon which the fundamental properties of cardiac muscle depend have been decomposed into their constituent ions. Now the extrasystole which has been experimen- tally produced throws the heart muscle into the "refractory phase" so that the next physiological stimulus of the rhythmic series aris- ing at the sinus node will reach the muscle cells lower down when they are inexcitable, hence it will be ineffective in producing a systole. The next systole will not occur until it is brought into being by the next spontaneous stimulus which is formed at the sinus node and which occurs exactly at the moment at which it would have occurred had there been no extrasystole. This lengthened diastolic period which follows the extrasystole is known as the "compensatory pause." When the time consumed between the last normal heart beat preceding the extrasystole and the normal beat following the compensatory pause is exactly equal to the time occupied by two beats of the normal rhythm, the long diastolic pause following the extrasystole is known as a "complete compensatory pause;" when the interval between the last spontaneous systole and the post-com- pensatory systole is less than the interval between two systoles of the normal rhythm, the compensatory pause is called "incomplete." A study of the compensatory pause in the mammalian heart re- veals the following facts: (a) When the sinus node is stimulated the extrasystole is not followed by a compensatory pause, (b) When the auricle is stimulated the compensatory pause is usually incomplete, (c) When the ventricle is stimulated the compensatory pause is complete. These facts may be explained on the following grounds : As soon as the stimulus material at the node is destroyed by its direct stimulation, the construction of the material is immedi- ately recommenced and reaches the explosive point at an interval just equal to the period of the normal rhythm. When the auricle is stimulated early in the diastolic period (see Figure 26) the stim- The Extk asystole 5'J V, ^^^ X Figure 26 Kxtrasystole arising from the auricle near the sinus. s s \ \ \ 5 AH EB Figure 27 Extrasystole arising from a point low down in the auricle. Ay ' 1 ' 1 1 j -i - i '1 ' 1 i ^i Figure 28 Extrasystole arising from a point in the ventricle. Diagrams to illustrate the mechanism of the extrasystole starting from various parts of the heart muscle. The arrows indicate the points of origin and the directions taken by the stimuli. Dotted arrows indicate the time at which the normal stimulus at the sinus node should reach maturity if its formation was not interrupted by the extrasystole. The thickness of the lines representing ventricular systole indicate the relative effect of the normal beat and the extrasystole in maintaining an adequate circulation. As = auricu- lar systole. A-V = auriculo-ventricular bundle. Vs — ventricular systole. 6o The Extrasystole ulllS is conveyed not only to the ventricle but also upward to the node and will destroy the spontaneously forming stimulus material at the node before it has reached the explosive point, hence the interval between the last physiological stimulus and the post-extra- systolic stimulus will be somewhat less than two cycles of the normal rhythm. When the auricular stimulation occurs somewhat later in diastole the retrograde stimulus may reach the node coincident with the explosion of the rhythmically formed stimulus material, hence in this instance the post-extrasystolic pause will be fully com- pensatory. When the ventricle is stimulated (see Figure 28) the retrograde stimulus reaches the sinus node during its refractory period just after its physiological stimulus and the post-extrasys- tolic stimulus will exactly equal the period between two beats of the normal rhythm and the post-extrasystolic pause will be fully com- pensatory. This explanation indicates how extrasystoles arising from different parts of the auricles may have compensatory pauses either complete or incomplete. It may be stated, as a general rule, that the nearer to the sinus node is the point of stimulation initiating an extrasystole, and the earlier it occurs in diastole, the shorter will be the post-extrasystolic pause ; and, conversely, the farther from the sinus node is the point of origin of the extrasystole and the later it occurs the more nearly will the post-extrasystolic pause be com- pensatory. Electrocardiographic studies have further shown that the stimuli originating extrasystoles may pass over the musculature of the heart by the normal paths (nomodrome extrasystole), or, since the stim- uli may originate from some point far removed from the normal path or may be shunted from this path by abnormal conditions of the muscles which form an obstruction to their passage, they may take an unusual course through the cardiac tissue (allodrome extra- systoles). A discussion of these abnormal paths and their varie- gated but characteristic electrocardiographic records will be left for a later paragraph. Extrasystoles have been produced experimentally in many ways other than the employment of electrical stimuli. Mechanical irrita- tion, heat, the application of irritating salts, obstruction of the great veins (Stassen), clamping of the aorta (Hering), ligation of a branch of the coronary artery (Lewis), the injection of digitalis The Extrasystole 6i and atropin (Cushny), adrenalin (Kahn), muscarine and physo- stigmine (Rothbcrgcr and Winterbcrg). Under proper conditions extrasystoles have been produced in the isolated perfused heart and in the mammalian heart in situ after all nervous connections have been severed, hence it is probable that their cause is an increased excitability of the muscle cells usually quite independent of nervous influences, though Kraus and Nicolai have produced them by vagus irritation. The conditions of the experimental production of extrasystoles have been set forth at some length since it is upon inferences from these data that our conception of the pathological conditions under- lying the extrasystole, as met with in man, is based. Very little indeed is known of the histological changes associated with the pro- duction of extrasystoles and there still remains here a field for care- ful and exhaustive research. Clinically extrasystoles are found far more frequently in those with slow hearts and often they may be made to disappear by moderate exercise which quickens the heart rate. The experimental evidence seems to indicate clearly that the extrasystole occurs because some cardiac muscle cells become more excitable than those of the sinus node and it is therefore on this ground, easy to understand why an increase in excitability should be more apparent during a slow rate, since in the faster rates the excitability of the node is greater than in the slow rates ; under such conditions the abnormal irritability of some portion of the auricle or ventricle must be considerable to make itself evident. It also seems fair to assume from the experimental evidence that nutritional disturbance may play an important part in increasing the excitability of heart muscle; an atheroma with a narrowing of the coronary artery or one of its branches may be the pathological counterpart of the ligation of the branches of the coronary which has been shown by Lewis to regularly produce extrasystoles. Numerous toxic agents are known to be associated with the pro- duction of extrasystoles ; they are quite common in many febrile conditions, notably in acute rheumatic fevers. One of the very common phenomena produced by the administration of large doses of digitalis (at least to patients having damaged hearts) is the ap- pearance of ventricular extrasystoles ; on the withdrawal of this drug they disappear. Nicotine is another of the cardiac poisons 62 The Extrasystole which is clinically prominent as a cause of extrasystoles. The "to- bacco heart" is one in which premature beats have become so frequent as to make themselves uncomfortably evident. Excessive tea drinkers are subject to this form of irregularity. Premature beats are found in persons of all ages ; they are rare in the first dec- ade of life and are most common after the age of 50. They are considerably more common among men than among women. Extrasystoles are probably very much more common than is gen- erally supposed; it has been estimated that a majority of persons reaching middle age have had extrasystoles at some period. They are frequently met with in those who afford other signs of impair- ment of the heart, such as valvular disease, myocardial degeneration and the cardiac complications of nephritis, but premature contrac- tions are also not uncommonly found in those whose hearts have no discoverable abnormality other than this irregularity. Premature contractions are exceedingly common in individuals of the neurotic type; they may sometimes be induced by irritation of the skin and in persons subject to this irregularity, merely plung- ing the hands into cold water is sufficient to develop it. They are often associated with digestive disturbances, particularly when ac- companied by flatulency. As has been mentioned exercise will fre- quently cause the temporary disappearance of extrasystoles, but if carried to the point of fatigue the irregularity is prone to become more evident than before. In those predisposed to them, suspen- sion of respiration for a few seconds will sometimes induce these premature contractions. When present in the upright position they will often disappear as soon as the subject lies down, even though this change in position is accompanied by a slight diminution in the rate of the heart. Extrasystoles are quite common during convales- cence from infectious diseases. IDENTIFICATION Clinically, the starting point for establishing the presence of the extrasystole is to determine whether the patient has a fundamentally normal cardiac rhythm, which is broken on occasions more or less frequently. When the interruptions occur at infrequent intervals, as is the case in the majority of these patients, the detection of the fundamental rhythm is comparatively easy. If one palpates the Tin-: Kxtkasystoi.k 63 radial artery there arc long periods during which the pulse is per- fectly regular, then occasionally this regular rhythm is broken by a pause which is too long to fit the fundamental rhythm, or one may detect a very small pulse wave followed by a pause longer than that ordinarily separating the waves of the normal rhythm. When one listens to the heart sounds they will be heard for long periods as a normal rhythmic scries until this series is broken by the occur- rence of one or two indistinct heart sounds which follow the last normal sounds too early and which arc in turn followed by a pause longer than that occupied by the interval between the heart sounds of the periods of normal rhythm. The small premature waves de- tected in the radial and the indistinct premature first for first and second) sounds heard over the precordium, each followed by a more or less complete compensatory pause, are our usual common evidences of the presence of extrasystoles. Whether one hears at the time of the premature beat a first and second heart sound or only a first heart sound depends, as has been pointed out in a preceding paragraph, on whether the extrasystolic contraction has, or has not opened the aortic and pulmonary valves. If murmurs are present during the periods of normal rhythm, they are much less distinct in the premature cycle and may be ab- sent. The mitral systolic is the murmur which can most easily be detected in the extrasystolic cycle; the presystolic is more rarely heard ; while aortic murmurs are absent or shortened in consonance with the action of the valve which may fail to open, or open only for a brief period. I have recently seen a case presenting extra- systoles in which no heart sounds could be heard, both first and sec- ond sounds being replaced by loud harsh murmurs. At the time of the extrasystole one could hear four murmurs following each other at equally spaced intervals. The first and second of these murmurs were louder and a little longer than the third and fourth ; the fourth murmur was followed by a considerable pause which was succeeded by a repetition of the two murmurs which constituted the auscultatory evidence of the ordinary rhythmic activity of the heart. Another type of rhythm which is easily recognized as due to extrasystoles is the so-called "bigeminus." Here the radial pulse shows a rhythmic series composed of a large wave, a short pause, a small wave and a long pause. This sequence is repeated again t>4 The Extrasystole and again. Tlie repeated recurrence of two pulse waves followed by a pause has given rise to the very expressive term "coupled rhythm." It consists of a wave of the fundamental rhythm fol- lowed by a premature beat and its compensatory pause. This rhythm is one of the common manifestations of toxic doses of digitalis. When an extrasystole occurs every third heat it gives rise to a rhythm that was formerly described as the "pulsus trigeminus." When extrasystoles occur quite frequently and at very irregular intervals it is sometimes more difficult to assure oneself, by the ordi- nary physical signs, that the irregularity is due to premature con- tractions, but careful observation will usually discover a fundamen- tal rhythm, interrupted by beats which occur too early, are followed by a pause and each time they appear give the impression of "coupling." Inspection of the jugular pulse is frequently an aid in making the diagnosis of an extrasystole. The two venous waves which one ordinarily sees during the fundamental rhythm are often replaced at the time of the premature contraction by a single venous wave larger than the others. This wave is due to the inability of the vein to discharge its contents into the auricle at this moment, since the pressure in the auricle is abnormally high, the ventricle being in systole and the auriculoventricular valves being closed. This is, of course, more in evidence when the origin of the extrasystole is in the ventricular wall and the auricle and ventricle contract simul- taneously. Whether an extrasystole is auricular or ventricular in origin can only be definitely decided by graphic records and yet the trained observer who has sharpened his powers of differentiation by corre- lating his physical signs with the evidence of the graphic records, can often, by noting the length of the compensatory pause and the character of the heart sounds of the premature beat, quite correctly assign a particular extrasystole to its proper category. A graphic record of the radial or of the apex beat is often suffi- cient evidence to establish the presence of the extrasystole. Such a record (Figures 30, 31 and 32) shows a series of similar waves re- curring at equal intervals. This rhythm is more or less frequently interrupted by a small wave which occurs too early to fit into the 'I HE EXTRASYSTOLE 65 0.2 second Figure 29 Auricular extrasystole at x. The compensatory pause is incomplete. Brachial 1.2 second Figure 30 Auricular extrasystole at x. a' of extrasystole superimposed on preceding r wave. The compensatory pause is incomplete. 66 The Extrasystole fundamental rhythm. It is followed by a pause longer than that between two bleats of the fundamental rhythm, which in turn is followed by a wave which is usually a little larger than the average wave of the rhythmic series and which is the first of a new^ series of rhythmic waves. In the case of an extrasystole which originates in the ventricle the post-cxtrasystolic pause is fully compensatory (see Figures 32 and 33). When the extrasystole has its origin higher up in the cardiac tissues, the pause i> "incomplete" ( Figures Jo, 30 and 31 ). The reason for this has been explained in a pre- ceding paragraph (page (>o). THE POLYGRAM Auricular 1 Extrasystoles. The jugular tracing throws additional light on the mechanism (Figures 29 and 30). Figure 29 shows a rhythmic series of waves a c i\ which is several times (at x) inter- rupted by a similar group which occur too early; it is clear that the auricle contracts too soon and is followed by a sequential contrac- tion of the ventricle. Another case of auricular extrasystole is shown in Figure 30; here the premature contraction of the auricle occurs earlier in the cycle than was the case in Figure 29, so that the auricular premature wave a' is superimposed on the v wave of the preceding group; the simultaneous contraction of the ventricle and the auricle causes an unusual temporary stasis in the jugular vein, hence this large wave (v a'), The extrasystole is followed by a compensatory pause which is "incomplete." The Nodal Extrasystole is illustrated (x Figure 31). In this in- stance our conception is that the premature contraction starts at a point in the tissues junctional between auricles and ventricles ; from this point the stimulus sweeps upward to the auricle and downward to the ventricle so that these chambers contract practically simultane- ously, hence the waves a' and c' of the jugular coincide. The retro- grade stimulation of the auricle has destroyed the usual stimulus material accumulating at the normal pacemaker ; the building up of stimulus material is, however, at once recommenced and this reaches maturity in the normal time which is shown by the fact that the time elapsing between the wave a' of the extrasystole and the suc- ceeding a wave is exactly the interval of the normal rhythmic series. 'I in. I'..-. I RASYSTOLE 67 %c **. S' fc *r5v ■ j \ Radial JUJlLLUlUJUJlLLUJuJUUlJlUUl^ Figure 31 Nodal extrasystole at x. In the jugular tracing the a and c waves of the extrasystole occur simultaneously. The compensatory pause is incomplete. Jugular Brachial 0.2 second Figure 32 Ventricular extrasystole at x. In the extrasystolic cycle the auricle and ventricle con- tract simultaneously (a' c'). The compensatory "pause is complete. 68 The Extrasystole Ventricular Extrasystoles are shown in Figure 32. The auricle, as represented by the a waves of the jugular record, contracts rhyth- mically, but occasionally (x) the ventricle contracts prematurely so that at these times the auricle and ventricle contract simultaneously and their activities are represented by a large wave (a' c') in the jugular tracing. The absence of the v wave in the extrasystolic cycle which is quite evident in the records is due to the empty con- dition of the ventricle at the time of the premature contraction. It is to be noted that the post-extrasystolic pause is fully compensa- tory. Figure 33, with its diagrammatic analysis, shows a ventricular extrasystole which occurs every thin beat giving rise to the so- called "pulsus trigeminus." Mixed types of extrasystoles are not infrequently seen in a single case. A tracing of such a patient is shown in Figure 34. Here one may make out the following sequence: normal beat, auricular extra- systole, ventricular extrasystole. The analysis of the polygraph in these cases is sometimes quite difficult. The analysis of the tracing shown in Figure 34 was subsequently verified by electrocardio- graphic records in which the analysis is much less difficult. THE ELECTROCARDIOGRAMS As a rule the identification of the kind and point of origin of the extrasystole is most accurately made by means of the electrocardi- ographic record. The most distinctive features of extrasystoles are that (1) they occur too early, and (2) they are followed by a pause greater than the normal intersystolic pause. To fix clearly the phenomena which the electrocardiogram dis- closes, upon which we base conclusions as to the point of origin of the extrasystole, let us recall just what the movements of the string of the galvanometer represent. At any given moment the deflection of the string indicates the algebraic sum of the differences of elec- trical potential of the heart as a whole. When the stimulus arises at the sinus node (the normal pacemaker) and passes over the heart in a sequential, orderly manner, a series of deflections occur which we have learned to recognize (see Chapter IV) as the normal differ- ences of electrical potential for successive instants of the cardiac cycle. If now the stimulus arises from some point of the cardiac musculature other than the "sinus node" it is quite evident that the TlUi EXTRASY! I "i.i. bg 0.2 second Figure 33 'Pulsus trigeminus" due to an cxtrasystole, which occurs every third beat. Ventricular and auricular a' c' — auricular extrasystole. Figure 34 extrasystoles in a single record. " — ventricular extrasystole. Jugular Brachial ;cond a C =^ normal cycle, yo The Extrasystole impulse passing by abnormal paths and reaching purl ions of the cardiac tissues at intervals quite at variance with the normal will produce differences of electrical potential at successive moments of the cardiac cycle quite different from the normal. How great are the variations in electrical potential which result from the extra- systolic contractions may best be appreciated by a study of the curves which are here reproduced. Auricular Extrasystoles. When the focus from which the extra- systole arises is at or near the sinus node the electrocardiographic complexes are usually of the normal form. Such a record is shown in Figure 35. It is composed of a series of complexes, each of which is practically of the normal type. Each cycle is opened by a P wave, which at its proper interval is followed by a normal ventricular com- plex, Q R S T. In the center of the record the fundamental rhythm is broken by a cycle ( x ) which, although normal in other respects, occurs prematurely and is followed by a pause which is not quite long enough to be completely compensatory. This premature con- traction must have arisen at or near the sinus node, since the vari- ous parts of the cardiac musculature have been stimulated by paths and in a sequence which is the normal one. The curve reproduced in Figure 36 shows an extrasystole which has arisen high up in the auricle near the sinus. Here the extrasys- tole has occurred so early that its P wave is superimposed on the T wave of the preceding cycle producing a wave which is equal to P -f- T. The pause following the extrasystole is incomplete. It has been shown by Lewis* that if the auricle of an animal is made to contract by applying artificial stimuli to various portions of the auricular tissue, the resulting electrocardiographic records will be greatly modified. When the point of stimulation is at or near the sinus node the P wave is upward in direction and of a form which we have come to regard as normal; as the point of stimula- tion is made more and more remote from the sinus the P complexes become irregular in form and may be directed downward or show a diphasic variation. We are therefore led to infer that in the human electrocardiogram an upward single P wave represents an auricular contraction originating at or near the sinus node; a down- ward directed P wave indicates an origin in the lower part of the ♦Heart, iqio, ii, 27. The Extrasystole 7i ifyl P T P ' T P T p T ;• Figure 35 Auricular extrasystole at x. Compensatory pause incomplete. P — auricular contrac- tion. R-T = ventricular contraction. Brachial tracing above. Figure 36 Auricular extrasystole at x. The auricular wave P of this extrasystole is superimposed on the T wave of the preceding ventricular complex. Figure 37 Extrasystole at x arising from a point low down in the auricle. P is directed down- ward in the extrasystole. P following extrasystole is diphasic. Below is brachial tracing. Figure 38 "Pulsus trigeminus" caused by an auricular extrasystole, which occurs every third beat at x. P is reversed in extrasystole, indicating a point of origin low down in auricle. Radial tracing above. 72 The Extrasystole auricle ; a notched or diphasic P wave indicates an intermediate point of auricular origin. An extrasystole which arose in the lower part of the auricular tissue is shown in Figure 37. The complexes of the ordinary rhythm are normal in form except that the P waves arc rather too broad and have summits which are slightly flattened; the extrasystolic cycle ( x ) is initiated by a P wave which is directed downward but is followed by a ventricular complex which is normal in form, indi- cating that the ventricular response to the premature auricular activity was the result of an impulse which passed down through the A-V bundle and over the ventricular musculature by the normal paths in a perfectly orderly manner. It may he noted in passing that the auricular complex which immediately follows the extrasys- tole has a form somewhat different from the P waves of the suc- ceeding normal cycles ; this is not an unusual occurrence and sug- gests that the auricle has not as yet entirely recovered its normal function. Figure 38 displays a rhythm which was formerly known as the "pulsus trigeminus." It consists of a series of two normal beats fol- lowed by an auricular extrasystole. The impression produced on the palpating finger by a pulse of this type is indicated by the radial curve taken simultaneously with the electrocardiogram. All the auricular (P) complexes of this record show an unusual diphasic form, suggesting that even those impulses which originated at the sinus node have taken an abnormal path through the auricular tissue. The P waves of the extrasystole (.r) are clearly reversed, indicating an origin low down in the auricle. The ventricular extrasystole presents in the electrocardiogram (Figure 41), a complex far removed from that of the normal ven- tricular contraction. The abnormal point of origin and the conse- quent abnormal path which the impulse follows usually produces a much greater difference of electric potential than does the impulse which descends from the auricle and follows the normal path through the A-V bundle and its branches. The auricle contracts at regular intervals, so that often when an extrasystole occurs the ventricular and auricular contractions are simultaneous. The little wave representing auricular activity wilf then occur during the time of ventricular activity and is usually relatively so small that it is Jul Extras^ tole d^'t^i^^F^ Figure 39 Lead II. Every P wave is of an abnormal form indicating an abnormal point of origin in the auricle or an abnormal path through the auricular wall. Figure 40 Auricular extrasystoles from a point low down in the auricle. Xote the short PR interval of the extrasystoles and the incomplete compensatory pauses. Lead I Lead II Lead III J^JU&jJ&U^h Jt^Jwto^yfc^ i Figure 41 Ventricular extrasystole at x arising from a point at the base of the left ventricle Showing similarity in the complexes obtained by leads II and III. Compare P R T = nor mal complex and extrasystolic complex x. 74 The Extrasystole submerged in the large waves of the ventricular complex. Figure 41 shows an electrocardiogram taken from a patient by the cus- tomary three leads. The first and last complexes of each lead are the normal for this individual, between these are seen the cxtrasys- toles. It is to be noted that the form of the extrasystolic waves are very similar in leads II and III, but that these differ very ma- terially from the extrasystole pictured in lead I. The similarity of form of the extrasystolic complexes of leads II and III is usual. The complex of lead I may be similar in form to that of lead II, but it is usually quite different. The submerged auricular wave which occurs during the extrasystole can be seen (only in lead II) as a small notch (P) in the final dip of the extrasystolic complex. Systematic studies of the electrical complexes obtained by stimu- lating various portions of the right and left ventricles both when the branches of the bundle of His are intact and when one of the branches has been cut, have shown that a comparison of the re- cords* taken by lead I and lead II will indicate the point from which the extrasystole has its origin. The prominent types are shown in Figures 42, 43, 44 and 45. The direction of the principal deflection in leads I and II with the points of origin of the extrasystoles may be tabulated as follows : TYPE DIRECTION OF PRINCIPLE DEFLECTION POINT OF ORIGIN OF STIMULUS. LEAD I. LEAD II. 1 3 4 up up down down up down up down Right ventricle near base " " apex Left ventricle near base apex A type of curve which is not infrequently met with is shown in Figure 46. Two ventricular extrasystoles appear in this record. Each is preceded by a P wave which occurs at its regular rhythmic *Rothberger and Winterberg: Archiv. fur die ges. Physiologic, 1913, cliv, P- 571- I.ra.l I Lead if 75 *.*■«* ^y^it^^f^ ^r^r* Figure 42 Type. 1. Ventricular extrasystole arising from a point in the right ventricle near the base. h^rfrf-*^ Figure 43 Type 2. Ventricular extrasystole arising from a point in the right ventricle near the apex. Above brachial tracing the extrasystole produces no arterial wave. Figure 44 Type 3. Ventricular extrasystole arising from a point in the wall of the left ventricle near the base. Radial tracing above. Figure 45 Type 4. Ventricular extrasystole arising from a point in the wall of the left ventricle near the apex. -6 The Extrasystole interval. At first sight one might regard this as an impulse which had its origin in the auricle and which was shunted off by an ab- normal path through the ventricular wall. One notices, however, that the length of the P-R interval of the normal complexes is unusu- ally long (over 0.2 second), while the interval between /' and the onset of the extrasystolic complex is very brief (0.1 second). It is therefore evident that insufficient time has elapsed between P and the onset of the extrasystole to permit of the passage of the stimulus from the auricle to the ventricle, and we must conclude that the ventricle has contracted in response to a stimulus initiated independ- ently in its own wall. A contrast to this case is shown in Figure 47. Here the ventric- ular extrasystole (at x) occurs relatively early and the auricular contraction P is seen as a step on the descending limb of the large extrasystolic wave. The arterial tracing which accompanies this as well as many of the preceding electrocardiograms shows the rela- tively small wave which is produced in the arterial tree by the extra- systole. This evident lack of efficiency of the premature contraction in maintaining an adequate circulation is due to two factors (1) the abnormal sequence of the stimulation of the muscle fibers of the ventricle results in a contraction which is relatively incoordinated, and the propelling power of the ventricles is less than under the normal conditions; (2) on account of the prematurity of its contrac- tion the ventricle is less well filled with blood, hence a smaller volume is expelled into the aorta. The nodal extrasystole. The majority of extrasystoles which one sees in the clinic have their origin in some portion of the ventricular wall. Auricular premature contractions are far less frequent. A still more rare form of extrasystole is shown in Figure 48. In this curve the extrasystolic complex is only slightly changed from the ventri- cular complex of the fundamental rhythm, the following pause is fully compensatory and the presence of P in its normal rhythmic position following the principal wave of the extrasystole shows that the rhythm of the auricle has not been disturbed. Since the ven- tricular portion of the extrasystolic complex has a form not unlike the ventricular complexes of the sequential rhythm and yet clearly is not the result of auricular activity, we conclude that its point of origin is at some point high up in the auriculo-ventricular bundle The Extrasystole 77 Figure 46 Ventricular extrasystole at x. The auricle contracts rhythmically, as shown by P waves. P-R interval = 0.3 second. The extrasystole does not originate in the auricle. 2 7» t ,. .. x » ^^-^^^ Figure 47 Ventricular extrasystole at x, showing submerged P waves. Brachial tracing above. Extrasystolic pause is fully compensatory. Figure 48 Nodal extrasystole at x. At time of ex- trasystole auricle and ventricle contract si- multaneously. Origin of ventricular im« pulse is high up in the A-V bundle. ^S The Extr vsystole anil that Its subsequent course through the ventricular wall follows the normal channels. This is known as the nodal extrasystole. The interpolated extrasystole is another rare form of premature contraction. An extrasystole always ventricular in origin occurs between two beats of the normal rhythm without otherwise disturb- ing the orderly course of either the auricular or the ventricular rhythm ( Figures 40. 50 and 511. In Figures 52 and 53 are shown two types of "pulsus bigeminus," each due to an alternation of normal cardiac contractions and extra- systoles; the extrasystoles of Figure 52 arise in the wad of the right ventricle near the apex; the premature contractions of Figure 53 arise in a point in the left ventricular tissues near its base. Extrasystoles of different points of origin frequently are met with in the same patients on separate occasions and sometimes in close succession. Figure 54 shows auricular extrasystoles at A and ven- tricular extrasystoles at x. The auricular extrasystoles have an in- complete, the ventricular a complete compensatory pause. Figure 55 shows an alternation of ventricular extrasystoles (x) and normal ventricular complexes. At the center of the record ( Y) the quence is further disturbed by the occurrence of a ventricular extra- systole from an entirely new point of origin. THE CLINICAL SIGNIFICANCE of the extrasystole is one of considerable importance. Most of us have followed the career of patients who have had occasional extra- systoles for a number of years and often we can secure a history of the existence of this form of irregularity for many years, antedating our own observations, yet we rarely see a case of cardiac insuffi- ciency which can reasonably be attributed to this irregularity per sc. The patient is often quite conscious of what they often describe as a "thumping" in the precordial region, "fluttering of the heart," or "palpitation." On examination a large number of these sensations can be shown to be due to the presence of extra- systoles. These sensations are often the occasion of considerable alarm to the patient particularly when they are first discovered and the physician who assures them that this irregularity in itself is of very little significance and rarely is the forerunner of more serious The Extrasystole 79 R UAmw^^A> Ai H Figure 49 Interpolated extrasystole. Figure 50 Patient G. Lead I. Interpolated extrasystole at X. Ventricular extrasystole type i. Figure 51 Patient G. (same as Figure 50.) Lead II. Interpolated ventricular extrasystole type 1. 80 The Extrasystole trouble docs the patient a great service in removing his grounds for anxiety. When, however, we see cases which show extrasystoles at very frequent intervals and particularly when the extrasystoles arise from more than one focus our prognosis should be much more guarded, such irregularities are evidences of more serious myocardial defects. The rapid and persistent increase in the number and a multiplication of the foci of origin of extrasystoles point to advanc- ing myocardial changes and are often associated with symptoms in- dicating cardiac insufficiency. Curiously enough some of the pa- tients in whom I have discovered extrasystoles occurring constantly and in great numbers were quite unconscious of cardiac irregular- ities. A more prolonged study of the different types of extrasystoles, their points of origin and their frequency may eventually lead us to modify our prognosis in accordance with such findings, but as yet our facts do not warrant more positive statements. Our prognosis ultimately rests on the extent of myocardial damage, and the extra- svstole is merely one of the symptoms which suggest that the de- fective muscle is little or much affected. The Extrasystole Hi Figure 52 "Bigeminus." The extrasystoles (x) arise from the wall of the right ventricle n< ar the apex (Type 2). Figure 53 "Bigeminus." The extrasystoles (x) arise from a point in the wall of the left ventricle near the base (Type 3). Figure 54 Extrasystoles from different points of origin. A = auricular extrasystole with incom- plete compensatory pause. X = ventricular extrasystoles with complete compensatory pause. tW ^>*W ' #{ *« *'&* ^■«* ***' ^- AwirtW * / ', ^KH*'^W ^»^» *^' fj***^ % Y Figure 55 Two types of ventricular extrasystoles. X arising from the right ventricle near the base. Y arising from the left ventricle near the apex (Types 1 and 4). CHAPTER VIII Tachycardia A heart rate of abnormal rapidity is one of the most frequent phe- nomenon observed by the physician. For purposes of the present discussion one may classify all such cases in two groups : I. ACCELERATED HEARTS. II. PAROXYSMAL TACHYCARDIA. The main clinical feature which distinguishes these groups is the manner in which the transition from the normal to the abnormal rate is accomplished. In the case of the accelerated heart the transi- tion from the slow to the rapid and from the rapid to the slow rate is gradual ; in a very brief period the heart cycle may become so shortened that the rate per minute is increased 50 per cent., and yet, as observed by palpation or auscultation, the length of any two suc- cessive cycles is so nearly identical that neither the finger nor the ear is able to detect the minute differences which go to make up the change. In the paroxysmal tachycardia the onset and the offset of the change in rate is abrupt and the observer and even the patient is usually able to detect the sudden transition without difficulty. THE ACCELERATED HEART ETIOLOGY AND PATHOLOGY It has already been pointed out that the rate of the normal heart is not fixed, but varies with the needs of the body at any particular moment. This rate adjustment is brought about through the regula- tory mechanism of the extra cardial nerves. In the conditions now to be considered the underlying factors are many and complicated, but we may recognize three important elements which individually or in association may produce an abnormal acceleration of the heart: (A) The outside demands on the heart may be excessive. A full discussion of the demands on the heart which originate outside of the cardio-regulatory nervous mechanism and the cardiac Tachycardia 83 tissues themselves, the nature of such demands and their modus operandi, important and interesting as they arc, would had us out- side of the limits which we have set in these chapters devoted to the suhject of myocardial function. However, this outside call for in- creased cardiac activity must never be lost sight of in analyzing the response of the cardiac tissues to these demands. A simple illustra- tion of the response of the heart to increased demand is seen in the effect of work. As a general rule it may be stated that the response to physical exertion of an individual with a good myocardium is shown in an increased blood pressure. One with a defective myocar- dium shows an abnormal acceleration of the heart rate. With a normal heart muscle under efficient regulation and a normal vaso- motor tone, moderate exercise causes an increase of cardiac rate, but with rest the rate should return to its usual level in the space of a very few minutes. That the demands of exercise produce an in- trinsic physiological effect on the myocardium is evidenced by the fact that the normal electrocardiogram constantly shows under such stress definite though small changes ; in addition to the shortening of the diastolic period (T-P) there is an increase in the size of waves P and T and a deepening of S\ (B) The extracardial nerves may be at fault in their regulatory capacity. It is quite evident in certain accelerated hearts that the fine nervous adjustments are unbalanced. The activity of the vagi are depressed or there is an excessive activity of the accelerators, such a lack of balance mainly affects the heart through its pacemaker, the sinus node. This is probably the mechanism of the rapid changes of rate in emotional conditions, the so-called "labile pulse" of neurasthenics and the more persistent rate increase in certain organic lesions of the central nervous system and of the peripheral nerves supplying the heart. (C) The heart muscle may be defective and responds to normal outside demands with abnormal acceleration. The direct application of heat to the myocardium is known to increase the cardiac activity. Bacterial and chemical toxins set free in many of the infectious dis- eases are recognized as efficient agents in causing functional or organic changes of the myocardium, which are the basis of a response in rate out of proportion to the stress. 84 Tachycardia While we can sometime? designate one of these particular factors, excessive outside demands, defective nerve regulation or myocardial damage, as the cause of the increased heart rate, the problem is usu- ally more complicated. No doubt frequently two or all of these ele- ments play a part. In the present state of our knowledge we are often at a loss in deciding which link in the chain is at fault, and, if more than one, their relative importance. Fever is nearly always accompanied by an acceleration of heart rate, and so uniform is this phenomenon that the well-known Lieber- meister's rule of an increase of 8 pulse beats for each degree of tem- perature above the normal is found approximately accurate, albeit, with many exceptions. Whether this is brought about by the in- creased temperature of the blood passing through the heart, or by the chemical action of associated toxins on the regulatory nervous mechanism, or on the cells of the cardiac muscle, is undecided. The increased heart rate of shock is undoubtedly due to local or general vaso-motor disturbance with its reflex demands on the heart to maintain an adequate blood pressure. A similar explanation seems probable for Graves' disease, and the excessive administration of thyroid extract in which the evidence points to the damaging effect of toxins on the vaso-motor apparatus, rather than the heart muscle. The "labile pulse," wide pulse pressure, flushing, local sweating and tremors characteristic of this disease suggest that the toxins chiefly attack the sympathetic nervous system, possibly incidentally produc- ing a hypertonus of the accelerator nerves, and probably act on the heart muscle only in an indirect manner. Pregnancy probably has only a reflex effect on cardiac activity. Exhausting diseases (tuberculosis, etc.) and convalescence from wasting diseases (typhoid, etc.), nearly always show some degree of increase pulse rate. Each one of these conditions, febrile or afe- brile, with toxic and nutritional disturbances may affect the outside demands on the heart, the functional balance of the extracardial nerves, or the cardiac muscle, and in each instance the effort should be made to determine and apportion the relative responsibility of each of these factors in the acceleration of the heart. The severe anemias, high grades of chlorosis, marked secondary anemias (as in malignant disease), and the primary pernicious forms are in- variably associated with an increase in heart rate. In the extreme Tachycardia 85 grades of anemia the cardiac muscle shows an advanced degree of degeneration with fatty infiltration and hemorrhages,* so thai have little hesitancy in ascribing the altered heart activity to the direct toxic or nutritional effect on the myocardium. In valvular disease the mechanical defect must he considered. The volume output is unusual and the normal bodily calls for blood are met by an increased heart rate. In the majority of these cases, how- ever, the disease which was the agent in distorting the valves has also injured the myocardium and this, in association with the change in cardiac tone resulting from dilatation and hypertrophy, are impor- tant influences in modifying heart rate. Changes in the myocardium are produced by acute rheumatic fever and other infections diseases with a resulting acceleration of heart rate. These changes may be chemical with no demonstrable histological abnormality, or there may be fatty degeneration and fibrous replacement, so that we meet with many degrees of functional impairment. MECHANISM The main link in the mechanism through which the increased rate of the "accelerated heart" is produced is the "sinus node," the nor- mal pacemaker of the heart. Here the fundamental properties of "stimulus formation" or "excitation" or both, become heightened. This change may be intrinsic, that is to say, the chemical processes of the muscle cells of the node are so changed that they form and explode stimulus material more rapidly, or the change may be brought about by the modifying impulses showered on the node by the extracardial nerves. The sinus node is particularly influenced by impulses brought to it by the right vagus and the right accelerator, v The distinguishing feature of the "accelerated heart" is that the sinus node retains its function as the pacemaker of the heart. This is shown by the graphic records which indicate that the impulse for- mation arises at the normal point and spreads through the auricle, the bundle of His and the ventricle in a normal orderly fashion. There are several facts, however, which indicate that, in these "accelerated hearts" other portions of the musculature may have their properties of "stimulus formation," "excitability," and perhaps also "conduc- *Lazarus : "Pernicious Anemia," Nothnagel's Practice, Phila., 1906, p. 283. fRobinson and Draper: Jour. Exp. Med., 191 1, xiv, p. 227. 86 TAcm CARDIA tion" heightened! It is known that the fibers of the left vagus and of the left sympathetic are in the main distributed to portions of the heart below the sinus node.f and experimental evidence indicates thai cutting the left vagus and stimulating the left sympathetic have a considerable effect in increasing the heart rate. Again in certain "accelerated hearts" it may be seen that systole, which in the normal heart has a very constant length, is shortened. This is onlv con- ceivable on the ground that one or more of the fundamental proper- ties of cardiac muscle mentioned above are quantitatively changed. The principal change from the normal in the cardiac cycle of the accelerated heart is a shortening of the diastolic period. From this it follows that the rest period of the heart is curtailed and the time allowed for the recovery of the property of "contractility" is con- siderably less than in the heart working at the normal rate, hence the contractile power is less. Furthermore there is less opportunity for the heart to receive its normal quota of blood, hence the volume out- put is smaller. It follows as a result of these two factors that the pulse is smaller in volume and of diminished force. IDENTIFICATION Little need be said of the clinical recognition of the "accelerated heart ;" the pulse may be counted either by palpation at the wrist or perhaps more accurately by auscultation at the apex. If one is pres- ent during the change from a slow to a faster rate this is best detected by counting the pulse in 10 second intervals, omitting every other 10 seconds. Neither the finger nor the ear can detect the small differ- ences in the lengths of the successive diastolic periods, but the varia- tions in length of the cycles separated by considerable periods is easily made out. The volume output of the heart is usually some- what diminished with the acceleration of the rate and the consequent diminution in the peripheral arterial wave may be quite evident. The polygram of the accelerated heart conforms to the normal except that the diastolic period is shortened. This is at times so marked that the a wave may be superimposed on the preceding v wave. The jugular tracings ( Figures 56 and 57) show a normal se- quence of waves, a, c, v. Figure 56 is a record of a girl, 15 years of age, suffering from rheumatic myocarditis and adherent pericardium. tCohn and Lewis: Jour. Exp. Med., 1913, xviii, p. 739. ACM Y< IARD1 A *7 Jugular Brachial 0.2 second Figure 56 Accelerated heart. Rate 145. Patient suffering from rheumatic myocarditis. C ' C O p *" c h Jugular Z~t">U:c\ Brachial 0.2 second Figure 57 Accelerated heart. Rate 138. Case of Graves' disease. NX T U HYl AklMA The rate at the time the record was taken was 145 and the rapidity was in part due to excitement, as hef pulse at rest was commonly 120. The slightest physical exertion at this time would send her pulse to 160, suggesting a marked instability of the sinus nodi'. In Figure ?y is shown a tracing of a ease of (iraves' disease; tin- rate is 138. It is evident from the jugular tracing that the normal pacemaker is in control and that the rapid rate depends upon the shortening of the diastolic period. Electrocardiograms of accelerated hearts are presented in Figures 58 and 59. Figure 58, from a case of Oaves' disease, shows a short diastolic period, hut the sequence of waves is normal. Figure 59 was ohtained from a case of cerebral hemorrhage, a few hours hefore death. The diagnosis was confirmed by autopsy and it seems clearly a case in which the nervous regulatory mechanism is at fault. The P and T waves in this record overlap. Careful measurement sug- gests that the earlier of the two peaks represents the auricular con- traction which occurs before the preceding ventricular systole is com- pleted. This curve simulates quite closely the records obtained experimentally during the stimulation of the right sympathetic gan- glion by Rothherger and Winterberg.* Till-: CLINICAL SIGNIFICANCE AM) PROGNOSIS of the accelerated heart depend on the underlying condition and to determine this, the responsibility of excessive outside demands, lack of balance between the elements of the nerve regulatory mechanism and defects of the myocardium, must be correctly apportioned. In general one may say that excessive outside demands and unbalanced nerve control acting on a heart with its myocardium intact, are usu- ally more readily corrected, and hence of less serious import to the patient than when the heart acceleration depends upon an intrinsic defect of the myocardium. But even a normal myocardium may be worn out by the excessive activity induced by extracardial condi- tions, and a defective myocardium properly handled may recover full functional efficiency. The tests by which we may gauge the integrity of the heart muscle and its reserve force will be discussed in a later chapter. ♦Archiv. f. (1. ges. Physiol., 1910, exxxv. p. 557, Fig. 18, d. Tachycardia 89 •L^r St+Lu. P - *-- "' J JL'^'* '^ « » 1 ' ' • » '- ». - ^ » .'. 1 Ftgure 58 Accelerated heart. Rate 148. Case of Graves' disease. — fj H IK Pt' pt t - 1- ^ Sfe *IF s|™ «l^ tf n%^W i Figure sq Accelerated heart. Rate 184. Terminal tachycardia of cerebral hemorrhage. CHAPTER IX Paroxysmal Tachycardia Acceleration of the heart rate, which lias been discussed in the preceding chapter, is exceedingly common and is important as a symptom associated with many conditions. Paroxysmal tachycardia, which we are now to examine, is relatively rare, and is associated with phenomena so distinct and definite that the syndrome deserves consideration as a clinical entity. This group is particularly characterized by the suddenness of the change in the rate of the heart. The acceleration in rate occurs as a paroxysm whose onset is abrupt and whose termination is equally sudden. The change in rate, both of the onset and off- set of the attack, occurs in a period of time less than that occu- pied by one normal cardiac cycle. The duration of the paroxysms are extremely variable. They may last for only a few beats or may continue for minutes, hours or days. The longest attack which has come under my notice was continued for 28 days. This varia- bility is the rule not only comparing different cases, but also in the successive attacks of a single individual. The relative time consumed by the paroxysms and the intervals of slow rate is very variable, but in nearly all instances the slow periods exceed the paroxysmal periods by a considerable margin. MECHANISM An analysis of the paroxysms shows that it is composed of a series of contractions having their origin in some part of the cardiac musculature other than the sinus node; in other words, a rapid succession of extrasystoles ; in some point of the heart wall ex- citability is raised to such a point that for a period stimuli are set free at an abnormally rapid rate, and, in accordance with the law that the most excitable portion of the heart sets the rate for the less excitable portions, this excessively irritable point usurps the function of the pacemaker, and for the time the normal pace- maker, the sinus node, is buried in the flood of stimuli arising from this new point of origin. Usually all of the contractions of a given paroxysm arise from a single point and spread over the heart 90 Paroxysmal Tachycardia 91 muscle by the same path. This is shown by the similarity of the waves obtained in graphic records. For the most part, the con- tractions arc rhythmic, hence their rate is to a degree a measure of the rate of stimulus formation and the excitability of the irri- table point. During the period of slowing, the sinus node regains its ascend- ency and sets the pace. Jf one studies carefully the periods of slow rate, one will almost invariably discover isolated extra toles occurring more or less frequently. These are usually of the same type as those which go to make up the beats of the parox- ysm, and are often of material assistance in determining the par- ticular point in the heart in which the extrasystoles of the paroxysms have their origin. It is conceivable that any portion of the heart muscle may be capable, under suitable conditions, of assuming the role of pacemaker for a limited period of time. We are certainly able to define paroxysms which have their origin in the wall of the auricle, in the region of the auriculo-ventricular node and in the right and left ventricles. Most of the paroxysms have an auricular origin. Ventricular paroxysmal tachycardias are com- paratively rare. When the point of origin is in the auricle, the ventricle usually responds promptly and in the usual manner to each auricular im- pulse. At times, however, the electrocardiographic records sug- gest that the stimulus has taken a path through the ventricle wall, somewhat removed from the normal, or again the exciting effects of the frequent stimuli may be seen in a depression of the bundle contractility, as evidenced by an abnormally long period between the auricular and ventricular contractions. It has been shown by Erlanger* that stimuli may pass over the conducting system of the heart in a direction opposite to the nor- mal. We have evidence that this occurs in paroxysms of ven- tricular origin, and that the auricular contraction is a response to stimuli reaching it from the ventricle. EXPERIMENTAL PRODUCTION In a previous chapter it has been pointed out that single extra- systoles may be produced experimentally by applying mechanical *Arch. Int. Med., 1913, xi, p. 362. 92 Paroxysmal Tachycardia or electrical stimuli to various portions of the cardiac musculature. If a properly spaced series of such stimuli are applied to the wall of the heart, a tachycardia will instantly result, composed of a succession of extrasystoles. During such an artificial paroxysm, the activity of the normal pacemaker is submerged by the stimuli set free from the new focus. When the artificial stimuli are with- drawn the tachycardia terminates abruptly. The normal pace- maker immediately regains its ascendency and the normal rhythm is resumed. Such paroxysms may be induced by stimulation of either the auricle or the ventricle. When the ventricle is thus excited, the stimuli are transmitted upward to the auricle, a direc- tion the reverse of the normal, and the contractions follow instead of precede the ventricular contractions. These retrograde stimuli pass the bundle of His with less velocity than those which pass over the heart in the normal direction, hence a part of them may be blocked and the auricle may fail to respond to each ventricular contraction. Tachycardias have been experimentally produced by the administration of aconitin (Cushny), muscarine (Rothberger and Winterberg), by an abrupt increase of the blood pressure (Hering), and by ligature of the coronary arteries (Lewis) ; a production of attacks of tachycardia by ligation of the coronaries particularly elicits our interest, since it more nearly approximates conditions which we may encounter clinically. Lewis* found that obstruction of the blood flow in the right coronary was usually, and that of the descending branch of the left coronary was in- variably, followed by isolated ventricular extrasystoles, as the nu- trition of that portion of the ventricular wall supplied by these vessels became progressively impaired, extrasystoles appeared at shorter and shorter intervals, until finally there was established a rapid series of rhythmically recurring extrasystoles, constituting a true paroxysmal tachycardia. Under these conditions the stimuli became retrograde and the auricular followed the ventricular con- traction. The extrasystoles were rhythmical and graphic records showed that in a given case all the extrasystoles had a single point of origin. In dogs rates between 300 and 420 per minute were obtained. The phenomenon occurred both when the vagi were intact and when they were sectioned, showing that the disturbance ♦Heart, 1909-10, i, p. 98. I 'aroxysmal Tachycardia 93 TTTTTTTfl J ^H ffi A-V \ Figure 60 Diagram showing mcclianism of auricular tachycardia. One isolated extrasystolc is indicated and a short paroxysm composed of a rhythmic series of similar extrasystoles. The temporary pacemaker is located in the wall of the auricle. The conduction time {A-V period) is lengthened during the paroxysm. As M ) B 5 5 H {((({(i(i T T T I I I T T Figure 6i Diagram showing the mechanism of ventricular tachycardia. One isolated ventricular extrasystole and a short paroxysm composed of a rhythmic series of similar extrasystoles. The temporary pacemaker is located in the ventricular wall. During the paroxysm the auricle contracts in response to "retrograde stimuli" passing upward from the ventricle, every other impulse from the ventricle is blocked. The arrows indicate the points of origin and the direction taken by the stimuli. Dot- ted arrows indicate the time at which the normal stimulus at the sinus node should reach maturity if its formation were not interrupted by the extrasystole. The thickness of the lines representing ventricular systole indicate the relative effect of the normal beat and the beats of the paroxysm in maintaining an adequate circulation. As = auricular svstole. A-V = time of transition from auricle to ventricle or the reverse. \"s = ventricular systole. ij4 Paroxysmal Tachycardia had its origin in the wall of the heart and could not be as- cribed to altered central innervation. When the ligature was removed and the circulation became re-established, the paroxysm abruptly ceased and the sinus node resumed its function of pace- maker. The diagrams, Figures 60 and 61, indicate the mechanism of the paroxysmal attacks. Figure <>o represents a focus of abnormal irri- tability situated in the wall of the auricle. The impulses are set free so rapidly that the stimulus material forming at the sinus node is destroyed before reaching maturity. As soon, however, as the abnormal irritability of the auricular wall is lost, the accumulation of stimulus material at the sinus node continues for the normal period and thus the node resumes its role of pacemaker. Figure Ci represents an abnormal focus in the ventricular wall, which, for a short period, becomes the pacemaker of the whole heart. Here the ventricular impulses become retrograde, that is, they passed up- ward over the A-V bundle and stimulated the auricle from below. These impulses are frequently blocked, as is indicated in the dia- gram, in which the auricle responds only to every other ventricular impulse. It might be supposed from this review of the mechanism of these disturbances that paroxysmal tachycardias would be frequent se- quela? of single extrasystoles. This is not the case. Isolated extra- systoles are extremely common. Probably most individuals reach- ing the age of 50 have had extrasystoles at one time or another, but attacks of true tachycardia are comparatively rare. On the other hand, it may be said that probably every true paroxysm is preceded by isolated extrasystoles. PATHOLOGY Little is known of the histological changes which may form the anatomical basis of paroxysmal tachycardia. In my own series only two cases have had a fatal termination, and in neither of these was a post mortem permitted. In the literature several autopsies have been reported and these have all shown more or less ex- cessive myocardial change — sclerosis, fibrosis, atrophy, and arterial degeneration, particularly of the coronaries. One does not feel that we have as yet evidence of any definite pathological lesion which Paroxysmal Tachycardia 95 is characteristic. Experimental evidence suggests that the cause may be found in the intracellular chemical change induced by vari- ations in the blood supply in the heart, which may or may not show degeneration of the myocardium. ETIOLOGY In no one of my scries of 33 cases of paroxysmal tachycardia have I been able to obtain a history of a similar condition in an ancestor or in any immediate relative. My youngest case was a girl who had her first attack when 9 years of age; the oldest a man of 69, whose paroxysms had annoyed him for 2 years. One patient, a man of 44, has suffered from attacks over a period of 20 years. The distribution by decades of the time of onset in my series is as follows: Decade Under 10 10-20 20-30 30-40 40-50 50-60 60-70 Number of Cases . . 1 486653 Among the 33 cases which I have observed, 23 were males and 10 females. The following tabulation indicates that the syndrome oc- curs about twice as often in men as in women. Hoffmann* Lewisf Men 6 18 Women 4 11 Hart Total 23 47 10 25 2 An analysis of my cases presents the following factors, which may have a bearing direct or indirect on the condition of the myo- cardium. Alcohol was used to excess by 4 ; tobacco by 2 of the men. Severe gastrointestinal disturbance had preceded the attacks for several years in 3 of the women; nearly all had a history of one or more of the infectious diseases of childhood; in one case the onset of tachycardia followed 6 months after a severe infec- tion of the middle ear ; in another yellow fever antedated the at- tacks by 2 years. There had been frank attacks of acute articular rheumatism, followed by endocarditis with valvular defects, in 4 cases ; a syphilitic infection was demonstrable in 4 cases, 3 of which *Die Electrocardiographic. Wiesbaden. 1014. tClinical Disorders of the Heart Beat, London, 1913. 96 Paroxysmal Tachycardia showed evidence of myocardial damage other than the attacks of tachycardia. Several of the scries had taken considerable doses of digitalis; in one a physician whose arrhythmia had been wrongly diagnosed as complete irregularity and auricular fibrilla- tion had taken very large doses, and it seems to me that this was undoubtedly an important agent in increasing the irritability of the heart muscles. The attacks in a young patient of my series, a hoy of ten, immediately followed a race in which he par- ticipated, at which time the physician who saw him found evidence of acute dilatation. A case of mild Graves' disease, in which the pulse averaged 100, has shown on several occasions paroxysms lasting only a few minutes in which the rate was between 160 and I/O. Valvular defects were present in 1 _' of my patients; the mitral valve was involved in 10, of which 4 were cases of well- marked stenosis; two patients had aortic insufficiency and one had defects of both the aortic and mitral valves; 15 cases showed various decrees of cardiac enlargement. In many cases the irri- tability of the heart muscle seems to require a very small excit- ing factor to induce an attack. The patient will usually ascribe the onset to flatulence, some emotional disturbance or unusual physical exertion ; any one of these is probably an efficient cause to call forth an attack in a myocardium suitably damaged. SYMPTOMS The symptoms associated with paroxysmal tachycardia arc of great variety, and show great differences from individual to indi- vidual. This is doubtless in a large measure due to the extent of damage present in the myocardium and the ability of the heart to meet the tax thus exacted. The patient is practically always conscious of the abrupt onset and termination of the attacks. They usually describe the attacks as beginning with one or two "thumps" or "throbs" in the precordial region, followed by a sensation of flut- tering in the chest, which is terminated by another "thump" or "flop," and the attack is over. The amount of anxiety is always greater in the early attacks; as the patient becomes more or less accustomed to the paroxysm he is less alarmed, and a momentary pause in his activities may be the only evidence to show that he knows the attack is on. This absence of alarm I have noticed Taroxysmal Tachycardia ( ji particularly in young adults who have had attacks for a number of years, but whose hearts show no anatomical abnormality and functional disturbance characterized only by the attacks of extra- systoles at more or less infrequent intervals. One of my patients, whose attacks have continued for several days, was quite unconcerned even when his heart was beating at 170. He rarely voluntarily assumed a recumbent position on ac- count of the attacks and it was difficult to convince him that rest at these times was important. In those who have an associated valvular lesion, and in those with evidence of marked arterial changes, a greater discomfort and attendant anxiety are closely associated with the symptoms re- ferable to the cardiac insufficiency which is induced by, or the precordial pain which accompanies, the attack. At the onset patients often complain of palpitation in the chest and a swelling and pulsation of the vessels of the neck. Often they have eructations of gas, nausea and vomiting. There may be a "gone," sinking feeling, and, if the attack is prolonged, sweat- ing, coldness, great lassitude and an intolerable feeling of weak- ness. They may have a sensation of palpitation or of bounding in the chest, shortness of breath or a sensation of suffocation. In one case under my observation attacks were invariably accompanied by a watery diarrhoea ; in another by frequent micturition. In the prolonged attacks, increase of the cardiac dulness to the left can sometimes be made out and the symptoms of circulatory em- barrassment terminate the picture. The veins are not properly emptied, but are engorged, and there is pronounced cyanosis. The liver may be increased in size and become tender to palpation. There may be edema of the extremities ; there may be cough with profuse thin, or blood-streaked, expectoration, with the physical signs of pulmonary congestion. The paroxysms are often attended with headache and dizziness, more rarely with momentary or prolonged periods of unconscious- ness, which may be explained on the basis of cerebral anemia. Pain is sometimes prominent. A feeling of oppression and of constric- tion of the chest accompanies the attacks in nearly all patients to a greater or less degree. The pain is usually precordial, and is sometimes sharp, suggesting a real angina, and may radiate into 98 Paroxysmal Tachycardia the arms and back: sometimes one can detect areas of hyperesthesia over the chest and arms, following the distribution of one or more of the upper thoracic and lower cervical nerves. A tew patients complain of numbness and tingling of the extremities. A progressive cardiac insufficiency may terminate in general anasarca, pulmonary edema, collapse and occasionally death. As a rule, however, the signs of cardiac insufficiency are very moderate, and even when present to an extreme degree clear up with great rapidity, following the abrupt ending of the rapid heart action. The absence of alarm, the facial change of expression from one of anxiety to complete calm ; the abrupt change from dyspnea to quiet breathing; the sudden cessation of pain; the subsidence of en- gorged veins of the neck coincident with the termination of the paroxysm present some of the most remarkable and agreeable clin- ical phenomena with which we are familiar. The signs of pulmonary congestion and edema of the extremi- ties may require a period of days for their subsidence, the rapidity depending to a considerable degree on the functional efficiency of the heart when it has resumed its normal rate. As illustrating the character of severe attacks terminating fatally, one case which I had the opportunity to observe closely for a period of months, may be described. A man, 55 years of age, who had a leutic infection 20 years earlier, had a heart moderately enlarged to the left and a faint systolic murmur at the apex. Between the attacks his pulse was about 70 with many extrasystoles. At all times there was evi- dence of a moderate degree of cardiac insufficiency. A descrip- tion of the attacks, obtained from the patient, was as follows: "The exact cause of these attacks of syncope and tachycardia, which come as often as twenty times in one day and have been ab- sent as long as 26 days, cannot be determined. Many times he has been wakened from his sleep by dizziness to become uncon- scious and have a typical attack. Again, a slight exertion, as walk- ing, going up stairs or straining to pass water, may be followed by an attack, but these same exertions, or even more severe ones at another time, may have no harmful effect. The attack comes on suddenly with dizziness, grayness before the eyes and a buzzing in the head like an organ. There are no premonitory symptoms, Un- Paroxysmal Tai [iycardia 99 iK'j'ar Brachial 3.2 second Figure 62 Normal. Rate 82. Respiratory rate 24. For paroxysm of auricular tachycardia in the same individual see Figure 63. fugular Brachial second Figure 63 Auricular tachycardia. Rate 182. Respiratory rate 30. For record of the same case Between attacks see Figure 62. Compare in the two records the volumes of the arterial and venous pulses. The jugular records are quite different in form, the large wave of ioo Paroxysmal Tachycardia consciousness follows rapidly, and when he comes to his heart is beating very rapidly, 200 to 250 to the minute. There is a chok- ing sensation, as if a hall were in the throat, and he is shaking all over. There is never any pain over the heart or down the arm. At times he has been struck down as if by electricity without warn- ing, again lie has simply had dizziness and grayness, without losing consciousness. The tachycardia lasts a varying length of time, sometimes for only ten minutes, at other times all day. During its continuance he has great gastric disturbance, with frequent vomit- ing. He cannot forecast the end of the attacks until it is at an end. Then, at times, a violent regular beating of the heart is suc- ceeded by two or three irregular beats, as if something shook the heart, and this is immediately followed by two or three tremendous throbs of the heart with each of which there is a feeling as if fresh air were forced into his throat and head and the attack stops suddenly as it began." His paroxysms of tachycardia continued for 5 years, becoming gradually more frequent, and he finally died during an attack. IDENTIFICATION The conditions other than paroxysmal tachycardia which afford a heart rate of over 160 are extremely rare. During the paroxysm the pulse is exceedingly small, often irregular in force and fre- quently cannot be detected at the wrist. Under these conditions our examination should at once be directed to the precordial region. The apex beat may be imperceptible to the touch or, when palpable, may give the impression of complete irregularity. The heart sounds may be indistinct and have a fetal character; often they are sharp and distinct ; as a rule, they are perfectly rhythmic, but so rapid that the rate can be only approximately estimated ; this is best ac- complished by counting short (5 seconds) periods. If one is for- tunate enough to be making observations at the beginning or at the termination of the attack, the change in rate is readily detected. The transitions are usually accompanied by one or two large forcible heats, with loud sounds and unusually large pulse waves. The change in rate is quite abrupt. In the absence of such an observa- tion the patient will frequently establish the diagnosis by his de- scription of the sudden onset and termination of the attacks. Valvu- Paroxysmal Taciiyi ardia ioi ■ I ! WW 0.2 second Figure 64 Rate 72. Between attacks same individual as Figure 65. At X is shown an extrasystole with an incomplete compensatory pause. Note the a wave is large and the a-c interval is of normal length. Jugular Brachial 0.2 second Figure 65 Auricular tachycardia rate 174. For slnw rate see Figure 64. The large venous waves are the result of the simultaneous contraction of the auricle and the ventricle. Each one of these waves belongs to two cycles. They are composed of a c wave of a cycle just com- pleted and an o wave of a cycle just beginning. The a-c" interval is abnormally long. ioj Paroxysmal Tachycardia lar murmurs, if present during the slow rate, sometimes cannot be detected during the paroxysm. In some rases a heart without mur- murs during the slow period will develop a loud systolic murmur during the paroxysms. During the slow periods extrasystoles followed by pauses, more or less fully compensatory, can usually be detected; sometimes they are very frequent, more often only occasional. Single extrasys- toles are quite common between paroxysms which are of short duration and which follow one another at brief intervals. During the paroxysms the veins of the neck are prominent, dis- tended, hard and pulsate with great rapidity. ( )ften two pulsations of the jugular may be seen to correspond to each systole of the heart. In most instances the attacks are not affected by the position as- sumed by the patient and continue whether he sits up or lies down without change in rate. When seen only between the attacks the diagnosis rests largely on the history, but the patient's description of the attacks is usually so clear that there is little difficulty in classifying the abnormal activity. The cases which present the most obscure diagnostic problems are those with very frequent short paroxysms separated by equally short periods of slow rate broken by frequently occurring extra- systoles. These are often wrongly classified as complete irregu- larity due to auricular fibrillation. They may usually be assigned to their correct category by means of a careful and prolonged study of the ordinary physical signs. Their status may be absolutely settled by graphic records. The polygram brings out clearly some features of the paroxysms which are observed with great difficulty by the ordinary means of eliciting physical signs. In Figures 62 and 63 are shown brachial and jugular tracings taken from a woman 35 years of age. Figure 62 shows the usual condition of her pulse; the rate is 82; the arterial pulse is of good size and well sustained; the jugular pulse shows a normal sequence of waves a, c and v ; the a-c interval is normal (less than 0.2 second). Figure 63 is a record taken during h C r second paroxysm, which lasted 2 days without interruption. At the time the tracing was 104 Paroxysmal Tachycardia secured the attack has been under way for 24 hour?. The heart at this time was beating rhythmically at a rate of 182 per minute. The small volume of the brachial pulse is in great contrast to that ot" the slow periods. The venous curve shows, in place of the well- defined waves of the slow heart rati', one large wave and one small notch to each cycle. The interpretation is that the auricle and the ventricle are contracting simultaneously, so that the veins are un- able to empty into the right auricle in the normal manner, ddie large jugular waves, much greater than the jugular \\a\es of the normal period, are due to a summation of the a and c waves. It will also he seen that during the paroxysm the a-c interval is con- siderably prolonged (over 0.3 second), indicating that there is a delay in the conduction of the stimulus from the auricle to the ventricle. This is not an uncommon feature in tachycardias, the excessive functional demand on the slender A-l' bundle leading to its partial exhaustion. In these two figures the respiratory curve is brought out in the venous tracing. That in this case the dyspnea was not very marked is evidenced by the facts that the breathing was 24 during the slow rate and only 30 during the attack, and that the excursion is not very much greater during the paroxysm. Tracings from another case of auricular tachycardia arc shown in Figures (»4 and 65. As in the preceding case, the contrasts be- tween the cardiac rates (72 and 174) and the arterial pulse volumes of the two periods are shown in the brachial tracings. During the paroxysm ( Figure 65) only one large wave appears in the jugular to each cardiac cycle. The slow period I Figure 64) is interrupted at one point ( .V 1 by an extrasystole with an incomplete compensatory pause, hence we may conclude that it probably had its origin in the auricular wall. It is a series of such extrasystoles which constitute the paroxysm. Figure 66 was taken from a man of 36 during a prolonged parox- ysm. The ventricular rate is 158 and is perfectly rhythmic. The jugular tracing shows the great venous congestion and the very large waves which are due to simultaneous contractions of auricle and ventricle; conduction is delayed. The exact point in the auricle which has become the temporary pacemaker for the whole heart cannot he definitely settled from the polvgraphic record. The Paroxysmal I achycardia !<>■■ T ift^A j*^^ ■_f — ■ ,.„,,„■ Normal. Rate 80 Figure 68 Same case as Figure 69. Lead II. „- T vr^. i nyf n '"P 1 . ■ i ,r. - r iTf Figure 60 Taken during a paroxysm, rate 167. Lead II. Same patient as Figure 68. Xote inversion of P, which notches the summit of T, Auricular tachycardia. The pacemaker of the heart is in the lower part of the auricle. nx> Paroxysmal Tachycardia respiratory curve upon which the large jugular wave? .ire super- imposed show that, in spite of the prolonged attack, the breathing is not greatly accelerated; at this time it was 22 to the minute, but quite irregular. A rare tracing from a case of ventricular tachycardia is repro- duced in Figure 67. The brachial shows at A the usual rate for this patient between attacks (92 per minute 1. At X isolated cxtra- systoles, each with a complete compensatory pause, occur; the premature beats are so weak that they make practically no impres- sion on the brachial pressure. At B are shown two short paroxysms of tachycardia, indicating the manner of the abrupt onset and termi- nation of the attacks. The a-C interval of the "normal" rhythm of this patient was always longer than that of a normal heart, meas- uring nearly 0.3 second. During the paroxysm the auricle contracted in response to the "retrograde stimulus" from the ventricle; this cannot be conclusively made out in the polygram, but is substantiated by electrocardio- graphic records (see Figure 80). The irregularity of this pulse is so extreme that it might easily have been mistaken for a case of "complete irregularity" and auricular fibrillation, had no graphic records been secured. The electrocardiogram gives us information in regard to parox- ysmal tachycardia which we can obtain by no other method. Through this agency we have discovered the real mechanism of the attacks. The knowledge acquired in this way tends to emphasize the importance of the muscle cell changes and to minimize the role played by the extra cardial nerves in inducing this change in cardiac activity. These graphic records convince us that a new point in the heart wall has become the temporary pacemaker of the heart. The proof is most clearly demonstrated, if we study the records of such a case as is shown in Figure Ho, where the evidence is com- plete in a single curve. This is from a case of ventricular parox- ysmal tachycardia, a condition ol extreme rarity, hence it will be bitter to first direct our attention to the more common forms, namely, tachycardias of auricular origin. Such a case is illustrated in Figure 69, which was taken during a paroxysm in which the heart rate was \()j. Figure 68 was se- cured from the same patient a few hours after the cessation of the Paroxysmal Tachycardia 107 ^W^JWtaJftvJtaJ^ Figure 70 Same patient as Figure 71. Rate 76 between attacks. Taken by lead II. P is slightly notched, otherwise the curve is normal. Figure 71 Auricular paroxysm, rate 174, lead II. From same individual as Figure 70. The small P wave is submerged in the large T wave. io8 Paroxysmal Tachycardia attack. This record shows a perfectly normal curve for a heart with a rate of 80. Both records were taken by lead II (right arm and left foot). If we >h<>ukl superimpose the ventricular portion (beginning of R to the end of / > of the cycles shown in Figure <>X on one of the cycles of Figure <»>. we would find thai they corre- spond in every particular, except that the summit of the T wave shows constantly a deep notch. If we compare the records further, we note that in Figure 69 then' is no wave which corresponds to the well-marked P wave of Figure 68. Careful measurement shows that the notch in the T wave ( Figure '>')) Occurs at exactly the time at which a /' wave of the normal rhythm should precede the R wave, hence we conclude that the positive P wave of the normal rhythm is replaced by a negative wave notching the T wave of the paroxysm. In studying the auricular extrasystole, it was shown that when tiie premature heat started from a point in the auricle at some distance from the sinus node, the P wave of the electrocardiogram was distorted in form, or even completely reversed in direction, hence in the records under consideration we are led to conclude that the paroxysm shown in Figure 69 is composed of a series ol extrasystoles having their origin at a point in the auricular wall considerably removed from the site of the normal pacemaker. Figure 70, taken by lead II, shows a normal electrocardiogram, except for a slight notching of the P wave. Figure 71 was taken from the same patient during an attack which lasted for one hour, during which the heart rate was 174. Here the ventricular por- tions of the two records are almost identical, except that the waves of the paroxysm are a trifle smaller than those of the slow rate. During the paroxysm no I' wave can he definitely located ; in this case it was probably so small that it caused no distortion of the relatively large T wave. F.lectrocardiograms of another case of auricular paroxysmal tachycardia are shown in Figures 72 and 73; both records were taken by had 111 (left arm and left leg). When Figure ~2 was taken the heart rate was j~> per minute. This record shows several abnormal features; the P wave is slightly notched and R is directed downward (the latter feature is quite usual in hypertrophy of the left ventricle), T is also directed down- Paroxysmal Tachy< ardia 109 p — — — r gf ^; 1 ' . — - — • -W- P P Figure 72 SI >w period, same case as L'"igure 73. Rate 75. Lead III. P is 11 itched, /<" and T liave a downward direction. Figure 73 Auricular tachycardia, rate 16S. Lead III. Same patient as Figure 72. Ventricular complex increased in size. T has become a positive wave. P is superimposed on 7\ no Paroxysmal Tachycardia \v;ml. During the paroxysm (Figure 73) the rate is 168. 7v is still directed downward and is increased in amplitude, suggesting a dila- tation oi the left ventricle. The slow wave between the R waves is an algebraic sum oi the waves P and T of the new rhythm. The next case, illustrated in Figures 74 and j^. shows some in- teresting features, during the slow period (rate 76 per minute) the /' wave is unusually broad. R is slightly notched and the rhythm is broken by an extrasystole, which is plainly of ventricu- lar origin. The paroxysm ^rate 188) is composed of A' waves fol- lowed by a depression, which in all probability are reversed P waves, having their point of origin in the lower part of the auricle, pos- sibly near the A-V node. The P-R interval is prolonged, measuring Over o.J second, exhibiting the delay in conduction which is not an uncommon feature of these cases. In this instance the com- plexes of the paroxysm probably represent extrasystoles of auricu- lar origin and do not conform to the type of the isolated extrasys- tole which interrupts the slow rhythm (Figure 74). Figures 76, jy and jS depict the mode of transition from the slow to the rapid and from the rapid to the slow rate in different cases. The onset of a paroxysm can be seen in Figure 76 and the dis- location of the pacemaker from the sinus node to a point low down in the auricle is indicated by the change in forms of the P Wave from a positive to a negative deflection. In the first cycle of the paroxysm the reversed P wave falls at the apex of the T wave, but subsequently notches the earlier portions of this part of the ventricular complex. The offset of a paroxysm is shown in Figure yj. The bizarre complexes which intervene between the paroxysm and the slow rhythm probably represent extrasystoles of unusual types, and are doubtless the kind of cardiac activity which give the patient the subjective sensation of "throbs" or "thumps" at the time of the transition. Another transition from a heart beat of 160 to one of 70 is shown in Figure 78. The curve is somewhat distorted by the move- ments of the patient produced by the sensations experienced at the time of the termination of his attack. The most convincing evidence of the nature of the mechanism Paroxysmal Tachycardia Figure 74 Rate of 76 interrupted by a ventricular extrasystole. Same individual as Fij/ure y- Lead 11. n a ** 3 — ' Figure 75 Paroxysm of tachycardia, rate 1R8. Lead II. From same case as Figure 74. Note reversal of P wave and prolonged P-R interval. Abnormal pacemaker probably situated near the A-V node. ii2 Paroxysmal Tachycardia in paroxysmal tachycardia is brought to view when we are fortu- nate enough to secure in a single record periods of slow rates in- terrupted by single extrasystoles, continued into periods of tachy- cardia. Such records are shown in Figures 79 and So. A short paroxysm of tachycardia (rate lUS), changing to a slow rate (86) broken by extrasystoles, is shown in Figure 79. The patient, from whom this curve was taken, was a physician, 65 years of age, in whom the diagnosis of "complete irregularity," due to auricular fibrillation, had been repeatedly made. The correct diag- nosis was hardly possible until electrocardiographic records were secured. The slow rate is interrupted by auricular extrasystoles (A',) and another type of extrasystole (A\.) which has Its origin in the ventricular wall. The auricular premature beats have their origin high up in the auricle, since the P wave of the extrasystole is a positive wave, as is shown by the waves which are clearly the sum of T and P. The paroxysm is composed of both kinds of extrasystoles, hut the auricular type predominates, which is also the case in the period of slower cardiac activity The electrocardiogram of a case of ventricular tachycardia* is shown in Figure 80. Tachycardias of this type are extremely un- usual. The bizarre forms of the complexes of his slow rate (80) are seen in the short diastolic (T-P) interval, the broad P wave, the long P-R interval and the unusual form of the R waves. These features alone suggest serious myocardial damage. From time to time there appear isolated ventricular extrasystoles (A'). The paroxysm (rate 200) is composed of complexes similar in form to those of the isolated extrasystoles. Between the large waves of the paroxysmal period are seen small waves (P) which occur with every other cycle. These undoubtedly represent auricular con- tractions due to retrograde stimuli arising in the ventricle. It ap- pears that every other impulse from the ventricle is blocked. This record conforms in many particulars to the curves obtained experi- mentally after tying one of the coronary arteries, hence a tentative diagnosis may be made of partial coronary obstruction. The pa- tient is still alive (3 years after the record was taken), hence the diagnosis has not been verified. *A complete record of this case will be found in Heart, 1012, iv, p, 128. Paroxysmal Tachycardia "3 ^^S^^-^T . W— w- W- Figure 76 Transition from slow rate to paroxysm. Note dislocation of pacemaker to a point low down in the auricle as evidenced by the abrupt change in the direction of the /' The ventricular complex is unchanged except as its contour is broken by the rever wave. Compare Figure 69. J K •* ^ J L- _ — , — _ , , , , Figure 77 Abrupt termination of a paroxysm. Transition distorted by extrasystoles of ventricu- lar origin. Pacemaker of paroxysm located near the A-V node. Compare Figure -5. FT J„1_T_T Vi/^glV^ T Figure 78 Auricular tachycardia, rate 160. Transition to rate of 70. Origin low down in the auricle. 114 Paroxysmal Tachycardia CLINICAL SioNiruwNii-: and prognosis There is little doubt that every subject of paroxysmal tachycardia has a defect of the myocardium that must be seriously considered. The prognosis is most difficult. Some patients over a period of many years have attacks which incommode them but little and the attacks become less severe, less alarming, and in some instances disappear altogether. Some have only a few attacks before the fatal termination. 1 have never seen a case that was fatal until a number of at- tacks had occurred, nor have I found such a case reported in the literature. The condition of the heart in the intervals between attacks is important as an aid in determining the seriousness in the individual case. If at these times the heart shows no abnormality other than occasional extrasystoles, one can be reasonably sure that there is no imminent danger. If, however, marked valvular defects are present, if there is evidence of an old inflammation of the peri- cardium, if there is a general arteriosclerosis, if extrasystoles con- stantly occur at very frequent intervals, and if the heart is embar- rassed in maintaining an adequate circulation in the periods of slow rate, the paroxysms will rightly be viewed with much appre- hension. The paroxysm is very exhausting to the heart. If the myocardial damage is made evident by the attacks only, the heart will probably successfully carry this stress; if, however, other evi- dences of myocardial damage exist, the strain of the paroxysm is a far more serious matter. The patients who do particularly well are young subjects with no evidence of cardiac abnormality be- tween attacks. Middle-aged and elderly individuals sooner or later invariably develop other evidences of myocardial insufficiency and, while they may have many and frequent attacks of tachycardia without serious manifestations, the ultimate outlook is less favorable. The frequency and duration of the individual attacks do not seem to be very important factors in determining the prognosis. Much more important is the severity of the attacks as estimated by the degree of circulatory embarrassment, cardiac dilatation, the congestion of lungs and liver and edema of the extremities. At- u6 Paroxysmal Tachycardia tacks associated with unconsciousness should be viewed with gravity. With a history of a moderate number of attacks over a number of years in a young adult, with intervening periods of normal heart action, one may usually give a good prognosis. When the patient is moie advanced in years and has paroxysms of increasing fre- quency and severity, and intermediate periods characterized by signs of cardiac insufficiency, the outcome of any particular attack is doubtful, the prognosis for the future is not good. There is another rare form of paroxysmal tachycardia in which the attack consists in a short period of auricular fibrillation. This will be discussed in the chapter on auricular fibrillation. CHAPTER X Auricular Flutter Closely allied to "auricular paroxysmal tachycardia," discussed in the last chapter, is an abnormal functional activity of the hearl usually designated as auricular flatter* The terms "auricular tachycardia" (Robinson), "auricular tachyrhythmia" (Hoffmann;, and "auricular tachysystole" (Rihl) have also been applied to this condition. The chief distinguishing feature of this group is the rapid, rhyth- mic, coordinated systoles of the auricle, the contractions usually occurring at a rate between 250 and 300 per minute. The auricular rate is so rapid that the ventricle is unable to respond to each im- pulse so that the ventricular rate is always slower than the auricular. The abnormal activity may occur in short paroxysms lasting only a few minutes or may be continued for days or weeks. It seems quite probable that this peculiar activity differs essentially from that of auricular paroxysmal tachycardia only in respect to the rate of the auricular contractions ; in paroxysmal auricular tachycardia the auricular rate usually does not exceed 250 per minute and the ven- tricles respond to each auricular stimulus ; in auricular flutter the auricular rate is much faster and the ventricles are unable to re- spond to each auricular stimulus. EXPERIMENTAL PRODUCTION As early as 1887 MacWilliam* described the phenomena which result from the application of a weak faradic current to the exposed auricular wall as follows : "It sets the auricles into a rapid flutter . . . the movements are regular : they seem to consist in a series of contractions originating in the stimulated area and thence spread over the rest of the tissue. The movement does not show any dis- tinct sign of incoordination: it looks like a rapid series of contrac- tion waves passing over the auricular wall." Under these condi- tions the ventricular rate is accelerated but is usually one-half or less than one-half of the auricular rate. In a heart beating 140 to *Jolly and Ritchie, Heart, 1910-11, ii, 77. ♦Journ, of Physiology, 1887, viii, 296. 117 i [8 Auricular Flutter iSo per minute such faradization may induce an auricular rate of 500 to 600 per minute while the ventricular rate may he 200 to 300 per minute, [f faradization of the auricles is Stopped the "auricular flutter" may continue fur a considerable time and then the auricle may resume its physiological rate. in the frog's heart "auricular flutter" lasting as long as two min- utes, starting suddenly and terminating abruptly, may he induced by a single induction shock applied to the sinusf or some portion of the auricle. $ While the auricles are in "flutter" vagus stimulation may change the flutter into a condition of "fibrillation" and slow the ventricle; it does not. however, slow the coordinated contractions of the auricle. It is possible, as suggested by Ritchie, that excessive stimulation of the accelerator nerves may he a factor in producing flutter in an otherwise healthy heart. MECHANISM Experimental and electrocardiographic evidence indicates that auricular flutter is characterized by a rapid rhythmic series of auricu- lar contractions having their origin in some point of the auricular musculature other than the sinus node. Nearly all paroxysms of auricular flutter are preceded and followed by extrasystoles which interrupt the physiological rhythm more or less frequently ; the extrasystoles are auricular in origin and prohably arise in the wall of the upper chamber at a point which becomes the pacemaker for the paroxysm. That the irritability of this point is very great may be concluded from the great rapidity of the auricular systoles. The mechanism is the same as that of auricular paroxysmal tachycardia but in flutter the auricular rate is so great that the capacity of the bundle of His to convey stimuli is exceeded and the ventricle re- sponds only to every second or third auricular impulse. In most cases the ventricular response is perfectly rhythmic and there is one ventricular contraction to two or three auricular contractions. Less commonly the ventricular contractions are arrhythmic and respond at one time to each second auricular impulse, at another time to each third or fourth impulse from the upper chamber. fLoven : Mitteilungen vom physiol. Laboratorium in Stockholm, 1886, iv, 16. JEngelmann; Arch. f. d. gcs. Physiol., 1897, lxv, 109. Auricular Flutteb ng A. ']/s 1111 1 111, 11 1 iniimT ninumiiininii N \ m Figure 8i Paroxysm of auricular flutter. During the attack tlie auricles contract rhythmically. The ventricles contract rhythmically at a slower rate, the ventricle responds to every third auricular impulse. iiuuiiumiuini mnrrrnrrnnrrrr Y, m ttl H s; Figure 82 Paroxysm of auricular flutter with irregular ventricular response. Such an extreme grade of ventricular irregularity may simulate the activity of auricular fibrillation, or a lower grade of irregularity may be mistaken for extrasystoles. The ventricle responds to the first, second, third or fourth auricular impulse. Diagrams to illustrate the mechanism of auricular flutter of different types. The arrows indicate the points of origin and direction taken by the stimuli. Dotted arrows indicate the time at which the normal stimuli at the sinus node should reach maturity if its for- mation were not interrupted by the abnormal impulse starting from a lower point in the auricle and traveling upward. The thickness of the lines representing ventricular sys- tole indicate the relative effect of the several contractions in maintaining an adequate circulation. The obliquity of the A-V line indicates the varying length of the conduc- tion time. As = auricular systole. A-V = conduction from the auricle to the ventricle. Vs — ventricular systole. i-'o Auricular Flutter The activity may be regarded as an auricular tachycardia with a functional depression of the property of conduction in the A-V bundle. We conclude that a real depression of conduction exists because we know that in "paroxysmal tachycardia" the ventricle mav- respond to the auricular impulses at a rate above -'30 per minute, yet in "auricular flutter" the rate of the lower chamber of the heart is usually not above 120; rarely it attains a rate of 160 per minute. Ritchie* has reported a patient with a ventricular rate at times under 40; in this case there was probablv an organic lesion of the bundle of His. Figure 81 shows in diagrammatic form the mechanism of a par- oxysm in which the ventricle responds rhythmically to every third auricular impulse; during the attack the ventricular rate is accele- rated but is only one-third the rate of the auricle. Each ventricular systole of the paroxysm is less forcible, since the property of con- tractility has not had the same time to recover as is permitted dur- ing the physiological rate. The exhaustion of the capacity of con- duction in the A-V bundle, due to the abnormal shower of auricu- lar impulses, is indicated by the obliquity of the line representing the period of the passage of the stimulus from the auricle to the ven- tricle. In Figure 82 are plotted the auricular and ventricular activities of a paroxysm of flutter in which the ventricular response is very irregular; the lower chamber follows the first, second, third or fourth auricular impulse in a seemingly haphazard fashion. The conduction period is variable and prolonged. The ventricular con- tractions have a force proportional to the preceding diastolic period. The difficulty of differentiating such a mechanism from that of "auricular fibrillation" is apparent. If the ventricular response had been rhythmic up to the time of the final beats of the paroxysm, it is easy to see how the pulse and heart sounds might suggest the occurrence of an extrasystole only. ETIOLOGY AND PATHOLOGY The reported cases of auricular flutter indicate that it occurs con- siderably more often among men than women. It may occur at any age; the earliest subject which has been put on record was 5 ^"Auricular Flutter," London, 1914, 36. Auricular Flutter 121 Jugular Carotid Brachial Figure 83 Auricular flutter with regular ventricular response. Auricular rate 276. Ventricular rate 92. Jugular Carotid Brachial Figure 84 Auricular flutter with irregular ventricular response. Auricular rate 2S0. Ventricle usually responds to fourth auricular impulse, at X it responds to second auricular impulse. [22 A.URICULAR FLUTTER years old. All the eases which I have observed, with one excep- tion (14 years), have been over 50 years of age. Ritchie in his analysis of 49 cases found that 70 per cent, occurred after the for- tieth year. Auricular flutter rarely occurs without some other evidence of damage t<> the cardiac tissues ; about a third of the cases show a de- fect of the mitral valve. Dilatation of the auricles is a common antecedent condition. Pericarditis has been present in several cases. General arteriosclerosis in which the coronaries have participated has been found in a number of instances. The acute infections, such as diphtheria and rheumatic fever, have been the evident causative agent in about 20 per cent, of the cases thus far reported. Evidence of a syphilitic infection is obtained in at least 10 per cent. It has been suggested that an abnormal balance of external ner- vous control may be an element in the production of auricular flut- ter, but no anatomical lesion which would indicate a removal of vagus influence or a hypertonic activity of the accelerators has thus far been demonstrated. Such evidence as is at hand leads us to believe that this abnormal activity has its origin in a lesion in the auricular wall which con- stitutes a focus of increased irritability. In the few post-mortems which have been reported, in those who have been the subjects of auricular flutter, histological examinations have failed to demonstrate a particular focus in the auricular wall to which one could ascribe the functional change, but general in- flammatory and degenerative changes of the myocardium are not wanting. Dilatation of the auricles with fibrous, fatty or lymphocy- tic infiltration of the walls is the most common finding. Atheroma of the coronaries and calcareous deposits in the arterial wall sug- gesting an interference with the nutrition of the heart musculature have been found in several instances. These lesions frequently in- volve a large part of the heart muscle and may include the sinus node and A-V bundle. Ritchie (Case III) found changes in the sinus node consisting of lymphocytic infiltration. Hemorrhage and granular degeneration of the nodes are reported by Hume.* I have obtained autopsies in three cases, men of 51, 54 and 55 years, re- ♦Hcart, 1913-14, v, 25. Auricular Flutteb ■R H MM ,JL. ********* ***■**. fatient II. S. Lead I. jflGURE 55 Auricular flutter. Time lines = 1/ Figure 87 Patient H. S. Lead III. Auricular nutter. Time lines = 1/^5 second. Figures 85, 86, and 87 taken from the same subject. Auricular rate 336 per minute. Kegular ventricular response to every fourth auricular impulse, ventricular rate 84. i_>4 Auricular Flutter spectively. Each showed sclerosis of the coronaries and extensive fibrous myocarditis; in each very little normal heart muscle could he found. Each had an old infarct of the left ventricular wall. IDENTIFICATION A careful history and physical examination may lead us to sus- pect "auricular flutter," but one can only be sure of the correctness of the diagnosis when fortified by the evidence of graphic records. The pulsation of the veins of the neck gives us certain information in regard to the activity of the right auricle, a very rapid rhythmic pulsation of the jugular vein, showing a continuous series of waves at absolutely equal time intervals and two or three times as rapid as the ventricular rate, as determined by auscultation, suggests an auricular flutter, but it is quite evident that by mere inspection it is most difficult to count and correctly determine the spacing of the small venous waves. In cases of established auricular flutter I have repeatedly tried to elicit auscultatory evidence of the rapid auricu- lar activity with complete failure. The ventricular contractions may be perfectly rhythmic and so accelerated that one may suspect a true "paroxysmal tachycardia" (see Chapter IX). As a rule, in "auricular flutter" the ventricular activity is less rhythmic and not as fast as is the case in "paroxysmal tachycardia." The irregular ventricular activity of "flutter" is most often mistaken for the far more common disturbance known as "auricular fibrillation" (see Chapter XI). In most cases of "auric- ular flutter" the arrhythmia is not as great as in "auricular fibrilla- tion" and in the latter the ventricular form of the venous pulse may aid in distinguishing the two conditions; however, without the assistance of graphic records the separation of these groups is prac- tically impossible. When the ventricular rate is only 40 or less and perfectly rhyth- mic, one at once suspects a condition of heart block. If in such a case the jugulars are pulsating rhythmically at a rate of 200 or more per minute, one can be reasonably sure that a condition of "auricu- lar flutter" coexists. There are certain types of irregular ventricular response when the auricle is in flutter which simulate forms of extrasystolic ac- tivity. For example, if for considerable periods there is a ventricu- Auricular Flutj i:i< [2< : : : . : 1 •R -R. *. s pj^i^ s iiii 1 Figure 88 Auricular flutter. Lead I. Auricular rate 332. Ventricular rate 166. As:Vs::2:i. Time = 1/25 second. , ■ — ■ j 1 . — 1 £ £dt*2JLE ****** Figure 89 Auricular flutter. Lead II. As:Vs::4:i. As = 492. Vs = 123. Time = 0.2 second. Figure 90 Auricular flutter with irregular ventricular response. Lead III. As = 280. Time = 0.2 second. [26 Auriculas Flutter lar response to every third auricular impulse and this established rhythm is broken by a ventricular response to the second auricular impulse, which is in turn followed by a ventricular contraction after four auricular systoles, the early beat and the succeeding pause may give one the impression of an extrasystole with a compensatory pause ( see Figure 82 |. The polygram is often of material aid in making a diagnosis of auricular flutter and the jugular tracing may demonstrate the rapid rhythmic activity of the right auricle. The analysis of the jugular curve is, however, often obscure, since the record of the waves of auricular activity is distorted by the c and v waves characteristic of the normal venous tracing. We should bear in mind that the a, c, :• and // waves of the normal jugular pulse do not follow one an- other at exactly equal intervals of time, and when we can detect in the jugular record such a rhythmic series of waves two, three or four times as rapid as the ventricular rate, we have strong grounds for suspecting a condition of auricular tachycardia. Figure 83 was secured from a case of "auricular flutter" in which there were regularly three auricular contractions to one ventricu- lar. The ventricular rate was 92, the auricular rate 276 per minute. One of the a waves of each cycle is simultaneous with the c wave. The ventricle contracts in perfect rhythm. A type of irregular ventricular response is shown in Figure 84. The jugular record is composed of a rhythmic series of a waves at a rate of 280 per minute, which can be picked out by careful meas- urement ; the pure auricular record is distorted by c and v waves of each cycle and the whole is superimposed on the respiratory curve. The ventricle is contracting at a rate of 102 per minute ; the ventricle usually responds to the fourth auricular impulse, but occasionally (at X) it responds to the second auricular impulse. This type of irregular ventricular response would strongly suggest occasional auricular extrasystoles were it not for the evidence obtained from the jugular tracing. The analysis of both of these polygrams was verified by electrocardiographic records taken at the same time. The electrocardiogram must be our final court of appeal in sub- stantiating a diagnosis of "auricular flutter." Even here the evi- dence is sometimes obscure, and it is wise to have records taken by the three standard leads in order to be certain of our interpretation. Auricular Flutter '-7 PHI ^*^^^\^^NnW^aI Auricular flutter. Lead III. Irregular ventricular response. One ventricular extra- systole. Time = 1/25 second. * R 7K K !^iJ^^I^Jf^J r ^!^^^ j Figure 92 Auricular flutter. Patient H. Auricular rate 388. Regular ventricular response rate 194. Time = 0.2 second. mm J'pwmmnmmt m&mmm I T* IK mmmm **mmmmmmrm A '- Figure 93 Time A = rI i2 Ia S econd! lati0n ' ^^ *""* ""* PEtient (H ° as Figure 9 "' but I5 da >" s Iaten 128 Auriculae Flutter Figures 85 (lead I), 86 (lead II) and 87 (lead III) were taken from the same patient at intervals of about one minute and indicate the differences in the records secured by different derivations. Us- nallv the analysis is most easily made from leads Jl and 111, but this is not always the ease. In these records the ventricle is beat- ing rhythmically at a rate of 84 per minute ; the auricle is contracting at a rate of 336 per minute. ( >ne of the auricular (P) waves of each cycle is submerged in the R defection of the ventricular cycle. The T wave of the ventricular complex is evident only in leads I and 11 as a slight distortion of the rhythmically recurring P waves. In Figures 88, 89, 90 and i)i are shown four records from four distinct cases of auricular flutter indicating the variations which such a group of cases may present. In l ; igure 88 is reproduced a curve taken from a patient by lead I. In this instance the ventricular rate is 166; the auricular rate is 332 per minute. The ventricular and auricular complexes are in part superimposed so that the analysis at first glance seems obscure ; by the aid of records taken by leads II and III (not reproduced) we could clearly establish a rhythmic rapid activity of the auricle at double the rate of the ventricle. The question arises in this case as to which of the auricular stimuli excites the activity of the lower chamber. We cannot answer this question positively but we have strong evidence for presuming that the earlier of the auricular stimuli (PJ is the one to which the succeeding ventricular contrac- tion is the response. If the response was to the stimulus delivered at P 2 the conduction time (P»-Q) would be abnormally short. While it is not inconceivable that in certain cases the property of conduction may be heightened, all our experience goes to show that in those cases of auricular flutter in which we have positive evidence, conduction is normal or depressed (usually the latter). It is never demonstrably shortened, hence we are led to believe that in every case the conduction time is longer than the normal and therefore in the instance shown in Figure 88 it is probable that the ventricle responds to P x rather than to P.. A case in which the lower chamber response follows four auricu- lar contractions is depicted in Figure 89. The ventricular rate is 1 23 ; the auricular rate is 492. Both chambers contract rhythmically, but the auricle four times as often as the ventricle. Auricular Flutter 129 ~~ ! 1 r*- u f"r^:"^T" 71 H "R R "R fiBl p P T> I p pi p p Figure 94 Patient K. Auricular flutter with irregular ventricular response and ventricular extra- systole. Time 1/25 second. Figure 95 Patient K. Sequential rhythm taken from same subject as Figure 94. Taken 11 days later. Note same type of ventricular extrasystole. Time 1. 25 second. , 130 Auriculas Flutter Irregular ventricular responses arc shown in Figures 90 and or. In Figure 90 the auricle is beating rhythmically 280 times per minute: the ventricle responds to every second or third auricular stimulus. In Figure 91 the response is to the second, third or fourth auricu- lar stimulus. This record is further complicated by an unusual com- plex indicating one ventricular heat having its origin in a point in the ventricular wall quite different from the other ventricular contractions, which are of supraventricular origin. A record from a case of "flutter" with a very rapid rhythmic re- sponse is represented in Figure < >2. The auricular rate is 38S ; every other auricular complex is submerged in a ventricular complex which occurs 194 times per minute. The ratio of the rate of the upper to the lower chambers is as 2 is to I. A record from the same case 1 Figure 93) taken 15 days later, after the patient had taken digi- talis, shows complete irregularity and a rate of 46 per minute. There are at this time no coordinated contractions of the auricle, but its activity is one of "fibrillation." CLINICAL COURSE AND SIGNIFICANCE Auricular flutter is occasionally the only evidence obtainable of a defective myocardium, though quite commonly extrasystoles pre- cede and follow the paroxysms. In such patients careful examina- tion fails to reveal any organic change in the valves, endocardium or pericardium, and the only evidences of functional disturbance are those elicited during the paroxysm. During the attack, which comes on abruptly and terminates suddenly, the patient may be very un- comfortable. He is conscious of an unusual commotion in the chest ; the accelerated and irregular activity of the ventricle may be the cause of considerable apprehension ; this may be accompanied by some dyspnoea, precordial distress and prostration if the paroxysm is prolonged. Some attacks may extend over days or even weeks, the earlier alarm and dyspnoea may subside, and the patient may re- sume his usual occupation aware only of the continuing "palpita- tion." In most cases there are other evidences of myocardial damage and the "auricular flutter" throws an additional load on a heart A [jriculab Flutter 131 1 1 T> P P P P P P P P P P .^/****» y^**** fa/"**""* d f .... f . ' '' ' ■? . . tm a,. „ y Figure 96 Patient M. K. March 11, 1912. Auricular flutter. Time 0.2 second. Figure 97 Patient M. K. December 12, 1914. Sequential rhythm. Time 0.2 second. Figure 98 Patient M. K. December 2S, 1914. Auricular fibrillation. Figures 96. 97 and 9S are taken from the same subject, the first of these was taken during an attack of pneumonia 2 1/2 years before the subsequent records. 132 Auricular Flutter already overtaxed. In such patients the general signs of cardiac insufficiency may have been present before the onset of the auricu- lar acceleration, or the unusual stress occasioned by the new rhythm may be too much for a heart barely able to preserve an adequate blood stream: its narrow margin of safety is quickly exhausted, and sigm and symptoms of cardiac insufficiency rapidly appear. The extent and severity of the symptoms depend to a very large degree on the condition of the heart before the attack; the auricular flutter may last for days or weeks, yet ultimately the heart may recover a normal rhythm and perform its work with reasonable efficiency; or in a short time there may develop dyspnoea, congestion of the liver and lungs, edema of the extremities, Cheyne-Stokes respiration, giddiness, unconsciousness and collapse. A patient may have many attacks of auricular flutter or it may appear only as a terminal event. Once established, the attacks are prone to recur and each one is apt to persist for a longer time. Oc- casionally one sees attacks of flutter alternating with periods of nor- mal rhythm; more often "auricular flutter" passes into "auricular fibrillation," which may persist indefinitely or may, in turn, give way to a physiological rhythm. With a return to a normal rhythm the symptoms usually improve. The tendency to resume a normal rhythm is seen in Figures 94 and 95, taken from the same patient at intervals of eleven days. Figure 94 shows auricular flutter at 300 per minute, with an ir- regular ventricular response interrupted at X by a ventricular extra- systole. In Figure 95 is seen the sequential rhythm of eleven days later interrupted by an extrasystole of the same type as that which occurred during the period of "flutter." Figure 96 was taken from a patient during her first paroxysm of flutter, which had its onset during an attack of lobar pneumonia in March, 1912. In December, 1914, she returned to the hospital with broken cardiac compensation. Her record taken at that time (Figure 97) shows a sequential rhythm. A few days later she be- gan to fibrillatc (Figure 98) and has continued this condition up to the present time (6 months later). The clinical significance of auricular flutter lies in the fact that it indicates a considerable degree of damage present in the auricu- lar wall. That the damage may be temporarily repaired is indicated Auricular Flutter [33 by the recovery of normal rhythm, but the tendency to repeated and more severe attacks suggests that usually the repair is incomplete. The welfare of the patient depends to a large degree on the dition of the ventricle. With a normal ventricular muscle the patient will withstand many attacks of "auricular tachycardia" with com- parative immunity. With a damaged ventricle the outlook is much less propitious. Unfortunately the myocardial damage is rarely limited to the auricle. In "auricular flutter" a slow, regular re- sponse of the ventricle is favorable; a rapid, irregular ventricular response makes the outlook more serious. The change to a condi- tion of auricular fibrillation and a slowing of the ventricle under digitalis are to be regarded as a favorable sequence of events. The return to a normal rhythm is to be welcomed but by no means as- sures complete recovery. CHAPTER XI Auricular Fibrillation The group which we arc now to consider is characterized by a "complete irregularity" of the pulse. Waves of varying sizes, large and small, separated by intervals long or short, follow each other in a confused succession. The pulse is absolutely devoid of rhythm. The closest study will not enable us to predict whether the next event in the series is to be a forcible, or a weak impulse, a pause short or long. We may have a series of small waves separated by unequal intervals occasionally mingled with large waves, or large and small waves and longer or shorter pauses may be jumbled to- gether in the utmost confusion. In the older literature this pulse has been described and labeled with many different names, "pulsus arhytlunicus," "deficiens," "iuacqualis," "intermittens," "irregularis/' it has been called the "mitral pulse." The pulse rate may be fast or slow, it may exceed 200, or may be under 40. The heart shows the same degree of irregularity, indeed by aus- cultation the absolute irregularity is made more apparent than by palpating the radial. The heart activity is, I think, best described by the now discarded term "delcrium cordis." The apex impulses are unevenly spaced, and forcible and weak thrusts are mixed in an erratic series. The heart sounds show the same absence of rhythm both in time and force. They vary greatly in intensity. Each contraction may be represented by a first and second sound, or at more or less fre- quent intervals the first sound alone is audible suggesting that the feeble contraction has failed to open the aortic valves. The credit of separating this type of disordered myocardial func- tion from others belongs in a very large degree to Mackenzie,* who pointed out the constant association of the "ventricular form of venous pulse" and "complete irregularity" of the ventricle. At this time he ascribed these phenomena to a paralysis of the auricles. Later he amplified his views in a paper based on the study of 500 ♦Study of the Pulse, London, 1902. 134 Auriculas Fibrillation 135 cases. f In a scries of subsequent: papers he modified liis theory of the underlying defective mechanism, and since he was led to bel that the auricle and ventricle contracted simultaneously, he assumed that a point near the A-V junction was the source of the impulse which simultaneously excited both the upper and the lower cham- bers. He further assumed that this abnormal pacemaker was lo- cated in the node of TawaraJ and therefore introduced the term "nodal rhythm"§ to designate this group. The real explanation of the activity of the completely irregular heart was made clear by the electrocardiographic studies of Roth- berger and Winterbergjj and of Thomas Lewis. || To these investi- gators, working independently, is jointly due the distinction of con- clusively demonstrating that in these cases there is no gross auricu- lar contraction, but that the auricular wall is in a continuous state of fibrillation. To those who are interested in the facts upon which their conclusions are based a study of the original papers is com- mended. EXPERIMENTAL PRODUCTION AND MECHANISM When the auricle of an exposed heart is faradized the coordi- nated contractions of the chambers as a whole cease, there is no auricular systole, and the muscle wall assumes the relaxed condition of diastole, the muscle mass is, however, not at rest, it manifests a continuous activity which consists of fine irregular waves with here and there a sharper twitching movement. The movement has been likened to the appearance of the squirming of a bunch of worms. This is what is known as fibrillation of the auricle. It is similar in appearance to the fine fibrillary movements which are not infre- quently seen in the tongue. When such a condition is produced experimentally it is accompanied by a complete irregularity of the ventricle, a venous pulse of the ventricular form and an electro- fAmer. Jour. Med. Sci., 1907, exxxiv, 12. JQuart. Jour, of Med., 1907-8, i, 39. §With our present clearer insight into the mechanism of the completely- irregular pulse, the term "nodal rhythm" should not be used in this con- nection. It should be reserved to designate a rare but definite cardiac activ- ity in which the pacemaker is located in the A-V junctional tissues. flWien. klin. "Wochenschr., 1909, xxii, 839. IJHeart, 1909-10, i, 306. 1 36 Auriculas Fibrillation cardiogram which shows a continuous scries of small irregular de- flections, which arc met with in no other condition, and arc un- doubtedly due to the abnormal auricular activity. Lewis studied 3 horses, each having complete irregularity, the electrocardiograms were similar to those obtained from nun with complete irregularity. On quickly opening the chest the auricles could be seen in a condition of fibrillation, and the ventricles were contracting in the characteristic irregular manner. Cushney and Edmunds,* who were familiar with the experimental production of auricular fibrillation, in discussing a case of complete ventricular irregularity in man were the first to suggest that this phenomenon might be associated with a iibrillating auricle. Auricular fibrillation has been produced experimentally by in- creasing the intra-auricular pressure (Lewis), by stimulating the vagus and accelerator nerves (Morat and Petzetakis) by the applica- tion of heat to the myocardium (Lagendorff) and by toxic doses of drugs, digitalis (Francois-Frank), nicotine (Pezzi and Clerc), pilocarpine (Busquet). It has been suggested by Lcwist that fibrillation is due to a highly irritable condition of many points in the auricular musculature, each of which "is independently and spontaneously elaborating hetero- genetic impulses," that is to say he views the condition as closely allied to the auricular extrasystole, but instead of there being one irritable point there are many, and the multiple impulses thus set free neutralize or reinforce one another in an utterly haphazard fashion. Recently GarreyJ has taken exception to this view, and substi- tutes the theory that the condition is due to many small blocks be- tween the fibers of the auricular musculature, so that the fibers re- ceive their stimuli not by the usual paths, but in such a manner that the stimuli pass slowly from cell to cell by a circuitous path, thus causing contraction waves in a shifting series of ring-like undula- tions. There is little question that the ventricular contractions are the result of irregular impulses received from the auricle for the electro- cardiographic ventricular complexes are usually of the form which *Amer. Jour. Med. Sci., 1907, exxxiii, 67. ^Mechanism of the Heart Beat, London, 191 1, p. 192. (Am. Jour. Physiol., 1914, xxxiii, 397. Auricular Fibrillai [on '37 are secured from stimuli arising in a point above the level of the junctional tissues. There arc several factors which may have an influence in determining the instant at which the ventricle shall re- spond: (a) it is conceivable that a stimulus is effective only when of a certain magnitude, and that such a size is only attained when a considerable number of minute auricular impulses bombard the junctional tissues at the same instant, (b) this constant shower of auricular stimuli may have a modifying effect on the excitability or the conductivity of the bundle, (c) the underlying disease which has caused the damage to the auricular musculature may not have left the A-V bundle unscathed. h w * » m » m • » » »» » ■ » ; »»»»*»»■ * ******** * * *. *.*** BE S^S3S WWW. \\. \ Figure 99 Diagram to illustrate our conception of the mechanism of auricular fibrillation. Aff dots of various sizes indicate stimuli of various magnitudes arising in many parts of the auricular wall neutralizing or reinforcing or blocking one another. When effective the impulse is transmitted through the junctional tissues (A-V) and the ventricle responds (Vs) at irregular intervals with a varying degree of force, roughly proportional to the length of the preceding diastolic period. It is to be noted that the auricle is in a state of continuous activity, but there is no coordinated contraction: also that the stimuli which call forth a ventricular contraction arises in a point above the ventricular tissues. The peculiar susceptibility of cases of auricular fibrillation to stimulationf of the left vagus and the drugs of the digitalis group suggests a distinct change in the functional activity of the junctional tissues. The force of the successive ventricular contractions depend mainly on the period of rest which precedes any particular contraction, thus permitting a more complete filling of the ventricle and a recovery of its contractile power, but as has been pointed out by Einthoven and Kortweg^ this relationship is not always maintained, hence other factors must be at work which are not completely understood. The accompanying diagram (Figure 99) portrays in a graphic manner the conception of the mechanism, the upper reaches of the junctional tissues are being continuously bombarded by a shower of fDraper and Robinson: Jour. Exp. Medicine, 1911, xiv, 217. JHeart, 1915, vi, 107. 1^8 Auricular Fibrillation small impulses from the auricular segments; at irregular intervals these stimuli become effective, and a ventricular activity, irregular iu time ami force, is the result. PATHOLOGY Every heart showing fibrillation of the auricles which has been exhaustively examined has given evidence of gross or histological damage of its tissues, but as yet no lesion has been described to which we may definitely attribute the abnormal functional activity. Grossly one finds valvular defects, most frequently mitral stenosis, hypertrophy and dilatation, pericarditis and coronary sclerosis. Mackenzie early in his studies pointed out the frequency with which dilatation and hypertrophy of the auricles is met with in these cases. Histological examination almost invariably reveals evidence of acute or chronic inflammatory changes of the myocardium, leucocytic in- filtration, or fibrosis and atrophy of the muscle cells. In several instances the blood supply of parts of the auricular wall has been found deficient. In some cases structural changes have been de- scribed in the sinus node or in the A-V node, in others these tissues have revealed nothing abnormal to the most thorough search.* The recognized fact that fibrillation of the auricles may be only temporary suggest that in a certain number of cases, the cause may be a toxin, or a temporary nutritional disturbance. Since it has been shown experimentally that over distension of the auricle may lead to fibrillation, it seems reasonable to suppose that an auricular wall damaged by disease, under the stress of a defective valve, or the demands of a general arteriosclerosis, may readily fall into fibrillation. This would explain the onset in a large number of the cases that are seen in the clinic. ETIOLOGY Auricular fibrillation is met with in all decades of life, but is ex- tremely rare in those under ten years of age. In a personal experi- ence with over 300 cases I have seen only one case under the age of ten. A curve of the age incidence (Figure 100) indicates that 89 per cent, of the cases occur between the ages of 21 and 60. The first *Colin : Heart, 1912-13, iv, 221. AUKICULAK FIBRILLATION '39 sharp elevation occurs during the years when rheumatism is preva- lent, the second elevation occurs in the decade when the rheumatic period overlaps the time at which arterio i< lerotic change bei ome a prominent feature. It is seen more frequently in men than in women, the proportion being about 2 to 1. The association with mitral disease is very noticeable, 60 per < ent. of the cases showed a mitral stenosis, with or without mitral incom- petence, in 5 per cent, there was evidence of mitral insufficiency Dfteth. I -10 11-r.O 1.1 - so ai-uo VI - So J~l - Imt (,1 - TO 71 -fo b» 1 / ^^ S i\ 1 > ; — J , r" Nr J ". ' \ I 1 I \ 1 I !/ ; I \ I -: 1- 1 J- i V -; ■ I /' J : \ I ' / ' ' I \ ' i / ! i 1 • \ _i / • «»_«._«_ -._> - - ■ — \ — — 1 J 1 1 1 1 ! \ i 1 S 1 ' V. ' 1 I ! J : ! |\ J ! ! 1 1 ! J — J Rheumatism Degenerative changes Figure 100 Age incidence of 300 cases of auricular fibrillation arranged by decades. without stenosis. In a few eases there was an aortic lesion as well as a mitral defect. In only 7 instances have we seen fibrillation in hearts with defects of the aortic valves only. Distinct evidence of one or more attacks of acute rheumatic fever was obtained in over one-half of the cases studied. The well-known frequency with which rheumatism affects the mitral valve is further evidence that this disease is the underlying cause of the myocardial defect. It is not, however, common to see auricular fibrillation dur- ing the first attack of rheumatic fever, the damaged heart does not usually go into fibrillation until some years after the evidence of a valvular defect has been established. This phase is further empha- 140 Auricular Fibrillation sized when we compare the age incidence of rheumatism and of fibrillation: according to Church* 57 per cent, of the mitral attacks of acute rheumatism occur under the age of 20. Our chart of the age incidence of fibrillation shows that in only 16 casest did the onset occur before the twentieth year, and only 149 casesj showed fibrillation during the first four decades. This suggests that fibril- lation points to a rather advanced degree of tissue damage. The stretching of the injured auricular muscle under the stress caused by a defective valve may well be an important factor in producing this type of abnormal function. We have seen fibrillation develop during the course of a lobar pneumonia on six occasion>.^ In several casts with mitral disease the original lesion could be attributed to an attack of scarlet fever. Attacks of influenza seem to be the only etiological factor that could be obtained in some of the patients. The most careful scrutiny of a case now under observation has given no explanation of a well- marked mitral stenosis and auricular fibrillation other than repeated attacks of grippe. We have seen fibrillation of the auricles in four cases of Graves' disease, two of these gave an old history of attacks of acute rheu- matic fever and each presented evidence of a mitral stenosis. Aside from the rheumatic cases, and those in which the myocar- dial damage may be attributed to one of the acute infections, there is a considerable group which includes those suffering from de- generative changes, such as general arteriosclerosis, chronic nephri- tis, emphysema, etc. This group is composed of patients who, for the most part, have passed their fortieth year, and in it males largely predominate. Syphilis and alcohol appear to be prominent etiological factors in this group. Many of these have no discoverable evidence of valvu- lar disease, a soft blowing systolic murmur in the mitral area is, ♦System of Medicine: Allbutt and Rolleston ; Vol. ii, Pt. 1, 603. |8 per cent, of those having a rheumatic etiology. X" per cent, of those of rheumatic origin. §In 126 cases of pneumonia carefully studied by Dr. A. E. Colin, fibril- lation occurred in 12 cases (personal communication). Auricular Fibrillation 141 however, not an uncommon feature. Several had dilatation of the arch of the aorta, and insufficiency of the aortic valves. IDENTIFICATION Clinical. Palpation of the radial pulse in most instances is suffi- cient to permit us to assign this group of cases to their correct cate- gory. The complete irregularity is at once evident, the pulse beats are irregular both in time and force. As a rule the stronger beats follow the longer pauses, but the disorderly sequence of large and small waves separated by intervals long or short, allows us to make a very strong conjecture as to the kind of abnormal cardiac activity with which we have to deal. There are other cases in which the complete irregularity is not so easily detected by palpation. When the pulse volume is diminutive, when the pulse pressure is relatively small, the recognition of the unequal size of the successive waves may be quite difficult. In cases with a rate of over 160 the pulse waves may show very insignificant differences in size, and the time intervals may show variations only to be detected by the most care- ful measurements secured by instrumental means. There are cer- tain patients with pulse rates between 70 and 80, and with the waves placed at such even intervals that an uncorroborated examination of the radial pulse is quite insufficient to classify it as one of complete irregularity. Before going farther we should emphasize the point that while practically every case of "auricular fibrillation" is characterized by a pulse of "complete irregularity," there are other conditions which may also afford a "completely irregular" pulse which can only be differentiated by exact instrumental methods, while in nineteen out of twenty instances a "complete irregularity" of the pulse correctly indicates a condition of "auricular fibrillation," the twentieth may be the result of an entirely different heart activity. The types which may notably give rise to this confusion are certain "sinus arrhythmias," and cases with very frequent extrasystoles, particu- larly when they arise from several points in the heart wall (Figure 120), or are interpersed with short runs of paroxysmal tachycardia (Figures 79 and 80). If the veins of the neck are prominent inspection will show that the jugular pulsations are synchronous with the apex beat, no pre- i4-' Auricular Fibrillation systolic wave can be seen, the venous pulse is of the ventricular form. Auscultation of the apex will corroborate the complete irregu- larity discovered in the pulse, and at times will make clear an irreg- ularity which was not discovered when palpating the wrist. The sounds vary greatly in intensity and follow one another at unequal intervals. ( U'ten the heart beats are far more numerous than the arterial pulsations, some contractions are too feeble to perceptibly increase the lumen of the radial artery, and others fail even to open the aortic valve. These latter are represented by a first heart sound only, the second sound is wanting. The question as to whether the aortic valves are or are not opened by any particular ventricular contraction depends on the rela- tive pressures in the aorta and the left ventricle. If the diastolic period is very short, the contractile power of the ventricle will have had little time in which to accumulate, at the same time the pressure in the aorta will be relatively high. Under such conditions the valves will not be opened. On the other hand given a longer pause the next succeeding ventricular contraction will have recovered its contractility to a greater degree, the aortic pressure will be relatively low, and the aortic valves will be opened. In some cases where the degree of irregularity is moderate, it may be difficult to distinguish this from a condition of extra- systole. It is helpful in such cases while listening to the heart beats to concentrate the attention on the beats which occasion- ally occur too early, and which simulate the premature beat of the extrasystole, the diastolic period following these early con- tractions of complete irregularity usually do not have the same length, nor as a rule do they have as long a duration as that which would constitute the "compensatory pause" of an extra- systole, and thus may be differentiated. If valvular defects are present murmurs are usually detected, but at times their character is cptite different from those heard before the inception of the complete irregularity. If the heart is beating very rapidly the murmurs are less intense, and the sharp snap of the first sound, so characteristic of mitral steno- sis, may become muffled. The intensity of the murmurs vary Figure 102 AJUUIJJUiJLLUJLLLUJLLUiJ-UJUJLLJUAJJJ^ Figure 103 JJuUUUlUlLLLULLLJULLUJJJJUL^ Figure 104 yLijcJ n i |i 11 j I iiil AAA k Lilt I LLLkJJJJL L L LI J I k M kL k I k l H H t t Figure 105 Arttrial tracings from cases of auricular fibrillation showing the great variety of pulses which are seen. All of these records show complete irregularity. 144 Auricular Fibrillation from cycle to cycle. The more forcible beats arc accompanied by relatively loud and harsh murmurs, the more frequent feeble contractions by murmur- of less conspicuous intensity. There is frequently an increase in the intensity and duration of the mitral diastolic murmur. It may also assume a rougher quality. This may be explained on the basis of the increased volume of blood under considerable pressure in the right auricle, which is possibly distended and is never emptied by an effective contraction. For the most part, the time relations of the murmurs remain as before the change to complete irregularity, systolic and dias- tolic murmurs continue to occupy their established position in cardiac cycle. Mackenzie long ago pointed out one exception to this general rule, namely, the disappearance of an established presystolic murmur in cases of mitral stenosis which changed from a physiological rhythm to one of complete irregularity. 11 is explanation of this phenomenon assumed that the presys- tolic murmur of mitral stenosis was due to auricular systole, and that the failure of the auricular contraction accounted for the disappearance of this murmur. While this phenomenon is frequently seen it is not invariable as has been evidenced both by the ordinary methods of eliciting physical signs* and by occasional graphic records of the heart sounds which may be found in the literature. Authorities are not at all agreed that this presystolic murmur is due to auricular systole, and the per- sistence of the murmur in certain cases of undoubted auricular fibrillation lends support to the view that other explanations of the mechanism of the production of this murmur may not be disregarded. The character of the complete irregularity of the arterial waves are clearly brought out by taking a tracing of one of the peripheral arteries (radial, brachial or carotid), and by means of a simple graphic record of this kind (see Figures 101, 102, 103, 104 and 105) one can hardly miss a correct diagnosis. The great variation in the size and time intervals of the ar- terial pulse waves is shown in Figures 101, I02 and 103. In Fig- ures 101 and 102 the waves are for the most part of large volume, ♦Hart, Med. Rec, New York, 191 1, lxxx, 2. Auricular Fibrillation i45 Jugular Brachial /J_AJUUUULAJlJUbULJUU^^ [0.2 second Figure 106 Auricular fibrillation. Great variation in the size of the arterial waves and the inter- vals between them. Jugular completely irregular, a absent, c and v waves fused. Depres- sion x absent. J^Cfu/ar 'ThhAV-* £™clufcl 0>\ MLt Figure 107 Auricular fibrillation. At certain places the form of the arterial record might suggest an extrasystole. In the jugular record note the "ventricular form" of the venous pulse, the a wave is absent. i^6 Auriculae Fibrillation but show considerable differences in force and time intervals. Fig- ure 103 shows a brachial pulse rate of 138. Many of the smaller waves could not bo detected by palpation of the radial artery, hence it is easilv seen how a count of the radial alone would have been very misleading in determining the rate of the heart heat. Figures 104 and 105 are both taken from cases of auricular fibrillation. They indicate an unusual degree of rhythmicity, but careful measure- ments will slmw that the uniformity is apparent rather than real. In both of these records there are waxes which a casual observer might mistake for extrasystoles, but close attention re- veals not only a lack of uniformity in what one might take to be wa\ es of the physiological rhythm, but further a period of very inconstant length both before and after the small waves which thus differentiate them from the intervals which one finds on either side of the extrasystole as commonly observed. Polygrams make the diagnosis still more clear (see Figures 106, 107, 108, 109 and no). In these records the arterial curves show in considerable variety the features that have already been dwelt upon. In addition to this, the jugular reveals features which are characteristic of this form of irregularity. It is itself completely irregular. The time intervals between the waves indicate a com- plete absence of rhythmicity. The size of the waves show great variations, which are quite independent of the phase of respiration in which they occur. Furthermore, the venous pulse is of the "ventricular form," that is to say all the positive waves occur during the ventricular systolic period, the a wave, the represen- tative in the normal jugular of auricular systole is absent, c and v waves may be made out, the c wave usually varying in size pro- portional to the synchronous ventricular contraction. The v wave is usually a large broad elevation which frequently begins earlier than the v wave of the physiological rhythm and may be fused with the preceding c wave (Figures 106 and 109). The explanation of this phenomenon is found in the distended con- dition of the auricle which is probably never effectually emptied, hence the ventricular pressure is more readily transmitted by way of this blood column to the large veins. This feature may be further emphasized by a relatively insufficient tricuspid valve. The V wave is promptly terminated by the opening of the tri- Auricular Fibrillation M7 J':;: ilat Brachial 0.2 sei 1 d Figure 108 Auricular fibrillation with a very rapid ventricular response. From a case of general arteriosclerosis with high blood pressure. Jugular Brachial 0.2 second Figure 109 Auricular fibrillation with slow ventricular response. Xote absence of a wave, absence of depression x, unusual depth of v, small oscillations during diastole iff). 148 Auricular Fibrillation cuspid valve, and the discharge of blood under abnormal pres- sure in the auricle into the ventricle. An examination of the several polygraphic records indicates the variety in the form and time of the beginning of the v waves. As a general rule the cases <>i' auricular fibrillation of long standing with overdistended auri- cles and veins show a tendency for the r wave to become fused with the c wave, and the depression x may entirely disappear. The unusually deep depression y seen in Figure 109 indicates an unusual fall of pressure when on the opening of the tricuspid valves the contents of the distended auricle are poured into a re- laxed and dilated ventricle. Figure 108 illustrates the kind of curves often secured from the cases of auricular fibrillation with a very rapid ventricular response in old arteriosclerotic cases, the pressure changes in the brachial and radial arc often quite small, and it is difficult to obtain good arterial tracings. A slow ventricular rate is recorded in Figure 109. The brachial waves are well marked and extremely irregular at a rate of 60 per minute. In the jugular tracing there are seen during diastole some very small waves marked ff. These minute fluctuations in venous pressure are not infrequently obtained in auricular fibril- lation when the ventricular response is deliberate, they have been ascribed to the undulating auricular activity, but it is quite probable that they are due to vibrations induced in the vein by the pressure of the cup used as a receiver. Synchronous records of the apex beat and carotid are repro- duced in Figure 110. At X are seen weak ventricular contrac- tions, which are barely forceful enough to overcome aortic pres- sure, and presumably would be too weak to be detected in the radial. The electrocardiogram usually merely corroborates the evidence of auricular fibrillation obtained by the simpler methods of exam- ination, but in certain obscure cases the electrical records are essential to a correct diagnosis. We have seen cases that have been carefully studied by skilful clinicians in which the irregu- laris was mistakenly interpreted as due to auricular fibrillation, and under vigorous treatment the patients grew worse rather than better. The galvanometric records disclosed the fact that Auriculas Fibrillai eon '49 'VJVJVJvJSw^jH^JV-Jv. > ' * — — 1 \ K. Carotid ' X w^t E ■ ■ ' MB ■■' ' H 1919 131! IS h f\ J\ ! Apex X .x -J\J N — M \J LLUJjLL/UJJjULLLUJJ-AJjU^ 0.2 second Figure iio Auricular fibrillation. Apex and carotid tracings. At x the weak ventricular contrac- tions are barely able to open the aortic valves. 150 Aubiculab Fibrillation these "complete irregularities" were not caused by "auricular fibrillation," and a proper revision of the treatment resulted in immediate benefit to the patient. The distinctive features of the electrocardiagram of auricular fibrillation are : 1. Complete irregularity in the time intervals between the ventricular complexes. 2. An absence of the P wave. 3. A series of small waves which are continuous throughout the whole cardiac cycle. If one examines a number of electrocardiograms from cases of auricular fibrillation such as are shown in Figures III, 112, 117, etc., the first thing that arrests our attention is the unequal spacing of the ventricular complexes. Some show this in a greater degree than others, but an absolute rhythmieity is al- most* never seen. The parallelism between the irregularity of tbe ventricle and the arterial pulse is shown in Figure in in which simultaneous curves of the galvanometer and the pres- sures from a cuff placed on the brachial are recorded. If we study the ventricular complexes carefully we are led to the conclusion that they have a normal form save for some dis- tortion produced by the small waves of auricular activity which are present during the whole cardiac cycle, both systole and diastole. The ventricular complex may or may not be introduced by a Q deflection, both the ascending and descending limbs of the R wave are sharp and abrupt, 5" may or may not appear. T is usually present, the curve which is the result of the contrac- tion of the lower chamber has the same characters and is of the same duration as is found in the same heart when the rhythm is of the physiological type. The records shown in Figures 121 and 122 were taken from the same patient, Figure 121, in June, 1910, when the auricles were contracting efficiently. Figure 122 was taken 10 months later, when the auricles were in fibrillation. A comparison of the ventricular portions of the two records show a marked similarity, the R and T deflections are of the same order, and of the same duration. We must therefore conclude *An exception to this general statement is seen in cases of auricular fibril- lation complicated by an .1-1' Mock. See Chapter XV. Auricular Fibrillation 15* Brachial Figure hi Auricular fibrillation. Note the complete irregularity in both time and force of the brachial waves. The ventricular complexes of the electrocardiogram show the same irregu- larity, the P wave is absent, the small oscillations (ff) vary greatly in size and duration, but are present throughout the whole cardiac cycle. *Uwm n n n ****** Figure 112 Auricular fibrillation with rapid ventricular response. R varies in height according as it coincides with the summit of one of the small waves or a depression between two small waves. i;- Auricular FIBRILLATION that even when the auricles are in a state of fibrillation the ven- tricles receive their stimuli from a point above the bundle of His, and that the stimulus travels over the ventricle by a path that is normal in all respects. The ventricle responds to a supraven- tricular impulse. The second feature of importance in establishing the nature of the cardiac activity from a study of these records is the absence of the P wave, the normal representative of gross auricular con- traction. In certain records ( Figures 117, [23 and 127) one might at first glance question whether in some of the cycles a wave pre- ceding the R deflections was not in reality a P, but an examina- tion of a number of cycles will soon convince one that the incon- stancy in the size, contour and time relation to the beginning of ventricular activity, make it necessary to find another interpre- tation. In the electrocardiogram of the normal heart it may be re- called that in the period from T to P, the diastolic interval, there is a line without any suggestion of deflection. In the records now under discussion (Figures 1 1 1, 112, 113, etc.) this period is evi- dently occupied by a continuous series of uneven oscillations. These are the representatives of the rapid, irregular fibrillary activity of the auricles. Further examination will convince one that these small deflections are not limited to the diastolic pe- riod, but are continued during systole as well, so that the whole curve is modified by an unending series of these small fluctua- tions. It is for this reason that in many of the records the ven- tricular complexes seem to lie of abnormal form. They are merely distorted by the superimposition of these representatives of unceasing auricular activity. The T wave being relatively small is frequently very much changed in appearance. The R deflection when large is only slightly modified, but will fluctuate in height ( Figures 1 1 1 and 112) according as it is coincident with a summit of, or a depression between the small waves. The oscil- lations are usually arrhythmic, and vary in frequency. When the rate can be estimated it will be found to be between 400 and 600 per minute : they are usually most conspicuous in records taken by the second and third leads. The great variety in the rate, size and rhythm of the waves Auricular Fibrillai eon i53 0.2 second Figure 113 Auricular fibrillation with ventricular response which is almost rhythmic. The auricular oscillations are small, but distinct, constant and quite uniform in size. I S5- TV !§ •R 4/ 0.2 second Figure 114 Very large waves of auricular activity which distort the ventricular complex to a marked degree. 154 Auricular FIBRILLATION of fibrillary activity a^ shown in the electrocardiogram indicates great differences in the algebraic sum of the electrical poten- tials developed from moment to moment in the same auricle, and in different auricles. The oscillations may be small and fairly rhythmic throughout the whole record, as seen in Figure 113, or large and very arrhythmic (Figure 114). Some curves show a great variation from cycle to cycle (Figures 11 1 and ii_>), others small fluctuations which are inconspicuous but quite constant (Figures 115 and 125). One may at times be confused by small rapid oscillations due to tremor of the skeletal muscles, when during the recording period the extremities are held tense and unrelated, these fluctuations are very fine and much more rapid than the waves of auricular fibrillation. They may be seen in Figures 116, 117 and 118, taken from the same patient on successive days before, during and after a paroxysm of auricular fibrilla- tion. These muscular tremors are met with in patients under excitement who make a voluntary effort to hold themselves quiet. If the rapidity of the oscillations are noted they should not be confounded with the waves of auricular fibrillation which have a much slower period of vibration. In cases such as are shown in Figures 113, 114 and 115, the ar- rythmia of the ventricles is only moderate, and it is plain that palpation of the radial or auscultation of the heart might fail to reveal the "complete irregularity." The graphic records, how- ever, make clear the nature of the abnormal activity. The ven- tricle is seen to be definitely arrhythmic, P waves are absent, and the continuous series of oscillations, large or small, are seen during the whole cycle. In Figure 115 a simultaneous jugular curve has been recorded. In this may be noted the absence of the a waves, the c and v waves participating in the ventricular arrhythmia, and an absence of the depression x due to the early onset of the v wave, the fine oscillations ff are also apparent, but as has been pointed out in an earlier paragraph these are prob- ably not characteristic of the fibrillating auricle, but are due to a venous thrill induced by the pressure of the cup used as a receiver. Auricular Fibrillation 00 i y *i i 4£ T T r *«w^i»i T * *T . ; . ..-,.., ■ Jugular jfl Electro- cardiogram 0.2 second Figure 115 From a case of auricular fibrillation with a slow ventricular response. The form of the ventricular complex indicates that the stimulus which called it forth originated in the supraventricular tissues. P is absent. R and T are but slightly distorted by the super- imposed oscillations of auricular activity (ff). Upper curve obtained from the right jugular vein, a is absent, c and v have coalesced. 156 Auriculas Fibrillation CLINICAL FEATURES Practically all patient? with auricular fibrillation suffer from some degree of cardiac insufficiency. The functional disability of the heart may show a very wide range in different patients, and in the same patient at different times it may vary from a condition of almost complete heart failure to one in which there is ordinarily no evidence of an inability on the part of the heart to maintain an adequate circulation, and in which symptoms of insufficiency develop only under unusual stress. The degree of circulatory embarrassment depends in a very large measure on the integrity of the ventricular muscle. The valvular defect which so often has preceded the development of fibrillation has thrown upon the ventricles abnormal work, and perhaps injury which may, however, have been completely met by a compensa- tory hypertrophy. More often the underlying disease which has damaged both valves and auricular walls has also attacked the ventricles, leaving them an easy prey to the stress which the inception of the new rhythm imposes. If therefore the ventricu- lar myocardium is extensively damaged one may expect the rapid development of the classical symptoms of cardiac insufficiency, lowered arterial pressure, increased venous pressure, slow capil- lary flow, cedema, cyanosis, dyspnoea, congestion of the lungs, liver, kidneys, etc., etc. On the other hand with a reasonably healthy ventricular muscle the strain occasioned by the disorder in the upper chambers may be supported with comparatively little evidence of abnormal blood distribution. Fibrillation once established usually persists to the end of life, hence the term pulsus irregularis perpetuus, which was formerly used to describe the arterial features. However, one sees cases from time to time in which the normal pacemaker reasserts its control, and a physiological rhythm is regained. This has oc- curred in 6 per cent, of the cases which have come under my observation. Such a case is shown in Figures 116, 117 and 118, taken on successive days, April 19, 20 and 21, 191 1. The records of the 19th and 21st show a sequential rhythm, on the 20th (Fig- ure 117) the auricles were in fibrillation. Auriculas Fibrillation '57 p "P ^ T P Figure 116 The two following figures were obtained from the same patient on successive days. April ii), 191 1. The rhythm is sequential. The heart is rhythmic, the auricle has its normal activity, as indicated by the regular appearance of the P deflection. Figure 117 Same patient as Figures 116 and 118. Obtained April 20, 191 1. At this time the auricle was temporarily fibrillating. Note the similarity in the form of the ventricular com- pleves in these three records. In this curve P is absent, there is complete irregularity, the small deflections (ff) due to the fibrillating auricle are present. E=$3 ? m *-* - -i- i: ■■: : :. I : Tl : ~ Hi A \ J A I T^JkJ m -/*/ mS * L . ■ff* f*f| ^^ ■■ 1 J& *rV Y^r / ^^» Tl Figure 118 Obtained from the same patient as Figures 116 and 117, on April 21, 191 1. The auricle has resumed coordinated contractions and the rhythm is again sequential. In all three of Khe above records note the fine rapid oscillations which are due to a tremor of the skeletal muscles. 158 Auriculas Fibrillation Under ''paroxysmal tachycardia" reference was made to an un- usual form of paroxysm consisting of a short run of auricular fibrillation, with a rapid irregular ventricular response interrupting an ordinary sequential rhythm. Such a paroxysm is shown in Fig- ure 119. The earlier portion of the record shows a number of cycles during which the sinus node is evidently the pacemaker. The rhythm is broken at A by an auricular extrasystole ; this is followed by a normal cycle, then a bizarre curve which it is difficult to classify, but which may possibly represent an abnormal ventricular contraction and two ectopic auricular contractions; these, in turn, are succeeded by a short period of auricular fibrillation with a rapid irregular ventricular response. The paroxysm of fibrillation lasted for about a minute and the sequential rhythm, broken by occasional auricular extrasystoles, reappeared. Patients showing this condition are very few in number, and in my experience it is very unusual to secure the graphic evidence of the transition from the sequential rhythm to the paroxysm of auricular fibrilla- tion. This curve was obtained from a patient seen in consultation bv Professor Longcope and was recorded by my assistant, Dr. Strong. These paroxysms may appear over a period of many years. A case reported by Cushny and Edmunds had attacks for twenty wars. Robinson* has reported careful studies in a case which had probably suffered from attacks for twelve years. The transitory character of the paroxysms has been somewhat difficult to explain. A number of patients in whom 1 have ob- served this phenomenon were suffering from lobar pneumonia ; here it is quite likely that the toxins of the disease had a direct action on the muscle cell. It has been observed in hearts which showed no other clinical evidence of a pathological lesion. Macken- zie! nas suggested that digitalis may be a possible factor in caus- ing the auricular fibrillation. Robinson has advanced the hypoth- esis that in certain cases the paroxysm may be due to an altera- tion in the blood supply to the auricular musculature. He also reports a casef which was directly attributed to poisoning with hydrogen sulphid. *Arch. Int. Med., 1914, xiii, 208. tHeart, 1910-1 1, ii, 295. n* m H! ft to 1 59 U 2 - 160 Auricular Fibrillation The patient is not necessarily conscious of the irregular heart action. At times they apply for examination <>n account of the sensation vi "fluttering" or "thumping" in the precordial region or complain of "palpitation." More frequently dyspnoea or oedema are the symptoms which bring them to the physician, and the erratic and tumultuous heart activity has passed unnoticed. Very few of them complain of anginal pains, but tenderness in the precordial region is a symptom frequently elicited during the ex- amination with the ringer, or the bell of the stethoscope. In cases which have been watched over a long period, one will often see the following series of events: (i) Several attacks of rheumatic fever with arthritis and endocarditis, most frequently involving the mitral valve. (2) Later extrasystoles, often auricular in origin. (3) The heart becomes gradually dilated under physical stress, and the auri- cles begin to fibrillate, and usually continue this activity up to the time of death, which may be postponed for many years. Such a sequence of events is shown in Figures 121, 122 and 123. The patient, a man of 50, had a sharp attack of rheumatic fever, followed by endocarditis, when he was 20 years of age. At that time he was seen by Dr. E. G. Janeway, who told him he had a mitral stenosis. I first saw him in 1909, when he became conscious of an irregularity of the heart. At that time the rhythm was se- quential, but he had occasional extrasystoles, which were verified by polygraphic tracings. On June 7, 1910, the curve shown in Figure 121 was obtained. It shows an extrasystole of auricular origin, and a split P wave. During an attack of pneumonia, in February, 191 1, his auricles began to fibrillate. Figure 122 was obtained on April 28, 191 1, and Figure 123 secured April 9, 191 5. This has continued up to the present time (July, 1916). He is now in excellent health, and is able to conduct a business involving large responsibility, but slight physical exertion. The rate of the heart beat in auricular fibrillation is extremely variable. One sees cases in which the rate does not exceed 40 a minute, and others which exceed 200. Under appropriate treatment it is not unusual to see a rate of 140 reduced to 100 in a very short time. tJour. Amer. Med. Assn., 1916, lxvi, 161 1. Auriculae Fibrillation JaJjI/ J&* — -J^^J^ c&ai FlGUKE 121 Patient B. S., June 7, [910. The auricle is contracting as a whole. P is broad and split. Kxtrasystule of auricular origin at x. Note fine tremor of skeletal muscles. Figure 122 Patient B. S., April 28, 191 1. The auricles are now fibrillating, the rhythm is rapid and very irregular. Figure 123 Patient B. S., April 9, 191 5. Figures ui, 122 and 123 are all from the same subject. The auricles are still fibrillating, but "the ventricular response is much less rapid and more evenly spaced. [62 Auriculas Fibrillation The palpation of the radial pulse is a very insufficient criterion of the condition of the circulation. While the palpation of the pulse alone may be sufficient to establish a diagnosis, and while by this method one immediately delects the complete irregularity in force and frequency which characterize this group, the count of the radial pulse may be misleading. Frequently the number of the impulses which can be counted at the wrist is far below the actual number of cardiac contractions. Only those waves which are of considerable volume and force can be felt at the wrist (see Figure 125), and many small ventricular contractions expend their force before reaching the radial, and some even fail to open the aortic valves. These small contractions are ineffectual in maintaining an adequate circu- lation, yet are exhausting to the heart muscle, for we know that, in accordance with the law discovered by Bowditch, every contraction of heart muscle is maximal, that is to say, if it contracts at all, it ex- hausts all of the energy stored as contractile material in its muscle fibers at any particular moment ; hence it is evident that however small a contraction may be, it must be taken into consideration in estimating the gravity of the condition of any particular heart. The inadequacy of the observations on the radial pulse alone is well illustrated in Figure 124. Here the lower margin of the shaded area indicates the radial count. If one were guided by this alone, one would have said that on admission the cardiac rate was under 70 and never above 100. The upper boundary of the shaded area is the count taken by auscultation at the apex, and represents much more accurately the true condition, the admission rate being 127; the gradual reduction to the neighborhood of 60 makes the real im- provement apparent. The term "pulsus deficiens" has for a long time been used in describing pulse phenomena (Traube, Hering, Wenckebach, etc.), but each author has used it with a different meaning ; some have considered it synonymous with "pulsus intermittens," others have applied it to an absence of ventricular contraction, wdiich breaks the ordinary rhythm ; it has been used in describing extrasystoles and pulse alternans. By "pulse deficit" we mean the difference between the number of cardiac contractions and the number of impulses which can be palpated in the radial artery. The best way of determining the pulse Auricular Fibrillation i6 3 1 01). 130 120 110 100 00 80 70 60 104 * 103 102. 10f- 100 i is I is ii it in u ii A J n. :!::: I ^MF^ft. ■ 1 ^^^> IP ^ Vfe, 98° I Hr :"fff thiJ«V— _oz! ::::::::::::::::::::::::::::::: :^ :__ oir.iT ALI9 INFUSION 4 6 6 C 6 G Figure 124 The shaded area represents the pulse deficit; the upper edge is the apex rate; the lower edge is the radial rate. Figures in digitalis column indicate dosage of the infusion in drams per twenty-four hours. Patient in bed during period represented in the figure. Rrachial Figure 125 Auricular fibrillation. Simultaneous records of the cardiogram and the brachial pulse. Showing the mechanism of the "pulse deficit." Every other heart beat has little or no effect in raising the pressure i.i the brachial artery. 164 auricular Fibrillation deficit is to have the apex counted by auscultation by one observer, while another is simultaneously counting the radial (these observa- tions must cover a period of not less than a full minute, on account of the extreme irregularity of the pulse in many of these cases a count of one-quarter or one-half minute only is much less accurate). When one is obliged to make these observations unaided, the apex and the radial counts may be made in successive minutes. This of course does not give an absolutely accurate deficit, but it is extraor- dinary how closely the counts of successive minutes will coincide even when the heart and radial show the most extreme degrees of irregularity. After a little practice one may be able simultaneously to auscultate the apex and palpate the radial, thus determining the number of beats which fail to reach the wrist in the period of a minute. In Figures 124 and 126 the upper margin of the shaded area represents the apex count, the lower margin the radial count, and the width of the shaded area represents the deficit at any particular point in the curve. The relative deficit. In many cases of auricular fibrillation, par- ticularly where improvement has occurred and the heart has become less irregular, slow, and fairly compensated, it will be found that the count at the apex and the radial are identical. Even in these c^-js the individual waves show a considerable variation in force and size. This is brought more clearly to view if the cuff of a blood- pressure apparatus is placed on the arm and the radial is counted while varying degrees of pressure are applied through the cuff. This difference in the pressure values of successive waves we have termed the "relative deficit," as contrasted with the absolute deficit, when without brachial pressure some waves fail to reach the radial. The following observation will serve to illustrate this point : The patient was a gentleman who had fibrillating auricles for something over two years, with at times an apex rate of 160 and an absolute deficit of over 50. Later his heart was fairly compensated, and he was able to supervise large business interests which required a daily attendance at his office of six to eight hours. When we last saw him Auriculae Fibrillai ion 16s tta_ iihsaf .d .;!:::;::!! ii:!::!;sii!;;ii....;;i..i .DIGITALIS' S 3 BL. P. SY3.1C0 ICO L^i :3 ICO 102 j ISO I : ] i/ii * .* I Figure 126 The shaded area represents the pulse deficit: the upper edge is the apex rate, the lower edge the radial rate. The hroken line indicates the "average systolic blood-pressure" (compare these values with the figures at the bottom of the chart, which show the systolic blood pressure determined by the usual method). Figures in digitalis column indicate drams of the infusion per twenty-four hours. if/. Auricular Fibrillation his apex rate was 64, radial rate 64, deficit o. On applying the brachial cut! the following counts were obtained : Brachial pressure Radial count per minute 140 nun. Ilg. 130 nun. 50 120 mm. 58 no nun. 62 IOO nun. 64 While he had no absolute deficit, his relative deficit was quite evi- dent when the pressure values of the waves of one minute were thus studied. This relative deficit may be detected in all cases of auricu- lar fibrillation ; it is rarely seen in other cardiac arrhythmias. We have found that such observations on the relative deficit are of real diagnostic value in corroborating a condition of auricular fibrilla- tion which palpation and auscultation have led us to suspect. The usual way of estimating blood pressure is entirely fallacious in auricular fibrillation. The accustomed method of obliterating the brachial artery by cuff-pressure and then by gradually lowering the pressure to determine the systolic blood-pressure by the height of the mercury column at which the pulse wave below the cuff is de- tected by palpation or auscultation is obviously of little value when practically each pulse wave has a different pressure value. If such a pulse is observed for a period of a minute it will be found that only a small fraction of the total number of cardiac con- tractions have a pressure value, approximating the systolic blood- pressure as determined by this method. Figure 126 illustrates the inaccuracy of this method in these cases. Systolic blood-pressure taken by the usual method would signify that the successive blood- pressures of this patient were 165, 160, 160, 162, 156, 155, 148, etc., and that as her condition improved the blood-pressure was lowered. As a matter of fact, only a few beats could be detected below the cuff when exerting a pressure at these levels, and while doubtless her systolic blood-pressure was momentarily at these levels, they in no way indicate the efficient pressure of the blood column. As we shall show later, her systolic blood-pressure really increased with the improvement in her condition. A much more valuable estimate of the force of the blood-slream Auricular Fibrillation 167 can be obtained by estimating the blood-pressure by another method ; the average systolic blood-pressure. To obtain what for convenience we have termed "the average systolic blood-pressure," the apex and radial are counted for one minute, then a blood-pressure cuff is applied to the arm, and the pressure raised until the radial pulse is completely obliterated; the pressure is then lowered 10 mm., and held at this point for one min- ute, while the radial pulse is counted; the pressure is again lowered 10 mm., and a second radial count is made ; this count is repeated at intervals of 10 mm. lowered pressure until the cuff-pressure is in- sufficient to cut off any of the radial waves (between each estima- tion the pressure on the arm should be lowered to zero). From the figures thus obtained the average systolic blood-pressure is calcu- lated by multiplying the number of radial beats by the pressures under which they came through, adding together these products and dividing their sum by the number of apex-beats per minute, the resulting figure is what we have called the "average systolic blood-pressure." The following two observations made on a pa- tient will indicate the method of computation : B.S., April 29, 1910. Apex, 131 ; radial, 101 ; deficit, 30. Radial count, o 13 I3X90="70 47— 13 = 34 X 80 = 2720 75 — 47 = 28 X 70=1960 82 — 75= 7X6o= 420 101 — 82 = 19 x 50 = 950 Apex= 131 )7220 Average systolic blood-pressure 55 plus Apex, 79 ; radial, 72 ; deficit, 7. Radial count, o 44 44 x 110 = 4840 64 — 44 = 20 x IO ° = 2 °oo 72 — 64 = 8 x 9° = 7 2 ° Apex =79)7560 Average systolic blood-pressure 95 plus Brachial pressure. 100 mm. Hg. 90 mm. 80 mm. 70 mm. 60 mm. 50 mm. B.S., May 11, 1910. Brachial pressure. 120 mm. Hg. no mm. 100 mm. 90 mm. ids Auricular Fibrillation The estimation of blood-pressure by this method gives us a sim- ple and approximate measure of this factor of the heart's work. The diastolic pressure may be roughly determined by taking a graphic record with the Erlanger or Uskoft" instruments and noting the pressure at which the average excursion of the pulse waves is maximal. Examined by this method, the two groups, rheumatic and arterio- sclerotic, show very different features. In the rheumatic-mitral stenosis group, one not infrequently sees an average systolic blood-pressure under 70 mm. of mercury ; these are usually cases with rapid rates (over 140) and a marked degree of cardiac insufficiency. With improvement the blood-pressure rises and may reach 120 mm., rarely 140. In the arteriosclerotic group with fair compensation the average systolic blood-pressure is usually 160 mm. or over, and only falls below this when insufficiency becomes evident ; in this group when the pressure, estimated in the above manner, falls below 140 mm. myocardial failure is very threatening. The irregular activity of the ventricle is unquestionably the re- sult of the peculiar activity of the auricles; while the upper cham- bers exhibit no gross contractions their walls show an incessant activity composed of irregular incoordinated contractions of the muscle fibers ; impulses from the auricles are showered upon the junctional tissues in an entirely haphazard fashion, and the ventri- cles respond in utter confusion devoid of rhythm, and with extreme variation in the force of the succession beats. In certain cases the junctional tissues between auricles and ven- tricles is somewhat damaged so that conduction between the cham- bers is depressed and fewer auricular impulses can reach the ven- tricles (Figure 113) ; under these conditions the ventricular rate is not excessive, and the contractions show more uniformity in force. Here one is impressed with the small amount of disability which results from the fibrillating auricle ; it is little more than a venous reservoir, and takes little part in moving the blood, and if the ir- regular impulses which are initiated in its wall do not disturb the ventricle too greatly, the circulation is maintained with a reasonable degree of efficiency. The fibrillary activity may be continued for years, and in itself is not at all incompatible with life or a proper distribution of the blood to the various organs. Auriculae Fibrillai con \< ,< , Figure 127 Auricular fibrillation. Fatient C. F. Heart very rapid and irregular (see Figure 128). Figure 128 Auricular fibrillation, patient C. F., taken one week after Figure 127. The auricles are still fibrillating, but the heart has become slow under appropriate treatment. This is a favorable response to therapeutic measures, hence in this case the prognosis is good. i7o Auriculas Fibrillation PROfiNO>TS This depends largely on two factors; first the integrity of the ventricular muscle, and second the facility with which the shower of impulses coming from the auricle can he blocked. With a weak, dilated ventricle showing irritability as evidenced by frequent ven- tricular extrasystoles arising from points in the ventricular tissue other than the A-V bundle, the outlook is bad, and yet under skill- ful treatment and favorable conditions, such a heart may occasion- ally recover a considerable degree of efficiency, and life may be prolonged several years. Mere dilatation of the ventricle if other- wise healthy need cause us much less concern if careful treatment is instituted soon after the beginning of the complete irregularity; but the longer the period between the onset of fibrillation and the employment of correct therapeutic measures, the more difficult is it to restore the damaged ventricle. In the majority of instances digi- talis will effectually block the erratic auricular impulses, and give the ventricle the lengthened diastolic period so necessary for its recuperation. In a few cases digitalis either cannot be taken in sufficient amounts, or fails to obstruct the stimuli from the upper chamber. In these the immediate prospect is exceedingly alarming. The degree of the response of the heart to treatment (see Figures 127 and 128), and the amount of reserve force which can be secured for it, are our best indications of what the future holds in store. Many of these hearts may be brought to a fair degree of efficiency, but the reserve force is never very great, and neglect of treatment, or over-exertion will almost invariably entail an attack of cardiac insufficiency. Each insult of this kind is met with greater difficulty and with each attack the outlook becomes more grave. Auricular fibrillation indicates a very serious myocardial defect; heart failure may be postponed for many years, but the majority succumb within ten years of its onset. The signs which point to a favorable prognosis are : — 1. The resumption of a physiological rhythm. 2. The maintenance of a rate under 70. 3. The absence of a pulse deficit. 4. The absence of extrasystoles. 5. An average systolic blood-pressure of over no in the rheu- matic group, and of over 160 in the arteriosclerotic group. Auricular Fibrillation 171 The symptoms which make the outlook grave are : — 1. A ventricular rate remaining for more than a few days above 130. 2. A persistent pulse deficit of 20 or over. 3. The occurrence of frequent ventricular extrasystoles. 4. A falling average systolic blood-pressure. 5. A ventricular rate which shows wide fluctuations under slight physical or emotional stress. The gravity of a given case is often indicated by the amount of treatment requisite to secure a slow ventricular rate without a pulse deficit ; some cases require very little treatment, and in these the immediate prognosis is good ; others yield only to the most active therapeutic measures applied over a very long period. In such the danger is about proportional to the therapeutic measures found necessary. VENTRICULAR FIBRILLATION Ventricular fibrillation has been recognized as a terminal event in experiments on animals. When an extreme degree of ventricular irritability is produced by faradization of the ventricle (Levy) or by cutting off its blood supply* the coordinated contractions cease. These are succeeded by ineffectual twitching of the muscle wall and finally by diastolic relaxation with fine undulatory movements of the surface, and in a few seconds the animal is dead. The con- dition has also been experimentally produced by introducing a bubble of air into the coronary artery. f In these observations the ani- mals occasionally recovered. In man, ventricular fibrillation, unless of only momentary dura- tion, is incompatible with life. Hoffmann| has reported, with elec- trocardiographic records, a condition which he interpreted as a period of ventricular fibrillation occurring at the end of a paroxysm of tachycardia ; the patient ultimately recovered. As far as I know, this is the only instance in which it has been suggested that such an outcome is possible, and it is not altogether clear that Hoff- *Lewis : Mechanism of the Heart Beat, London, 1911, p. 160. fAlorat and Petzetakis : Compt. rend. Soc. de Biol., 1914. lxxvii, 222, 377. JHoffmann: Heart, 1911-12, iii, 213. i7- Ventricular Fibrillation matin's records may not be interpreted a? a series of ventricular extrasystoles arising from several points of origin. Ventricular fibrillation, as a terminal event, has been studied by Robinson* and by 1 talsey.f It seeems not at all improbable, as McWilliams:;: suggested, that in a certain number of cardiac cases Midden death may be due t<> the abrupt onset of ventricular fibrillation. Levy§ has shown that the administration of low percentages of chloroform, by inhalation to animals, produces a high degree of ventricular irritability. Under this condition small reflex sensory stimulation or the struggling of the animal is sufficient to induce ventricular fibrillation and sudden death. If adrenalin was given intravenously to an animal under light of chloroform anaesthesia, ventricular fibrillation at once ensued. Levy believes that the cause of chloroform death in man is the onset of ventricular fibrillation and has collected from the reports of sudden death under chloroform a number of cases which strongly support his view. The period of danger is at the time the patient is getting very little chloroform, at the beginning of its administration or when it is given intermittently. To avoid this danger, all nervous ex- citement for the patient must be excluded. No manipulations must be attempted until he is well under the anaesthesia. The chloro- form must be given continuously and in considerable amounts. Adrenalin should not be used in conjunction with chloroform. ♦Jour. Exp. Med., 1912, xvi, 291. ^Tleart : 1915, vi, 67. tBrit Med. Jour., 1889, i, 6. §Heart, 1912-13, iv, 319. CflAITKK XI f Auricular Flutter, Tachycardia and Fibrillation These forms of arrhythmia have been discussed in separate chap- ters, but it may not be amiss to say a few words about their close association and to examine the slight modifications in mech- anism which may lead to the transition of one into another. In 1887, McWilliams,* in investigating the activities of the dog's heart under different experimental conditions, called attention to the variation in the nature of the response of the auricles to faradic currents of greater and less intensities. lie found that (i) when he stimulated the auricular tissues with a weak faradic current the auricles contracted at a very rapid rate in perfect rhythm. If, however, the strength of the stimulating current was increased, (2) the auricles ceased to contract as a whole, the walls relaxed and assumed the diastolic position, but the muscle movements did not stop ; the whole surface of the auricles took on an undulatory, incoordinated activity with irregular twitching, but with no actual systole of the upper chamber. Finally, (3) when stimu- lating current was withdrawn, the auricles resumed their accustomed deliberate coordinated contractions. In the first instance, the ven- tricles responded rhythmically, in response to each auricular con- traction or more often to every other auricular impulse. Under the conditions of the second stage of the experiment, the ven- tricles responded in a haphazard fashion with complete irregularity. Finally, when the auricles recovered their accustomed activity, the ventricles responded in a normal manner. Since these earlier observations, these different activities have been elaborately studied and are now recognized as "auricular flutter," "paroxysmal auricular tachycardia" and "auricular fibril- lation." McWilliams' observations have been verified by a num- ber of other investigators. Hirschfelderf was able to produce at will "auricular tachycardia" or "auricular fibrillation," according to the strength of the faradizing current. The same phenomena *Jour. Physiol., 1887, viii, 296. fBull. Johns Hopkins Hosp., 1908, xix, 2 22 - 173 174 Auriculas Flutter, Tachycardia and Fibrillation were observed by Robinson,* who found, further, that if the right vagus was stimulated during a period of experimental tachycardia there was a transition to auricular fibrillation, while stimulation of the left vagus did not inhibit the auricular tachycardia, but blocked a portion of these impulses so that the ventricle failed to respond to every auricular contraction, lie helieves that in the experi- FlGURE 129 Figure 130 mental animal faradization of the auricles produces a mixed effect which is a comhination of "flutter" and "fibrillation." If one examines a number of electrocardiograms taken from a series of patients with complete irregularity, one is at once impressed with the great variety in the size and the rhythmicity of the waves representing the auricular activity In one they are so small as to be almost imperceptible and show no tendency to rhythmicity; *Jour. Exp. Med., 1913, xviii, 704. Auricular Flutter, Tachycardia and Fibrillation 175 Figure 131 f r^ FFf=^ HSBE prr prrr m i' n=rr P^T— pzr CT= , ' .'i , ' ■ ; . 'in r -_ — ^ft ±rrr #3= ■ 'i ^E r— -f- ■ 1 "~~j ^zj IS i^j^Ji 1 i ' : ■■! I i : ■ -: . 'i Figure 132 Figure 133 Figures 129-133. — Records from five different cases of complete irregularity. Arranged to show gradations in the size and rhythmicity of the undulations representing auricular activity and the ventricular response. i7'' Auricular Flutter, Tachycardia and Fibrillation in another these wave? may he very large and reenr at quite defi- nite intervals. A series of records of this kind is shown in Figures l-'o, 130, 131, [32 and [33. They have been arranged to show the grada- tions that are seen in a collection of such curves. They vary from small irregular deflections to those of considerable size and degree oi rhythmicity. < me may say that, as a rule, as the auricu- lar waves increase in size, the tendency is for them to become rhyth- mic, and also for the ventricle to respond to the auricular impulses at more regular intervals. When one examines the fust record ( Figure 129) of this series, it conforms quite definitely to our conception of the classical pic- ture of auricular fibrillation with the minute, very irregular fibril- lary manifestations and the complete irregularity in ventricular response. In the last record of the series (Figure 133) the undulatory waves are very much larger and quite rhythmic. The ventricular response is irregular, but not more so than might be seen in a case of "auricular flutter" with a block of varying degree. An inspection of the intervening records show gradations which sug- gest that, under various pathological conditions which are not under- stood, and at present cannot be differentiated, there may be all grades of auricular activity, such as the incoordinated contraction of individual muscle fibers, contractions in which a group of fibers are coordinated and contractions resulting from a coordinated ac- tivity of the entire musculature. The close relationship of "auricular flutter" and "auricular fibril- lation" may be further inferred from the ease with which, in the individual patient, the activity may change from one form to the other. Instances of this transition have been illustrated in the chapter on "auricular flutter" (Figures 92, 93, 96, 97 and 98). It has been suggested that in "auricular flutter" the auricular contractions arise not from the normal pacemaker, the sinus node, but from some point of abnormal irritability in the auricular wall ; in other words, that they are true auricular extrasystoles. If such is the case, it would bring our ideas of the mechanisms of "auric- ular flutter" and "auricular tachycardia" into a very close relation- ship. Such a conception is borne out by a study of the records Auricular Flutter, Tachycardia and Fibrillation 177 p p p p p ^.^■A^&flSMMlMlrif&f&ftf*! Figure 134 Record of T. K. showing transition from complete irregularity Cauricular fibrillation) to rhythmic auricular flutter with a 2 to 1 ventricular response fl's= 120, As = 340; and the return to ci mplete irregularity. Figure 135 Record of T. K. taken a few minutes after Figure 134, showing rhythmic tachycardia (Vs = 240). The ventricle responds to each auricular impulse. Figure 136 Transition from auricular flutter with irregular response to rhythmic tachycardia [I s = 1S0.) 178 Auriculas Flutter, Tachycardia and Fibrillation (Figures T34, F35 and 13; I from a patient who was under obser- vation For a period of less than two hours, during which these curves and a number of others were secured. The beginning and the end of the electrocardiogram (Figure 134) ran lie interpreted as auricular fibrillation. In the center of this record there is a rhythmic period during which there appears an auricular flutter, with a ventricular response, to every other auricular impulse. A few minutes later this passed into a period of rhythmic auricular tachycardia (Figure 135). during which the ventricular rate is jusl double the rate of the rhythmic period of Figure 134. It seems evident that the auricle is still in flutter and that now the ven- tricle is responding to each auricular contraction. Figure [37 is a polygraph secured from the same patient a few minutes later and shows the transition from a period of flutter, with, irregular ventricular response, to one of rhythmic tachycardia. The electrocardiogram of another patient showing a transition from an auricular flutter, with an irregular ventricular response, to a typical paroxysm of auricular tachycardia, terminating again in auricular flutter, is presented in Figure [36. This patient was under observation for many weeks and her heart recovered a nor- mal rhythm. During none of this time was it possible to obtain any conclusive evidence of auricular fibrillation. Such observations suggest that there is a very close relationship between these types of abnormal auricular activity. Auricular Flutter, Tachycardia and Fibrillation 179 Jugular Brachial o.z second Figure 137 Polygraph of T. K. taken immediately after Figures 134 and 135, showing transition from auricular flutter with irregular response to rhythmic tachycardia. CHAPTER XU1 Alternation The palpation of the arterial pulse often presents to the clinician a series of waves which alternately vary in size. The waves recur with perfect rhythmicity for considerable periods. There is a large wave, then a small wave, another large wave Eollowed by a small wave, and so on for hours or days. This condition is known as alternation of the pulse. The term alternation is not confined to this pulse phenomenon, but is also used to designate a similar al- ternating activity of the heart and of the jugular veins. The term alternation requires further definition than the mere statement that large and small pulse waves follow one another. Alternation should he reserved for that activity of the heart in which forcihle and weak contractions succeed one another rhyth- mically, and in which the interval between the large and small beats is equal to or greater than the interval between the small and the large beats. It is to he distinguished from the pulsus bigeminus, in which every other cardiac contraction is an extra- systole, and also from the pseudo-alternans detected in both veins and arteries, which is directly dependent on respiratory movements. EXPERIMENTAL PRODUCTION AND MECHANISM Alternation has been studied extensively in both cold- and warm- blooded animals. In the course of experimental studies of various kinds, it occurs spontaneously and has also been produced by utiliz- ing various poisonous substances. It has been seen in the isolated and perfused heart and in the heart exposed by removing a por- tion of the chest wall. In the suspended heart, it has been pro- voked by withdrawing the supply of Ringer's or Locke's solution, by the substitution of carbon dioxid for the oxygen, by the intro- duction of hemolytic serum, etc., etc. This activity has been in- duced in the heart in situ by the introduction of digitalis and aconi- tine (Cushny) and antiarin (Straub) and glyoxylic acid (Ilerirg, Rihl, Kahn and others). Alternation may appear during the ap- 180 Alternation i Hi plication of electrical stimulation to the myocardium rind while the extracardial nerves arc being manipulated. The difference in the successive waves may be in their contour, rather than their size. Their dissimilarity is practically alv. demonstrable by a time pressure curve, but the electrocardiogram furnishes evidence of alternation only on very infrequent occa- sions. When this is present, it consists in an alternating height of the R wave, more rarely in a change in the elevation of the / wave. The mechanism of alternation is still a matter of considerable speculation. The majority of investigators ascrihe this abnormal function to a defect in the contractility of the heart. It has been supposed that under pathological conditions different muscular fibers have different refractory periods, so that at one time all the fibers are active, at another only a portion take part in the contraction (Wenckebach, Mines). A view that has received con- siderable support is that the cardiac fibers differ in their excitability and, hence, respond to stimuli at uneven intervals (Gaskell, Kron- ecker). The abnormal activity has also been thought to be de- pendent on a defect in conductivity (Engelmann, Muskens). It is clear that as yet the evidence is not conclusive in regard to the fundamental properties of cardiac tissues which are at fault in the production of this irregularity. On clinical grounds, it seems to me that in alternation we are dealing with a phenomenon which may be produced by a defect of contractility at one time and at another time by a defect of conductivity. I believe that further study will permit us to segregate our cases of alternans into groups, each of which may be shown to be due to a different defect. A presentation of the various theories of alternation and a crit- ical review have been published by Gravier* in a recent thesis. PATHOLOGY There are reported in the literature about twenty autopsies in subjects in whom alternation of the heart has been a prominent feature and in whom this arrhythmia has been verified by graphic methods. Some of these reports are not at all complete; others give in considerable detail the histological findings obtained from *L'Alternance du coeur, Paris, 1914. 1 82 Alternation a very exhaustive Study of the cardiac muscle. Practically all of the hearts thus examined have presented anatomical lesions of greater or less extent. 'There is usually an hypertrophy, particu- larly of the left ventricle, with some degree of degeneration of the muscle fibers ^h\^ to a perivascular sclerosis. These lesions are, as a ride, quite extensive and are not limited to any special part of the cardiac tissues. In some, the lesions have involved portions of the conduction system, but this finding is not at all constant. We may conclude that, as yet, we have no evidence which permits us to assign this functional disturbance to a special anatomical lesion. The ease with which alternation may he provoked in the normal cardiac tissue of experimental animals by the administration <>i toxic substances, such as aconitine, digitalis, glyoxylic acid, stro- phanthin, veratrin, etc., has suggested that this functional abnor- mality may be the result of a cell intoxication. Digitalis must al- ways be thought of as a possible factor, but one frequently sees alternation in patients who have never had this drug. Hering has described alternation in a man poisoned with strychnine. As alter- nation is not an uncommon accompaniment of advanced nephritis, it has been suggested that it is a manifestation of uremic poisoning. The remarkable properties of glyoxylic acid in producing alter- nation experimentally, and the fact that this acid may be a product of abnormal metabolism, gives us a hint of another possible source of an auto-intoxicant. ETIOLOGY Our ideas of the frequency of the occurrence of the various arrhythmias of the heart is changing very greatly. The routine painstaking examination of large numbers of patients has demon- strated that irregularities which were once believed to be very exceptional are in reality not uncommon. This, for example, has been our experience with "auricular flutter." At one time this was regarded as a very unique finding ; today it is not unusual to have more than one such case always under observation. A similar transition has occurred in our notions of the frequency of alter- nation. Xot long ago it was thought to be rather a rare symp- tom ; to-day, according to the statistics of some observers, it ranks Alternation i Hr.v hial 0.2 second Figure 138 Alternation in brachial and jugular. Note variation in amplitude of a waves. Taken from same case as Figure 139, only a few minutes separate the two records. ^ V J'<'\J a Mttk-JX— _rfWL_L J^JLti rfMn t\ ttk tk ^JK^k^ -AA. ^ 6.2 stcondi , *■ :.. Jujju!ar Figure 139 Jugular and electrocardiogram taken simultaneously. By palpation the radial was alternating at this time. There is no evidence of alternation in the electrocardiogram. Same case as Figure 138. 1S4 Alternation in frequency only second to the extrasystole. In a recent study of three hundred cardiac cases. White,* during a period of eight months, discovered no less than seventy-one cases of .alternation, lie found this irregularity in thirty-three per cent, of all the cases showing any degree of cardiac decompensation in which he se- cured graphic records. Alternation is more frequent in the old than in the young, but has been observed in all ages from fifteen to seventy-five years. It is a common manifestation in myocarditis with hypertension. In my own experience it has most often been seen in cases of chronic nephritis or general arteriosclerosis, which have recently been admitted to the hospital wards. Alternation is rather uncommon in the course of the acute in- fections, but it has been noted in pneumonia, diphtheria, typhoid fever and rheumatism. It is seen in cases of chronic valvular dis- ease and pericarditis which are of rheumatic origin. Alternation has been observed in acute dilatation ( Mackenzie) in a case showing myocardial infarcts (Gallavardin) and in strych- nin poisoning (Hering). White obtained a positive Wassermann reaction in fifteen per cent, of his cases, and a history of overindulgence in alcohol, tobacco and tea was notable. In an analysis of forty-five cases of alternation, Windlef observed that the associated conditions presented the following order of frequency: (i) Arterial and myo- cardial disease; (2) chronic heart disease due to rheumatism; (3) pneumonia, and (4) acute rheumatic carditis. In a considerable number of patients showing alternans, this is by no means the only evidence of myocardial defect. In asso- ciation are found many other types of cardiac arrhythmia. A lat- ent alternation often becomes evident when the heart rate is accel- erated, hence alternation is a very common accompaniment of very rapid hearts, particularly those showing paroxysmal tachycardia (Figures 140, 150 and 151). Many also present signs of imper- fect conduction. Alternation is quite common in cases of "auric- ular flutter" (see Figure [46) and this is not surprising when we recall that in the latter condition conduction defects and tachy- ♦Amer. Jour. Med. Sc, 1915, cl, 82. ■rQiiart. Jour. Med., 1912, vi, 453. Alternation Jugular Apex Radial 0.2 second Figure 140 Alternation of apex, radial and jugular. Tachycardia rate 200. i86 Alternation cardia are very often in evidence. The association of extrasystoles is a Frequent finding and an alternation which may have been quite unnoticed may become very pronounced in the cycles immediately following an extrasystole. This is so common that it has been given a special name, the "post-extrasystolic alternans." It seems to me that the evidence is very suggestive that in cer- tain cases of alternans the exciting cause of this irregularity is really a lack of proper nutrition of the myocardial calls. Under conditions of stress, the tissues have too little oxygen or there is an accumulation of CO a or possibly other toxins which may be the intermediary products of abnormal metabolism. [DENTIFICATK IN The more pronounced types of alternation may be detected by palpation of one of the peripheral arteries. This is naturally more easily accomplished when the large and small arterial waves show a considerable difference in the systolic blood pressures. This dif- ference usually does not exceed ten millimeters of mercury, but occasionally may be as much as twenty millimeters (Rihl). With the smaller variations in pressure this important type of irregularity often passes unobserved, but if one is constantly on the outlook for it in cases in which it may be suspected, such as nephritics, general arteriosclerotics, etc., it will be discovered with consid- erable frequency. There are several simple means which may aid in the detection. Palpation of the pulse should always be made with the tips of several fingers, not with one ringer alone, and while one is making the observation the pressure exerted on the arterial wall should be changed, as this often accentuates the dif- ferences in the size of the waves. A latent alternans may fre- quently be made more evident by partly occluding the artery above the palpating fingers. This may be accomplished by exerting pres- sure on the brachial artery by means of the cuff of a sphygmonan- ometer or by digital pressure of the axillary artery (Gallavardin and Gravier). The pressure thus applied should be varied in amounts, as it is difficult to predict in advance what degree of pressure will best accentuate the pulse differences. A little exertion to in- crease the rate of the heart may be of service in rendering the alternation more evident. Ar.TKKNATION 187 Figure 141 Radial tracing showing alternation and probably one extrasystole. Figure 142 Radial tracing showing alternation. While this record was being taken a pressure of 85 mm.Hg. was applied to the brachial artery through a sphygmomanometer cuff in order to bring out the differences in amplitude of the successive waves. i88 Alternation In palpation the attention must be directed not only to the varia- tion in amplitude of the successive waves, but also to their spacing; if the impression is obtained that the interval between the small and succeeding large wave is greater than the interval between the large wave and succeeding small wave, the irregularity is more probably an extrasystolic "bigeminus" than an alternation. This is the irregularity which has most often been confused with alternation. Palpation of the precordial region may give evidence similar to that secured from palpation of the peripheral arteries, but this is usually an uncertain aid. Auscultation of the heart rarely re- veals a difference in the intensity of the sounds of the strong and weak beats. When murmurs are present, they occasionally vary in intensity, but a change in heart sounds normal and pathological are far more characteristic of the extrasystolic irregularities and auricular fibrillation than they arc of alternation. In rare cases of alternation, inspection of the venous pulse shows a great variation in amplitude of every other cycle, thus giving us a clue to the type of the irregularity (see Figure 140). Unless instrumental means are employed as a routine, many cases of alternation will escape recognition. Painstaking observa- tions with the sphygmograph are our only sure means of detect- ing pulsus alternans in a very large number of instances. These records, taken under the various conditions outlined in discussing palpation of the pulse, present to us the minute variations in the amplitude and spacing of the succession waves, which will often escape even the highly cultivated tactile sense of the expert. Typical sphygmograms are presented in Figures 141 and 142. In these records the difference in the amplitude of the alternate waves and their rhythmic spacing is well illustrated. Figure 141 is a radial tracing from a case in which the alternation was quite evident from palpation of the pulse. Figure 142, also taken from the radial pulse, was only brought out distinctly when a brachial cuff, with pressure 85 mm. Hg., was applied. Some cases of al- ternans have been published with graphic records in which the successive waves differ in duration rather than amplitude.* Graphic records of the apex beat are, as a rule, rather unsat- *Gravicr, loc. cit., p. 44. Alternation ,89 1 Apex Radial 0.2 second Figure 143 Polygram showing alternation in radial and apex. iyo Alternation is factory in detecting this condition. It is, however, fairly well shown in Figures 140 and 143. In these records the alternation in the radial is quite evident. The alternation in the apex activity is indicated by the notching of every other wave of the cardio- gram. 1 [ering has pointed out that tracing, taken in the precordial region near the base of the heart, sometimes shows an alternation when it is absent in records taken near the apex. The respiratory movements of the chest are prone to affect the contour of the waves of the cardiogram, but in these records the evidence is quite conclusive that the variation in the waves is quite independent of the breathing. It may be noted in this con- nection that in cases with a slow pulse and rapid respiration, when the pulse rate is approximately double that of the respiration, the peripheral arteries may show a difference in the size of the suc- cessive beats which simulates alternation. The pulse wave coin- cident with inspiration is smaller than that corresponding to ex- piration. This pseudo-alternans is easily differentiated by having the patient hold his breath when the amplitude of the pulse waves at once becomes uniform. Alternation may or may not appear in the venous tracings and may assume several forms. There may be alternation of the c waves, of the v waves or of the a waves. In Figure 144 is shown a well-marked alternation in the arterial record, but no evidence of this irregularity in the jugular. Respira- tory movements are much more likely to distort the phlcbogram, hence in cases of doubt it is always a wise precaution to secure the record during a period of suspended breathing. Alternation in the c wave is quite evident in Figure 145. Here the large c wave corresponds to the large wave of the brachial, which is quite what one would expect. Occasionally one sees cases in which the small c wave corresponds to the large peripheral ar- terial wave. The explanation of this phenomenon is difficult. Alternation of the auricle is seen in experimental work and may be diagnosed in the clinic by an alternating amplitude in the a wave of the jugular tracing. Such a record is exhibited in Figure 138. On the whole, evidence of venous alternation is rather rare and its significance has not been carefully studied. Alternation 191 Jugular Brachial 0.2 second Figure 144 Alternation of brachial, no alternation in jugular. Jugular Brachial 0.2 second Figure 145 Alternation of brachial and of c wave of tracing taken from above the clavicle. iy_> Alternation A very beautiful exhibition of alternation involving radial apex and jugular curves, is shown in Figure 140. This record was se- cured from a man suffering from advanced myocardial disease Several months before his death. This curve was taken during an attack of paroxysmal tachycardia, during which the rate was 200 per minute. The phlebogram is difficult to analyze, since the a, C and ?' waves are fused together. At other times there was also evidence oi a prolonged a-C interval, so this element also compli- cates the analysis. It would seem that there is in this case alterna- tion of the X' wave, due to alternating ventricular activity, which is very prominent on account of an insufficient tricuspid valve. There also would appear to be an alternation of the auricle, as evidenced by the differences in amplitude of the a waves, but this is less certain. The electrocardiogram rarely shows evidence of alternation. The differences in amplitude of the waves of the peripheral arteries may be quite evident, and yet the successive cycles of the heart, as portraved by the galvanometric curves, may present great uni- formity (see Figures 139, 146, 148 and 149). In Figure 146 are presented simultaneous curves of a radial pulse and the electro- cardiogram. The latter record shows that we are dealing with a case of auricular flutter with an irregular ventricular response. The radial waves distinctly alternate in amplitude, but it would seem that their rhythmic spacing is due to a delay in the transmission of the smaller waves to the periphery, rather than to a true alter- nating cardiac activity. Figure 147 was secured from an old gentleman with cardiac de- compensation and a pulse which, on palpation, closely simulated an alternans. The combined record shows that the irregularity is really not due to alternation, but to ventricular {Vx) and auricu- lar (Ax) extrasystoles. A true alternans, which is complicated by a single premature beat, is presented in Figure 148. The abnormal form of the usual ventricular complex suggests a lesion of one branch of the A-V bundle. Rarelv one obtains electrocardiographic evidence of alternation of the heart. This may consist in varying amplitudes of the R or of the T waves. Two such curves are shown in Figures 150 Alternation "J3 Radial FlGXJRE 146 Radial showing alternation. The electrocardiogram shows auricular flutter with irregular ventricular response. ~ * Brachial Figure 147 Pseudo-alternation of brachial due to ventricular (Vx) and auricular (Ax) extrasystoles. 194 Alternation and 151. Figure [50 was from a woman suffering from parox- ysmal tachycardia ; between the attacks neither radial tracings nor the galvanometer showed evidence perform work of which it is hardy capable. In cases of paroxysmal tachycardia, in which on the strength of other evidence we feel reasonably sure that the ventricular muscle is not seriously damaged, an alternation of the heart is of much less sig- nificance than when it appears in a heart with a slow rate. [f we consider only these hearts with a slow rate, our personal experience would agree with that of Yaquez,* who finds three degrees of alternation which may he arranged in the order of their prognostic value, as follows: (i) Prolonged continuous alterna- tion; (2) post-extrasystolic alternation; (3) transitory alternation. A fatal termination may he expected in continuous alternation within a few months. I know of no case of this kind in which death has been delayed more than two years. *XVTI, Intcrnat. Congress of Medicine, London, 1913, vi, 164. CHAPTER XIV The Influence Exerted by the Extracardial Nerves In discussing the theories of the nature of the heart beat, it was pointed out that the cells of the myocardium intrinsically possess the fundamental properties through which the activities of the heart are initiated and maintained ; these are modified and adapted to the momentary needs of the body through the agency of the extra- cardial nerves. It is conceivable that a departure from the normal efficiency of this adjustment may arise in two quite distinct ways: (i) The muscle cells may be so changed that one or more of their fundamental properties may be more than normally sensitive to nerve influences; (2) the nerve mechanism may be defective, and modifying influences abnormally large or small may thus be brought to bear on the cells of the myocardium. It is, therefore, important that we should examine the manner in which the myocardial activities are modified by the extracardial nerves and the clinical manifestations which are the result. ANATOMY AND PHYSIOLOGY The extracardial nerves which modify the activity of the heart are the cardiac branches of the two vagi and branches of the cervi- cal sympathetics. The vagus arises from nuclei lying in the medulla in the lower part of the floor of the fourth ventricle, passes out of the medulla in a groove between the restiform and olivary body, escapes from the skull through the jugular foramen and passes down the neck in the sheath of the carotid artery. About the level of the lower border of the thyroid cartilage the nerve is joined by branches of the sympathetic; at the level of the first rib the cardiac branches are given off; on the right side they follow the sheath of the innominate artery and on the left pass in front of the aorta, thus reaching the cardiac plexus. The sympathetic fibers come from the spinal cord bv way of the four or five upper thoracic spinal roots and pass through the first thoracic ganglion either to the inferior cervical ganglion or 199 200 Influences Exerted ijv the Extracardial Nerves directly to join the main vagus trunk. The fibers derived from the sympathetic arc known as the accelerator nerves of the heart. The cardiac plexus is composed of nerve fibers which can be traced over the posterior surface of the auricles and over the auricnlo-ventricnlar groove to the ventricles. The ultimate dis- tribution of the vago-sympathetic fibers is not entirely clear, bul the recent work of Keith and Flack, < )|>]>enheim, Dogicl and Colin strongly suggest that some of them terminate in the muscle cells of the sino-auricular node, while others end in the node of Tawara or follow the bundle of His and its branches into the muscle cells of the ventricles. These histological studies suggest that the spe- cialized muscle cells of the nodes and .-]-/' bundle play an impor- tant role in receiving the modifying impulses conveyed to the heart by the vago-sympathetic nerves. Stimulation of the vagi causes (i) a slowing of auricles and ventricles, (2) a depression of conductivity, and (3) probably a diminution in force of the contractions of the left ventricle. Stim- ulation of the sympathetica causes an acceleration of the heart rate. Studies on the activities of the extracardial nerves have revealed marked functional differences in the right and left vagus and in the two sympathetica. These differences are qualitative, as well as quantitative. Thus, in his experimental work on dogs, Cohn* found that stimulation of the right vagus usually caused the arrest of all the chambers of the heart, but appeared to have very slight direct influence either on conduction or the activities of the ventricle. On the other hand, stimulation of the left vagus had only a moderate slowing effect on the auricles, but a very definite depressing influ- ence on the rate of conduction between auricles and ventricles. His conclusions as to the differences in the distribution of the fibers of the right and left vagi are shown in Figure 152. Rothberger and Winterbergf have shown that a corresponding difference exists in the distribution of the right and left sympathetic fibers, stimulation of the right stellate ganglion caused an increased auricular rate without conduction changes, while stimulation of the left stellate ganglion shortened or abolished the conduction time, calling forth the suggestion that the irritability of the A-V node *Jour. Exp. Med., 1912, xvi, 72> 2 - tArch. f. d. ges. Physiol., 1911, cxli, 217; 1910, exxxv, 506, 559. Influences Exerted by the Extracardial Nerves 201 ■RIGHT SrMTATHCTC I'M •I!:! LEFT 4rriPA7HETlC I'iii Figure 152 Diagram after Cohn (modified) indicating the distribution of the fibers of the right and left vagi and the right and left sympathetics.. It is to be noted that the right vagus and the right sympathetic are in the main distributed to the sino-auricular node and the auricle. The left vagus and the left sym- pathetic have a preponderating influence over the auriculo-ventricular node and bundle. The data upon which this diagram is based were obtained principally from the conclu- sions drawn from their experimental work by Cohn and by Rothberger and Winterberg. 202 [NFLUENCES EXERTED BY Tin: EXTRACARDIAL NERVES had been thus increased so that it had assumed the role of pace- maker for the heart. The inferences as to the distribution of the fibers cit" the sympathetic, drawn from the observations of Koth- berger and Winterberg, have been incorporated in the diagram | Figure [52). Antedating the experimental work above outlined, Robinson and Draper J had shown that in man right and left vagus pressure pro- duced distinct qualitative differences. Their method was to make digital pressure over the carotid sheath sufficient to obliterate the carotid pulse. They concluded from their electrocardiographic studies that the right vagus had a more evident influence on the rate and force of ventricular contractions, and that the left vagus had a pronounced effect in modifying conduction. Clinically, vagus pressure should be employed only on one side at a time; alarming standstill of the heart may result from bilateral pressure. The contrast in the effect of the activities of the right and left vagi are shown in Figures 153 and 154. Both of these records were obtained from a case of paroxysmal tachycardia. The arrows indicate the time at which vagus pressure was made. Figure 153 was taken during pressure on the right vagus; Figure 154, during pressure on the left vagus. The tachycardia was caused by a very rapid auricular activity to which the ventricle made a corre- sponding rapid response. Pressure on the right vagus (Figure 153) immediately changed the rate of the pacemaker from 172 to 56 per minute. In Figure 154 is shown the effect of left vagus pressure: the ventricular rate is immediately changed from 172 to 86, but it is evident that the mechanism of the altered function is quite different from that shown in Figure 153. The auricular rate is unchanged, hut the ventricle responds only to every other auricular impulse. Alternate auricular impulses are blocked, hence the ven- tricular rate is halved. Flere it is evident that stimulation of the right vagus exerted its influence mainly on the auricle, stimulation of the left vagus had no effect on the auricle, but modified the A-V junctional tissues in such a way that a partial block was induced. Numerous attacks of tachycardia, while this patient was under ob- servation, permitted us to repeat these observations on a number of occasions. tjour. Exp. Med., 191 1, xiv, 217; 1912, xv, 14. ! h. 1 Ihf* saLLk I: iilKl will ; , 2^ « Eg pti ££ c3 s «5 203 .j C u J04 Influences Exerted by the Extracardial Nerves Ashner* first observed that pressure on the eyeball caused a slowing of the pulse. He traced the course of these nerve im- pulses through the trigeminus to its nucleus and thence by fibers to the vagi. This oculocardiac reflex has been studied by many observers; a digest of their work may he found in Levin's paper. f In general, when the nerve tracts are intact, right and left ocular pressures correspond rather closely in their effects to right and left vagus pressures (Figures 155 and 150). CLINICAL TYPES The "accelerated heart" and its relation to vagus and sympathetic activities have been discussed in a preceding chapter and need not detain us at the present. The slow regular heart, with a rate of 60 or somewhat less, is a type often seen. It has been referred to in an earlier chapter (VI) and is usually due to excessive vagus influence constantly at work. It has little significance, except as an indication of a high degree of vagus tone. The slow heart, with or without sinus arrhythmia, significant of heightened vagus activity, is not infrequently met with in associa- tion with other symptoms suggestive of excessive vagus influence. These symptoms are: paleness of the face, tendency to myopia, low blood pressure, moist skin, asthma, gastric hypersecretion, hyper- chlorhvdria, rapid gastric motility, spasmodic constipation, etc. Patients presenting this symptom complex have been grouped under the term "hvpervagotonic." Over against the group comprised in this syndrome one sees many patients presenting an opposing series of symptoms : tachycardia, flushing of the skin, gastric hyposecre- tion, etc. It is believed that these patients are the subjects of increased sympathetic activity, hence they have been classified as "hvpersympathicotonics." These groups may further he distin- guished by their reaction to drugs. The "hypcrvagotonic" group react: to the administration of atropine by increased pulse rate, relief of asthmatic breathing, diminished gastric secretion, motility, etc., to pilocarpin with sweating, salivation, etc. The symptoms of the "hypersympathicotonics" are aggravated by the administration *Wien. klin. Wochnschr., 1908, xliv, 1529. fArch. Int. Med., 1915, xv, 738. ttril 205 M\ ¥ t : fe 2o6 Influences Exerted by tiie Extracabdial Nerves of atropine : they do not react to pilocarpin, but respond to epine- phrin with tachycardia, hypertension and glycosuria. As a rule, the "hypervagotonics" show a marked response to vagus ami ocular pressure; in the "hypersympathicotonics" these reflexes are dimin- ished or absent. Such studies assist us in formulating our impres- >ions as to the relative importance of the extracardial reflexes in modifying the cardiac activity in the individual case. With such abnormal tone either of the vagus or of the sympathetic mechanism, one may feel less suspicion that an altered myocardium is respon- sible for the changed heart activity. Figures 155 and 156 are parts of a continuous curve and afford a record of the effect of right ocular pressure secured in a young man of 22 of the hypervagotonic type. His usual heart rate was under 60, with a moderate degree of sinus arrhythmia. He was the subject of attacks of asthma, gastric hypersecretion and hyper- acidity and constipation. At the point in the electrocardiogram marked by the arrow, (1) pressure was made on the right eye- ball, which was released at (2). After the beginning of the pres- sure there was one normal heart beat; from this point until the pressure was released, the auricle was in complete arrest, as indi- cated by the absence of the P wave. After a complete cardiac standstill of 3.4 seconds, there is a "ventricular escape," (a) fol- lowed by two similar phenomena (b) and (c) with intervening periods of standstill each somewhat over two seconds. The "ventricular escape" is of such a form that we feel assured that it originated from a point high up in the A-V bundle, prob- ably in the region of the A-V node. It is another illustration of the ability of the cells of the myocardium other than the sinus node to initiate contractions. On the removal of the ocular pressure, the sinus node resumes its pacemaking function and auricular contractions (P) reappear. The most common irregularity of the heart which is due to vagus influences is the "respiratory sinus arrhythmia" of children and of young adults (Figures 157, 158, 159 and 160). This is fre- quently discovered when palpating the radial. It consists in a rhythmic lengthening and shortening of the heart cycles coincident with the respiratory movements of the chest; the longest cycles usually appear in expiration ; during inspiration the cycles are per- Influences Exerted by the Extracardial Nerves 207 ration Brachial 0.2 second Figure 157 Respiratory sinus arrhythmia. Upper curve respiratory movements. Lower curve brachial pulse. Time 0.2 second. Jugular Figure 158 Respiratory sinus arrhythmia. Upper curve jugular pulse. Lower curve brachial pulse. Time 0.2 second. Rhythmic variation in length of cycles vanes with respiration. The auricle participates in the irregularity, the a-c interval is normal. jo8 Influences Exerted by the Extracardial Nerves ceptibly shortened. Forced respiration may produce an arrhythmia hitherto unnoticed or may exaggerate an irregularity which has horn present during natural breathing. The most pronounced modifica- tion can be secured by having the patient take a full inspiration and hold the breath for 15 to 30 seconds; while holding the in- spired air the pulse becomes slow and suddenly quickens when respiration is resinned. Figure i<>i i> the electrocardiogram of a boy of i-> who ordi- narily showed a mild degree of sinus arrhythmia. To verify the nature of the irregularity, under instructions he drew a deep in- spiration at (I) and held his breath; at (3) expiration was al- lowed. The slowing of the auricles and of the whole heart is quite evident. There was a distinct change in the form of the P wave while the breath was held (2) and this did not recover its normal contour until natural breathing was resumed (4). This is the only common forme of cardiac irregularity met with in young children and, hence, has been named by Mackenzie the "youthful arrhythmia." It is also not infrequently seen in young adults, particularly in those with a rather unstable nervous organ- ism. The irregularity is due to changes, induced by varying de- grees of intrathoracic pressure, in the vagus influences conveyed to the sinus node, thus modifying the rate of impulse formation of the pacemaker of the heart. This irregularity is sometimes in evidence in patients showing abnormal types of respiration. Figure 162 was obtained from a man of 50 with an advanced grade of nephritis exhibiting Cheyne- Stokes respiration. The change in pulse rate during the transi- tion from deep breathing to a period of apnoea is illustrated in the tracing. During the active respiratory movements, the heart cycles occupied 1.4 seconds; during apncea, the rate increased so that each cycle consumed approximately 0.6 second. It is prob- able that in this case the change in vagus tone is central in origin, depending on the accumulation of carbon dioxide in the blood; the heart has endeavored thus to compensate for the disordered respiratory function. The graphic records of a case in which the arrhythmia was due to peripheral stimulation of the vagus, are presented in Figure 163. This was secured from an extremely neurotic young man of % 1 \m m - £' E fe " 209 ff - (H — , • 5 ^1 jio Influences Exerted by the Extracardial Nerves 22, who was seen in consultation because it was thought that he was suffering from auricular fibrillation on account of the com- plete irregularity of the pulse. The upper curve of the record was obtained by placing a receiving cup over the upper part of the neck. The movements are due to the efforts of the patient to swallow and expel air from the stomach. The change in the cardiac cycles are clearly synchronous with these irregular movements of the (esophagus. Electrocardiograms showed conclusively that the complete irregularity of the heart was not due to auricular fibril- lation, but was caused by the varying rate of stimulus production in the normal pacemaker, induced by the spasmodic muscular move- ments during "cribbing." The identification of this form of irregular pulse is usually a simple matter. The rhythmic change in the length of the cycles is synchronous with respiration, and may be exaggerated by forced respiratory movements. The pulse waves usually show very slight variations in size ; the only noticeable departure from the normal is the rhythmic variation of the intervals between the beats. The cardiac irregularity is of the same nature, first and second sounds follow each other at normal equal intervals, but the time interval between the second and first sounds shows a rhythmic change in length. The venous pulse (Figure 158) shows a normal succes- sion of a, c and v waves, but the intervals between these groups show the same grade of irregularity as the arterial pulse. The electrocardiogram (Figures 159, 160 and 161) presents a series of normal auricular and ventricular complexes. The ventricular curves are of normal duration, and the irregularity shows a departure from the usual physiological rhythm only in a variation in the length of the diastolic period. From the evidence presented in regard to the relative influences of the right and left vagus nerves on the sinus node and on the junctional tissues, it may be inferred that the right vagus is the most important factor in producing this irregularity. Exceptionally one meets with a case of "sinus arrhythmia" in which the poly- gram shows an a-c interval of varying length, the electrocardio- gram a similarly changing P-R interval. This indicates that the passage of stimuli from the auricle to the ventricle has been de- layed and in these one is led to the conclusion that the tone of 21 I ~ a ni o — — 5-s S«H 1 J 5 i E rt K 3 IJl:- "i Q^ : ^:$ u a 212 Influences Exerted by the Extra< vrdial Nerves the loft vagus also is being rhythmically modified, thus affecting the rate of the ventricular response. rhe clinical significance of "respiratory sinus irregularities" is mtv slight. The importanl element is the recognition of their true character, thus distinguishing them from the forms of abnor- mal cardiac activity of a more serious nature. Patients showing this arrhythmia do not develop cardiac insuffi- ciency which can be attributed to the irregularity. Ii is frequently met with in neurasthenics in whom no other evidence of cardiac abnormality can be found at the time, or subsequently. In the majority of children it will spontaneously disappear before puberty. It has been studied in robust school hoys, soldiers in training and other healthy individuals. It is not indicative of myocardial dis- ease and requires no treatment. No drugs or other therapeutic measures are needed, nor should those who present this symptom limit their customary activities. Then- is another considerable group of sinus arrhythmias which hear no relation to the respiratory movements. These disorders of the heart mechanism have been classified in subgroups by Lewis as follows: (i) sudden cessation of the whole heart heat; (2) phasic variations of pulse rate, in which a retardation and subse- quent gradual acceleration of the whole heart occurs; (3) an ir- regularity of the whole heart in which shorter and longer pauses are mingled indiscriminately. (1) Sudden cessation of the whole heart heat. This is a form of irregularity which is seen with extreme rarity. It has been known as "sino-auricular block," since, on rather theoretical grounds, it was supposed to be duo to an interference with the passage of the impulse from the sinus node to the auricular tissues. The phenomenon consists in the dropping out of a single heat; that is to say, there is a pause during which there is no evidence of activity of any part of the heart. The length of this pause is commonly a trifle less than two heats of the usual rhythm. Since at present we have no means of detecting the activity of the sinus node other than the effects which it has on the auricle, there seems to be no direct way of establishing the fact that the node continues its normal activity hut that its stimulus is inter- rupted on the way to the auricle. From the close similarity which 2/3 1 p 6 £ 1 H 1 6 u 1 d. 1 E nj PI * g 3 u »3 a I o S (>. Ih o Figure 162 pper curve respir ut 43 per minute. PS §8 •- c « & .is £ D.T3 4; u_t 1- ^ to c rt >> u° ■58 0. in rt .tS tj) Js.s 3 CO (*- +■* n) °o C3 ■ -M4 Influences Exerted by the Extracardial Nerves this phenomenon seems to bear to the irregularities (phasic folia- tions oj pulse rate) discussed in the next paragraph, since these two types of irregularity are seen in the same patient, since in certain cases (Eyster and Evans)* it can be induced by pressure on the right vagus nerve and abolished by atropine, it seems to me there is little doubt that it is a vagus effect and the term "sino- auricular block" should be dropped as inconsistent with the evi- dence which we possess at the present time. This irregularity can be surely recognized only by instruments of precision. The polygraph shows an absence of ventricular activ- ity in both arterial and venous tracings. The jugular record shows no evidence of an a wave during the pause. The electrocardiogram merelv shows a pause nearly or quite equal to two cycles of the usual cardiac rhythm without evidence of either auricular or ventricular activity. This irregularity is usually associated with other evidences of abnormal cardiac function, most of the reported cases have shown some degree of auriculo-ventricular block. Figure [65 is the record (lead 1 ) of a man of 55 with evidences of myocardial degeneration. At other times he had showed ex- treme grades of cardiac arrhythmia with many ventricular cxtrasys- toles, paroxysmal tachycardia, etc., etc. At the time the record was taken he had recovered to a considerable degree and the heart was for him fairly regular and for weeks showed only the abnor- malities here presented. It is to he noted that the P wave is slightly diphasic, that the R wave is reversed, that the whole ven- tricular complex has a very abnormal form and the P-R interval is excessively long. One "dropped beat" is evident in the electro- cardiogram. The interval including the "dropped heat" ( R., to R t ) is a trifle less than the length of two cycles of his usual rhythm (R, to R,). The record (Figure 164) of a young girl suffering from rheumatic pericarditis shows a prolonged standstill of the heart. At other times the change in the length of the cardiac cycles was less abrupt, so that one would have included her arrhythmia under group 2, "phasic variations of the pulse rate"; indicating, as we have already suggested, that no sharp line may fairly be drawn between these •Arch. Int. Med., 1915, xvi, 832. FlGUKE 164 Sinus arrhythmia nnt respiratory. "Dropped beat, rheumatic pericarditis. P-R interval = o.2 second. From a younf? woman with Figure 165 (< From a man 55 years old with myocardial degeneration. "Dropped beat." So-called sino-auncular block." All the complexes are very atypical (see text). P-R intervals 0.22 second. Time 0.2 second. Figure 166 Records from above downward jugular tracing, electrocardiogram, brachial tracing, time 0.2 second. From a young woman with hyperthyroidism. The arterial pulse is completely irregular, but both the jugular and electrocardiographic records indicate an auricle with irregular but otherwise normal contractions. jio Influences Exerted by the Extracardial Nerves groups. The somewhat prolonged P R interval suggests a hyper- tonus of the left as well as of the right vagus. z. Phasic variations of pulse rate (Figures 1^7, 168 and 169). 1 [ere there are alternating periods of rapid slowing and equally rapid acceleration of the heart. In some cases this change is quite rhyth- mic, the heart beating 10 or 15 times between the individual cycles of the maximum length, in other cases the time elapsing between similar phases is very variable. The variation in the length of the individual cycles is always quite independent of respiratory move- ments. Wry little is known of the mechanism of this form of irregu- larity, but the evidence seems to point to vagus influences acting on a sinus node which is functionally damaged. 1 believe the mech- anism responsible for its production is quite similar to that of the single dropped heat described above. The identification may be sus- pected when a rhythmic series of quickening and slowing heart beats is detected by palpation or auscultation. The type of irregularity is securely established by graphic records. Figure [67 is the record of a man with general arteriosclerosis, with a rhythmic change which occupied about 18 heart cycles. Fig- ure 168 is from a girl of eleven with acute endocarditis; when the acute process subsided the arrhythmia disappeared. The electro- cardiogram of a boy of fourteen with acute rheumatic endocarditis and arthritis is reproduced in Figure 170. The varying length of the P-K interval in this record is suggestive either of excessive activity of the left vagus or of an A-V node peculiarly susceptible valescence, but reappeared coincident with a recurrence of the arthritis. 5. Irregularity of the whole heart in which shorter and longer pauses arc mingled indiscriminately. This arrhythmia closely sim- ulates the pulse features of complete irregularity of auricular fibril- lation of the slow type (Figures 163 and 166). But the mechan- ism of its production is quite different. The sino-auricular node acts as the pacemaker of the heart, but the rhythmic character of the formation of stimulus-material is disturbed, probably due to the reception of impulses varying in intensity which reach the sinus node through the right vagus. The auricle responds irregu- 217 I 1 m £ 1 I 218 Influences Exerted by the Extracardial Nerves larly and the ventricle follows the auricular contractions with a cor- responding arrhythmia, hut with no other abnormal features. In short, the whole heart assumes the arrhythmia of the pacemaker, hut the chambers respond sequentially and otherwise normally. Recognition of this type of irregularity by the ordinary physical signs is difficult. If the pulsation of the veins of the neck are prominent, one may he able to detect the presystolic a wave, in- dicative of coordinated, hut arrhythmic, auricular activity. Barring this resort must he had to graphic records. Both polygrams and electrocardiograms show nothing ahnormal except the unequal dias- tolic periods. The a, c and v waves of the jugular record show the normal relationship (Figure [66 and [69). The auricular and ventricular complexes of the electrocardiogram have a normal se- quence and the usual form ( Figures K>() and 171 ). The polygram is to he distinguished from that of auricular fibrillation by the pres- ence of the auricular as opposed to the ventricular form of venous pulse; the electrocardiogram shows a P wave of normal type and an absence of the small diastolic oscillations so characteristic of auricular fibrillation. The condition is to be distinguished from the auricular cxtrasystole by the absence of intervals which repre- sent pauses of a compensatory character and by the normal contour of the P wave in the galvanometric records. The polygraphs (Figures 166 and 169) show the complete ir- regularity of the arterial pulse, an auricle which is active and equally arrhythmic, a considerable variation in the length of the diastolic period and the normal sequential relation of auricle and ventricle. Figure 166 was from a young woman of 20 with symptoms which suggested hyperthyroidism, but with no evidence of myocardial dis- ease other than the arrhythmia. The electrocardiogram ( Figure 171) was obtained from a woman of 25 during an attack of acute rheumatic endocarditis. CLINICAL FEATURES AND SIGNIFICANCE Sinus irregularities which hear no relation to respiration are seen more frequently in the young, but are not limited to this period of life. They may be discovered accidentally in those who show no other evidence of disease. They are occasionally seen in the period of convalescence following the acute infectious diseases. They are Influences Exerted by the Extracardiai, Nerves 219 Jugular Brachial 0.2 second Figure 169 Brachial and jugular tracings from a young woman with a completely irregular pulse. Sinus arrhythmia independent of respiration. 220 Influences Exerted by the Extracardial Nerves sometimes associated with the administration of large doses of digitalis. These irregularities are usually seen in association with a slow pulse rate, sometimes they are abolished by exercise or a febrile condition in which the pulse is accelerated. Most of them show a very prompt response to vagus or ocular pressure < Figures 155 and 156). Frequently they disappear under the administration of atropine. At the Presbyterian Hospital, in the routine examinations dur- ing the past \ear, we have studied and recorded graphically seven- teen cases of sinus arrhythmia in which the irregularities were quite independent of respiratory movements. Eight of these cases were associated with other forms of arrhythmia suggesting a myocardial defect, such as extrasy stoles, partial auriculo-ventricular block, etc. The nine remaining cases belonged exclusively to the type of ir- regularity now under discussion. Among these there was one adult and one seventeen ; the rest were all under fourteen years of age. Six were males and three females. Of these nine cases, five had physical signs of definite endo- or pericardial lesions ; one was an overgrown athletic boy with a moderate degree of cardiac hyper- trophy, one had chorea ; the remaining two showed no definite signs of disease, although one was slightly dyspneeic and the- other was of a high-strung, nervous temperament. In two of these cases the irregularity disappeared, in the others it still persisted at the time of the last examination. Clinically, it is important that we should recognize the nature of these arrhythmias and distinguish them from the types of more serious moment with which they may he confounded. Such an activity of the heart is in itself, 1 believe, not a serious matter, hut my present impression is that it indicates a definite myo- cardial change which may he very transitory, hut which may well bear careful observation. The exciting causes are undoubtedly the nervous impulses con- veyed to the heart through the vagi, but these are probably peculiarly effective, since they are acting on a heart which is damaged and, hence, unusually susceptible to outside influences. — 1 - 1 W £ Pi o o .•a rt o S3« 1 *~1 tt. o CHAPTER XV Mixed Arrhythmias In the preceding pages the arrhythmias have been discussed as individual types. This is the usual form in which they are seen in the clinic and it is, perhaps, simpler to study them primarily from this standpoint. It has been pointed out from time to time how close is the asso- ciation of some of the types; for example, that a single heart may pass through the phases of extrasystole, auricular flutter, fibrilla- tion and paroxysmal tachycardia and repeat any one of these abnor- mal types of functional activity. There are other instances by no means rare in which the arrhyth- mia depends upon the alteration of more than one of the funda- mental functions of the cardiac muscle. Changes in the rate of stimulus formation at the sino-auricular node are not infrequently associated with a defect in the capacity of conduction in the bundle of His. Increased irritability of various portions of the muscula- ture, as evidenced by extrasystoles or fibrillation, is often found associated with a depression of the property of conduction. One might spend considerable time in enumerating the various combina- tions which are seen, but it will suffice us to discuss several of the more common and distinctive types of the mixed arrhythmias, bear- ing in mind that these by no means exhaust the assortment that are encountered. Perhaps the most common type of the mixed irregularities are those in which a definite sinus arrhythmia is associated with a defect in the conductivity of the A-V bundle. The electrocardio- gram of a well-marked case of this group is shown in Figure 172. The lower line of numerals represent the measurements in frac- tions of a second of the P-R intervals, the upper the P-P intervals. The P-R time was usually excessive in this case and in the rec- ord shows a variation in length from 0.18 to 0.43 second. The P-P intervals, which indicate the rate of stimulus formation at the sinus, also presents a variation in length with a tendency to a rhythmic, gradual increase followed by a diminution in the length of these 222 9 inSP 224 Mixed Arrhythmias intervals. The extreme differences are about one-third of a sec- ond. The ventricular arrhythmia is the roultant of these two fac- tors and the cycles occupy from 0.69 to 1.01 seconds. The arrhyth- mia was accentuated by forced respiratory movements. Just before this curve was secured the patient took a deep inspiration and held the breath; the slow expiratory movement is indicated l>v the por- tion of the respiratory curve in the latter half of the record. It is quite probable that the arrhythmia is in a large measure due to vagus influences, the sinus activity varying with the tone of the right vagus, the conductivity of the bundle changing with the tone of the left vagus (see Chapter XIV on the Influence of the Extra- cardial Nerves). In Figures 173 and 174 are exhibited the electrocardiograms of two cases in which sinus arrhythmias arc associated with changes in the contour of the P leaves, indicating a shifting of the pace- maker from the sinus node to some other point in the auricular wall. In Figure 173 a small, but definite, change in the P deflec- tion (1, 2, 3, 4) is accompanied by a shortening in the P-R inter- val; at 5 the P wave recovers the form characteristic of the normal pacemaker and the P-R interval measures 0.2 second. Figure 174 presents less variation in the P-R interval, but a more marked dislocation of the pacemaker is suggested by the com- plete inversion of the auricular complex. A functional abnormality of this character indicates a mild de- gree of auricular myocardial defect, not in itself sufficient to em- barrass the patient but which serves as a signal to the physician that unless stationary it may be the forerunner of more serious damage, with corresponding mischief to the circulation. A mixed arrhythmia, which is extremely common, is the asso- ciation of ventricular extrasystoles with auricular fibrillation. It is met with not infrequently in subjects with auricular fibrillation to whom digitalis has been administered in considerable doses. It is also seen in those who have never received digitalis. Most often the extrasystoles occur at infrequent intervals and are all of one type. The record shown in Figure 175 was obtained from a patient who was not taking digitalis. It presents rather an extreme degree of the irregularity. The extrasystoles are of three distinct types, indicating as many points of abnormal ventricular irritability. By 225 a z — — 226 Mixed Arrhythmias means ol the ordinary methods of physical examination, one may find considerable difficulty in correctly interpreting this type of ir- regularity. < me who has studied a great many hearts of this kind learns to distinguish by auscultation certain contractions which dif- fer from the majority by their "flopping" character, and these he may suspect to be extrasystoles. They can only be surely analyzed with the aid of electrocardiographic curves. The appearance of a large number of ventricular extrasystoles in a case of auricular fibrillation indicates that, in addition to an irritable auricle, we have an abnormally irritable ventricle. The muscle damage is very extensive. When the extrasystoles arise from many foci, we must conclude that the lesions are even more widely distributed. Nearly all of these patients have a severe grade of cardiac insufficiency which is extremely difficult to control. In discussing the prognosis of auricular fibrillation, it was pointed out that the future of the patient depended to a very large degree on the integrity of the ventricular muscle. Here we have clear evi- dence that the ventricular wall is extensively diseased. The grav- ity of the prognosis increases with the multiplication of the num- ber and types of ventricular extrasystoles. AURICULAR FIBRILLATION AND HEART BLOCK In 1909 James Mackenzie* described a group of four cases pre- senting a slow rhythmic pulse which suggested a complete heart block, but in which polygraph curves failed to reveal any auricular activity. He suggested that there was also in these cases a brady- cardia of the auricle and that the auricles and ventricles were con- tracting simultaneously in response to a stimulus arising in the region of the A-V node. Accordingly, he designated this type as "nodal bradycardia." This acute observation was soon followed by an exhaustive study of one of the cases of this group by Lewis and Mack.t using Einthoven's galvanometer. They were able to show that the auricle was in a condition of fibrillation and that the ven- tricles had assumed the slow ideo-ventricular rhythm ordinarily seen in complete heart block. The post-mortem examination of this ♦Heart, 1909-10, i, 25. tQuart. Jour. Med., 1909-10, iii, 273. M [xed Arrhythmias 227 Jugular Brachial Figure 177 Auricular fibrillation, complete A-V block and ventricular extrasystoles. Rate 35. For electrocardiogram of this case see Figure 176. ' Jugular Brachial Figure 178 Auricular fibrillation and complete A-V block. Note rhythmicity of ventricular complexes 228 M IXED ARRHYTH M IAS heart i revealed a lesion completely severing the bundle of Ilis, and organic damage to the auricular wall sufficient to explain the ex- istence of auricular fibrillation. It has been my fortune to observe two cases | resenting this symptom complex. ( >ne of these died while under observation, but permission for an autopsy could not be obtained. The mechanism of this rather unusual functional activity seems reasonably clear. There are no coordinated contractions of the auricles; they are in a state of fibrillation and, as is usual in this condition, irregular impulses are being constantly showered on tin- functional tissues. Since, however, there is a complete functional severance of the .-/-/' bundle, all these impulses are blocked and none of them reach the ventricle. Thus cut off from stimuli de- rived from the upper portions of the heart, the ventricle initiates its own stimuli and a typical ideo-ventricular rhythm becomes established. Among the etiological factors found have been syphilis, rheuma- tism and general arteriosclerosis. As in other conditions of block, the association of mitral disease is more common than other valvu- lar lesions. The effect of digitalis and drugs of the same order in producing a complete block in cases of auricular fibrillation will be consid- ered in another place. Of the cases reported in the literature only one ( Mackenzie, case 4) was under fifty years of age, the others were from fifty-one to sixty-eight years old. It is seen less frequently in women than in men. Complete block will, of course, be inferred when the ventricles are found to be beating rhythmically at a rate in the neighborhood of thirty per minute. When a rhythmic pulsation of the jugulars two or three times the rate of the ventricles is absent, an associated auricular fibrillation may be suspected. In the polygraph the arterial records show a slow rhythmic rate of about thirty per minute and a corresponding rhythmic jugular of the ventricular form. All a waves are absent and there is no evidence of gross auricular activity (Figure 177). The electrocardiogram (Figure [78) presents a slow rhythmic tCohn and Lewis: Heart, 1912-13, iv, 15. Mixki) Arrhythmias 229 contraction of the ventricle characteristic of complete block, an absence of all P waves and the small undulations | // ) pathog- nomonic of auricular fibrillation. The galvanometric record of another case is shown in F'gure 176. Here the activity is further complicated by ventricular con- tractions (.x'j, x 2 ) originating- in abnormal points in the ventricular wall, indicating an excessive irritability. The record is suggestive of the effect, of digitalis when administered in large doses to cases of auricular fibrillation, but, in this instance, neither digitalis nor any other drug of this group was being given. The abnormal activity was entirely due to the myocardial defects. In this case the administration of atropine produced a considerable increase in the ventricular contractions of the normal type (R). Further details have been reported in a paper on "Functional Heart Block."* A polygram secured from this same patient is re- produced (Figure 177). The arterial pulse is slow, 35 per min- ute, and rhythmic, except toward the end of the curve, where two extrasystoles appear. The jugular tracing shows an absence of all a waves and is of the ventricular form. Most of these cases present signs of a considerable degree of cardiac insufficiency, and it is evident that the defective myocardium is unable to maintain an adequate circulation. In neither of the two cases which I have had under observation have there been at- tacks of unconsciousness or convudsions, but several of the re- ported cases have exhibited phenomena which allow them to be grouped under the Adams-Stokes syndrome. The convulsions are due, as in other cases of heart block, to cerebral anaemia follow- ing an abrupt lowering of the heart rate. In these cases the myocardial damage is so extensive that it makes the prognosis exceedingly grave. The termination may occur at any time in a convulsive seizure or, as in the two cases which I have been able to follow, the course may be a progressively weak- ening heart with ultimate failure. Probably three or four years would be the longest period of life which could be expected after the discovery of such serious myo- cardial defects. *Hart: Amer. Jour. Med. Sc. 1915, cxlix, 62. 230 Mixed Arrhythmias HEART BLOCK AND EXTRASYSTOLES Aii unusual phenomenon occasionally met with in cases of com plete block is presented in Figure [79. This was taken from a case, seen in consultation with Dr. Frank Grauer, of Adams-Stokes disease, who died in a convulsion two years after these observa- tions were made, llis usual ventricular contractions were per- fectly rhythmic and at a rate of thirty per minute, the auricular rate was 86. At rare intervals there appeared a single premature ventricular heat, sometimes two of these presented in succession. That the origin of these extra contractions must have been in the region of the A-V node, or, at any rate, high up in the A-V bundle, may be inferred from the form of the ventricular complexes of the electrocardiogram (Figure 180), taken on the same day. There are two possible explanations of this activity : ( 1 ) The block, which is ordinarily complete, occasionally becomes partial and the ven- tricle responds with a delay in the conduction period to an auricular impulse; the complete character of the block for most of the time makes this explanation seem improbable. (2) The A-V node or bundle is excessively irritable at times and the usual ideo-ventricular rhythm is interrupted by what may be called a nodal or bundle extrasystole. On theoretical grounds, one might assume that such a quickening of the ventricular activity would be an event favor- ing an improved distribution of the blood. My observations on this patient were not sufficiently prolonged to determine whether such was the case. The graphic records of another case of heart block are pre- sented in Figures 181 and 182. The polygraph shows a perfectly rhythmic activity of the auricles at a rate of 78 and of the ven- tricles at a rate of 37, but with a complete dissociation of the upper and lower chambers of the heart. This curve would suggest the ordinary type of complete heart block. When, however, we come to examine the electrocardiographic record (Figure 181) it presents some unusually interesting features. Here, again, there is evi- dence of complete dissociation of auricles and ventricles. The P wave is, however, quite abnormal in form. Instead of a single positive wave, it is diphasic and it is, therefore, probable that the auricular pacemaker is a point in the muscle at a considerable dis- MIXED Arrhythmias 23; ■^^^1 n 9k |MH . - nl R^H^^H l9M IV LS 1 KREB Em HH9S uflml ^H Ira Bra ffSyjPjpfr 1 /'•■.."/■■' m !5©3fik< ipn PWI ffi^ ■jBJWj 4 ™J", ™ ^■/■lW.1 iwMwJWjH ■^^■^^^w^^i Jugular Brachial 0.2 scconu Figure 179 Complete A-V block. As rate — 86. Vs rate = 30. Complicated by extrasystoles c', c", c"'. For electrocardiogram of this cj.se see Figure iGa. F ' ! ■ 1 ..... i 1 . . . .1 1 1 ■'". A p p ■P -■ ■ ' • ■ ' ... • ©.2. £lC9v%cL _ Figure 180 Complete A-V block ?"d nodal extrasystoles. As rate =: polygram of this case see Figure 179. 5. Vs rate = 30. For z$z Mixed Arrhythmias tance* from the sino-auricular node. Still more interesting is a study of the ventricular complexes. These arc similar in form, but arc readily distinguished from the curve of a normal ven- tricular contraction. The records taken by leads I and II (not here reproduced) showed ventricular complexes of an abnormal type. In lead 1 they were directed upward, in lead II and lead III ( Figure [8i ) they were directed downward. These complexes con- form to the type obtained experimentally by Eppinger and Roth- bergcr,! through a destruction of the left branch of the bundle of His. We, therefore, conclude that in the case under discussion there existed a lesion dividing the main stem of the A-V bundle, causing a dissociation of auricular and ventricular activities, and, further, that there was a destructive lesion in the branch of the A-V bundle which is distributed to the left ventricle. The ideo- ventricular rhythm, therefore, probably arose, not as is usual from a point in the main stem of the bundle, but in the right ventricular wall. It is interesting to observe how widely is distributed the prop- erty of rhythmicity in the heart muscle. This heart, with a ven- tricular pacemaker very remote from the normal site, maintained an almost perfect rhythmic activity over long periods of time and, on many occasions, when he was under observation. ♦Lewis: Heart, 1910, ii, 27. T/tschr. f. klin. Med., 1910, lxx, 1. M [XED ARRH y'I II Ml AS 233 Figure 181 Complete A-V block with destruction of the left limb of the A-V bundle. Note diphasic P complex. For polygram of this case see Figure 182. .2 second Jugular Radial Figure 182 Complete A-V block. As rate=78. Vs rate=3^. For electrocardiogram of this case see Figure 1S1. CHAPTER XVI Position of the Heart and Changes in the Disposition of the Muscle Mass A discussion of changes in position of the heart in the chest cavity would lead us outside of the limits which we have set to the subject matter of these pages. Since, however, we have laid considerable stress on the use of the electrocardiogram as a means of studying myocardial function, and have utilized not a small por- tion of our space in describing the various characters of these rec- ords and the means for their analysis, it becomes necessary to ex- amine certain deviations from the usual type which arc due to changes in the position of the heart and which, therefore, must be distinguished from those which are due to intrinsic myocardial alternations. The amplitude and direction of the records obtained by the three leads usually employed in clinical work depend on the algebraic sum of the currents developed in the heart at any given moment, but any one of the leads will record only those currents which pass in the same plane as the line connecting the points from which the particular lead is secured. Einthoven* has shown that if the strength and direction of the current developed by the heart is rep- resented by a line of given length and direction the relative size of the deflections obtained by the three leads will be proportional to the projection of this line on the sides of an equilateral triangle whose sides represent the connections of the points from which the current is derived from the body. This conception is illustrated in the diagram (Figure 183) reproduced by permission from a paper by Pardee. t In this diagram the line xy represents the strength and direction of the original current arising in the heart. The amount of current recorded in each of the leads is measured by the projection of this line on the sides of the triangle formed by connecting the points from which the current is led off. The magnitude of the deflections of leads I, II and III will be pro- portional to the lines Xjy lt x..y. and .r 3 y a . In the normal heart the ♦Lancet, 1912, i, 853. tjour. Amer. Med. Assn., 1914, lxii, 131 1. 2 34 Changes in Positn III. I I I. API Figure 183 After Pardee. Diagram illustrating- the relative size of the waves of the electro- cardiogram in the different leads obtained from a current which is represented in force by the length and in direction by the position of XY. RA right arm; LA left arm; L left leg. Roman numerals designate the leads represented by the sides of the triangle. ■*! 3"l> - r 2 3'2 an d X Z J'3 indicate the relative amplitudes of the reflections secured from the three leads. Figure 184 After Pardee. Diagram illustrating the variations in direction of the current in the different leads caused by differences in direction of the current developed in the heart. 236 Changes in the Disposition of the Muscle Mass waves of lead II arc larger than those obtained by either lead 1 or lead II. Einthoven, Fahr and I)e Waart* and Williams f have demonstrated mathematically that reckoned from a fixed point in the cardiac cycle lead 11 minus lead 1 equals had III. and if two of these values are known the third can be correctly calculated. The direction of the waves of a given lead depends on the direc- tion of the flow of the current in the heart. This is illustrated by the diagram (Figure 184), in which the effect on the direction of the current in the three leads, due to a difference of direction of currents in the heart, is shown by comparison. The most common variations which one sees are differences in the relative amplitude of the deflections clue to changes in the axis of the heart caused by respiration or an alternation in the position of the body. During inspiration the waves R and T are smaller in lead I and larger in lead III. When the body is turned from the left to the right side there is a deepening of the S wave in lead II. (Irani has found that the 5" wave of lead II was made greater by pathological conditions (left pleural effusions, etc.) which displaced the heart to the right. The records of a case showing an extreme change in the cardiac- axis is shown in Figures 185, 186, 187, 188, 189 and 190. The patient had complete transposition of the viscera and the heart was on the right side of the chest. The records were obtained by the following leads: I = right arm — left arm, II = right arm — left foot, III = left arm — left foot, IV = left arm — right arm, V= left arm — right foot, VI = right arm — right foot. It is plain that by leads I, II and III (those usually employed) the waves de- part from the normal in direction and in amplitude in the different leads. By reversing the electrodes (leads IV, V and VI) the elec- trocardiogram of a normal heart is secured. A one-sided hypertrophy of the heart produces a change in the electrical axis and, hence, a corresponding change in the .u r al- vanometric records taken by the three customary leads. This ob- servation was first reported by Einthoven.l who called attention to the fact that in many cases of left hypertrophy the R wave in ♦Arch. f. d. ges. Physiol., 1913. cl, 275. tAmer. Jour. Physiol.. 1914, xxxv. 292. JZeitschr. f. klin. Med., [909, lxix, 281. Arch. Internat. de Physiol., 1906, iv, 132. 1 ' • *V . 3 \ :'" [iit: ■■''-.. | \ ! . • £ 1 238 Changes in the Disposition of the Muscle Mass lead 1 was increased in size and in lead 111 was diminished or even directed downward, while in right hypertrophy R was small or negative in lead 1 and increased in amplitude in lead 111. The constancy of this phenomenon has been questioned by Hering and others and a number of apparent exceptions have been discussed in a recent paper by Bridgman.f It is probable that some of the discrepancies in the correlation of the heart condition and the changes in the electrocardiograms have been due to insufficient evidence as to the relative masses of the right and left chambers of the heart. In a very careful study of this ([notion. Lewis$ has pointed OUt that the usual methods of examination are quite in- sufficient to determine the relative degrees of hypertrophy of the right and left ventricles. As a rule, he found that his cases of mitral and pnlmonary stenosis, with clinical evidence of right-sided hypertrophy, showed the characteristic electrocardiograms of right hypertrophy, as indicated by Einthoven, while cases of hypertension and aortic insufficiency, with signs of left hypertrophy, showed the graphic evidence ascribed to left hypertrophy. There were, how- ever, a number of discrepancies and these he explains on the ground that the clinical evidence of right or left hypertrophy was not conclusive. In a small number of cases, which he was able to study by separating the chambers by dissection and taking their weights he was able to show that the electrocardiographic records corresponded to the degree of preponderance of the right or the left heart. Fraser* produced experimental right and left hypertrophy in rab- bits by the injection of adrenalin, spartein and bacterial toxins, and was able to show a correlation between the changes in the elec- trocardiograms and careful post-mortem examinations. It seems to me that the evidence is reasonably conclusive that right ventricular predominance is characterized by a diminution in the size of R and a deepening of 6" in lead I, an increase in R and a lessening of .V in lead 111, while left ventricular predominance is shown by an increase in the amplitude of R and a decrease in 5* in lead I, and a shortening of R and a deepening of S in lead III. fArch. Int. Med., 1915, xv, 487. tlleart, 1914. v, 367. *Jour. Exp. Med., 191 5, xxii, 292. -3V 240 Changes [N the Disposition" of the Muscle Mass A comparison of the records obtained in right and left ventricular predominance are shown on pages 239 and _• \ 1 . Figures mi . 192 and [93 were secured from a ease of long-standing hypertension ( -'-'5- 260 mm. Hg.), with physical signs and radiographic evidences of marked left ventricular hypertrophy. Figures 104, i<)5 and 196 are from a patient with mitral stenosis and clinical and radio- graphic evidences of right-sided hypertrophy. Lewis has called attention to the fact that infants under three months of age show an electrocardiogram of the right ventricular hypertrophy type which gradually changes to the normal type. "Sf I i n 11 1 111 i II Hi J H III illitlllllttlllri mil- ' o — fa '5 24 1 fa 5 fM^HHlfH-n ■ ■ »■..;..:.: .::■!:,.!. CHAPTER XVII Treatment GENERAL PRINCIPLES The object of the treatment of myocardial disease is the restora- tion of function. This may be accomplished by ( i ) the removal of an abnormal structural condition of the heart muscle, or, fail- ing this, (2) maintaining a proper relation between the amount of work performed by the heart and its functional capacity. Functional abnormalities are usually the result of organic struc- tural changes; there is little question that we can correct these to some extent and possibly in certain instances restore the muscle cell to the normal. In other instances the functional derangement is dependent on chemical rather than histological changes in the muscle cells or nerve endings, these too are often capable of com- plete correction. An adequate circulation may be secured by improving the con- dition of the heart itself, or by reducing the demands on the heart to a point where a defective myocardium may still be able to per- form the necessary work. It is obvious that etiological studies are of vital importance in determining the means suitable to be employed in the removal of the particular lesion. For example, the acute infections, rheuma- tism and syphilis, each present their individual problems and a corresponding solution. Taken in hand in the early stages, myocardial changes due to such toxins may often be repaired and frequently complete restora- tion of function may be attained. However, as we know only too well our early efforts to avert fixed structural changes are all too frequently unavailing. Diphtheria has left behind degenerative changes, the active inflammatory reaction of rheumatism has sub- sided, but the bands of fibrous tissue separating or replacing muscle cells remain. An active syphilitic process may have been controlled, but the gumma may be replaced by scar tissue interrupting the continuity of functionally active myocardial tissue or may have produced changes in the walls of the blood vessels materially affect- Trkatmknt 243 ing the nutrition of otherwise healthy contractile areas. Advancing years have brought with them blood vessels atheromatous and studded with calcareous deposits and tin- elasticity of their walls is all hut gone. The outside demands of excessive physical exer- tion of the contracted kidney or of a general arteriosclerosis have left in their train dilated cardiac chambers with the myocardium over-stretched or thickened. The recognition of such structural changes demands that we meet the problem by a different method and by new agencies. Though we frankly admit that we cannot dissolve calcareous deposits or replace connective tissue with new muscle cells, we have by no means exhausted our opportunities of service to our patient. There are at our disposal a number of measures which may help to improve the myocardium and an even greater number through which we may influence the demands on the heart and thus limit the stress to the capabilities of the organ damaged beyond possibilities of restoration to the normal. INDIVIDUALIZATION Success in the treatment of myocardial disease is primarily de- pendent upon individualization. It is in this sphere that the newer methods of investigating the myocardium, to which such a con- siderable portion of this book has been devoted, are of greatest value. Up to the present time these studies have been in a large measure directed to discovering the nature of the abnormal func- tion and in designating in each instance the fundamental property of the muscle cell which is at fault. Thus we are able to say with considerable certainty that in one case a defect in conduc- tivity, in another abnormal irritability and in a third a change in contractility, is primarily the basis of the functional change. The effect of drugs and other remedial measures on these fundamental functions of cardiac tissue have been less completely investigated, but such studies as have been made have already furnished infor- mation of great value in determining the mode of their activities and in pointing the way to their employment in abnormal func- tional states. It is needless to suggest that further research along these lines is most desirable and should be a fruitful source of information. It should serve to extend our knowledge in a very useful field and to correct many of the notions now in vogue in J44 Treatment regard to the treatment and management of those suffering from diseases of the heart REST The most important single measure at our command in the treat- ment of diseases of the heart is a curtailing of the work that the heart is called upon to perform. This does not mean that every case showing a defect of myocardial function needs rest, and it is one of the important duties of the physician to determine in each instance whether the demands on tin- myocardium are too great and if so to what degree they should he modified. When the body is at rest, the heart liberates only a small part of the force of which it is capable; the remainder is called the "reserve force." This factor of safety is very considerable in the normal heart and it has heen estimated* that the reserve force of the heart renders it ahle to perform thirteen times the amount of work which it accomplishes when the hody is at rest. A mod- erate amount of physical exertion calls upon the heart for the expenditure of four times as much work as is required in a state of bodily inactivity, hut the normal heart will readily perform this task year after year if its work is alternated with proper intervals of rest. The insufficient heart is one in which the "reserve force" is below the normal. The depletion of the reserve may have been due to excessive demands on a normal heart or normal demands which cannot he met by a damaged heart. It is evident that the term "insufficient heart" is a relative one. The exhaustion of reserve strength may be very slight or of a degree that is barely com- patible with life. When the heart is insufficient and the reserve force is depleted to a marked degree, rest is always indicated. The first object attained by bodily rest is a diminished demand on the heart for work, i.e., the drain on the reserve force is cur- tailed. Important as is this factor, there are other associated bene- fits which should not be lost sight of in reckoning the value of this mode of treatment. Physical inactivity usually entails a slow- ing of the heart. This is brought about by reflex nervous influ- ences affecting the pacemaker. In a normal heart beating at a rate of 70, the cardiac cycle occupies 0.862 second. In such a *Lewy: Ztschr. f. klin. Med., 1896-97, xxxi, 320. Treatment 245 heart Edgren has estimated that duration of systole is 0.379 sec ~ ond, diastole 0.483 second and the time occupied in diastole in a twenty-four hour period is, therefore, over thirteen hours. In the accelerated heart the shortening of the cycle is almost entirely at the expense of the diastolic period, the length of systole remaining practically unchanged. In a heart heating 140 per minute, the total time occupied hy diastole in twenty-four hours is reduced to less than four hours. The diastolic period is the time in which the myocardium obtains its rest and the above figures sufficiently in- dicate the great variations in this period of recuperation with different heart rates. During diastole the molecules are built up, upon which depend the fundamental properties of the muscle cell, and, other things being equal, the longer this period of recovery the more mature will be these molecules and the more effective their dissociation during systole. Thus the contractile power of the muscle cell is proportional to the period of rest preceding its utiliza- tion. The above is illustrative of the advantage to the heart of conditions permitting the fundamental properties of the muscle cell to reach their optimum during each cycle, and for this physical rest is one of our most useful agents. Another important benefit to the muscle cell attained by pro- longing its period of rest is dependent on the fact that the myo- cardium receives its nutrient supply of blood during diastole ; it, therefore, follows that a lengthening of an abnormally short dias- tolic period affords a better opportunity for the muscle cells to receive their full quota of nutrient material, upon which must depend a normal functional activity and the storing of an adequate reserve. The development of cardiac hypertrophy, so desirable in many cases, is dependent on an adequate blood supply, which can best be secured by prolonging the diastolic period. The question may now be asked in what patients, the subjects of abnormal myocardial function, is rest* indicated and to what degree must it be employed? To such a question no categorical answer can be given, but a few suggestions will be offered which may help the physician in formulating the policy suited to the needs of the individual case. *We would define "rest." as used in the present discussion, as any curtail- ment of the physical activity to which the individual is accustomed. 246 Treatment rhe object to be attained is to prevail myocardial damage or, if this is in process, to limit its extent; to maintain a normal dis- tribution of the blood throughout the body, and to accomplish this without permanently reducing the reserve force, or, it' the reserve force is already curtailed, to afford an opportunity for its restitution. Absolute rest in bed is advisable in all eases where an active in- fective process is localized in the heart substance and in the active stages <>i all infectious diseases, the toxins of which are prone to attack the cardiac tissues. It is also indicated in the early Stages for a heart which has become insufficient from any cause what- ever, the insufficiency being suggested by a greater or less degree of dyspnoea and other evidences of improper blood distribution. Frequently, when the reserve force of a heart is only moderately depleted, a period of confinement to bed, while sometimes not absolutely necessary, will allow the patient to shorten materially the time required to recover his balance. In cases of acute or chronic severe cardiac insufficiency, with complete exhaustion of reserve force, absolute rest in bed is imperative. Many mild infections and febrile conditions, such as bronchitis, indigestion, diarrhoea, etc., not ordinarily considered of serious im- port, attain a new significance when they occur in a subject with a weak cardiac muscle; such patients should be confined to bed until the complication has cleared up. Few patients with extreme myocardial insufficiency can he kept flat in bed and some are far more comfortable and will improve quite as rapidly if they are allowed to spend all their time in a chair. The length of time that a patient should remain in bed is often rather a difficult matter to decide. I think the more common error is to allow the patient up too soon, but in a certain number the confinement to bed may be overdone and there is a more rapid improvement if the heart is given the extra work which the change in position entails. The patient should he confined to bed until it i- quite evident that the extreme insufficiency has disappeared and until he has accumulated enough reserve force to change his position and make certain simple movements without inducing symp- toms of exhaustion of the reserve force. Changes to an upright position and the transition to walking and other exercises should Treatment 247 be very gradual and should depend on a study of tin- reaction of each individual to the work thus newly imposed. All advance should be made only under the explicit written directions of the physician. Many cases of mild chronic myocardial insufficiency do not need to go to bed, limitation of their usual physical activities, change in occupation and definite periods of enforced inactivity are suffi- cient to allow the heart to recover a reasonable amount of res< force. In arranging a program for each patient, the ingenuity of the physician will often be greatly taxed. Our prescription must be one which the patient can follow. If merely correct in theory, but impossible of accomplishment, it will be as little creditable to the sagacity of the physician as it is of benefit to the patient. We can do better than to advise a poor man, who has to climb three flights to his two-room tenement, to install an elevator. A tem- porary interruption or a change of occupation may be imperative, but the psychological, as well as the physical, effect on the patient must be carefully considered before this is advised. Our discussion has hitherto contemplated conditions in which myocardial defects are associated with cardiac insufficiency. There are a vast number of patients with disorders of myocardial func- tion, some undoubtedly due to real organic changes, who show no evidence of cardiac insufficiency. In the majority of these rest is not indicated, indeed they are better oft following their usual mode of life, provided this does not involve excessive physical exertion, rather than modifying this and thus introducing a con- tinuous state of introspection which may ultimately unfit them for both the work and the pleasures of life. There are a certain num- ber, however, whose activities should be curtailed, at least for a temporary period, with the object of warding off a subsequent con- dition of exhaustion of the reserve force or of correcting a func- tional derangement which is a source of apprehension to the patient, or his friends. Such individuals are greatly helped if we can as- sure them that the course of treatment is temporary and for the purpose of bringing about a complete restoration of the normal cardiac functions. It is the duty of the physician to sift care- fully these cases, using all the facilities which modern methods have placed at his disposal, and, backed by the evidence thus ob- 24S Treatment tained, assist his patient l>v advising a mode of life suited to the individual conditions. Fear and apprehension arc very Frequent accompaniments of myo- cardial disorders. The most potent influence that can be employed in correcting such psychological states is the kindly but firm as- surance, based on real knowledge, given by the physician to the patient. Mental rest is, to some patients, as important as physical rest. Worry and excitement, acting retlcxly through the extra- cardial nerves, accelerate the heart or exert their influence un- evenly, rendering an irritable heart less able to preserve its rhyth- mic activity and thus reducing its efficiency. The method to he employed to combat such conditions again calls for the most pains- taking efforts of the medical adviser in offering advice suited to the individual. Withdrawal from business or other usual occupations will, in many cases, augment rather than relieve nervous tension. Change of surroundings and mild, suitable diversions may serve our purpose in one case and utterly fail in another. Hence, the study of the psychology of each individual becomes an important part of the physician's duty. In other portions of this book the significance of special dis- orders and the amount of rest suited to each is discussed. EXERCISE The indications for and method of transition from a state o\ complete bodily rest to movements requiring moderate muscular exertion have been touched upon in connection with the discus- sion of rest. It remains for us to consider the advantages which may be secured by exercise, the class of cases upon which regu- lated activities have a favorable effect and the methods which should be utilized in applying this form of treatment. The most evident effects of moderate exercise on a normal heart are an immediate increase in rate and the blood pressure. If the exercise has not overtaxed the heart, its rate and the blood pres- sure will return to normal a few minutes after the cessation of the exercise. In general, the insufficient heart reacts to exercise in the same manner as the normal heart, provided that it too is not over- taxed. In order that a heart may not be overtaxed, the demands put upon it must fall below its maximal working capacity, which consists of the sum of the force necessary to carry on the cir- Treatmeni 249 dilation while the body is at rest rind its reserve force. The dif- ference in the working capacity of the normal and the insufficient heart is a difference in the amount of reserve force. There is no advantage to an insufficient heart in the increase of rate produced by exercise, but if the acceleration is not excessive and the period of its duration is brief, it usually has no detrimental effect. T1k heightened blood pressure in the first part of the aorta increases the amount of blood passing through the coronaries, and this furnishes more nutritive material to the myocardium. As a result of this, the individual muscle fibers become larger* and actually increase in number.f Hence, there is a thickening of the musculature which we recognize as hypertrophy of the heart. Exercise increases the work of the heart. The heart reacts to this increased work with hypertrophy. Hypertrophy means, at least for a time, an increased reserve force. Aside from the direct effect on the myocardium, exercise facilitates the return flow of the blood from the extremities and reduces the work of the heart ordinarily expended in this direction, while at the same time there is an increased flow of blood to the right side of the heart. A discussion of the benefits to the patients from exercise other than those directly affecting the circulatory apparatus are beyond the scope of the present papers. But such items as the relief of congestion of the various organs of the body, the improvement in appetite and digestion, the betterment of the excretory activities of bowel, kidneys and skin, the betterment of respiratory condi- tions, etc., etc., should not be forgotten in estimating the value of this form of therapeutics. In considering the classes of patients who may be benefited bv a course of graded exercises, it may be well first of all to enu- merate those in which any measures of this kind are absolutely contraindicated : 1. Acute infectious diseases in which a myocardial involvement has commenced or may be apprehended. 2. Acute dilatation after overexertion. 3. A heart which is not compensated during complete bodily rest. 4. Angina pectoris. ♦Goldenburg: Virchows Arch., 1886, ciii, 88. fZielenko : Ibid., 1875, lxii, 29. 250 Treatment 5. Cardiac asthma. <>. Chronic nephritis. 7. General arteriosclerosis with high blood pressure. Among those to whom we may be confident thai properly reg- ulated exercises will be of benefit, arc: 1. Young people with disproportionate small hearts. We see this condition not infrequently in young persons who have grown rap- idly, but whoso cardiac development has apparently failed to keep pace with the vest of the body. It occurs not only in those of sedentary habits, but also in boys who are exercising vigorously. These may show signs of cardiac insufficiency of a mild grade, with no discoverable abnormality other than a myocardium that is relatively small. These patients should not be deprived of their exercise, but for their irregular and often too violent activities a course of regular and carefully graded training should be substituted. 2. Those of sedentary habits whose cardiac tissues are sufficient in quantity; but deficient in quality. Here exercise acts as a direct stimulant to cardiac metabolism and the results of its employment are most gratifying. 3. Young persons with sinus arrhythmia. The instability of the pacemaker and its sensitiveness to reflex nervous influences, are often favorably affected by properly controlled exercise. 4. ( >bese patients in whom the cardiac reserve is not sufficient to support the extra burden of overweight. In these a strict dietary should play an important part. In the very aged, or when arterio- sclerosis is present, exercise should be used with great caution. Lying midway between the group in which exercise is distinctly contraindicated and the group in which we may invariably expect favorable results from its employment, art' many cases in which the results of exercise cannot be as confidently predicted. We should always individualize, but in the cases under consideration a minute study of each patient's condition and his reaction to exer- cise is particularly required. For the most part, these arc patients wdio are convalescing from an acute myocardial process or chronic cases whose hearts have become decompensated; all of them show a greater or less impair- ment of reserve force and a period of rest must precede any meas- ures directed toward increasing the work of the heart. This is Treatment 251 especially the case in those in whom the reserve force has been depleted hy physical exertion which has exceeded the maximal work- ing capacity of the heart. After a period of rest, during which the heart will have had an opportunity of adding something to its reserve force, massage or the mildest forms of resistance move- ments may he tried for brief periods; if the reaction of the patient to these mild procedures is favorable, they may he continued and gradually increased in the manner indicated below. If, however, the cardiac response is bad, rest must he continued and all forms of activity deferred to a subsequent and more propitious occasion. The chief advantages of the introduction of a course of graded exercises are that both passive and active movements of this kind can be more accurately measured than in the case of voluntary indiscriminate activities, which the patient will undertake when not under close supervision. Progress is more uniform and con- valescence is less apt to be interrupted by frequent temporary set- backs due to thoughtless excessive demands on the reserve force, and is therefore shortened. In order that the patient may receive benefit from this form of treatment, it must be conducted under the closest supervision of the physician. The physician must either carry out the treatment in person or must be present during each of the earlier treatments and at intervals during the later stages, in order that he may observe the patient's reaction and advise as to the rapidity witli which advances shall be made. When the effect of treatment is established, the physician may by degrees avail himself of the assist- ance of a trained attendant always working under his direction. On a number of occasions I have seen considerable harm as the result of the well-meaning, but injudicious, efforts of an attendant ignorant of the limits which should be imposed. The physician must prescribe the kind of exercise, the length of treatment and the intervals of rest in each instance and vary these in accordance with the changes in the reserve force. The physician is guided in measuring the amount of exercise desirable by the reaction of the patient. This does not mean the subjective sensations of the patient, as these are often misleading. The best guides are a study of the pulse rate and blood pressure. One can- not lay down actual figures, but the increase in pulse rate during 2 5- Treatment the exercise should never be excessive. A good reaction, as indi- cated by the pulse rate, is one in which the rate increases during exercise (not over 20 beats per minute) and returns to the pre- exercise rate or below this within 3 minutes after the cessation of the exercise. Systolic blood pressure should show a maximum in- crease on the completion of the exercise. If the pressure rise is prolonged after the pulse rate begins to decline, it indicates that the work to which the myocardium has been subjected is excessive. The most important principle to be observed in planning a course of graded exercises is to regulate the demands on the heart so that they shall never exceed its reserve force. If the treatment is commenced very early, that is, before the patient is allowed out of bed, or even when he is beginning to sit up, at a time when the reserve force is still small, a start should be made with gentle massage of the extremities, always working from the periphery toward the trunk. Short periods of massage (10 minutes) should alternate with ten-minute periods of rest, and the whole treatment should not consume more than half an hour. As the reserve force increases, the massage may include the whole body. The periods of rest may be shortened and the duration of treatment lengthened, but it should never exceed one hour. Following the course of massage, passive exercises may be introduced. Here the patient relaxes completely and his extremities are gently moved by the attendant. Next are added simple voluntary movements made by the patient at first slowly without resistance, later more rapidly and against resistance furnished by the attendant. This may, in turn, be followed by exercises involving self-resistance, in which certain muscles are contracted by a voluntary effort against resist- ance introduced by opposing sets of muscles (e.g., the patient imag- ines he is lifting a weight with one hand, etc., etc.). All these exercises should be employed for short intervals only, alternating with periods of rest, and a period of complete relaxa- tion in the horizontal position for half an hour or more should follow each treatment. Along with these exercises the patient should be taught the proper method of breathing, a very important element in facilitating blood flow. Patients with a fair amount of reserve force should be allowed Treatment 253 to walk short-measured distances on the level, later the distant e may be increased and climbing may be tried. The changes should be very gradual and always controlled by a study of the effect which the prescribed exercise produces. A patient with a permanently damaged heart must be taught that there arc definite limits to the stress with which his heart can definitely cope, and he must learn to live within these limits or pay the penalty. What the limits may be can only be determined by a careful study of the indi- vidual. The degree to which some patients with severe grades of myocardial insufficiency can improve is extraordinary. They may reach a point where they can do a surprising amount of heavy manual labor with impunity. In selecting the form of exercise suitable for a patient whose heart has attained a fair degree of strength, it is often helpful to ascertain the kind of exercise in which he is proficient. On the links a trained golfer will make much less demand on his reserve than the beginner, even riding may be permissible for a skilled horseman. It has been our purpose to outline the principles involved in ap- plying systematic graded exercises, the details of the various meth- ods as advocated by Herz and Zander, Oertel's Terrain cure, Schott's modification of the Swedish movements as used at Nau- heim, Barringers dumbbell exercises, etc., etc., are best studied in the original papers or in special treatises devoted to these subjects. BLOOD-LETTING Under ordinary conditions, the hydrostatic pressure in the vas- cular system tends to make the blood in the veins rise to the same heights as in the arteries. The force of the heart, assisted by the suction action of respiration and the muscular pressure on the veins, returns the blood to the heart at the same rate at which it is sent out. A prominent feature of many cases of cardiac insuffi- ciency is an abnormal distribution of the blood. A weak myo- cardium, with loss of muscular tone, predisposes the cardiac chambers to dilatation ; when the right ventricle is thus affected and tricuspid insufficiency ensues, the back pressure leads to an overfilling of the veins and right heart. It is under these condi- tions that bleeding: is often of great value. The volume of the 254 Treatment blood brought to the heart is reduced and the embarrassment of the right heart is at leasl temporarily relieved. Venesection lias an effeel thai is essentially mechanical. It de- creases the amount of blood brought to the right ventricle, hence this contracts more completely and more efficiently and forces more blood into the left heart, which, in turn, sends more blood into the aorta. This increases arterial pressure and, incidentally, the blood flow in the coronaries, thus improving the nutrition of the myocardium. The indications for venesection arc an overdistended right heart and venous engorgement in a patient whose condition demands prompt interference, where there is no time to wait for the action of drugs or other remedial measures or where these have failed. The procedure will often afford a respite during which other meas- ures may have an opportunity to act. I deeding is best accomplished by opening a superficial vein at the bend of the elbow after applying to the upper arm a bandage sufficiently snug to obstruct the venous return. By puncturing the vein with a good-sized aspirating needle, to which is attached a rubber tube leading to a flask, much of the disorder incident to the cruder methods may be avoided. The blood flow may be facili- tated by gentle mouth suction by the operator on another tube lead- ing from the flask. The blood flow is also increased by getting the patient to close and open the hand, thus forcing the blood through the veins by muscle contraction. The best results are usually secured by the removal of 300 to 500 cubic centimeters of blood. DIET There are few general principles which can be laid down as a guide in regulating the diet of those suffering from myocardial disease. The relation of protein intoxication to the degenerative changes of various organs, is a subject pregnant with interesting possibilities, but as yet our knowledge is but a step advanced be- yond the sphere of pure speculation. If our therapeutics are to be used with a conviction which is based on a reasonable logic, the application of these hypotheses to the treatment of our patients must await the discovery of further facts which may link together the fragments which at present can only be called suggestive. Treatment The beneficial effects of the administration of large quantitie of sugar is based on evidence secured by perfusing the isolated heart with fluids containing sugars of varying amounts'*' and is supported by a considerable amount of rather unconvincing clin- ical evidence. f My own experience with this procedure has been limited and thus far inconclusive. Regulation of the diet is important, but should be directed toward the correction of conditions frequently very remote: from the hearl and which influence the myocardium in ways indirect, but often efficacious. Among such conditions the patient's weight should receive con- sideration as a factor of first moment. Excessive weight is a very common complication of chronic heart disease, because, as a rule, restriction in the amount of food has not paralleled the reduction in bodily activity. The requirements of the body at rest are less than twenty-five calories per kilogram of body weight. Those whose activities call for great physical work often utilize 50 calories per kilo. When a patient's mode of life is suddenly changed from one of severe physical exertion to one of comparative inactivity, the tendency is for him to continue taking the quantity of food which habit has established. As a result, the body requirements are more than supplied and the surplus is stored as fat, which soon is an additional burden to be carried by a heart whose reserve already shows too narrow a margin. It follows that when a physician curtails the physical activities of a patient with an in- sufficient heart, the diet should be restricted as a prophylactic meas- ure. When an excessive diet has already produced a condition of obesity, the overweight must be gotten rid of by a carefully insti- tuted reduction cure. The details of a regime suited to the needs of the various types which we meet need not detain us, but we should bear in mind that dependence must be placed almost en- tirely on the restricted caloric value of the ingested food. Exer- cises can be employed to only a very limited extent and drugs are worse than valueless. The weight should be reduced very gradually. I believe the best results are obtained when the loss is about one pound a week. *Locke and Rosenheim : Zentralbl. f . Physiol., 1905, Xo. 20. Dec. 30. fA. Goulston : Cane Sugar and Heart Disease, London, 1914. 256 Treatment The antitheses to these ohese patients are not infrequently seen. They are below average weight and are poorly nourished. Most often they are young persons \\ln> are growing rapidly. Some- times they have had repeated attacks of rheumatic fever. The whole musculature is below par and the myocardium has suffered along with the other muscles of the body. To these judiciously forced feeding is of great value. Patients suffering from chronic nephritis with high blood pres- sure and a heart laboring beyond its capacity are best treated dietetically with foods, the end products of which make the least demand on the eliminative capacity of the kidney. The kind of food best suited to the individual case can only he determined by a careful study of the functional activities of the kidney in each case. Those with infectious diseases running a febrile course with inter- current myocardial involvement should be fed with small quantities of nutritious food at frequent intervals. The management of the diet does not differ from that of the uncomplicated disease, except that, as a rule, it is well to keep the administration of fluids within reasonable bounds. In general, patients with well-marked cardiac insufficiency do better when given small meals at frequent intervals ; five or six feed- ings in the twenty-four hours are usually better than three meals. The majority of the diet should consist of solid food. Quite as important as the proper direction of the kind and quan- tity of the food is the regulation of the water balance. The rela- tion of cedema, ascites, pleural effusion, etc., to myocardial insuffi- ciency is intricate and a full discussion would lead us far afield. The volume of the circulating blood undoubtedly has a considerable influence, not only on the amount of work which the heart is called upon to perform, but also must be reckoned with as a direct factor in producing dilatation and hypertrophy. The most notable example of this condition is met with in the so-called "beer heart." Here the myocardial changes may be the result of several elements, such as the alcohol and carbohydrate content of the beverage, the severe physical exertion to which most of these patients have been sub- jected and the increased volume of the blood following the inges- tion of enormous quantities of fluid. Practically all competent ob- servers are agreed that the latter is the most important factor Treatment 257 in inducing the change in the hear! muscle. The aspiration of tin- pleura, or the removal of ascitic fluid, will often relieve the -train on a laboring heart and furnish the starting point for the recovery of its reserve force. The disappearance of oedema is frequently the forerunner, rather than the result, of improved heart action. With this end in view, the stimulation of kidney activity and the reduction of the sodium chloride intake may he of considerable indirect benefit to the heart. As a general rule, those suffering from myocardial insufficiency should not take over one and a half liters of fluid a day. Many, particularly those having oedema, are greatly benefited by a more restricted fluid intake. We are not as yet in a position to designate the exact types which will respond favorably to an extreme limi- tation of fluid ingestion, but not infrequently the employment of this method yields brilliant results. The diet suggested by Karell* *Karrell Diet. For the first five to seven days, milk 200 cc. at 8 and 12 a.m., 4 and 8 p.m. No other food or fluid. Eighth day : milk as above and at 10 a.m. one soft-boiled egg; at 6 p.m., two pieces of dry toast. Ninth day: milk as above and at 10 a.m. and 6 p.m. one soft-boiled egg and two pieces of dry toast. Tenth, eleventh and twelfth days: milk as above, and at 12 m. chopped meat, rice boiled in milk and vegetables ; 6 p.m., one soft-boiled egg. (No salt is used throughout the course. Salt-free toast and butter used. Small amount of cracked ice allowed with diet. All meat can often be advantageously omitted.) From Dr. Herbert S. Carter's Diet Lists, Saunders, Phila., 1914. is one of the most satisfactory means of securing the desired fluid restriction. During such a course the patient should be confined to bed. Not infrequently a patient who has shown a prompt im- provement on a Karell regime may be benefited by later using such a diet one day each week. BEVERAGES The regular use of alcohol in those suffering from functional or organic disease of the myocardium, is to be deprecated on theoret- ical grounds. There is little doubt that its habitual use affects favorably neither the heart muscle nor its controlling nervous mech- anism. And yet I think there are many patients accustomed to the use of malted and spirituous liquors by years of habit in whom the entire withdrawal of all alcoholic beverages is a distinct detri- ment. To young adults, all alcoholic drinks should be forbidden : elderly people accustomed to its use often do better if allowed _'5S Treatment moderate quantities. Light wines, good whiskey or brandy are to be preferred to malted drinks representing an equal amount of alcohol. These should be taken at meal-time and in amounts defi- nitely prescribed. Tea and coffee should be regulated much in the same way as alcohol, tlu-\ are not to be indiscriminately forbidden and in certain instances the effect dt" the contained caffeine is of distinct value. < OLD APPLICATIONS The application of cold to the precordium, l>v means of an ice- bag or a Leiter's coil, often seems to be of advantage in rapid, overacting hearts and in tachycardias of sinus origin. The rational explanation of such a procedure present difficulties. We know that the formation of stimulus-material is slowed hv a direct applica- tion of cold to the sinus region, but it is hardly conceivable that a precordial icebag will produce a degree of cold sufficient to penetrate to such a depth. The precordial poultice and hot fomentation are frequently com- forting to the patient. It is doubtful whether they have any more profound therapeutic effect. BATHS In a certain number of patients suffering from myocardial dis- ease, a course of baths seems to be of considerable value. Waters containing carbon dioxid and simple brine have been employed with satisfactory results. The reaction of the individual patient must be studied. The first bath should be a weak one, just below body temperature and should last not over six minutes. It the patient is comfortable, if there is no increase of dyspnoea, and if the pulse .and heart action are improved, the baths may gradually be made stronger, the temperature lowered and the time length- ened. The method is almost wholly empirical and we have little knowledge of the physiological processes through which the bene- ficial results are obtained. Nervous reflexes, following cutaneous stimulation and altered vaso-motor tone, are probably elements of importance, but much careful observation and scientific study is necessary before we can offer a logical explanation of the modus operandi and a more accurate outline of the indications for and a' r ahiNt these measures. Treatment 259 SPA TREATMENT The value of spa treatment, I believe, has been greatly over- estimated. The benefits derived from a visit to a well-organized resort arc due mainly to the ordered regime to which the patienl is subjected under the watchful care of a skilful physician, the relaxation from the cares of business and home, the change of scene and opportunities for properly regulated pleasures. The spe- cific value of special waters and complicated apparatus are of very minor importance. The miraculous cures which are often claimed in the name of the spa may be equalled in the experience of any skilful practitioner. Most patients are much more readily controlled in a place re- moved from accustomed ties and responsibility, and where it is the fashion to follow the minute directions of the medical adviser. The conscientious physician, in considering the probable value to be derived by his patient from spa treatment, must take into account the long journey, its attendant fatigue and expense. He must see to it that his patient is placed under expert medical care and is not allowed to drift into the net of the unbalanced faddist or the unscrupulous charlatan, who unfortunately are not less in evidence at the most famous cures than elsewhere. CHAPTER XVIII Treatment DRUGS In the present discussion of drugs in the treatment of abnormal- ities of myocardial function, we will limit ourselves to a consid- eration of a very small number and will examine only their direct action on the myocardial tissues or their indirect action through the vagUS and accelerator nerves. It is often most important in treating myocardial disorders to correct or modify the condition of organs other than the heart. Thus a change in kidney function or an alteration in the size of the peripheral arteries may he a far more efficient means of im- proving cardiac function than anything which we can do to the heart muscle directly. It is not, however, our purpose to discuss drug activity from this standpoint. We will, therefore, confine our attention to those drugs which have a direct action on the myocardium and will omit a consideration of the effect of the drugs of our selected list upon other organs of the body. These aspects are presented in the proportions which they deserve in the standard works on pharmacology and works devoted to the broader discussion of diseases of the heart. An excellent resume of the experimental work has been compiled and discussed by Win- terberg* and should he consulted by those particularly interested. The graphic methods of recording circulatory changes have greatly improved the detail and accuracy of our clinical observations. By these means we may discover minute alterations which have been hitherto impossible of detection. It is probable that the next few years will add much to our knowledge of the usefulness and use- lessness of drugs. ADRENALIN The extract of the suprarenal gland finds its chief effect on the wall of the peripheral blood vessels. There is considerable evi- ♦Handb. d. Path., Diagnostik, u. Tlicrap. d. Herz. u. Gefasskrankungen, Leipzig, 1914, iii, H. 2. 260 Treatment 261 dence that it also has an influence in increasing the activities of all of the fundamental properties of the myocardial cells, notably heightening the irritability and the contractility, it may be thai this is due to a direct action on the muscle cell or, indirectly, through its effect on the sympathetic nerve for which this drug seems to possess a selective activity.* In large doses and under special conditions (see "ventricular fibrillation") adrenalin may produce extreme myocardial irritability and many types of arrhythmia. f On account of its influence in increasing the contractility and the tone of the heart muscle, it has been recommended in acute dila- tation and in conditions of surgical shock. Until our knowledge is more complete, I believe that we should employ adrenalin with great caution in conditions of acute heart failure, recalling that in association with anaesthesias of light degree^ it has a tendency to produce great irritability, which may result in ventricular fibril- lation and a fatal outcome. There is considerable experimental evidence which indicates that, while adrenalin acts as a constrictor on most of the peripheral arteries, it produces a widening§ of the lumen of the coronaries. ALCOHOL The effect of alcohol on myocardial activity is probably purely reflex and the result of functional changes in the central nervous system and modifications of vasomotor control. The slowing of the heart, following the administration of alcohol in febrile affec- tions, is probably due to its influence in diminishing cerebral ex- citement. Alcohol has no effect on muscle when brought to it in the blood stream, but when applied directly to the muscle it weakens its contractions (Cushny). AMMONIA probably has no direct effect on the myocardium. Its influence in reducing heart rate is by reflex nervous inhibition. Its effect is quite rapid and disappears in a few minutes. *Rothberger and YVinterberg : Pfliiger's Arch., 191 1, cxlii, 461. fKahn: Arch. f. d. ges. Physiol., 1909, exxix, 379. tNobel and Rothberger: Ztschr. f. d. ges. Exp. Med., 1914. iii. 151. §Janeway and Park: Jour. Exp. Med., 1912, xvi, 532, 541. _•<._• Treatmi n r ATROPINE modifies cardiac activity through its effect on the vagus nerve con- trol. It probably lias no direct influence on the myocardial cells, although given in toxic quantities to experimental animals it is said to depress the property of contractility (Ringer). The first effect of atropine is to stimulate the vagus through its center in the medulla and thus cause a slowing oi the heart. This effect is very slight and quickly passes off. It is succeeded by an increase in heart rate due to a paralysis of the inhibitory terminations oi the vagus nerves. That the influence is due to its action on the nerve endings is indicated by the fact that after its administration stimulation of the vagi has no effect on cardiac activity, whereas it" the action were central stimulation of the vagi should still slow the heart. The accelerators are not affected by atropine. Children show very little cardiac response to atropine. The reac- tion to the drug gradually increases with maturity and reaches its maximum in those about thirty years of age. In advanced years the reaction is less marked than in middle life. In man the slow- ing of the heart occurs about five minutes after the subcutaneous administration. This disappears in a minute or two. The maxi- mum increase in heart rate appears twenty to thirty minutes alter its exhibition. From this tune the rate gradually lessens and re- turns in an hour or two to the rate which preceded its administration. Atropine is useful in correcting a heart action which is too greatly slowed by an overacting vagus. Thus, in a heart block which is due to a hypertonic vagus, the block may he promptly broken by its administration. The slowing effect of morphine may he neutralized by atropine. When digitalis has been given to excess, a part of its influence may he promptly opposed by a hypodermic of atropine. Its administration is a useful diagnostic means of distinguishing the vagal influences in heart block and cases of sus- pected hypervagotonicity from those in which the defect is intrin- sically in the muscle cell. If the disordered myocardial function is due to an excessive activity of the vagus, the atropine will speed- ily remove this influence. In an adult with a heart rate under 60, 1.3 milligrams ( i/5° grain 1 may he given subcutaneously and may he repeated when the effect has disappeared. Unfortunately, the drug is not well Treatment 263 suited for prolonged therapeutic effects, for if the dosage is con- tinued at a level to maintain the vagus paralysis other symptoms, such as dryness of the pharynx, dilatation of the pupil, etc., make the patient very uncomfortable. CAFFEINE and the closely related substances, theobromine and theophyllin, exert an influence on both the extracardial nerves and on the muscle cells of the heart. In experimental animals caffeine may slow the heart by central stimulation of the vagus and depression of the accelerators (Fredericq). \n man such an effect is very incon- stant. Small doses in animals usually accelerate the heart by in- creasing the irritability of the sinus node (Cushny and Naten*). This effect is independent of any action on the regulatory mechan- ism of the heart, since it is seen when the accelerators are cut and when the vagus is paralyzed by atropine. In dogs large doses produce auriculo-ventricular dissociation (depression of conduc- tion). In animals in which an artificial heart block has been pro- duced by a destruction of the bundle of His, caffeine augments the irritability of the ventricle so that the ideo-ventricular rate is increased and many extrasystoles appear.f The evidence as to the effect of caffeine on contractility is somewhat conflicting, but in- clines toward the view that in moderate doses it improves the working efficiency of the heart. In a few patients to whom I have administered theocin as a diuretic, there have appeared immediately thereafter large num- bers of extrasystoles and in one case a paroxysm of tachycardia, which, as far as could be determined, was unique for this indi- vidual. These observations have led me to be cautious in the use of caffeine and closely related drugs in myocardial conditions show- ing a high degree of irritability. It suggests that the excessive use of tea and coffee in susceptible individuals may be the cause of extrasystoles. CAMPHOR is one of our drugs which has long enjoyed a reputation as a direct stimulant to cardiac muscle. We have at present no con- clusive evidence that it favorably affects the heart muscle. Its use *Arch. Internal:, de Pharmodyn et de Therapie, 1901, ix, 169. fEgmond : Pniiger's Arch., 1913, cliii, 39. 264 Treatment has been advocated in auricular fibrillation, but recent reports make it appear that it is of doubtful value in this condition. CHLOROFORM acts on the heart indirectly by stimulating the vagus center, thus slowing the heart, and also has a direct influence on the muscle cells of the heart. Chloroform depresses conductivity to such an extent that at times an auriculo-vcntricular block is established. It may greatly increase the irritability of the ventricular wall so that mam extrasvslolcs appear which may pass into a ventricular tachy- cardia and thence to ventricular fibrillation which is uniformly fatal. The observations of Levy* seem to indicate that the most detrimental effects to the myocardium are wont to occur during light aiuesthesia, so that arrhythmias are most common when the patient is in the early stages of anaesthesia or is beginning to recover from its effects. The dangers of the use of adrenalin, in conjunction with chloroform, have already been noted (see "ven- tricular fibrillation" and "adrenalin"). DIGITALIS Digitalis obtained from the purple foxglove is the most impor- tant member of a group of drugs which have a similar action on the heart. In this series are included strophanthus, squills, helle- bore, convallaria, apocynutn and several others less well known. Of this group of drugs digitalis has received by far the greater study and, since all the members of this series affect the myocardium in a similar manner,f our discussion will be in the main limited to digitalis and the alkaloids which are derived from it. The glucosides obtained from digitalis include digitoxin, digitophyllin, digitalin, digitalein and digitonin. All of these glucosides are pres- ent in the infusion; digitonin, being insoluble in alcohol, is absent from the tincture. Pharmacological studies indicate that digitalis acts in a twofold manner on the functional activities of the heart. It has a direct effect on the muscle cells and an indirect influence through the vagus nerves. The influence on the fundamental properties of the muscle cells has been analyzed to some degree. Tunc: this ♦Heart: 1913, iv, 319. tCushny: Jour. Exp. Med., 1897, ii, 233. 265 Figure 203 Digitalis effect. Delayed conduction. a-c intervals — 0.4 second. Figure 204 Digitalis effect. 2 to 1 block. Auricular rate 80. Ventricular rate 40. Jugular Brachial Jugular Brachial 0.2 second Jugular Brachial 0.2 second Figure 205 Digitalis effect. Coupled rhythm in a case of auricular fibrillation. 266 Treatment property is distinctly modified by digitalis, its direct action on the muscle is to increase its tone and to render relaxation less com- plete, the heart becomes smaller in s] stole and dues not dilate .so fully in diastole. Hand in hand with this direct action on the muscle, digitalis exerts a stimulating effect on the vagi, through this influence the heart is slowed and the tendency to diastolic re- laxation is increased. Hence, the effect of digitalis on cardiac tone is the resultant of these two opposed factors and the tonicity will he increased or diminished according as the direct muscle effect or the indirect vagus effect is predominant. In a like manner the efficiency of the heart to empty itself will depend on the rela- tive degree to which each of these factors comes into play. Con- ductivity is depressed so that one often sees in the experimental animal a complete auriculo-ventricular block. The depression of conductivity is due in part to vagus influences, since the block can at times be removed by cutting the vagi. However, there is some evidence which suggests that the dissociation is also due to a direct action of digitalis on the cells of the myocardium. The irritability of the heart muscle is increased by digitalis. Thus, in the isolated heart which has ceased to heat, the addition of digitalis to the perfusion fluid may induce rhythmic contractions. All these modifications of the fundamental properties of the heart muscle which have heen ohserved in the experimental animal may be seen in man. We have as yet no accurate means of meas- uring the tonicity of the heart in the human subject, hut most clinicians believe that it is increased by the administration of drugs of the digitalis group. A depression of conduction, even to the degree of complete auriculo-ventricular dissociation and increased irritability (as evidenced by the production of extrasystoles), are common sequela: of the exhibition of digitalis in the clinic. While the experimental study of digitalis has afforded us much valuable information in regard to the nature of its activity, it should be remembered that such investigations must of necessity he car- ried out on hearts with a myocardium approaching the normal or the damage which has been artificially produced is an acute change which is probably quite different from the myocardial changes which are commonly seen in the clinic and checked up at the post-mortem examination. -'7 I • : PR VR *f* t f**{**f*f*"f Hi ^^ S 5 Figure 2nt> February 24, 1916. Before digitalis. PR -pn ^f*" f*^f**"*P~*f**f** f m "( Figure 207 March 9, 1916. Sinus slowing. LTZHF rr 1 r P R R P PR -P * a Figure 208 March 13, 1916. Complete block. Figure 209 March 15, 1916. Complete block and coupled rhythm. Every other ventricular beat is an extrasystole. All these records are from the same patient and show the progressive effect of con- siderable doses of digitalis in a myocardium susceptible to its influence. All of these records were taken by lead III. 268 Treatment It is, therefore, most fortunate that the polygram and electro- cardiogram have come to <>ur aid in the study of the effects o\ this and other drugs in man under the conditions which arc seen in health and disease and which it is impossible to reproduce in the experimental animal. The alterations in the rhythm of the heart under the influence ol digitalis are: (i) a slowing (due to a depression of stimulus for- mation at the sinus node induced by vagal influences) ; (2) a slow- ing and development of arrhythmia, with modification of the prop- erty of conduction (due to change in the A-V junctional tissues through a direct effect on the myocardium and an indirect effect through the vagus), and (3) an increased irritability causing new forms of irregularity to appear (extrasystoles, fibrillation, etc.). Some of these changes may be detected by the ordinary methods of physical examination. The change in rate of sinus origin is usually only of moderate degree; when due to alteration in con- duction, the slowing may he much more marked, so that, with complete hlock, the ventricular rate may he reduced to 30 a min- ute. These conduction changes may sometimes he verified by ob- serving the rate of the jugular pulsations in the neck and comparing them with the apex impulse (see "conduction defects," Chapter VI). The increase in irritability is identified by watching for the development of complete irregularity (see "auricular fibrillation," Chapter XI) or of extrasystoles (see Chapter VII), notably the so-called "coupled rhythm," in which two beats are followed by a pause: the second of these beats is an extrasystole and the pause is the ordinary "compensatory pause" which is associated with extrasystoles. At first this digitalis effect may he observed as oc- casionally occurring extrasystoles, later every other heart contrac- tion is an extrasystole with a compensatory pause and this is man- ifested as the "coupled rhythm." The polygram helps us in detecting these digitalis effects and is a much more accurate indicator of the changes in heart rhythm than inspection, palpation and percussion. Records from three cases under the influence of digitalis may be seen in Figures 203, 204 and 205. In Figure 1 the a-c inter- val is greatly prolonged and measures 0.4 second. In the case whose curve is shown in Figure 204 the brachial pulse rate is Digitalis 269 Figure 210 Coupled rhythm. Digitalis effect in a case of auricular fibrillation. Figure 211 Coupled rhythm. Digitalis effect. Every other ventricular beat is an e.xtrasvstole. Case of auricular fibrillation. 270 Treatment perfectly rhythmic and only 40 a minute; the auricular rate is 80 and the slow ventricular rate is due to a 2 to 1 block. The patient whose tracing is presented in Figure 205 was a case of auricular fibrillation which showed the toxic effects of digitalis by the development of the coupled rhythm; the brachial shows a rate dt 67 per minute, hut examination of the jugular curve shows that the ventricle was beating at a rate of ij.| per minute, hut only every other one of these heats makes an impression on the brachial curve. 'The second heat of the couple is a ventricular ex- trasystole and is followed by a compensatory pause. A rhythm of this character and of such a rate indicates a high grade of irri- tability of the ventricular muscle and is a warning that digitalis must he immediately discontinued. The electrocardiograms bring out these changes even more clearly. Figures 206, 207, 208 and 20<; are all taken from the same patient at intervals of a few days during the administration of digitalis. Figure 206 presents the rapid rate ( 145) with a normal P-R interval hefore digitalis was commenced. (All these figures record lead 111, in which in this case the .V wave was abnormally deep, suggesting left ventricular preponderance; see Chapter XVI.) In Figure 207 is seen a slowing of the whole heart 1 sinus effect) and prolonged P-R interval (.-/-/' conduction delay). Figure 208 shows still greater sinus slowing and a partial block. Figure 209 portrays an even less rapid sinus activity, complete block and the "coupled rhythm," in which the second heat of each pair is a ventricular extrasystole, indicating a high degree of myocardial irritability. Records of two cases of auricular fibrillation, with different grades of ventricular irritability, are presented in Figures 210 and 211. It is quite evident that the irritability of the heart recorded in Figure 211 is very extreme, much more than that shown in either Figures 209 or 210. There is another very interesting change in the electrocardiographic records under the administration of digi- talis which has been recently described by Cohn, Fraser and Jamie- son.* This consists in a change in the contour of the T wave. A T wave which is positive in direction before the use of digitalis becomes smaller, diphasic or even directed downward when the *Jour. Exp. Mod., 1915, xxi, 593. _7- l'ki' \TMKNT heart becomes digitalized. This is well shown by comparing Fig- ures 212, 213 and J14, the three leads taken before and Figures 215, 216 and -17 secured after the administration of digitalis. This sign is a valuable guide in determining whether the heart muscle is being affected by the digitalis. The discoverers found it as the earliest evidence of digitalization in 34 out of 36 cases. They also call attention to the fact that influences other than digitalis may, on rare occasions, produce a similar modification of the size and direction of the T wave. There is considerable clinical evidence that digitalis acts both on the muscle cells of the heart directly and indirectly through the vagi. The changes which occur in the T wave suggest this.* If the heart is brought thoroughly under the influence of digitalis, and tlie vagal influences are removed by administering atropine which paralyzes the terminals of the vagus in the myocardium, cer- tain digitalis effects will still persist.! Digitalis has a greater in- fluence on the damaged than on the normal heart muscle. This is particularly true of hearts which have been injured as the re- sult of rheumatic fever and those which show conduction defects. Digitalis is particularly indicated in the dilated heart with a re- duced muscle tone and in cases of tachycardia, where the rapid ventricular rate is due to impulses arising in abnormal foci in the auricles which are showered upon the A-V junctional tissues (auricular fibrillation and auricular flutter) ; here it is given with the purpose of blocking, partially or completely, the stimuli from the upper chambers. Digitalis is usually contraindicated in those showing frequent ex- trasystoles, unless it can be shown by careful observation that it does not increase the myocardial irritability. It is rarely of value in tachycardias of sinus origin such as are seen in certain forms of auricular paroxysmal tachycardia, Graves' disease and in the acute infections. In hearts showing a partial block the abnormality is usually increased by digitalis administra- tion. It is not contraindicated by hypertension. When a digitalis action is desired, it should be given until some physiological effect becomes apparent, but in pushing the dosage *Cohn: Jour. Amer. Med. Assn., 1915, lxv, 1527. fCushny, Morris and Silberberg: Heart, 1912-13, iv, 33; Talley: Amer. Jour. Med. Sc, 1912, cxliv, 514. Treatment 273 the possible dangers should never be forgotten. Evidences of heart block and excessive irritability must be watched for and their de- velopment are the signs which should at once put us on guard. The most important elements in selecting particular preparations of digitalis for administration are: (i) a high degree of physio- logical activity; (2) uniformity of physiological activity, and (3) familiarity on the part of the physician with the physiological ac- tivity. One and two can only he secured hy obtaining the drug from reliable manufacturers who carefully select their digitalis leaves, employ a uniform method of extracting the active prin- ciples and standardize their product by physiological tests. The third element is secured by confining one's attention to the study of a small number of preparations and using these to the exclu- sion of all others. In my own practice a potent infusion, a stand- ardized tincture, tablets of digipuratum, ampoules of digipuratum and crystalline strophanthine are the preparations which I have found satisfactory and which meet my needs. No rules for the amount of the drug which should be given can be laid down. Each case, in this respect, is a law unto itself, and the amount can be gauged only by studying the physiological effect in the individual. The maximal doses which may be used are: of an active infusion (freshly prepared) 30 cc. (1 ounce) in 24 hours; of a good tinc- ture 4 cc. (1 fluiddram) in 24 hours; digipuratum by mouth 0.4 gram (6 grains) in 24 hours, intramuscularly 0.1 gram (1^2 grains) three times a day; crystalline strophanthine intravenously Yz milligram dissolved in 8,000 parts of normal saline, not more often than once in 24 hours. Unless there is special urgency, digitalis should be given by mouth, as all of the active preparations are very irritating to the tissues when administered subcutaneously. Hatcher and Eggles- ton* have shown that the nausea and vomiting which are produced by digitalis is due to their action on the central nervous system, rather than a local irritant effect on the stomach, hence the intra- muscular or intravenous administration causes these symptoms as readily as when the drug is given by mouth. The toxic dose of strophanthin given intravenously is not far removed from the therapeutic dose, hence it should never be given to a patient who *Jour. Pharm. and Exp. Therap., 1912, iv, 97. 274 Treatment has been recently taking any drugs of the digitalis series, and is indicated only in extreme emergencies. The experimental work of Voegtlin and Macht,* who found that digitonin relaxes, while other alkaloids of digitalis constrict, the coronar\- arteries, suggests that in coronary spasm the infusion which contains digitonin should he a more useful preparation than the alcoholic extracts which contain no digitonin. Digitalis is a drug of great power, our most potent agent in correcting certain defects of myocardial function, hut its promiscu- ous use is not without danger and may be the direct cause of myo- cardial damage. In some cases it is absolutely contraindicated, in others it should be used boldly and with confidence. In those in which its use is of doubtful value, it should be administered with extreme caution. OPIUM and its alkaloids are not contraindicated by myocardial lesions po- se, although the associated derangement of other organs (e.g., the kidneys) may make their use inadvisable. Their effect on the heart is probably entirely due to a stimulation of the vagus center in the medulla. In animals large doses of morphine slow the heart rate. This effect may be prevented or abolished by cutting the vagi or by the administration of atropine. It may produce|| a sino-auricular or an auriculo-ventricular block and other forms of arrhythmia, notably sinus irregularities. It is believed that these changes are entirely due to vagus influencesf (some hold that the accelerators are also depressed) and that morphine has no direct action on the muscle of the heart. In man therapeutic doses of morphine produce bradycardia in susceptible individuals. Morphine is of considerable value in some cardiac emergencies, such as the paroxysmal tachycardias and other rapid hearts asso- ciated with conditions of great excitement and restlessness. According to Macht, i the various alkaloids of opium differ in their effect on the coronary arteries. Thebain, heroin and codeine have little influence on controlling the lumen of these blood ves- *Jour. Pharm. and Exp. Therap., 1913-14, v, 76. ||Eyster and Meek: Heart, 1912, iv, 59. tCohn : Jour. Exp. Med., 1913, xviii, 715. tMaclit: Jour. Amer. Med. Assn., 1915, Ixiv, 1489. Treatmeni 275 sels ; papavcrin causes a marked relaxation and, therefore, should be useful in anginal pains due to coronary spasm. THE NITRITES in man cause a considerable acceleration of the pulse through reflex influences acting on tbe vagus center. This activity may be so marked that apparently the vagus is completely inhibited so that the condition simulates full doses of atropine. It seems pretty well established, however, that these influences are exerted on the medullary center and not, as is the case with atropine, on the terminations of the vagus nerve. Experiments on animals and clinical observations have failed in affording evidence that the ni- trites have any direct action on the heart muscle. Hence, when it is indicated by reason of its other activities, it is not contraindi- cated on account of any action detrimental to the myocardium. Extracts of the posterior lobe and the pars intermedia of the pituitary gland have a considerable effect on the peripheral arteries and, aside from this, probably a direct action on the heart muscle. According to Wiggers,* they slow the heart, decrease its amplitude and increase its muscle tone. STRYCHNINE has no direct action on the cells of the myocardium. Its effect on the heart is an indirect one only and, therefore, it cannot fairly be classed as a drug useful in correcting intrinsic heart defects. *Amer. Jour. Med. Sc, 1911, cxli, 502. CHAPTER XIX Treatment INDICATIONS AFFORDED BY THE DIFFERENT TYPES OF RHYTHM It is well to emphasize at the outset thai the individual arrhyth- mias do not constitute distinct entities. They are merely symptoms of abnormal myocardial activity. At times an arrhythmia is the only means through which we may detect functional disorders of the heart, at others it is merely one of a large group of signs which demonstrate the defective character of the method in which the heart is performing its work. Their special value is found in the fact that they often reveal the particular fundamental prop- erties of the muscle cells which are at fault, and thus suggest a new point to be attacked by therapeutic measures. The treatment of symptoms is often of very great value not only because a symptom in itself may at times actually endanger life, but also because its removal may be the starting point which leads to the correction of the more fundamental defect. The relief of pain during an acute infection may afford the rest which the body needs to reorganize its forces to combat successfully the toxins which are threatening its life. A bradycardia or a tachycardia may, through its intensity or frequent repetition, jeopardize life quite aside from the intrinsic influence which the underlying lesion may have on the circulation. For these reasons I think we are fully justified in considering the arrhythmias in separate groups, both for the sake of such clues as may thus be afforded for their correction, as well as for the light which such a classification may throw on the conditions more fundamentally at fault. It is needless to say that there is no drug or therapeutic measure which is a specific in correcting all irregularities of the heart. One form of treatment may be most beneficial in one type of arrhyth- mia and absolutely contraindicated in another type. This becomes perfectly apparent when we consider that to produce the different irregularities, modifications of different fundamental properties of the myocardial cells are necessary. A measure which may satis- 276 Treatment 277 factorily control one form of arrhythmia may increase or even bring into being another type of irregularity. HEART BLOCK is the type of abnormality which indicates that there is an inter- ference with the conduction of stimuli from one portion of the myocardium to another. Fundamentally, the objeel for treatmenl is to restore to the normal the functional capacity for conduction. The methods to be selected in the treatmenl of heart block depend upon the etiology, the degree of the impairment of the property of conduction and the functional efficiency of the heart. One most often sees a condition of delayed conduction, or of partial block, in the course of one of the acute infections, notably in cases of rheumatic fever. Usually this functional disturbance is transitory and passes off with the elimination of the toxins of the acute process. The treatment is entirely directed toward the general disease, antitoxin in diphtheria, salicylates in rheumatism, etc., free elimination in all. No treatment is especially indicated by the myocardial defect, which doubtless is frequently a chemical alteration rather than any histological change. If the conduction abnormality persists after the acute stages of the disease and into the period of convalescence, the patient should limit his activities for a considerable time, in the hope that the heart, not unduly taxed, may recover its normal function. If, after a reasonable period, the defect appears to have become permanent, the patient may graduallv resume his usual activities, but under the careful observation of his physician, in order that an increased degree of block or anv cardiac insufficiency may be detected at once and be corrected by appropriate measures. The change from partial to complete block is, of course, always abrupt, but there are certain cases which show what we may desig- nate as a transition period; that is to say, a very moderate block may become a partial block of marked degree and then return to a block of less severe type, or a partial block may become complete and in the course of a few hours the rhythm may revert to the partial type. As has been pointed out, it is during this period that the patient is most likely to develop syncopal attacks and hence is in a condition pregnant with considerable danger. -'7 N Treatmen r During this period, resf in bed should be insisted upon; this not only minimizes the possible dangers from the attacks of unconsciousr ness, but also reduces the demands on the heart to the lowest degree, thus possibly preventing a more advanced type of block and avoid- ing the attacks of syncope. It is in this period that atropine may often be used to advantage. ( u" tins mine will be said in a later paragraph. Digitalis is contraindicated. Those in whom complete dissociation is thoroughly established usually can resume a moderate degree of activity, unless this is found to reduce the ventricular rate or to induce attacks of Syn- cope. Those who are subject to attacks of unconsciousness must limit their activities, hut are not, as a rule, confined to bed. They should he warned of the dangers which the fits entail and should never go about unattended. Some of these syncopal attacks seem to have a definite exciting cause, such as the stress of over-exertion or a reflex induced by gastrointestinal disturbances. Such causes should be thoroughly searched for, and the necessary measures for their avoidance instituted. There are reports in the literature which seem to indicate that some attacks of unconsciousness can be warded off or aborted by the use of atropine. We have no other means of relieving the syncopal attacks and I see no reason why atropine should not be tried. With ivw exceptions, complete block, when once established, continues until the patient dies. From our knowledge of the pathol- ogy, we can rarely expect to restore the tissues to a normal capacity for conduction ; however, the possibility of a syphilitic lesion and its removal should never be overlooked. In the presence o! the his- tory of infection and a positive W'assermann reaction, a vigorous course of antisyphilitic treatment is always indicated and even those in whom the evidence of lues is less convincing are entitled to the benefit of the doubt. The administration of mercury and potassium iodide should always precede the exhibition of salvarsan, which should be introduced cautiously and in small doses, which may gradually be increased. Success in securing a return of com- plete conductivity has been reported in some cases. The failure of antisyphilitic measures to restore the normal function does not prove that the scar which remains may not have been of syphilitic origin. Nearly all grades of block are associated with a greater or less 2 7 'J -f Figure 218 November 20, 10.51 a.m. Complete block. As = 85; Vs = 46. 1 f -ff ♦» ■ — ^ Figure 219 November 20, 10.56 a.m. Delayed conduction: twenty-five minutes after atropine P-R interval = 0.4 second. As = 85; Vs = 85. — - "-„ "H - ! 1 1 " U. ... ^ 1 . . 1 S^*--^ •iflSSlff**^ i,Q,tStC. "' Figure 220 November 20, 11.01 a.m. Conduction slow. P-R interval = 0.22 second, .4.$ = 85; Vs - 85. .:_: — : :„:::i. * * x - "H — « 5j 5 _ ««" ! "" i . ^ j Ui.Cvl ^.^ C ' ^w - ^. , u--' ^. i ^ c Figure 221 November 20, 11.06 a.m. P-R interval = 0.2 second: As = So; Vs = So. Complete block broken by tbe administration ot" atropine. 280 Treatment degree of cardiac insufficiency. Tin's docs not necessarily parallel the severity of the dissociation. This factor requires quite as much attention as the block, and for each patient appropriate measures must be employed to improve this phase of his difficulty. As has been pointed out in another place, the activity of the vagus is sometimes an clement in producing block. Although 1 believe it must be unusual for a vagus block to occur without other myocardial defect, it should always he taken into consideration as a possible factor. The administration of atropine may he used to remove vagUS influences and thus determine their relative impor- tance. For this purpose it may be employed subcutaneously in closes of 1.3 mg. (1/50 grain). Its effect should be apparent within thirty minutes. The effect of atropine usually disappears in a few hours. In some cases it is desirable to continue its in- fluence and for this purpose 0.7 mg. (1/100 grain) may be given by mouth or subcutaneously at six-hour intervals for several days. The prolonged administration is apt to cause the patient considerable discomfort; his mouth becomes dry, and he cannot use his eyes on account of the loss of accommodation, hence its use must be discontinued. Atropine is useful to counteract the effect of digitalis, when this has been given to a point where its toxic effect has become evi- dent through the development of heart block. Here it probably influences only the vagus part of the digitalis action. The graphic evidences of the effect of the administration of atropine are shown in Figures 218, 219, 220 and 221. These records were obtained from a man who entered the hospital with signs of marked cardiac insufficiency, mitral incompetence and a dilated left ventricle. His heart was rapid and rhythmic, but showed a prolonged conduction interval (P-R = 0.2 second). He was given digitalis and after four days of its administration the heart suddenly became very slow (rate 46). An electrocardiogram taken at this time (Figure 218) presented the evidences of a com- plete heart block. He was given 1.3 mg. atropine subcutaneously, and the effect is shown in the succeeding records. Figure 219, taken twenty-five minutes after the atropine was given, indicates that there is no longer a block, although the conduction time is very long ( P-R = 0.4 second) and the ventricular rate has increased to Figure 222 November 18, 3.40 p.m. Complete block. Before atropine. As — y^; Vszztf. -- . * — - wfrfam&mfik : — o.a s» v . -'— ■_-_^_'_^_'_^^ i ^'_j_ ■ _-_-_'_d Figure 223 November 18, 4.07 p.m. Complete block twenty-five minutes after atropine. As = 00; Vs = 52. - ; ; — — — IZ . .... , ■ ml 1 * T ■ I 7; ?t9t . ^^ =z= — -— i^ ^J«, , Figure 224 November 18, 4.10 p.m. Complete block. As = 100: J's = 6c ' '"" . . - - — . _ , 1 p > ?! ,- ■p t B V -P" T » p ■pi v I 4P PI » ■p - ■ ' '. _ . 1 ' '_!' • 'j^ - - /" O O •": O.X J^c. - ■ _■- Figure 225 November iS, 4.1JP.M. Complete block As _= 100; f'j = 60. A case of block not removed by atropine administration. 282 Treatment 85 per minute. Five minutes later (Figure 220) the heart rate had not changed, hut the P-R interval was reduced to 0.22 second. Thirty-five minutes after the atropine | Figure 221 ) the ventricu- lar rate was So, the P-R interval 0.2 second. This was the maxi- mum atropine effect, which gradually whit away until, at the end of eight hours, complete block again appeared. The results of the administration of atropine to another patient with a complete heart block (cause unknown) is presented in Fig- ures ---, 223, 224 and 22^. It will be seen that atropine did not abolish the block which remained complete throughout the period of observation. It did, however, cut off the vagus influences, with the result that both the auricular and ventricular rates were increased.* 'Idle question of the administration of digitalis to patients show- ing defects of the property of conduction must be studied in each individual, To many showing signs of cardiac insufficiency and dilatation, its use is beneficial. In eases of established complete block, it is not eontraindicated unless it produces excessive ven- tricular irritability and extrasystoles. In cases of delayed conduc- tion, it may be given with caution. To those with partial block, it is usually harmful. Every patient with conduction defects to whom digitalis is given, should be under the close observation of his physician until its effects are fully established. EXTRASYSTOLES Our present knowledge indicates that an extrasystole represents an increased irritability of some portion of the myocardium. Whether this is due to a chemical alteration of the muscle cell, histo- logical changes in the cell or to extracardial nervous influences which increase the excitability of the cell, is not altogether clear. From the evidence at our disposal, we may make the assumption that in different patients exhibiting extrasystoles the cell modi- fications are not necessarily of the same nature and that in one it may be a true histological, in another a chemical change and in a third a nerve influence. The object of therapeutic measures is to reduce the myocardial irritability and the assumption that the change in this property may be the result of such diverse influ- *Hart : Amcr. Jour. Med. Sc, 1915, cxlix, 16. Treatment 283 ences afford us several points of attack which may be considered in each case according to its individual merits. There are certain substances which have an undoubted influence in the production and maintenance of extrasystoles. They prob- ably act as direct toxins to the myocardial tissues. These arc tea, coffee, tobacco and certain drugs, such as digitalis, theocin, adrena- lin, chloroform, etc. The reason for the susceptibility of some- hearts to these substances is entirely unknown. Some individuals can apparently use excessive quantities of tobacco with entire im- punity, while in others a small amount of nicotine will produce a high degree of myocardial irritability. This I have repeatedly seen in susceptible individuals who have been closely observed to deter- mine this point. In the same way certain patients show a similar tendency with digitalis in small doses, while others will take very large amounts without evidence of increased myocardial irritability. The first attempt to reduce the excessive cardiac irritability should consist in the withdrawal of all such toxic substances. In many instances the discontinuance of the use of tea, coffee or tobacco will result in the disappearance of extrasystoles, in others the cure is not so simple, but it is not fair to condemn this method until it has been given a prolonged trial. Another apparent source of myocardial irritability is an abnor- mal condition of the gastrointestinal tract. Whether such digestive disturbances act by producing substances which are direct toxins to the heart muscle or by purely reflex nervous influences is not known, but it seems very clear that in a certain number of in- stances the extrasystoles will disappear with a correction of the gastrointestinal disorder. It is also wise to search for other possible sources of endogenous toxins or irritants which may cause an abnormal reflex and to remove them when possible. A distinction should be made between the extrasystoles which are associated with other evidences of myocardial damage and those which occur as the sole evidence of disturbance of heart function. In the former case our treatment may be mainly directed to a correction of the more fundamental cardiac defect and often the extrasystoles will become less evident with the improvement of the other features. These are the patients in whom we are justi- 284 Treatment Red in trying the effect of digitalis, but it should be used with care, only under close observation and should be discontinued if it increases the irritability out of proportion to its otherwise bene- ficial effect. In those in whom extrasystoles are the only sign of abnormal cardiac activity, digitalis is contraindicated ; they are often made worse by its administration. These patients should be told that they have no serious heart lesion, they should not cur- tail their ordinary physical activities and, if they are leading a sedentary life, they should be introduced to regular exercise in the fresh air and take a course of carefully graduated physical exercises, which in a very large number of instances will abolish the extrasystoles altogether. I know of no drug which will directly improve the cardiac condition, although the use of one of the bro- mides or valerian may be of service in tiding over a period of anxiety and apprehension. While the patient's mind should be put at rest and he should be reassured, 1 think it is a matter of some importance that we should get rid of the extrasystoles if we can by the simple hygienic meas- ures which we have outlined above. I have the impression that by allowing extrasystoles to go unchecked the abnormal focus in the myocardium acquires, as it were, a habit of assuming the role of pacemaker for the heart, and this, if uncontrolled, tends to become fixed and may lead to the development of abnormalities of more serious moment. THE ACCELERATE > HEART In seeking methods of slowing the heart that is beating at too rapid a rate, we should always endeavor to single out the cog in the mechanism which is defective. When the demands of physi- cal exertion exceed the capacity of the heart muscle, it must be curtailed; if it has led to actual heart strain and dilatation, the patient must be put to bed and digitalis may be found of benefit. [\ the excessive stress arises from the abnormal functional activity of other organs, these must be corrected as far as possible, and during the process the heart strength must be conserved by rest. When the increased rate is due to excessive accelerator influences, the cause may often be found in the deranged function of some organ remote from the heart. By rectifying this disorder, the Treatment 285 abnormal reflexes will be excluded and the tachycardia will dis- appear. In these conditions sedatives, such as the bromides and valerianates, are often of considerable service. It is probable that by far the greater number of simple tachy- cardias are due to poisons which destroy the balance of the extra- cardial nerves or more often actually increase the irritability of the sinus node, such, for example, are tea, coffee, tobacco, alcohol, thyroid extract and the toxins of bacterial infection. The indica- tion is clear that the absorption of these substances musl be cur- tailed and their elimination facilitated. Beyond this, rest and the application of cold to the precordium are the means which afford the best results. Drugs such as digitalis, strychnine, aconite, etc., will be found of distressingly little value. PAROXYSMAL TACHYCARDIA Since our conception is that these attacks are due to the exces- sive irritability of some point in myocardial tissue, which, there- fore, assumes the role of a pathological pacemaker, our efforts are directed to reducing this irritability to the normal. With this end in view, we study the condition of the heart between the paroxysms and correct, as far as may be, such abnormal functional activities, adjusting the patient's mode of life to the amount of stress which his heart is able to support. We endeavor to remove elements which may act as exciting causes to the paroxysm, such as sudden physi- cal exertion, emotional excitement and gastrointestinal disturbances. We put the patient in the best possible physical condition in the hope that the attacks may be less frequent or that he may be better able to cope with the paroxysms when they arise. When the attack comes on, the patient should at once go to bed ; this they usually do without advice, but exceptionally one sees an individual who will interrupt his activities only for a moment at the beginning of the seizure and will then go on with whatever he may be doing with seemingly little discomfort. The paroxysms are prone to terminate spontaneously, and are so variable in length that it is exceedingly difficult to estimate the value of measures employed to arrest them. One fact is very cer- tain, we have no one single means which invariably stops the attacks. In certain individuals the attacks can be stopped by various muscu- 286 Treatment lar movements or by assuming some special posture. The patients themselves will often discover the "trick" by which this end is attained or the physician may find one suited to the patient's needs by testing the methods which have proved successful in others. The following are a few of the means which may be tried: holding the breath after deep inspiration; strong deglutition movements (as has been suggested by Vaquez, this may be accomplished by having the patient swallow several large cachets containing some inert drug or other substance); assuming various hodilv attitudes, such as lying on a couch with the head projecting hcvond the edge and thrown hack as far ;is possible, or Hexing the head forward and bringing it down between the legs with the body curled up; slap- ping tin- chest; a long drink of very cold water; vomiting induced by tickling the pharynx or the administration of an emetic, such as mustard, zinc sulphate or the syrup of ipecac; cold applications to the chest wall. It is probable that all these methods act by stimu- lating the vagus either by mechanical pressure or by reflex influ- ences. ( hie can frequently stop an attack temporarily, sometimes permanently, by direct vagus pressure. This is accomplished by making digital pressure over the carotid sheath just below the angle of the jaw. Right vagus pressure is usually much more efficacious than left vagus pressure (see Figures 152 and 153): the nerves should he manipulated one at a time, compression should never he applied to both vagi at the same moment, as there is a possibility of causing serious arrest of the heart. Ocular pressure may he tried, hut it is, as a rule, less effective than vagus pressure. Digitalis is of little or no value in the short paroxysms, hut in attacks lasting several days it may be pushed to the physiological limit. In the tachycardias of auricular origin we may hope to induce an A-V block; in those rare paroxysms, which arise from a focus in the wall of the ventricle, digitalis is contraindicated. The intravenous use of crystalline strophanthine has been found succe>>ful in arresting the paroxysms on a number of occasions. A single dose of one-half milligram, dissolved in 8,000 parts of normal saline, may be given. This dose may he repeated after an interval of twenty-four hours. No one of the above measures is always successful. Some paroxysms resist all the attempts made to arrest them and ulti- Treatment 287 mutely stop spontaneously. Under these circumstances the patient must be made as comfortable as possible I te is allowed to assume the posture in which he is most at case. Quiet and resl are attained by the administration of bromides, valerian, or, in conditions of great distress and restlessness, a hypodermic of morphine. There is a long list of drugs which have been reported to be efficienl in stopping the attacks, among these are aconite, amy] nitrite, strych- nine, veratrine, hypophysis extract, etc., etc. These probably are without any real effect and owe their reputation to the coincidence of their administration with the time of the spontaneous termina- tion of the paroxysm. SINUS ARRHYTHMIAS We have seen that cardiac irregularities arising in the sinus node- are due to a condition of the nodal tissue which makes it peculiarly susceptible to vagus influences. When the rhythmic changes are synchronous with the respiratory movements, we may regard them as entirely physiological, and as such they require no treatment. They do not indicate an abnormal condition of the myocardium, hence there is no reason for subjecting the individual presenting this irregularity to unusual restrictions or for limiting his accustomed activities. The irregularities of simts origin, which are independent of the respiratory movements, have a somewhat different significance. Here, I believe, that the cause of the instability of the nodal tissue is usually a true myocardial defect of which the functional change of the sinus nbde is often the earliest evidence. It is certainly wise that these patients should be closely watched, with the pur- pose of detecting at the earliest possible moment further signs of myocardial damage, should these present. In themselves, these irregularities are of little consequence ; they do not demand treat- ment. These patients never show cardiac insufficiency without pre- senting signs of abnormalities of the heart other than this arrhyth- mia. When the irregularity is first discovered, the patient's activ- ities should be moderately restricted, in order that the heart may not be subjected to any considerable stress pending the determina- tion of the extent of the myocardial damage. If at the end of a reasonable period it appears that the irregularity is the only evi- 288 Treatment dence of disturbed function, the restrictions may be gradually relaxed. AURICULAR FLUTTER Auricular flutter indicates an exceedingly irritable condition of the auricle, which is contracting rhythmically at a very rapid rate. It is usually associated with a defect in the .-/-/' junctional tissues, so that a part of the auricular impulses are blocked and the ven- tricle responds only to every other stimulus originating in the upper chamber. Hence the object of our therapeutic measures is first to increase the degree of block and thus reduce the number of the auricular stimuli which are able to reach the ventricle, and, second, to diminish the irritability of the auricular tissues so that the sinus may regain its ascendency and resume its role of cardiac pacemaker. During the attack the patient should be in bed and as nearly horizontal as possible. Frequently the patient breathes more easily, if the head is somewhat elevated, and during urgent dyspncea it may be necessary to allow him to sit up in a chair. He must be kept as quiet as possible and all friends and sources of emotional excitement must be excluded. Sleep and rest may be secured by the administration of bromides and valerian or even morphine, if the restlessness is excessive. Food should be given frequently in small amounts and in an easily digested form. As a rule, large amounts of fluid should be avoided. As in the case of "paroxysmal tachycardia," which seems to bear a very close relationship to auricular flutter, stimulation of the vagus will sometimes slow the ventricles and even arrest the paroxvsm. A number of methods for attaining this result have been detailed on page 286, and need not be repeated here. The effect of vagus stimulation is, however, usually transitory and is unreliable as a lasting therapeutic measure. On theoretical grounds the stimulation of the left vagus should have a greater effect in slowing the ventricles, while the right vagus should better control the auricular tachycardia. That this is not always the case is shown in Figures 226 and 227. These are portions of records secured from a man of forty-nine during an attack of auricular flutter last- ing several days. His auricles were contracting at a rate of 300 per minute; his ventricular rate was 150 per minute. At the point in Figure 226 indicated by the arrow, digital pressure was made 289 """ TTT ]?J3i — 2 v -j. — |j *> ». or^ , 2(p Treatment on the right vagus nerve and continued for ten seconds. During this time the ventricles did not contract, the auricular activity was not affected. < >ne second after pressure was discontinued the ven- tricles resumed their contractions at a rate of 25 per minute. This rate gradually increased and at the end of five minutes the ven- tricular rate had returned to 150. The effect of left vagus pres- sure is shown in Figure 227. Mere again it is evident that the auricular tachycardia is unchanged. There was a ventricular escape at the end of 2.4 seconds and the intervals rapidly short- ened and a ventricular rate of [50 per minute was attained in nine seconds, while vagus pressure was still being made. The drugs which are of most value in auricular flutter are digi- talis and others belonging to this group. The ohject to he sought is an increase in the degree of auriculo-ventricular block, so that a portion of the impulses originating in the irritable auricle may be obstructed and the ventricular rate reduced. In order to secure a prompt effect digitalis must be administered in large doses. It may be given subcutaneously if the patient is in great distress, or if immediate relief is demanded strophanthin may be given intra- venously, observing the pracautions that have already been sug- gested in the use of this powerful alkaloid. Exhibited by mouth in full doses, digitalis may require several days to reduce the ven- tricular rate to the normal, but a considerable slowing is usually seen in forty-eight hours. When the ventricular rate reaches about 70 per minute, although the auricles are usually still in a condi- tion of flutter, the digitalis may be stopped, in the hope that a physiological rhythm may be recovered. If the ventricle shows a tendency to increase its rate, digitalis should be resumed. It is quite probable that soon after this the auricles will begin to fibril- late, but often the physiological rhythm will reappear with no intervening period of fibrillation. The question has been debated as to whether the fibrillation is due to the administration of the digitalis. This seems quite probable, hence it would seem wise to employ this drug only to a point where it controls the ventricular rate within reasonably normal limits, and from time to time to discontinue it, carefully observing the functional condition of the heart. A typical favorable reaction to digitalis is shown in Figures 228, FlGURE 228 April 6. Refore treatment. Auricular flutter with irregular ventricular contractions 150 per minute. m_u.l:.l I : "rn~T - nst- - ----- FIGURE 229 April 9. Ventricle irregular rate 100. Z= ^ :: ■—'- I - ■ : — '^— 4— l I II I - i - • I ! I ' : ■ ■ : FlGURE 230 April 15. Ventricle regular, rate 75. Auricles still in flutter. After this digitalis was stopped. FlGURE 2 31 April 22. Regular sequential rhythm. Auricular flutter has stopped. The above four records show the effects of well-regulated digitalis administration in a case of auricular flutter. _•.,_• Treatment 229, 230 and 231. ' 'n April 6, before treatment | Figure 228), the ventricular rate was 150 per minute; under large doses <>i" digitalis the rate was reduced to 100 (Figure 229). The quantity of digi- talis was then reduced, and <>n April 13 the activity was that pre- sented in Figure -'^o. The auricles wire still in flutter, with rhythmic contractions at the rate of about 300 per minute; the ventricles were also perfectly rhythmic, but responded only to every fourth auricular impulse. At this point digitalis was discontinued and a few days later the heart returned to a sequential rhythm ( Figure 231). At no period was auricular fibrillation observed in this patient. Ah' Hit one-half of the cases of auricular flutter recover a physio- logical rhythm, many of them pass into auricular fibrillation and, in a considerahle number, this is continued for the remainder of life. The use of potassium iodide, in association with digitalis, has given favorable results in some cases.* It" there is evidence of a syphilitic infection, a course of mercury and iodide is indicated. AURICULAR FIBRILLATION It is most generally held that this condition is caused by a highly irritable condition of the auricular wall. The disturbances of the circulation are almost entirely due to the secondary effects on the ventricles, which are induced by the abnormal stimuli showered upon the junctional tissues by the frenzied activity of the auricles. The purpose of treatment is, therefore, to reduce the irritability of the auricles, in the hope of securing coordinated contractions of the auricular muscle. Failing in this, we should attempt to obstruct a portion of the impulses set free in the upper chamber and thus relieve the ventricles of the stimuli, which lead to such rapid and ineffectual contractions. Our means to reduce the excitability of the auricular muscle are limited and most often unavailing, yet I believe that in every case of auricular fibrillation discovered near the time of the inception of the new rhythm, an attempt should he made to bring the auric- ular activity hack to the normal. It has been pointed out that .-1 sudden increase in intra-auricular pressure is probably an impor- tant factor in inducing the onset of fibrillation in a heart previously ♦Ritchie: Auricular Flutter, 1914, p. 132. Treatment 293 damaged by disease. Anything which we can do to prevenl venous congestion and overfilling of the auricles of a hearl in which we suspect myocardial defects, should be employed as a prophylactic against fibrillation. It" fibrillation has commenced, resl in bed is at once indicated, and in cases with evident venous stasis and over- distension of the auricles, a prompl phlebotomy may sometimes relievo the increased pressure and permit the auricle to resume a physiological activity. The active elimination of the toxins of the acute infections or of other poisons may be accompanied by the reap- pearance of normal auricular contractions, if the ventricular rate becomes very rapid, digitalis may be employed in full doses until the ventricles are slowed to about 90 a minute, but it should then be discontinued, for digitalis, undoubtedly, has the effect of increas- ing the irritability of the muscle cells of the heart, and in these early cases it is wise to remove this influence in the hope that the auricles may recover their normal coordinated contractions. As has already been stated, our efforts to reduce auricular excita- bility and to secure a return to a normal rhythm are usually unsuc- cessful, auricular fibrillation becomes established and will probably continue to the end of life. It is in these cases, however, that the treatment of abnormal myocardial function obtains its most brilliant successes. The attention of the physician must be centered on the ven- tricular activity, if the rate of the lower chamber is not over 75 per minute, and the heart is well compensated little need be done for the patient other than to see to it that his mode of life con- forms to the limited amount of force which such a heart has in reserve. Physical and emotional strain must be avoided, the exces- sive use of tobacco, alcohol, tea and coffee are forbidden, gastro- intestinal disturbances must be corrected and exposure to infections shunned. With a more rapid and irregular ventricular rate, the indica- tions for treatment are quite different. The patient should be put to bed at once and kept as quiet as possible. Food should be given at frequent intervals in easily digested forms, the amount of fluids taken should usually be restricted. Rest may often be secured by one of the simple hypnotics, veronal, trional, etc. The most important object to be attained is to block a portion of the hap- 294 Treatment hazard auricular impulses, so that these may erase to vex the over- acting ventricles. This can nearly always be secured by the admin- istration of digitalis or strophanthus. In a considerable number nt" these hearts the myocardial damage is not limited to the auric- ular wall, but has also involved the ./-/' bundle. This makes them peculiarly susceptible t<> digitalis influences, and with this drug it is usually easy t<> produce a considerable degree of auriculo- ventricular block. While rest in bed is essential to the successful treatment of these cases, it is quite easy to demonstrate thai this alone is not sufficient, in the majority of instances, to reduce the ventricular rate to the desired point, outside demands in ex< of the functional capacity of the heart are only partly responsible for the increased rale. This is due in a very large degree to the abnormal auricular activity and until this influence is checked the ventricles cannot be satisfactorily controlled. Hence, the admin- istration of digitalis is practically always a necessity. 1 low much digitalis must we give? This question can be answered only by studying the individual patient. We must give it in suffi- cient amounts to secure its physiological effects, and this can be determined only by observing the reaction of each heart to the drug during its administration. The method which I have found most satisfactory is to begin by giving by mouth a good infusion or the tincture. I use 30 c.c. (i ounce) of the infusion or 4 c.c. (no minims) of the tincture in each twenty-four hours until a definite physiological effect is observed. This is usually seen in from three to five days. The beneficial effects of rest and the administration of digitalis arc shown in the graphic records of the brachial pulse, taken at inter- vals of two or three days from a single patient ( Figures 232, 233, 234, 235, 236 and 237). I think the hest method for watching the effect of the drug is to make frequent estimations of the apex rate, the radial rate and the pulse deficit, as described in the chap- ter on auricular fihrillation (page 164). When the rate of the heart, determined by auscultation over the apex, falls below 90 and the pulse deficit is less than 10, the dosage may he gradually diminished, hut should he continued in sufficient amount to effect a still further slowing of the heart and a diminution in the pulse deficit. As a rule, I find that these hearts are most efficient if 295 FIGURE 2^3 January 25. Rate 115. FIGURE 235 January 29. Rate 96. FIGURE 237 February 5. Rate 54. A series of records taken from a case of auricular fibrillation showing the progressive effect of digitalis administration. 296 Treatment the rate is kepi between 00 and 70 per minute with no deficit. When patients are observed in this way, it is very rare to see the disagreeable toxic effects formerly so common in digitalis therapy; nausea and vomiting are very infrequent, and it is almost never necessary to discontinue the drug on account of these symptoms. Excessively slow rates and the "coupled rhythm" are so unusual that they are curiosities. Notwithstanding the infrequency of the development of the signs of digitalis intoxication in patients to whom the drug is administered by this method, they occasionally arise and, should the heart rate fall below 50 or the "coupled rhythm" appear, digitalis must he stopped at once. When the rate has increased to 70, digitalis should he resumed in a smaller dose. The patient should he kept in hed for a week after the rate has reached 70. He may then hi- allowed to slowly resume his activ- ities. Any notable acceleration of the heart or increase in the pulse deficit is a warning that he is exceeding the stress which his myocardium may safely support and his exertions must he correspondingly reduced. It is usually necessary to continue small doses of digitalis for an indefinite period. I have patients who have not missed their daily dose of digitalis for five years. If the physical exertion is increased very cautiously and the heart rate is not allowed to exceed 70 a minute, hypertrophy will grad- ually develop and in some individuals the myocardium will recover an extraordinary capacity for work-. While a majority of those suffering from auricular fibrillation respond to a course of treatment as outlined above in a satis- factory manner, there are some who are exceedingly difficult to handle. These are usually cases of long-standing fibrillation which have been untreated, or those who have been treated intermittently with intervening periods of cardiac decompensation. They usually present evidences of extensive myocardial damage extending into the ventricular tissues and often show frequent ventricular extra- systoles. The polygrams of such a case are shown in Figures 238, 239 and 240. The effect of digitalis in these cases is to cause a great increase in the number of ventricular extrasystoles without materially slowing the ventricular rate. Figure 239 shows the record obtained on the second day of the administration of our usual initial dosage of digitalis. On account of the coupled rhythm, 2n April 18 (Figure 245) the rate fell to ^J and the increased irri- tability of the ventricle was evidenced by the occasional appear- ance of extrasystoles. At this time digitalis was discontinued and Auricular Fibrillai eon 299 cardii : days. Figure 241 Patient "G." Auricular fibrillation. Rate 104. Digitalis had been taken for two H T A. pw ww^ r\+mmm Jugular Electro- cardiogram Brachial Figure 242 Patient "G." Fourth dav of digitalis therapy. Note •'coupled rhythm," every other ventricular contraction is an extrasystole which does not affect the jugular or the brachial pressures. 300 I'ki \i mi \ i on May 4 (Figure J40) extrasystoles had completely disappeared and the heart rate was 94 per minute. 'This series ol records also shows the influence of digitalis in modifying the form of the T wave. The effect of digitalis on blood-pressure, in auricular fibrillation, has long been a matter of contention. Thirty years ago it was thought that the administration of digitalis elevated blood-pressure, but this view was controverted by many subsequent observers, such as Christeller, Frankel, Ileike, Hansen, Gross, Potain, and others. Their opinions have been summarized by Janeway,* who says: "All of the above observers fail to find any relation between the arterial tension and the circulatory improvement from digitalis." Our present evidence justifies us in asserting that in the cases of cardiac insufficiency, where digitalis is of most value, it raises blood-pressure by slowing and increasing the force of ventricular activity. The failure of former observers to recognize this fact was de- pendent on two elements: (1) That it was not then known that the benefits of digitalis administration are mainly evident in cases of auricular fibrillation, and (2) that they had no satisfactory method of estimating the blood-pressure in these cases, in which the successive contractions of the heart vary so greatly in force and time. Mackenzie says, in his "Monograph on Digitalis": "In our observation, even when the drug was pushed and caused nausea and heart irregularities, we could detect no appreciable effect upon the blood-pressure (except in one case)." Since we have come to recognize that digitalis finds its chief usefulness in cases of auricular fibrillation, and have applied our method of estimating the ''average systolic blood-pressure" to the study of this group, it has become clear to us that hand in hand with the improvement in the patient's condition the average sys- tolic blood-pressure is elevated. This is best made evident by the presentation of several charts, which have been selected from a considerable number, all ot which show the same features. figure [26 shows the effect of rest and digitalis on a case under observation in the Presbyterian Hospital for two weeks. The dimi- *The Clinical Study of Blood-pressure, New York, 1904, p. 210. JOl - Figure 243 April 15. Rate i*8. (The " control curve" was made artificially to standardize the galvanometer string by introducing one millivolt of current into the circuit. All of tin- recordf standardized in this way.) z=z. — 1 1 \-_ • BE !Er H - , 1 1 . :ir i~' ' 1 1 — ■ — - ; : _ Figure 244 April 15. Rate 100. FIGURE 24^ April 18. Rate 57. Ventricular slowing, appearance of extrasystoles and change in form of T wave. FIGURE 246 May 4. Rate 94. Digitalis stopped on April 19. Effect of digitalis in a case of auricular fibrillation. 3<>2 Treatment nution in the deficit and the gradual increase in the average sys- tolic blood-pressure is quite clear. During this period all of the patient's symptoms improved, and she was able to leave the hos- pital to return to her home. ddiis chart also shows how misleading would have been the sys- tolie blood-pressure estimations made by the ordinary method (see figures at the bottom of the chart), for at these brachial pres- sures only four or five waves per minute reached the radial during the three days following her admission. The diagram indicates that the full digitalis effect is not obtained for four or five days; this we have found to be quite usual. Figure 247 is the chart of a man who, during the whole period of observation, insisted upon following his ordinary occupation. 1 le was not confined to bed at any time, although we should have considered this the wisest course when he was first seen. He, therefore, illustrates the effect of digitalis independent of the influ- ence of any considerable amount of rest in the horizontal position. The rise in blood-pressure coincident with a slowing of the pulse and diminishing deficit and the fall of pressure corresponding to an increase in the pulse rate and deficit stand out clearly. The observa- tions cover a period of nineteen months, and the changes in the deficit and the blood-pressure could be closely correlated with his other symptoms. Whenever there was any considerable deficit or the blood-pressure fell this w T as associated with more or less dysp- noea, a lack of vigor and feelings of lassitude. Figure 248 is that of a woman who was in the Presbyterian Hospital during the whole period of observation as represented by the diagram. The initial deficit on admission, which showed a marked and sudden diminution with the administration of a freshly made infusion of digitalis (an ounce was given on October 17), the first setback induced by getting out of bed, her subsequent im- provement under rest and digitalis, the second setback brought on by an attack of hemorrhoids and the variations in blood-pressure, associated with the various stages of her progress, are all indicated in a graphic manner. ALTERNATION is a positive indication for limiting the work which the heart is called upon to perform. Although we may not as yet agree to Treatment 3"3 " Aprlltfiy *»"« "<*■ """• c i il a J £ Dn. J»nT'h. M»r. »f»r 4 -. - •/. o ir N 1 1 1 II inUII I 12 8 12 21 4 II IH 25 1(1 I loo m, «* Mm m ' Wk m m -_.-_- ^kl u ! Bl ^r iWv r ^^aB • Hn ^ M ■ TrV'-rbsJ ! ■ , t ' so :_:::::«:::::tt±:- ' illKKlMllllIKU' . A*4 L ■ wm - ' ' ' ' ' vj to t :•: - ; - Tjj W •' l\ 1 : IP'- ■-' ™ TVS Z "• ' W 'M l \ m rs - p-t - - ^^ T i 1 ( in ' ! r m T± i T^ t ' iP^h" 50 \_->n I ±111 X t ■ ! M *^"^ i H ■ 1 ; ! ; 40 «"?,'; r ~ c -' TAUb 60 oo 8 4 8 4 4 4 15 „ , , | , , , , , 15 15 15 3 3 8 8.1 8 4 4. 1 8 i j 8 S S 1 S i8 ao„J 1 1-1 W Figure 248 The shaded area represents the pulse deficit; the upper edge is the apex rate; the lower edge is the radial rate. The broken line indicates the range of the "average systolic blood pressure." Digitalis figures indicate minims of the tincture and drams of the infusion. October 13, admitted to hospital. November 3. up in chair one-half hour; November 9, up in chair two hours. December 4, up in chair four hours; at this time she had a crop of external hemorrhoids which caused much distress. 304 Treatment the exact mechanism underlying this form of irregularity, it is pretty generally conceded that it indicates a normal myocardium that is being overtaxed or more usually a very much damaged heart muscle for which even a moderate stress is too great. The soundness of this view is shown by the facts that rest in bed fre- quently is associated with at least the temporary disappearance of the alternation and that an alternation which is often very much in evidence when the heart is beating at an excessive rate may no longer be capable of detection when it is measurably slowed. Alternation is often a persistent matter, and it may he impossible and unwise to keep a patient in bed until it disappears. But when first discovered the patient should have the benefit of an absolute rest for at least a few days. This should he followed by gradually increasing exercise, the amount to he determined by the observations of the physician as to its effect on the activity ot the heart. It has been pointed out that while alternation is regarded by the majority of observers as an indication of defective contractility, it has not been conclusively proved that this fundamental property is alone at fault, ft is certain that many cases are at least asso- ciated with a defect of one of the other properties, such as con- ductivity or irritability. It is also known that we can rarely produce a change in one of these fundamental properties without modifying the others. Hence, it is possible that by inducing a change in the irritability or the conductivity we may indirectly affect the properly of contractility. The .above may explain the divergent views in regard to the use of digitalis in alternation. It is advocated by some workers and discountenanced by others. My own observations lead me to be- lieve that it is of distinct value in some cases of alternation, and I have never seen harm done which I could directly attribute to the digitalis. In a case of alternation associated with auricular flutter, which I had the opportunity to follow for many months, digitalis was of undoubted value. In those cases in which digitalis slows the ventricular rate, it will often abolish an alternation. Digi- talis is usually contraindicated in the psuedo-alternans due to extra- systoles. My custom is to use digitalis in moderate doses, watching the TkhA'l MEN! 305 effect closely and stopping if after a rea onable period, if the heart docs noi respond favorably. hi view of the lad thai alternation is experimentally readily produced by certain poisons, it serins logical thai we should reel as far as possible disorders of metabolism or other sources of toxins, or at least secure their elimination as rapidly as may be. The correction of kidney and bowel functions not only assist in removing poisons, but also tend to diminish the work winch the heart is called upon to perform. According to Lewis, patients witb alternation are not favorable subjects for general anaesthesia. If an anaesthesia must be used, ether, rather than chloroform, should be employed. BIBLIOGRAPHY BOOKS AND MONOGRAPHS Cusiiny: Pharmacology. Third edition. Philadelphia. 1903. Cyon: Les Nerfs du Caeur. Paris. 1905. Cyriax: Kellgreris Manual of Treatment. London. [903. Gravier: L'Altemance du Caeur. Paris. [914. Hirschfelder : Diseases of the Heart and Aorta. Second edition. Philadelphia. 191 3. Hoffmann: Die Electrocardiographic. Wiesbaden. 1^14. Hofmann: Remedial Gymnastics for Heart Affections. New York. 1 y 1 1. I vgic: ( Editor) Handbuch dcr Pathologie, Diagnostik and Thera- pie Herz and Gefdsserkrankungen. Leipzig. 1914. Kaiin: Das Electrocardiogram. Wiesbaden. i«M4- Kraus i'.m) NTicolai: Das Electrocardiogram des gesunden und kranken Menschen. Leipzig. 1910. Krehl: Die Erkrankungen des Herzmuskels mid die nervosen Herzkrankheiten. Second edition. Wien. 1913. Le Clerq: Maladies du cceur et de I'aorta. Paris. 1914. Lewis: Mechanism of the Heart Beat. London. 191 1. Lectures on the Heart. New York. 191 5. Mackenzie: The Study of the Pulse. London. 1902. Diseases of the Heart. Third edition. London. 1914. Meyer: Die Digitalis Therapie. Jena. 1912. Meyer und Gottlieb: Die experimentelle Pharmakologie. Wien. 19 1 4. Nicolai : Die Mechanik des Kreislaufs. Nagel's Handbuch der Physiologie des Menschen. Braunschweig. 1909. Ritchie: Auricular Flutter. New York. 1914. Tawara: Das reizleitende System des Sdugethier-Herzens. Jena. 1 906. Tigerstedt: Human Physiology. Third edition. Translated by Murlin. New York. 1906. Wenckebach : Die Arrhythmia als Ausdruck bestimmter Func- tionsstorungen des Herzens. Leipzig. 1903. W'iggeks: Circulation in Health and Disease. Philadelphia. 1 y 1 5 . 306 Bibliographv HEART BLOCK Rachmann: Jour. Exp. Med., 1912, xvi, 25. BARRINGER: Arch. Int. Med., [909, iv, 186. Cohn: Heart, 1912-13, iv, 7; 1914, v, 5. Christian: Arch. Int. Med., 1915, xvi, 341. Edes: Trans. Assn. Amcr. Phys., igoi, xvi, 521. Eppinger und Rothberger: Ztschr. f. klin. Med., [910, lxx, 1. Erlanger: Johns Hopkins Hosp. Bull., 1905, xvi, 234. Jour. Exp. Med., 1905, vii, 676; 1906, viii, 58. Amer. Jour. Physiol., 1905-6, xv, 153. Amcr. Jour. Med. Sc, 1908, exxxv, 797. Eyster and Meek: Heart, 1914, v, 1 19. Faiir : Virch. Arch. f. path. Anat., 1907, clxxxviii, 562. Geriiardt: Dent. Arch. f. klin. Med., 1908, xcii, 485. Hart: Amer. Jour. Med. Sc, 1915, cxlix, 62. Herrick : Amcr. Jour. Med. Sc, 1910, exxxix, 246. Hewlett: Jour. Amcr. Med. Assn., 1907, xlviii, 47. James: Amcr. Jour. Med. Sc, 1908, exxxvi, 469. Krumehaar: Arch. Int. Med., 1910, v, 583; 1914, xiii, 390. Univ. Penn. Med. Bull., 1908. Lea: Lancet, 1915, i, 1289. Lewis and Oppenheimer: Quart. Jour. Med., 191 1, iv, 145. Neuhof: Amcr. Jour. Med. Sc, 1913, cxlv, 513. Jour. Amcr. Med. Assn., 1914, lxiii, 577. A. Oppenheimer and R. S. Oppenheimer: Proc X. Y. Patli. Soc, 1913, xiii, 123. Oppenheimer and Williams: Proc. Soc Exp. Biol, and Med.. 1913, x, 86. Pardee: Arch. Int. Med., 1913, xi, 641. Price and Mackenzie: Heart, 1911-12, iii, 233. Thayer: Arch. Int. Med., 1916, xvii, 13. Wilson: Jour. Amer. Med. Assn., 191 5, lxv, 955. extrasystoles Danielopolu: Arch. d. mal. du cceur, 1914, vii, 174. Dresbach and Munford: Heart, 1913-14, v, 197. Erlanger: Amcr. Jour. Physiol., 1906, xvi, 160. Ferralis and Pezzi : Arch. d. mal. du ca-ur, 1916. ix, 1. 308 BlBLldiJRAPHV Flemming: Quart. Jour. Med., [911-12, v, 318. Gallavardin and Gravier: Lyon Med., [914, cxxii, 830. LaSLETT: Heart. l'Mi-lo, i. 83. Levi : Heart. [913-14, v, 299. Lewis : Heart, [910, ii, 27. Quart. Jour. Med.. [9] i-u. v, 1. Heart, 1913-14, v, 335. Lewis and Silberberg: Quart. Jour. Med.. 1912, v. 333. Lewis and White: Heart. [913-14, v, 335. Mackenzie: Quart. Jour. Med.. [907-8, i, [31 ; 481. Rothberger and Winterberg: Arch. f. d. gcs. Physiol., [912, cxlvi, 385 : [913, cliv, ^j 1. Zentralbl. f. Physiol., [906, xxiv, 1. VlNNIS: Heart. [912-13, iv, 123. Wilson: Arch. Int. Med., [915, xvi, 989. TACHYCARDIA Cohn: Jour. Exp. Med., [912, xv, 49. COHN AND FrASER: Heart. H)i; v V, 93. Gallavardin: Arch. d. mal. du ea-ur, 1916, ix, 45. I I \kt : Heart. [912-13, iv, 128. 1 [UME : Heart. [9] [-12, iii. 89. Lea: Proc. Royal Soc. Med. (Lond.), 1913. vi, U- Lewis and Schleiter: Heart. [911-12, iii, 173. Lewis and Silberberg: Quart. Jour. Med.. [911-12, v, 5. LlAN: Arch. d. Dial, du ea-ur, 1915, viii, 193. Parkinson and Mathias: Heart, [914-15, vi, 27. Riiil: Dcut. med. Wchnschr., 1907, xxxiii, 632. Robinson: Areli. Int. Med., [915, xvi, 967. Rothberger and Winterberg: Zentralbl. f. Physiol., 1907, xxv, 1. Arch. j. d. i/es. Physiol., [911, cxlii, 461. auricular flutter Fulton: Arch. Int. Med., 1913, xii, 475. Hay: Lancet, 1913, ii, 986. Hertz and Goodhart: Quart. Jour. Med.. [908-9, ii, 213. Hewlett and Wilson: Arch. Int. Med.. [915, xv. 786. Hirschfelder : Bull. Johns Hopkins Hosp., [908, xix. 322. I llBLIOGRAP] I , 309 Hume: Quart. Jour. Med., [913, vi, 235. Heart, [913 14, v, 25. Jolly and Ritchie: Heart, [910-11, ii, 177. LEVINE AND FrOTHINGHAM : Arch. Int. Med.. I'jI.S. xvi, 818. Lewis : Heart , igi 2, iv, 171 . M. c Willi am s : Jour. Physiol., [887, viii, 296. Mathewson : Edinb. Med. Jour., [913, xi, 500. Morison : Lancet, [909, i, 39; 77. Neui-iof: 7I/V(/. Record, [915, lxxxviii, 995. Parkinson and Mathias: Heart, [915, vi, 27. Rii-i'l: Ztschr. f. exp. Path. u. Therap., [9] i, ix, 277. Ritchie: Edinb. Med. Jour., ](>\2, ix, 485. /'roc. Royal Soc. Edinb., 1905, xxv, 1085. Robinson: 7oMr. y^.r/'. Med., u)\t,, xviii, 704. White: ^;t/;. /;//. Med., 191 5, xvi, 517. auricular fibrillation Agassiz: Heart, 1912, iii, 353. Busquet: Presse uied., 1914, xxii, 41. Cohn: Heart, 1913, iv, 221. Cohn and Lewis: Heart, 1913, iv, 15. Cowan: Glasgow Med. Jour., 1914, lxxxi, 128. Cushny and Edmunds : Anicr. Jour. Med. Se., 1907, exxxiii, 66. Draper: Heart, 1911-12, iii, 13. Eiirenreich : N. Y. Med. Jour., 1914, xcix, 269. Einthoven and Korteweg : Heart, 1915, vi, 107. Falconer and Dean : Heart, 1912, iv, 87. Fredericq: Scalpel, 1914-15, lxvii, 49. Garrey : Amer. Jour. Physiol., 1914, xxxiii, 397. Hart: Med. Record, 1911, lxxx, 2. Hart and James: Amer. Jour. Med. Sc, 1914. cxlvii, 63. Hering: Munch, med. Wchnschr., 1912, lix, 750; 818. Hewlett: Heart, 1910, ii, 107. Arch. Int. Med., 1915, xv. 786. Kilgore: Arch. Int. Med., 1915, xvi, 939. Lea: Quart. Jour. Med., 1911-12, v, 388. Lewis: Heart, 1909-10, i, 306; 1912-13. iv, 273. Jour. Exp. Med.. 10 12, xvi, 395. jio Bibliography Lewis and M a< k : Quart. Jour. Med., [910, iii. 273. Lewis and Schleiter: Heart. [912, iii, 173. Mackenzie: Brit. Med. Jour., 1911, ii. 869; 969. Quart. Jour. Med.. [907-8, i, 38. Atner. Jour. Med. -V(-., I«K>7. exxxiv, [2. Morat and Petzetakis: Compt. rend. Soc. i 4, lxxvii. ■ . . ■ . ■> - — . _ vV . Pardee: /cur. Atner. Med. Assn., 1915, Ixiv, -057. .!/('■<■//. />//. Med., 1914, xiii, 298. Rothberger ami Winterberg: Arch. f. d. ges. Physiol., 1910, exxxi. 387. Wien. klin. Wchnschr., 1909, xxii, 839. Wenckebach : Arch. f. Anat. 11. Physiol., 1007, 1-24. Wiggers: Arch. Int. Med., 1915, xv, jj. Winterberg: Arch. f. d. ges. Physiol., 1901;, exxviii, 471. VENTRICULAR FIBRILLATION GUNN : Heart, KJ13-14, v, I. Halsey : Heart, 11)15, v '- 67. Hoffmann: Heart, 1912, iii, 213. Levy: Heart. 1912-13, iv, 319; 1913-14, v, 299. /owr. Physiol., 191 4, xlix, 54. Levy and Lewis: Heart, 1912, iii, 99. McWilliam: Brit. Med. Jour., 1889, i, 6. Morat ami I'i.tzetakis: Compt. rend. Soc. de Biol., 1914, lxxvii, 222 ; 237. Nobel ami Rothberger: Ztschr. f. _>. Robinson: Arch. Int. Med., [915, xvi, 967. Robinson and Draper: Jour. Exp. Med., 1911, xiv, 217; 1912, xv, 14. ROTHBERGER AND WlNTERBERG : Arch. f. d. ges. Physiol., I9IO, cxxxv, 506; 559; I'll 1. cxli, 217; 343. Wilson: Arch. Int. Med., 1915, xvi, 1008. ALTERNATION Esmein : Arch. d. mal. du cceur, 1913, vi, 385. Gallavardin am> Gravier: Arch. d. mal. du carur, 1914, vii, 497. Lvo« Mi (/.. i«)ii. 1 )ec. [9. (i M.1.1 : Arch. d. mal. du Civur, [916, ix, 40. Hering: Ztschr. f. exp. Path. u. Therap., 1912, x, 14. Herrick: Jour. Amer. Med. Assn., 1915, Ixiv, 739. Joachim: Munch, med. Wchnschr., 1911, lviii, 1951. Kahn: Arch. f. d. ges. Physiol., [911, cxl, 471. Lewis: Quart. Jour. Med., 1910-1 1, iv. 141. Muskens: Jour. Physiol., 1907, xxxvi, 104. Pezzi and Douzelat: Arch. d. mal. du cceur, i 9~- (See also "hypertension" ) in auricular fibrillation, 167, 303. Arterio-sclerosis, 114. 228, 2 and alternation, 186. and fibrillation, 139, 140, [68 Asphyxia, 34. Asthma, 250. Atheroma, 35. Atropine, 32, 61, 214, 220, 262. and digitalis, 280. heart block in, 50, 229. hypervagotonics in, 204. Auricular canal, 13. Auricular fibrillation, 38, 102, 116, [34. age incidence, 138. and arterio-sclerosis, 139, 140, [68. and block, 226. and extrasystoles, 141, 160, 170, 171. 224. and flutter, 173. and rheumatism, 139, 160, 168. and sinus arrhythmia, 218. and tachycardia, 173. and vagus, 137. and valvular disease, 138, 140. arterial tracings, 143. clinical features of, 156. digitalis in, 136, 137, 268, 270. 272, 293, 300. due to toxins, 138. electrocardiograms, 148, 151, 153, 155- etiology, 138. experimental production, 135. heart rate in, 160. His' bundle in, 152. identification. 141. mechanism, 136. murmurs in, 142, 144. paroxysmal, 158. pathology, 138. polygrams, 145, 146. prognosis in, 170. pulse deficit in, 162. treatment. 170, 292, 300. Auricular flutter, 117, 120, 182. age incidence, 120. and extrasystoles, 118. and fibrillation, 118, 120, 124, 130, 13^. 173- and heart block, 124. and tachycardia, 173. auricular rate, 117. bundle of His in. 118. 120. clinical course of, 130. conduction in, 120, 128. contractility in, 120. coronary arteries in, 122, 124, digitalis in, 272. duration, 130. 315 l.M'l X trocardiograifis, 123, 125, 126, 129, 131. etiology, 120. experimental production, 1 1 ~- identification, 124. mechanism, 118, 1 19- pathology, 120. polygrams, 121, 126, 179. significance of, 132. treatment, 288. vagus eff< d on, 1 18, 122. Auricular tachycardia, 117. >7''. [78. Auricular tachyrhythmia, 1 1 r- Auricular tachysystole, 1 1 r - Auriculo-ventricular bundle, 4. 5. 14 26, -•:. i Si <■ also I lis' bundle > branches, 5. Auriculo-ventricular node, 4. 5i -'■ 30. .1-1' bundle, ( Sir "I li-* bundle" I in auricular fibrillation, 168. defects in, 222. digitalis effect on, 268. Bathmotropic influences, 10. Baths, 258. Beer heart, 256. Beverages, 257. Blood-letting, 253. Blood pressure, 166. average systolic, 167, 171. 300. digitalis effect on. 300, 303. in alternation, is<>. 194. in auricular fibrillation, 165, 170. litch's Law, II, 12, 102. Bradycardia. 27, 31. nodal. 226. Bromides. 284, 287. r wave, 15, 16. Caffeine, 263. ( Calcareous degeneration, 35. ( amphor, 263. ( lardiogram inverted, 18. bral hemorrhage, 31, 88. turners. 31. Cheyne-Stokes respiration, 132. Chloroform, 172, 204, 284, 305. in heart Mock. 51. Chronotropic influences, 9. Classification of myocardial disturb- ance - Coffee, 283, 285, 293. ( '■ 1*1 applications, 258. Compensatory pause, 58, 66. complete, 58. incomplete, 58. 66. Complete irregularity, 27, lo r >, 141, 154- (See aUo "auricular fibrillation") of sinus origen, 216, 219. Conduction, 27, 33. 1 S( <■ "stimulus conduction" 1 after digitalis, 266. delayed, 34, 47. impaired, 36, 120. 12S, 181, 2-2. increased, 85. rati- of, 20. Conductii n system, 5. 35. path of, 29. Contractility, 8, 9, 1 1. 24. 26. abolished, 13. diminished, 86, 181. in auricular flutter, 120. Convallaria, 204. Coronary arteries, 92, 94 ti2. in auricular fibrillation, 138. in auricular flutter, 122. 124. in ventricular fibrillation, 171. Coupled rhythm, 64, 268, 296. Cribbing, 210. 213. Dclerium cordis, 134. Dextrocardia, 237. Diet. 254. Karell, 2^7. Digitalis, 27. .,4. 36, 38, ',<>. 264. and atropine, 280. and blood pressure, 300, 303. and sinus arrhythmia, 220. bigeminus, 64. coupled rhythm. 64. dosage, 273. effect on T wave. 270, 300. in alternation. 180, 304 in auricular fibrillation, 13 >. 170, 224. 293, 294, 300. in auricular flutter, 130. 133, 290. in extrasy stole, 60, 61. 283, 284. in heart block, 50. 228. in tachycardia, 286. trigeminus, 64. Dilatation. 1, 12, 85, 170. acute. 2 |o. Diphtheria, 36, 54. 12-'. 184, Dissociation, 32. complete, 33. incomplete, 34. Dromotropic influences, n. Dropped beat, 34. 42, 40. 56, 215. /; interval. 1 7. Einthoven's ( ralvanometer, 10. electrodes, 20. standardization, 20. 21. Electrocardiogram, 15. after atropine. 279, 281. after digitalis, 207. 269, 271, 291, 299. compared with polygram, 24, 25. comparison in different leads, 24. 234- I ;, i >{■.:■: V7 method of taking, 10. normal, 23, 24. of accelerated heart, 89. "i" alternation, [83, tp3, [95, 107- of auricular fibrillation, tip, i.;i . [51, 153, 155) l 57) ''". [ °3< 169, 174, 175, 240. of auricular flutter, [23, 125, 127, 1 21 1, [31, 29 1 . nf block and extrasystoles, 231, of delayed conduction, 47, 223, 267. of dextn cardia, 237. of extrasystole, 68, 71, 72, 73, 75, 77, 70, 81, [29, 159, [61. of fibrillation and Mock, 225, 227. of fibrillation and extrasystoles, 225, 299, 301. of flutter and tachycardia, 177. of heart block, 44, 45, 48, 49, 279. of hypertrophy, 239, 241. of infants, 240. of lesion of limb of His' bundle, 233. of paroxysmal tachycardia, 105, 107, 109, in, 113, 115. of sinus arrhythmia, 209, 211, 215, 223. of vagus pressure, 203, 289. standardization, 20. Electrocardiograph, 2, 19. Electrodes, 20. Embryonic heart, 3. Epinephrin, 206. Erlanger apparatus, 18. Escape of the ventricle, 34, 206. in heart block, 46. Esophageal records, 19. Excitability, 8, 9, 10, 11, 14, 26, 32. abolished, 13. increased, 61, 85, 90. Exercise, 83, 248, 304. and extrasystoles, 62. Extracardial nerves, 30, 32, 83, 85, 199. (See also "vagus" and "accelera- tors") anatomy, 199. distribution, 201. physiology, 200. Extrasystole, 27, 38, 56. after digitalis, 268. allodrome, 60. and block, 230. auricular, 58, 65, 66, 70, 73, 176. bigeminus, 63. clinical significance, 78. electrocardiograms, 68, 71, 72, 73. /5. 77, 79- etiology, 57. experimental production, 60. identification, 62, 218. in Mm ill.ii ion, 224. interpolated, 78, 79. mi 1 hani tm, 9, nodal, 66, 67, 76, 77, 78. noi modrome, 60. pathology, $7. polygrams, 65. prognosis, 80. treatment, 2X2. trigeminus, 64. types, 74, 75, 81. ventricular, 58, 67, 68, 69, 72. 73, 74, 71, 77, 296. Fear, 248. Fevers, 31, 36. 53, 84, 249. and alternation, 184. and fibrillation, 140. ff oscillations, 152, 154. Fibrosis, 35, 94. Frog's heart, 3, 13. Galvanometer, 19. electrodes, 20. standardization, 20, 21. Glyoxilic acid, 180, 182. Graphic records, 15, 27, esophageal. 19. Graves' disease, 84, 87, 96, 272. and sinus arrhythmia, 215. fibrillation in, 140. h wave, 15, 16. Haemolytic serum, 180. Heart action current of. 19. change in position, 234. cycle. 245. disposition of muscle, 234. frogs, 3, 13. hypertrophy, 236, 245, 249. insufficient. 244. irregular, 27. normal, 28. outside demands on. 82. rate of. 14, 27. 28, 38. regular, 27. reserve force, 244. 246. rhythm. 27, 28. small, 250. valves of, 1. Heart block, 31, 32. (see also dissociation.) a-c interval, 44. Adams-Stokes syndrome, 40. 42, 230. and extrasystoles, 230. and fibrillation. 226. and sinus arrhythmia. 46. 220. atropine in, 278. auriculo-ventricular. 14. clinical features, 50. :i8 t~NDEX complete, 3 course, 53. dropped beats, 46. electrocardiogram in, 44. 47. 4S, .40. etiology, 36. following digitalis, 268, 278. identification, 38. jugular vein in, 40. partial, 33, 34, 277. pathology, 34. »f, 42, 54- 43- polygram < prognosis, rati-. 38. significance, 50. treatment, 277. Hellebore, 264. His' bundle, 4. 5, 14. 26, 27, 33, 34, 200. auricular-^ entricular t See also bundle ). branches, in auricular in auricular 232, 233. fibrillation, 152, 168. flutter, 11N, 120. in heart block, 50. 1 [ypersympatheticotonics, 204. Hypertension, .}_'. 92, -'411. 250, 256. digitalis in, 272. Hypertonus, 30, 84. Hypertrophy of heart, 1, 85, 296. left, 236. rijjit. 237. 1 1\ pervag tonics, -'04. [deo-ventricular rhythm, 14, 2^2. Influenza, 53. Inotropic influences, 11. Intermittent pulse. 56. Irregular heart. 27, 29. Irritability, 24. after digitalis, 266, 268. Jaundice. 31. Jugular pulse, 15, 40. ventricular form. 134, 142, 140. Jugular vein. in alternation. 190. it- heart Mock, 40. pressure, -'5. records, 15. Karell diet. 257. Labile pulse, 83, 84. Law of "all or ni tie." 11, 12. Leucocytic infiltration, 35. I i' bermeister's rule. 84. Mackenzie cup, 18. Maximal contractions: law of. 11, 12. Meningitis, 31. Mitral pulse, 134. Mitral stenosis, 138, 139. murmurs. I4_\ 144. Muscarine, 34. 61. 02. Muscle tremors, 154, 157. Myocardium, 1. abnormal function, classification .if, 2''. anatomj . 3. function. 1. fundamental properties of, 7, in accelerated heart. 83. infarct- of, 124. [84. Myogenic theory, 7. Nephritis, 31. [82, - alternation in. [86, [96. diet in. 256. fibrillation in. 140. Nen 1 5. see "accelerators." see "extracardial nerves." see "sympathetic." see' "vagUS." Neurogenic theory, <>. Nicotine, 61, 05, 285, 2_•. in alternation, [84. Tonicity, 8, n. 12, _■<>. Treatment, 242. adrenalin. 26b. alcohol, 261. ammonia, 261. atropine, _'<>-*. baths, 258. beverages, 2?j. M'" id letting, 253. caffeine, 263. camphor, 263. chloroform, 264. cold applications, 258. diet, J54. digitalis, 264. drugs, 260. exercise, 248. general principles. 242. heart block, 277. individualization, 243. massage, 252. modified by types of rhythm, 276. nitrites. 27'-. obese, 250. of accelerated heart, 284. of alternation, 302. of auricular fibrillation, 202. of auricular flutter. 288. of extras} stole, 282. of paroxysmal tachycardia, 285. of sinus arrhythmias, 287. opium, 274. resistance exercise, 2-2. rest, 244. spa, 259. strychnine, 275. sugar in, 255. Tubei miosis. 84. Typhoid fever. 31, 36, 53, 84, 184 / ' wave, 22. Uskoff apparatus, t8, V wave. 15. id, [46. Vagus, 6, 30, 32. 34. 3 6 . 38, 92. [99 202, 216. and extrasj stoles, 61. atropine effect on, 280. in accelerated heart, 83, So. in auricular fibrillation, [36, 173. in auricular flutter, [l8, 122. 173. in heart block, 50, 51. 280. in sinus disturbances, 22 \. pressure, 202, 214, 220, 286, _>sx. Valerian, 284, 287. Valves, 1. Valvular disease, 85, 96, 114. and auricular fibrillation, 1.58, 139, 140. and block, 228. and hypertrophy, 241. Vaso-motor disturbances. 84. Venesection, 254, 293. Ventricular fibrillation, 171. and extrasystoles, 172. due to adrenalin. 172. due to chloroform, 172. Veratrin, 182. Vertebrate heart, 3, 13. Water balance, 256. Waves. cause in electrocardiogram, 22. size of, 18. time relations of. 16, 18, 25. Waves of electrocardiogram. amplitude of, 236. /'. 21, 22. 24. ". 21, 22, 24. A'. 21. 22. 24. S, 21. 22, 24. / 21 22 24 U, 22. Waves of polygram. a. 15, 16. c, 15. 16. /'. 15. 16, v, 15. r6. .!'. I :, [6. V. 15. I''. Weight, 255. (see also "obesity"). under, 256. .v wave. 15, to. V wave, 15, [6. Tie copyright of this hook, in oil English-Speaking countries, is owned by Rebman Company, Nctu ) or/.-. H25 Copy 1